The IACLE

Contact Lens
Course

MODULE 7
Contact Lens-Related
Complications
First Edition
 Module 7: Contact Lens-Related Complications

Published in Australia by
The International Association of Contact Lens Educators

First Edition 2004

”The International Association of Contact Lens Educators 2004

All rights reserved. No part of this publication may be
reproduced, stored in a retrieval system, or transmitted in
any form or by any means without the prior written
permission of:

The International Association of Contact Lens Educators

IACLE Secretariat,
PO Box 6328 UNSW
SYDNEY NSW 1466
Australia

Tel: (612) 9385 7463

Fax: (612) 9385 7467
Email: iacle@iacle.org

ii IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Complications

Table of Contents
Page
Acknowledgments..................................................................................................... iv

Contributors................................................................................................................ v

Educators’ Guide to the IACLE Contact Lens Course ........................................... vi

Symbols, Abbreviations and Acronyms Used in the IACLE Contact Lens

Course ...................................................................................................................... viii

Summary of Module 7: Contact Lens-Related Ocular Complications ................. xi

Request for Feedback .............................................................................................. xii

Unit 7.1 1
Course Overview 2
Lecture 7.1 Patient Symptoms and Clinical Signs 3

Unit 7.2 13
Course Overview 14
Lecture 7.2 Soft Contact Lens Complications and Their Management 15

Unit 7.3 191

Course Overview 192
Lecture 7.3 RGP Contact Lens Complications and Their Management 193

Unit 7.4 315

Course Overview 316
Lecture 7.4 Diagnosis and Management of Dry Eye in Contact Lens Wear 317

IACLE Contact Lens Course Module 7: First Edition iii

 Module 7: Contact Lens-Related Complications

Acknowledgments
The IACLE Curriculum Project is the result of a desire to raise the standard of eyecare
education, to make contact lens wear safer and more successful, and to develop the contact
lens business by creating the educational infrastructure that will produce the teachers,
students, and practitioners of the future.
The concept of the world's best educators making available their most creative educational
contributions for the common good without any recompense, other than a sense of
satisfaction, was born out of IACLE's idealism.
The Curriculum Project could not be successful without the assistance and generosity of a
large number of talented and dedicated people. To all those contributors of lectures,
laboratory notes, videos, slides, etc., we say thank you. Your generosity of spirit will benefit
many educators, hundreds of thousands of students, and millions of patients throughout the
world.
Since IACLE’s inception, IACLE’s Vice President, Professor Desmond Fonn, has made a
tremendous contribution. More recently, he has applied his considerable expertise to the final
editing stage of the Curriculum. This project was commenced under Professor Brien
Holden’s leadership. The original plans and layout for the Curriculum were prepared by Ms
Sylvie Sulaiman, IACLE’s former Director of Education. Sylvie's dedication and excellent
understanding of practitioner and community requirements, gave the project focus and depth.
More recently, the Curriculum Project has benefited from the work of Dr Lewis Williams,
IACLE’s Manager: Educational Development.
Kylie Knox and Peter Fagan have done an excellent job as Project Editors. To complement
the efforts of the editors, layout and production coordinators Barry Brown and Shane Parker
have done an admirable job. The Cornea and Contact Lens Research Unit (CCLRU) at the
University of New South Wales has contributed substantially to this project through the
donation of time, resources, and editorial support.
The IACLE Secretariat, including Project Coordinator, Gail van Heerden and Special Projects
Officer, Pamela Capaldi, have managed expertly the considerable tasks of production and
distribution.
No acknowledgement page in an IACLE document would be complete without a reference to
its major corporate sponsors Ciba Vision, Johnson & Johnson, and Bausch & Lomb; together
with supporting corporate sponsors AMO (formerly Allergan), Ocular Sciences Inc; corporate
contributors Alcon Laboratories, CooperVision; and donor Menicon Europe, who have
generously supported the development costs for this Module of the IACLE Contact Lens
Course.
IACLE is a cooperative effort and none of its activities are more collective than the Curriculum
Project. The IACLE Contact Lens Course resulting from this project is provided to assist
educators in accredited institutions to impart eyecare and contact lens knowledge. All the
contributors deserve recognition for their selflessness and talent. I am proud to be associated
with them.

Deborah Sweeney
President of IACLE

iv IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Complications

Contributors

Desmond Fonn, Dip Optom, MOptom Editor-In-Chief

Associate Professor
School of Optometry
University of Waterloo
Waterloo Ontario Canada N2L 3G1

Robert Terry, BOptom, MSc x Patient Symptoms and Clinical

Cornea and Contact Lens Research Unit Signs
School of Optometry and Vision Science x Soft Contact Lens Complications
UNSW and Their Management
Sydney NSW 2052 x RGP Contact Lens
Australia Complications and Their
Management
x Diagnosis and Management of
Dry Eye in Contact Lens Wear

Lewis Williams, AQIT(Optom), MOptom, x Patient Symptoms and Clinical

PhD Signs
IACLE Secretariat x Soft Contact Lens Complications
PO Box 6328 UNSW and Their Management
Sydney NSW 1466 x RGP Contact Lens
Australia Complications and Their
Management
x Diagnosis and Management of
Dry Eye in Contact Lens Wear

With Additional Input From:

Rènée du Toit, Dip Optom, MPhil x Diagnosis and Management of
(Optom) Dry Eye in Contact Lens Wear
Cornea and Contact Lens Research Unit
School of Optometry and Vision Science
UNSW
Sydney NSW 2052
Australia
Adrian Bruce, BScOptom, PhD x Soft Contact Lens Complications
Clinical Vision Research Australia and Their Management
Victorian College of Optometry
Cnr Keppel and Cardigan Sts
Carlton Vic 3053
Australia
Richard Lindsay BScOptom, MBA x RGP Contact Lens
Richard Lindsay & Associates Complications and Their
5th Floor, 376 Albert Street Management
East Melbourne Vic 3002
Australia

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 Module 7: Contact Lens-Related Complications

Educators Guide to the IACLE Contact Lens Course

Overview
The IACLE Contact Lens Course is a comprehensive package of educational
materials and other resources for teaching the subject of contact lenses. This
package was designed to encompass The IACLE Contact Lens Course Syllabus and
consists of 360 hours of lectures, practicals, and tutorials in ten modules. It contains
material at basic, intermediate, and advanced levels.
The teaching resources have been designed for flexibility. They allow the educator to
select the materials appropriate to the students' knowledge and the educational
requirements of the class, school, institution, or country.
The English language reference used for the IACLE Contact Lens Course is: Brown L
(Ed.). The New Shorter Oxford English Dictionary. 1993 ed. Clarendon Press, Oxford
(UK). The only spelling exception is mold and mould. The Oxford dictionary suggests
mould in all contexts. We chose to use mold for manufacturing-related matters and
mould for fungi since both meanings and spellings appear regularly in contact lens
literature. This differentiation is based on common usage. Where words are
‘borrowed’ from a language other than English, they are reproduced in their native
form where possible.
Where standards have been ratified by the International Organization for
Standardization (ISO), or where draft ISO standards are at an advanced stage, their
relevant terminology and symbology are used. Système International (SI) units of
measure are used wherever possible.
Many major contact lens textbooks from around the world, and some important
journal articles, are referenced in the Course, and copyright illustrations are
reproduced with permission of the original publishers and/or copyright owners. The
References section at the end of each unit details the information sources used
throughout.

Teaching Resources - Module 7

Module 7 of the IACLE Contact Lens Course consists of the following materials:

1. Contact lens manual

The contact lens manual, containing:
x Course overviews
x Lecture outlines and notes
x Practical outlines, exercises and notes*
x Tutorial exercises and notes*
* Not all units contain all these sections.

The recommended allocation of time for the lecture, practical, and tutorial
components of the module are outlined in the Summary of Module 7 on
page xi. In the interests of standardization, this manual provides
recommended activities, references, textbooks, and evaluation techniques.
Ultimately however, the design and methodology of the course is left to the
discretion of the contact lens educator.
vi IACLE Contact Lens Course Module 7: First Edition
 Module 7: Contact Lens-Related Complications

2. Slides for lectures, practicals and tutorials

All slides are numbered according to the sequence in which they appear in
each lecture, practical, or tutorial, e.g. 28. Each slide is also identified by a
code based on a cataloguing system in use at the IACLE Secretariat, e.g.
7L497400-281. The identification code(s) should be used in any
communication with IACLE regarding slides.

NIBUT:
CORNEA vs SOFT LENS
For example: 100
CCLRU data
Pre-Lens Tear Film
Pre-Corneal Tear Film
80
60
60 50

To re-order this slide please quote 40

BUTs in SECONDS

its identification code 25

15
25

20 10
5 5 5
0 0 0
0
0-4 5-9 10-14 15-19 20-24 25-30
97400-172S.PPT

7L497400-172

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 Module 7: Contact Lens-Related Complications

The IACLE Contact Lens Course: Symbols, Abbreviations, and Acronyms

SYMBOLS
n increase, high { collectively produced by

p decrease, low } collectively produces

o produces, towards ™ sum of

m produced by, from ± plus or minus the value of

l no change, not obvious + plus, add, include, and

nn significant/great increase – minus, reduce

pp significant/great decrease | approximately

% percentage = equal to, the same as

< less than, earlier than & and, as well as
> greater than, after xq degrees: e.g. 45°

t equal to or greater than @ in the meridian of

d equal to or less than D dioptres

? unknown, questionable X axis: e.g. –1.00 X 175. –

1.00D cylinder, axis in 175°
meridian
n, nsub, nsub´ refractive indices ' prism dioptres or difference

v proportional –
x mean of data

ABBREVIATIONS
Pg micrograms (.001 mg) min minute, minutes

PL microlitres (.001 mL) mL millilitres (.001L)

Pm micrometre (.001 mm) mm millimetres

(<1968: micron)

Pmol micromoles, micromolar mmol millimole, millimolar

cm centimetres (.01m) mOsm milliosmole

-9
d day, days nm nanometres (10 m)
Endo. endothelium Px patient
Epi. epithelium Rx prescription
h hour, hours s second, seconds
Inf. inferior Sup. superior
kg kilograms t thickness
L litre

viii IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Complications

ACRONYMS
ADP adenosine diphosphate LPS levator palpebrae superioris
ATP adenosine triphosphate NADPH nicotinamide adenine dinucleotide
phosphate
ATR against-the-rule NIBUT non-invasive break-up time
BS best sphere OD right eye (L.: oculus dexter)
BUT break-up time OO orbicularis oculi muscle
CCC central corneal clouding OS left eye (L.: oculus sinister)
CCD charge-coupled device OU both eyes (L.: oculi uterque, or
oculus uterque - each eye)
cf. compared to/with PD interpupillary distance
CL contact lens PMMA poly(methyl methacrylate)
Dk oxygen permeability R right
DW daily wear R&L right and left
e.g. for example (L.: exempli gratia) RE right eye
EW extended wear RGP rigid gas permeable
GAG glycosaminoglycan SCL soft contact lens
GPC giant papillary conjunctivitis SL spectacle lens
HCL hard contact lens TBUT tear break-up time
HVID horizontal visible iris diameter TCA tricarboxylic acid
i.e. that is (L.: id est) UV ultraviolet
K keratometry result VA visual acuity
L left VVID vertical visible iris diameter
LE left eye WTR with-the-rule

IACLE Contact Lens Course Module 7: First Edition ix

 Module 7: Contact Lens-Related Complications

ACRONYMS: Module 7
AI Asymptomatic Infiltrates IK Infiltrative Keratitis
AIK Asymptomatic Infiltrative LCP Lens Care Product
Keratitis
CLARE Contact Lens-induced Acute MGD Meibomian Gland Dysfunction
Red Eye
CLPC Contact Lens-induced Papillary MK Microbial Keratitis
Conjunctivitis
CLPU Contact Lens-induced RH Relative Humidity
Peripheral Ulcer
CNPU Culture Negative Peripheral SEAL Superior Epithelial Arcuate Lesion
Ulcer
FB Foreign Body ST Surface Tension

x IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Complications

Summary of Module 7: Contact Lens-Related Complications

Course Program

Lecture Practical Session Tutorial (Small Group Teaching)

Title Hrs Level* Title Hrs Level* Title Hrs Level*
L 7.1 1 1
Patient Symptoms and
Clinical Signs
L 7.2 2 3
SCL Complications and
Their Management
L 7.3 2 3
RGP Lens
Complications and Their
Management
L 7.4 2 3
Diagnosis and
Management of Dry Eye
in Contact Lens Wear

* Level 1 = Basic: essential knowledge

Level 2 = Intermediate: desirable knowledge
Level 3 = Advanced: useful knowledge

Course Time Allocation

Level Lecture Practical Tutorial Total Hours
(Laboratory) (Small Group Teaching)
Basic 1 0 0 0
Intermediate 0 0 0 0
Advanced 6 0 0 0
TOTAL 7 0 0 7

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 Module 7: Contact Lens-Related Complications

Request for Feedback

As this is the first edition of the IACLE Contact Lens Course, it is our intention to
revise and update it periodically. To ensure each revision is an improvement on its
predecessor, we request your help. We invite you to provide feedback in the form of
comments, corrections, or suggestions that you believe will enhance the accuracy or
quality of the Course. Such feedback may then be incorporated in subsequent
revisions. We are particularly interested in receiving corrections to, and suggestions
for improvements in, the text and slides of the lectures.
To facilitate this feedback process, a pro forma is included on the next page. This
can be photocopied. Please complete your contact details as the team may wish to
discuss your suggestions in greater detail, or even seek your assistance with any
revision resulting from your input.

xii IACLE Contact Lens Course Module 7: First Edition

 The IACLE Contact Lens Course
Feedback / Corrections / Suggestions Form
Name: Date:
(yy-mm-dd)
Institution:
Address:

Module: Unit: Page Number:

Slide Code: Section:

Comments:

Thank you

Please return this form to: IACLE Secretariat Office Use Only:
PO Box 6328 Response #: _________
UNSW Sydney NSW 1466 Forward to: ___________
AUSTRALIA Action:
 Unit 7.1: Patient Symptoms and Clinical Signs

Unit 7.1
(1 Hour)

Lecture 7.1: Patient Symptoms and

Clinical Signs

IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Ocular Complications

Course Overview

Lecture 7.1: Patient Symptoms and Clinical Signs

I Introduction to Patient Symptoms
II Introduction to Clinical Signs
III Introduction to Assessment of Patient Signs
IV Introduction to Problem Solving

2 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.1: Patient Symptoms and Clinical Signs

Lecture 7.1
(1 Hour)

Patient Symptoms and Clinical Signs

IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Ocular Complications

Table of Contents

I Symptoms and Signs in Contact Lens Wear.........................................................5

References.................................................................................................................12

4 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.1: Patient Symptoms and Clinical Signs

I Symptoms and Signs in Contact Lens Wear

1 Patient Symptoms and Clinical Signs
The ideal contact lens should:
x Be indetectable in use.
x Restore/provide normal vision.
PATIENT SYMPTOMS x Permit unlimited wear.
AND CLINICAL SIGNS
x Not produce harmful side-effects.
(after Burnett Hodd, 1984).
However, in general contact lens practice it is not
unusual to encounter contact lens wearers who
97100-1S.PPT
experience some difficulties when wearing their
7L197100-1 lenses. These difficulties range from the
inconsequential to the clinically very significant. If
long-term success and satisfaction is to be
achieved, the contact lens practitioner must manage
all problems as they occur. Furthermore, steps
must be taken to prevent foreseeable problems
arising. This preventative approach applies to the
initial supplying/dispensing of lenses as well as to
any treatment of subsequent problems.
Managing these problems successfully requires:
x Careful and close questioning of the patient.
x A meticulous examination of the eyes.
x A careful and detailed inspection of the contact
lenses.
A symptoms is defined as:
A physical or mental phenomenon, circumstance or
change of condition arising from, or accompanying,
a disorder and constituting evidence of it; a
subjective indication perceptible to the patient.
A sign is defined as:
An objective indication of disease; evidence; an
indication of a present state (after The New Shorter
Oxford English Dictionary, 1993).
2 Patient Questioning and History Taking
HISTORY TAKING To manage contact lens-associated complications
effectively, the practitioner should begin by taking a
• Key to solving most problems
thorough wearer case history. Frequently, the
• Pertinent and probing initial questions information obtained during such questioning
provides the key to what action might be appropriate
- how, what, where, when and why? to minimize, or prevent a recurrence of, the original
• Open-ended questions (open probing) and/or related complications.

• Listen to the wearer’s own words History taking is a consulting room skill that is
refined and evolved only through experience. It is
• Follow-up questions important for the wearer to be given the opportunity
to use their own words when answering questions
97100-2S.PPT

7L197100-2 as this usually enables the practitioner to determine

what is of concern and/or of greatest concern to the
wearer.
It is impossible to overstate the importance of taking
and recording a good wearer history. Not only is it
important to patient problem solving, but it is also

IACLE Contact Lens Course Module 7: First Edition 5

 Module 7: Contact Lens-Related Ocular Complications

3 central to any legal defence a practitioner may have

to rely on should legal proceedings be initiated by a
dissatisfied wearer. These and related practice
HISTORY TAKING
management issues are covered more fully in
• An acquired skill Module 10: Business Aspects of Contact Lens
Practice.
- requires practice

• Assists in differential diagnosis

• Information must be recorded

- a legal requirement

97100-3S.PPT

7L197100-3

4 Solving the Problem

While endeavouring to resolve problems associated
PROBLEM SOLVING with contact lens wear, the practitioner usually
• Follow a routine considers possible causes while eliminating those
that have no possible bearing on the condition.
• Consider the simple before the complex Although the answer to some problems is obvious,
• Commence with high-probability causes
others require extensive investigation before a
solution is found.
• Rule out possible causes In many cases, management of the problem can be
commenced without having resolved the causative
- arrive at a differential diagnosis
issues fully, provided adequate follow-up is given
97100-4S.PPT
and the investigation is continued.
7L197100-4 In some cases, while the solution may be obvious
the cause may never be elucidated.
An example:
x A wearer experiences an uncomfortable,
unilateral red eye.
x The symptoms are relieved by lens removal.
x The condition returns upon lens reinsertion.
x The relevant contact lens appears to be in
good condition and is not particularly old.
It is apparent that the lens itself is implicated. In this
case it is probable that a new lens should be
supplied even before/while a detailed investigation
of the old lens is undertaken. Further, it is possible
(even likely) that subsequent investigation of the
troublesome lens will fail to reveal the actual cause
because our current knowledge of the
immunological aspects of lens wear is incomplete.
Furthermore, the determination of the presence of
immunological factors in a contact lens is unlikely to
become a consulting room procedure in the
foreseeable future.

6 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.1: Patient Symptoms and Clinical Signs

5 Assessment of Patient Symptoms

A symptom is an indication of a disorder expressed
SYMPTOMS by the sufferer to their practitioner or other enquirer,
• Described by the patient (subjective)
i.e. it is a subjective report (complaint) of a
condition, experience or feeling.
• Generally, a main symptom is reported Except in psychotic conditions in which symptoms
are reported but no physical basis can be found, a
- this is the chief complaint
symptom serves as evidence of a condition.
• Usually have an organic or functional basis The expressions used by the contact lens wearer
form the basis of the interaction between the
• Manifestation(s) of injury or disease
practitioner and wearer that is aimed at solving their
97100-5S.PPT
problems.
7L197100-5 In most cases, the wearer will report one symptom
that is of prime importance to them even though
multiple symptoms may be elicited. This chief
6 symptom or complaint must be dealt with by the
practitioner even when other, important problems
SYMPTOMS may exist.
• Real or imagined

• Physical and/or physiological

• Psychological basis?

• May or may not be associated with signs

• Type, time of onset, duration, course

97100-6S.PPT

7L197100-6

7 Assessment of Patient Signs

Signs are manifestations of an underlying process,
SIGNS
abnormality, injury or disease. They can be
detected objectively and may or may not result in
• Detectable manifestations of injury or
symptoms being experienced or reported by the
disease ‘sufferer’.
Signs of problems associated with contact lens
• Seen by patient and/or practitioner wear vary between those that are easy to detect and
those that are so subtle that a thorough examination
• May or may not be associated with by the practitioner is required. The slit-lamp
symptoms biomicroscope is the principal instrument used for
97100-7S.PPT
wearer assessment (slide 9).

7L197100-7
In many cases it is the sign of a problem, e.g. an
obviously red eye, rather than the resulting
symptoms, e.g. some eye discomfort, that prompts
8 the wearer to seek the care and advice of their
practitioner.
DETECTION OF SIGNS

• Requires skill and experience

• Main observational tools are:
- illumination
- magnification
• Specialized techniques may be required

97100-8S.PPT

7L197100-8

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 Module 7: Contact Lens-Related Ocular Complications

7L10513-98

10 Examination Skills
If problems are to be resolved to both the wearer’s
PRACTITIONER SKILL and practitioner’s satisfaction, the practitioner must
Ability to: employ all their relevant skills when dealing with
- investigate lens wear-related difficulties. While the level of
experience in the contact lens field may influence
- deduce
the speed, quality of assessment, and the efficacy
- analyse of advice given, there is still a role for knowledge of
- diagnose the subject. The latter is not necessarily experience
- solve problems dependent.
- educate The following aspects should be included in an
97100-9S.PPT
examination of the wearer:

7L197100-9 x Subjective response of the wearer to

questioning (symptoms).
x Objective examination of the condition of the
11
wearer (signs).
PRACTITIONER SKILL x Analysis of the condition.
Employ SOAPE: x Development of a plan to manage the problem.
- Subjective x Education of the wearer to ensure that they
- Objective
understand the nature of the problem, the
method(s) of resolving it, and the means by
- Assessment which they can prevent it from recurring.
- Plan
- Education
97100-10S.PPT

7L197100-10

12 Symptoms Occurring in Contact Lens Wear

A wide range of symptoms can be associated with
SYMPTOMS IN CONTACT LENS WEAR contact lens wear. Nearly all wearers will
experience some symptoms during the early
• Adaptive or normal symptoms
adaptation period of lens wear.
• Abnormal symptoms The practitioner should counsel the patient about
• Dictate course of action what to expect and to anticipate some adaptive
symptoms as a normal part of the adaptation
- monitor process (see Module 4, Lecture 4.4: Conducting
the After-Care Visit). However, care must be
- intervention
taken not to supply the wearer with a ‘shopping list’
97100-11S.PPT
of potential problems and symptoms from which a
plausible problem or symptom can be chosen.
7L197100-11
Abnormal symptoms such as ocular pain during
lens wear require the wearer to seek advice from

8 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.1: Patient Symptoms and Clinical Signs

13 their practitioner promptly. The line separating

normal (adaptive) and abnormal symptoms may be
CAUSE OF SYMPTOMS very fine (subtle). Both the wearer and practitioner
Mandell, 1988 should err on the side of caution when deciding if an
• Adaptive problems assessment is required during contact lens wear,
• Procedural error by wearer i.e. a conservative approach should be taken by
• Extraneous sources of irritation both parties.
• Psychological problems Some possible causes are presented in slide 13
• Physiological problems (after Mandell, 1988).
• Lens fitting error
• Lens defect
97100-12S.PPT

7L197100-12

14 Symptoms in the Presence of Ocular Signs

Any description of symptoms by the contact lens
SYMPTOMS WITH SIGNS wearer during history taking provides the
• Easier to detect cause of problem(s)
practitioner with potential evidence of the cause(s)
of any complication associated with lens wear.
• Counseling of wearer often easier In cases where symptoms are accompanied by
specific signs such as upper palpebral conjunctival
• Modify lens usage and/or wear mode changes (slide 15), ocular redness and lacrimation,
the task of the practitioner is made somewhat
• Wearer understands the need to change easier as the problem is obvious.
While the problem may be obvious, the cause(s)
97100-13S.PPT
may not always be apparent immediately.
7L197100-13
Regardless of this, the wearer can readily
appreciate that the eye-lens combination is
inadequate in some way or for some reason.
15

7L10394-97

16 Symptoms Without the Presence of Ocular

Signs
SYMPTOMS WITHOUT SIGNS
In those cases in which there are no signs (slide 17)
• A thorough history is assumed to accompany the symptoms reported by the
patient, the practitioner must investigate the
• Are symptoms normal or abnormal? patient’s history more thoroughly. Additional
detailed questioning is usually necessary to
• Practitioner intervention is required understand the experiences of the patient more
• Wearer’s concerns need to be allayed fully, i.e. a targeted extension of normal history
taking is required.
• Close monitoring required A psychotic explanation is one of the least likely
97100-14S.PPT scenarios in the absence of ocular signs but the
7L197100-14 possibility needs to be ruled out rather than simply
ignored.

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 Module 7: Contact Lens-Related Ocular Complications

17

7L1097-99

18 Ocular Signs Without the Presence of

Symptoms
SIGNS WITHOUT SYMPTOMS During routine after-care, the practitioner may
• Careful assessment requires: detect significant signs in either eye, the contact
lenses, or both. In some cases, the wearer may
- observational skills have also noticed the same signs but not be aware
- routine follow-up of any unusual symptoms, e.g. red eye. Under
these circumstances, the practitioner should
• Extensive history taking question the patient in greater detail to obtain
• Prevention of problems information that the patient may have either
forgotten, failed to detect, or failed to associate with
• Careful patient education
contact lens usage.
97100-15S.PPT

7L197100-15

19
Signs that are only observable with the slit-lamp
may indicate the need to alter the contact lenses in
some way if the risk of problems occurring later is to
be reduced. Slide 19 shows a localized region of
dense staining in the superior epithelium. If the
wearer is asymptomatic and therefore unaware of
the existence of any problem, it is important for the
practitioner to explain carefully the reasons for
making any changes to their lenses, solutions,
wearing schedule, etc.

7L10367-97
20 Clinical Judgement and Practitioner Intervention
CLINICAL INTERVENTION A major component of contact lens practice is the
after-care provided by the practitioner following the
• Practitioner judgement dispensing of lenses. After-care visits provide the
practitioner with an opportunity to examine both the
• Need to counsel patient
worn lenses and the wearer’s eyes in detail (slide
• Follow-up to confirm 21). It is also an opportunity to educate or re-
educate the wearer about any deficiencies that
expected improvement
become apparent and to advise them appropriately
• Resolution of problem(s) should any modification to their contact lenses, lens
wearing, or their behaviour be required.
Subsequent assessments are needed to ascertain
97100-16S.PPT

7L197100-15 whether the problems experienced by the patient

have been resolved satisfactorily.

10 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.1: Patient Symptoms and Clinical Signs

21

7L10305-98

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 Module 7: Contact Lens-Related Ocular Complications

References
Ball GV (1982). Symptoms in Eye Examination. Butterworth, London.

th
Mandell RB (1988). Contact Lens Practice. 4 ed. Charles C Thomas Publisher, Springfield.

McMonnies CW (1997). After-Care Symptoms, Signs and Management. In: Phillips AJ, Speedwell L
(Eds.). Contact Lenses 4th ed. Butterworth-Heineman, Oxford.

12 IACLE Contact Lens Course Module 7: First Edition

 Unit 7.2: SCL Complications and Their Management

Unit 7.2
(5 Hours)

Lecture 7.2: Soft Contact Lens

Complications and Their
Management

IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Ocular Complications

Course Overview

Lecture 7.2: Soft Contact Lens Complications

I Introduce Contact Lens Complications
II Detail complications related to:
x Hypoxia and corneal oedema
x Inflammation and infection
x Lenses, and lens fit
x Hypersensitivity and allergy
x Solution toxicity
x Non-compliance
x Lens deposits
x Reduced vision

14 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

Lecture 7.2
(5 Hours)

Soft Contact Lens Complications

and Their Management

IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Ocular Complications

Table of Contents
I Introduction to Contact Lens Complications................................................................17

II Complications Related to Corneal Oedema and Hypoxia .......................................... 21

II.A Corneal Oedema .................................................................................................. 21
II.A.I Striae .................................................................................................................... 23
II.A.II Folds And Black Lines .......................................................................................... 25
II.B Epithelium: Microcystic Oedema........................................................................... 30
II.C Epithelium: Epithelial Microcysts........................................................................... 32
II.D Stromal Thinning .................................................................................................. 39
II.E Endothelial Polymegethism................................................................................... 41
II.F Endothelial Bleb Response................................................................................... 43
II.G Epithelium: Slach/Reduced Epithelial Adhesion.................................................... 48
II.H Corneal Exhaustion Syndrome (Ces).................................................................... 51
II.I Corneal Vascularization ........................................................................................ 53
II.J Corneal Oedema-Induced Refractive Changes .....................................................58

III Inflammation and Infection.......................................................................................... 63

III.A Effects: Ocular Discomfort .................................................................................... 63
III.B Effects: Ocular Hyperaemia.................................................................................. 69
III.C Endothelial Bedewing ........................................................................................... 74
III.D CLPC.................................................................................................................... 76
III.E Meibomian Gland Dysfunction (MGD)................................................................... 85
III.F Corneal Infiltrates ................................................................................................. 91
III.G Corneal Abrasions/Erosions ............................................................................... 100
III.H Microbial Keratitis (MK)....................................................................................... 104
III.I CLARE ............................................................................................................... 112
III.J CLPU & CNPU ................................................................................................... 116
III.K Corneal Scarring..................................................................................................122

IV Lens and Lens Fit-Related Complications............................................................... 126

IV.A Lens Fitting Problems ......................................................................................... 126
IV.B SEALs ................................................................................................................ 130
IV.C ‘Smile’ (Inferior, Arcuate, Epithelial) & Desiccation Staining................................ 137
IV.D Solution Sensitivity.............................................................................................. 142
IV.D.I Solution Sensitivity: General ............................................................................... 142
IV.D.IISolution Sensitivity: SLK ..................................................................................... 144
IV.E Non-Compliance ................................................................................................. 147
IV.F Lens Case Contamination................................................................................... 149
IV.G Lens Deposits: Front........................................................................................... 151
IV.H Lens Deposits: Back ............................................................................................154
IV.I Mucin Balls ..........................................................................................................156

V Vision Problems.......................................................................................................... 159

V.A Vision Problems: General ................................................................................... 159
V.B Lens/Corneal Wrinkling ...................................................................................... 162
V.C Vision Problems: Changes in Refraction............................................................. 165
V.D Vision Problems: Residual Refractive Error ........................................................ 166
V.E Vision Problems: Poor Optical Quality ................................................................ 168

References........................................................................................................................172

16 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

I Introduction to Contact Lens Complications

1 Soft Contact Lenses and Their Management

SCL COMPLICATIONS AND

THEIR MANAGEMENT

97200-1S.PPT

7L297200-1

2 Causes of Contact Lens Complications

Numerous factors can play a role in the aetiology of
COMPLICATIONS: AETIOLOGIES contact lens wear-related complications.
• Physical, including lens fit Perplexingly, a particular problem can be caused by
more than one factor. When trying to determine the
• Lens back vertex power (BVP)
aetiology of a particular problem, all possible causes
• Lens dehydration need to be considered. Despite considerable effort,
there is no guarantee that an answer will be found.
• Surface deposits/poor wettability
Some of the possible root causes are categorized
• Altered blinking generally in the slides opposite.
• Hypoxia
97200-2S.PPT

7L297200-2

COMPLICATIONS: AETIOLOGIES
• Pre-existing systemic or ocular disease
• Environmental
• Chemical
• Microbiological
• Immunological
• Patient non-compliance
97200-3S.PPT

7L297200-3

4 Complications: Physical Factors

COMPLICATIONS: When translated to the ocular surface, mechanical

PHYSICAL FACTORS
forces acting on a contact lens during wear, have
the potential to induce changes. The main forces
• Lens:
relate to lens fit and lens movement, as well as the
- fit
movement of the eyelids over the surfaces of the
- surface properties
lens and eye.
- lens condition
- lens shape (design) The physical condition of a lens is important
• Blinking: because the interaction of the lids with its front
- completeness surface and edges, when combined with its fitting
- lid tonus relationship, govern its on-eye behaviour.
97200-195S.PPT

7L297200-195

IACLE Contact Lens Course Module 7: First Edition 17

 Module 7: Contact Lens-Related Ocular Complications

5 Complications: Visual Factors

Usually, the primary purpose of contact lenses is to
COMPLICATIONS: correct refractive error. Should lenses with
VISUAL FACTORS inappropriate back vertex powers be dispensed,
• Accuracy of Rx prescribed monocular as well as binocular vision problems can
ensue. The Rxs ordered should be the balanced
• Reproducibility/optical quality
binocular refraction results. Corrections for vertex
• Accuracy of Rx dispensed distance must be made for spectacle lens powers
• Binocular vision a complication? (in the spectacle plane) >±3.75 D.
• Incipient presbyopia
Incipient presbyopia is a possible cause of visual
• Distance vs near (esp. torics) dissatisfaction, particularly in the case of higher
97200-196S.PPT
myopes (see Module 2, Lecture 2.3, Section IV
Accommodation with Contact Lenses).
7L297200-196
A more subtle form of visual problem is the lens
rotation that can accompany convergence while
wearing toric soft lenses. Rotations of 10 to 15° are
relatively common. Compensation for this rotational
behaviour that is effective at all working distances is
not possible, and compromises need to be made.
A less subtle form of visual disturbance arises from
mislocation, or worse, variable location, of toric
lenses under normal viewing circumstances.
6 Complications: Physiological Factors
Arguably, the oxygen transmissibility of a lens is its
COMPLICATIONS: most important physiological parameter. For a
PHYSIOLOGICAL FACTORS detailed discussion of this and related issues, see
• Dk/t Lectures 6.1 to 6.3 in Module 6 of this course.
• Water content Another important lens factor is water content.
- factors affecting water content Water content varies with lens material, as well as
• Blinking with the environmental circumstances in which a
- frequency lens is used. Both ocular and external
- completeness
environmental factors, particularly relative humidity,
play a significant role in soft lens
• Environment
97200-197S.PPT
hydration/dehydration (Opdahl et al., 2003), and
therefore wearer comfort.
7L297200-197
Blinking (tear exchange) is not an important
physiological consideration with DW SCLs but it
must be sufficient to remove post-lens tear debris.
Regardless of lens type, the blink rate of many
wearers is altered by contact lens wear. Blink
frequency may increase or decrease, and
completeness of blink may also be altered
adversely.
7 Complications: Pathological Factors
Commonly, bacterial keratitis in non-lens wearers is
COMPLICATIONS:
due to infection by Staphylococcus aureus, whereas
PATHOLOGICAL FACTORS
infections in contact lens wearers are frequently
• Condition of lenses caused by Pseudomonas aeruginosa (Aswad et al.,
- micro-organisms 1990).
- immunological issues Pseudomonas aeruginosa and Staphylococcus
aureus are two relatively common ocular pathogens
• Chemical
that have been found attached to contact lenses.
• Environmental Dart and Badenoch (1986) found that S. aureus, but
not P. aeruginosa, attached preferentially to
• Pre-existing ocular pathology
97200-198S.PPT
hydrophobic surfaces, e.g. to PMMA rather than soft
lenses, but attachment to both was possible (clean
7L297200-198
PMMA surfaces are not hydrophobic). Further,
Miller et al., (1987, cited in Fleiszig et al., 1992)
18 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

found that the attachment of P. aeruginosa

decreased with increasing water content, a finding
in agreement with Fletcher and Loeb (1979) and
Pringle and Fletcher (1986) (both also cited in
Fleiszig et al., 1992).
Generally, soft contact lenses are more susceptible
to deposits on, and sometimes within, their
material’s matrices. This is primarily due to their
material’s affinity for tear components, especially
tear proteins. One study has shown that the
adherence of micro-organisms to contact lenses is
not enhanced by lens surface deposits or
irregularities (Dart and Badenoch, 1986). Further,
at least two other studies have shown adherence is
deterred by the surface coating that results from
lens wear (Refojo et al., 1990, Boles et al., 1991).
Other investigations have not provided such clear-
cut results, or have contradicted Dart and
Badenoch’s findings, e.g. Stern and Zam (1986),
Duran et al. (1987), Slusher et al, (1987), Aswad et
al. (1990).
Liotet et al. (1983) suggested that lens deposits are
secondary to colonization and not a precursor of it.
Fleiszig et al. (1992) suggested that bacteria that
remain attached to a contact lens despite adequate
washing, are unlikely to detach and be released
onto the anterior eye. However, the offspring of
these attached bacteria are potentially a threat and
the eye’s antibacterial mechanisms are the first line
of defence against these.
In addition to the wearer’s hands, the other sources
of micro-organisms that come in regular contact
with lenses are the lens case (except those
disposed of daily), and the solutions used therein.
McLaughlin-Borlace et al. (1998) reported a high
correlation between lens case biofilms, and
bacterial and amoebic infections. The effects of
contact lens wear on the ocular biota are covered in
Module 6, Lecture 6.4, Section V Ocular Biota and
Contact Lens Wear.
Micro-organisms may also induce immunological
reactions. However, other sources such as
denatured tear proteins on used lenses, and certain
ingredients in lens care products, are probably more
significant and more common causes of such
reactions.
8 Complications: Wearer-Related
Non-compliance has long been acknowledged as
COMPLICATIONS: being a major contributing factor to negative
WEARER-RELATED outcomes of contact lens wear.
• Non-compliance:
- misunderstanding Non-compliance takes many forms and ranges from
- ignorance and carelessness the unintentional to a deliberate failure to follow a
- deliberate deviation prudent course of self-care.
- little or no care of lenses Not availing oneself of the opportunities for
• Failure to attend after-care visits preventative or curative care by failing to attend
• Swapped lenses after-care appointments is also common because,
• Poor personal hygiene in most cases, lens wear, even novice lens wear, is
97200-199S.PPT
uneventful. To the naive wearer, uneventful
7L297200-199 equates to ‘no further practitioner involvement is

IACLE Contact Lens Course Module 7: First Edition 19

 Module 7: Contact Lens-Related Ocular Complications

required’ and the requests from the practitioner for

after-care visits go unheeded.
While other issues of little consequence such as
swapped lenses are relatively common, it is
somewhat surprising just how often the possibility is
not considered and a consultation is requested to
solve the vision problems that ensue.
9 Preventing Contact Lens Complications
In routine contact lens practice, a number of steps
PREVENTING COMPLICATIONS can be taken to prevent, or at least minimize, the
• Patient selection risk of complications.
• Lens selection It is important for the practitioner to control each
phase of the process if an optimal outcome is to be
• Patient education realized.
- preventative measures Of all the controls that can be enacted, it is probable
- signs, symptoms, action that patient education is the most ‘efficient’ in that a
little effort invested early in the process can prevent
• After-care and appropriate intervention
potentially calamitous outcomes.
97200-18S.PPT

7L297200-18

20 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

II Complications Related to Corneal Oedema and Hypoxia

II.A Corneal Oedema

10 Corneal Oedema: Introduction

Corneal oedema was observed as a side-effect of
CORNEAL OEDEMA: INTRODUCTION contact lens wear by the original contact lens
pioneers Fick and Muller (circa 1888). However, all
• Mild oedema is a natural consequence of sleep
people experience mild corneal oedema resulting
• Recognized as contact lens-induced since from eye closure during sleep because the oxygen
introduction of CLs (1888) available to the cornea is reduced by approximately
• Measured indirectly by corneal swelling two-thirds by the coverage of the lids. Figures for
overnight swelling range from 2.9% (du Toit et al.,
(pachometry)
1998) or 3% (Sweeney, 1991) to 5.5% (Harper et
• SCL-induced oedema involves the whole of the al., 1996).
cornea and is diffuse
Generally, SCL-induced corneal oedema involves
97200-235S.PPT
the whole of the cornea and is diffuse in nature.
7L297200-235 Usually, such oedema is greater centrally than
peripherally, and occurs in an anterior-posterior
direction.
The low level of oedema resulting from most current
contact lenses is difficult to detect with a slit-lamp.
Corneal oedema results in corneal swelling and an
instrument such as a pachometer (optical,
ultrasonic, or OCT [Optical Coherence
Tomography]) is required to establish the presence
of subtle corneal thickness changes.
11 Corneal Oedema: Signs
The oedema caused by contact lens wear can affect
CORNEAL OEDEMA both the structural and functional capacity of the
SIGNS
cornea. All layers can be involved but the signs of
• Diffuse corneal oedema are more likely to be seen in the
• Structural and functional changes
posterior layers. Certain signs are visible with the
slit-lamp and these include:
- involve all layers x Hazy tissue. This is believed to be due to
- subtle to obvious
changes in the collagen bundles that makes
them appear to be whitish (Ruben, 1978).
• More central than peripheral x Increased visibility of stromal nerve fibres when
97200-54S.PPT
the stroma is oedematous (Ruben, 1978)
(probably because of an altered refractive index
7L297200-54 difference between the nerve fibres and the
altered stroma).
12 x Stromal striae.
x More oedema apparent in the mid-peripheral
cornea in the case of moderate to high minus
Rxs mirroring the regions of greatest lens
thickness (lowest Dk/t ). Conversely, central
oedema is more likely to be obvious in
moderate or high plus Rxs (after Ruben, 1978).
However, central and mid-peripheral swelling is
invariably greater than peripheral swelling (see
later this section).
x Folds in Descemet’s membrane. In the more
obvious cases these are sometimes referred to
as ‘black lines’ because of their appearance.
7L20513-97
However, black lines are indicative of a very
significant level of corneal oedema, e.g. Grade
3, involving a •8% increase in thickness, with 5
or more striae visible (Efron, 1999). This level
of corneal alteration is seldom seen with

IACLE Contact Lens Course Module 7: First Edition 21

 Module 7: Contact Lens-Related Ocular Complications

13 modern contact lenses and is only likely in

conventional soft lenses with very high plus or
high toric Rxs.
Slide 12 shows an extreme example of oedematous
corneal haze seen through a slit-lamp.
This level of haze is uncommon and is unlikely to be
seen with any contact lens marketed in the last
decade. It is much less likely with the newer
generations of RGP, soft, or siloxane hydrogel
lenses.
Slide 13 shows a very oedematous cornea in optic
section (narrow slit, direct illumination). The stroma
appears to be granular rather than diffusive
although it exhibits diffusive properties as well. This
appearance is a result of very significant corneal
swelling and is more likely to be seen in cases of
corneal pathology than contact lens wear.

7L20960-91

14 Topographical Corneal Swelling

Although the whole of the cornea is involved in
TOPOGRAPHICAL SWELLING
20
corneal swelling during soft lens wear, the cornea
SOFLENS 04 (Holden et al., 1985)
does not swell uniformly across its diameter (Holden
CORNEAL SWELLING (%)

15
– 9.00 D
– 6.00 D
et al., 1985, Bonnano and Polse, 1985, Bonnano et
– 1.25 D
al., (1986), Herse et al. 1993, Erickson and
10 Comstock, 1995, Erickson et al. 1996).
5
)
(%
IG
W
S
L
A
E
N
R
O
C

In these studies, much less corneal swelling was

found in the periphery than in the centre. It was
0
concluded that the anchoring or ‘clamping’ of
5 4 3 2 1 0 1 2 3 4 5 6
Temporal Nasal peripheral corneal thickness by the adjacent limbus
CORNEAL LOCATION (mm)
97200-200S.PPT
and scleral rim was the most likely explanation
(Holden et al., 1985B, Bonnano and Polse, 1985,
7L297200-200 Bonnano et al., 1986, Doughty, 2001).
Holden et al. also studied the cornea’s swelling
behaviour across the same corneal zones using
anoxia (humidified nitrogen) applied in a goggle. A
similar finding to the lens studies was made, adding
weight to the peripheral ‘clamping’ theory. They
also noted that the difference was more apparent
with greater levels of central swelling and with high
minus Rxs (slide 14).
These findings suggested that peripheral tear
circulation and poorer physiological performance
under the lens’ mid-periphery, were not factors in
their observations of less swelling in the periphery.
Bonnano and Polse, using similar lenses and BVPs
to Holden et al., found 25 to 50% less swelling in the
corneal periphery.
Following an analysis of open-eye central and
peripheral corneal swelling over 3 hours with SCLs
of wide-ranging powers, Bonnano et al. (1986)
22 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

suggested that significant lateral diffusion of oxygen

or epithelial metabolites may be occurring between
corneal regions of induced high and low oxygen
partial pressures.
On the other hand, Erickson et al. (1996), during a 4
hour, closed eye (patched and awake) study of SCL
wear using lens powers spanning ±6D, found that
over the central 7 mm of the cornea, the corneal
swelling was influenced by both local and regional
lens thickness.
II.A.I Striae

15 Corneal Oedema: Striae: Introduction

CORNEAL OEDEMA: STRIAE Commonly, corneal striae seen in or near
INTRODUCTION Descemet’s membrane occur in numerous
• Appear in the posterior stroma inflammatory, traumatic, and degenerative corneal
• Occur in: conditions (Polse and Mandell, 1976).
- inflammatory conditions
- traumatic conditions Striate corneal lines (slide 16) resulting from
- degenerative conditions hydrogel lens wear were first reported by Sarver in
- CL wear (hypoxia & other CL effects) 1971. Sarver reported 6-12 irregular, fine vertical
• Usually vertically oriented lines that were apparently located in the posterior
- 1-3 mm in length stroma adjacent to Descemet’s membrane and
- whispy white lines
- usually thicker than nerve fibres
which proved to be reversible over 2-4 days of no
97200-234S.PPT
lens wear. Both Sarver (1971) and Wechsler
(1972) reported that striae could be made to
7L297200-234 disappear by the application of digital pressure to
the globe and that from their observations, the
incidence could be a high as 50% of hydrogel lens
wearers, a figure also reported by Polse et al.,
(1975). Kerns (1974) reported a lower incidence
overall (36%) and noted a lower incidence in PMMA
wearers. It is noteworthy that the lenses worn at
that time were either PMMA or relatively thick (tc =
0.2 to 0.3 mm) low water (38%) hydrogel lenses.
Because more recent contact lenses have improved
physiological performance, striae are now a rare
clinical observation.

IACLE Contact Lens Course Module 7: First Edition 23

 Module 7: Contact Lens-Related Ocular Complications

16 Corneal Oedema: Striae: Signs and Aetiology

When viewed in direct illumination, striae appear as
fine, whispy, greyish, whitish or translucent corneal
lines in the central to mid-peripheral, posterior
stroma (slide 16). Striae may be single or clumped
together. Usually, their orientation is vertical or near
vertical (Sarver, 1971, Wechsler, 1972, Polse et al.,
1975, Polse and Mandell, 1976) although horizontal
and oblique orientations have been reported
(Holden and Swarbrick, 1989).
Since a vertical orientation is more common, it is
relatively easy to differentiate striae from corneal
nerve fibres whose arrangement is essentially
radial. Furthermore, nerves extend some distance
across the cornea, are longer, and branch. This
differentiation becomes more critical when dealing
with keratoconus or possible keratoconus, because
of the increased corneal nerve conspicuity in that
condition.
Striae were postulated to be the result of stromal
oedema (Wechsler, 1974) and have been shown to
result from corneal oedema (Polse and Mandell,
1976). The level of corneal swelling required to
produce striae is of the order of 4-6% (Holden and
Swarbrick, 1989).
7L22015A-95 When viewed under conditions of fundal retro-
illumination, striae may appear as black or dark
lines (after Efron, 1999) (see below). However, the
17 line can be expected to appear thicker using retro-
illumination than when viewed in direct illumination
CORNEAL OEDEMA vs STRIAE because retro-illumination shows the whole of the
(La Hood & Grant, 1990)
25
Striae (number) refractile extent of a corneal feature, not just its
striae = 1.45 x oedema – 6.5 more obvious aspects.
20
n = 192
r = 0.88 These refractile (optical) effects are believed to be
p < 0.001
15 due to increases in the separation between some
10
posterior stromal collagen fibrils. The separation is
due to stromal oedema and the resulting buckling of
5
the posterior stroma and Descemet’s membrane.
0 Posterior buckling is probably the result of
0 5 10 15 20 25
93005085.PR3 Oedema (%) differential swelling behaviour of the posterior
(greater) and anterior (lesser) stroma (Lee and
7L293005-85 Wilson, 1981). Corneal swelling has been shown
to occur in a posterior to anterior direction
(Bergmanson and Chu, 1982) which may also offer
18 a partial explanation of the apparent location of
STROMAL STRIAE striae.
AETIOLOGY Striae become more conspicuous and more
numerous with higher levels of corneal swelling
• Corneal hypoxia causes stromal oedema
probably due to the increasingly disordered
arrangement of the stromal lamellae.
• Minimum of 5% corneal swelling required
La Hood and Grant (1990) quantified the
relationship between corneal oedema as measured
• Separation of lamellae by pachometry and the incidence of striae as
observed with a slit-lamp. They found that a count
• Refractile effect of 10 striae represented 11% ±2% corneal swelling.
97200-71S.PPT
The relationship they found is shown in slide 17.
7L297200-71 The advent of siloxane hydrogels has lowered
further the incidence of striae in contact lens
wearers.

24 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

19 Corneal Oedema: Striae: Management

STROMAL STRIAE Striae are indicators of physiological corneal stress.

MANAGEMENT Their presence warrants some form of clinical
intervention by the practitioner.
• Intervention is warranted This usually involves increasing the amount of
oxygen available to the cornea during contact lens
wear to reduce the stress and minimize the risk of
• Increase lens Dk/t
striate formation.

• Reduce wearing time The oxygen transmissibility of the lens must be

optimized for the individual patient. The obvious
solution is to refit the wearer with a siloxane
97200-72S.PPT
hydrogel lens. Striae will be found to be
7L297200-72 increasingly uncommon as use of siloxane hydrogel
lenses becomes more widespread.
If, despite a practitioner’s best efforts or the lack of
a suitable siloxane hydrogel lens, striae are still
detectable, lens wearing time must be reduced to
prevent any long-term changes in the structure and
function of the cornea.
II.A.II Folds and Black Lines

20 Corneal Oedema: Folds and Black Lines:

Introduction
CORNEAL OEDEMA: FOLDS & BLACK
LINES - INTRODUCTION The level of corneal swelling required to produce
folds (slide 22), and possibly black lines (slide 23),
• Terms used somewhat interchangeably
is usually given as 7% to 12%. While the two terms
• Buckling of the component layers resulting from are often used somewhat interchangeably, the term
corneal oedema ‘black line’ is usually reserved for the more extreme
• Limbus constrains lateral corneal expansion manifestation of this phenomenon which is a
buckling of the posterior stromal tissue and/or the
• Require 7 to 12+% corneal swelling
endothelium. Regardless of the terminology used,
- black lines result from swelling at the higher folds and black lines should be regarded as part of
end of this range a continuum, with the actual appearance being
97200-233S.PPT
influenced by observation conditions, and individual
7L297200-233 characteristics of the cornea involved. This buckling
is the result of very significant corneal swelling in a
viscoelastic tissue, particularly posteriorly, that is
21 constrained by the sclera at the limbus (after Cogan
in Stocker, 1971 and Wechsler, 1974).
CORNEAL OEDEMA vs FOLDS According to Holden and Swarbrick (1989), swelling
(La Hood & Grant, 1990)
25
Folds (number)
of 15% or more is required in some cases for black
20
folds = 1.33 x oedema – 9 lines to appear. For folds, Efron (1999) presented a
n = 166
r = 0.87 figure of 8% or more, with stromal haze and a
15 p < 0.001 granular appearance being apparent by 15%
10
swelling (see slide 16). Black lines should be
regarded as a clear sign of oedema exceeding
5 clinically acceptable levels (Holden and Swarbrick,
0
1989).
0 5 10 15 20 25
93005088.PR2 Oedema (%) Although hypoxia-induced corneal striae and folds
are transient, some diabetic patients may exhibit a
7L293005-88
more ‘permanent’ form of posterior stromal folding
(reported by Waite and Beetham, 1935, Leopold,
1945, and Henkind and Wise, 1961, all cited in
Kerns, 1974) that is stable over a period of months
(O’Donnell and Efron, 1995). A suitable history
should help to differentiate these two presentations.
In addition to quantifying striae, La Hood and Grant
(1990) quantified the relationship between corneal
oedema and the incidence of folds. They found that
IACLE Contact Lens Course Module 7: First Edition 25
 Module 7: Contact Lens-Related Ocular Complications

a count of 10 folds represented 15% ±3% corneal

swelling. The relationship they found appears as
slide 21.
22 Corneal Oedema: Folds and Black Lines: Signs
Corneal folds (stromal and/or endothelial) may start
out as corneal striae (see previous section). Once
corneal swelling approaches 7% to 8%, the
significant stresses generated within the cornea
result in folds appearing in the posterior stroma
adjacent to Descemet’s membrane (slide 22).
These folds may also be accompanied by striae.
Should greater swelling be realized, the folds
become more apparent and may also widen
(broaden). The folds appear as long, almost
straight, black lines when viewed with a slit-lamp.
These lines may be single and discrete or
occasionally crossed. Their orientation is nearly
vertical in most cases.
Should swelling reach or exceed the 10% to 15%
range, the appearance of the folds may change to
that of black lines (slide 23).
Individual corneal characteristics also play a role in
the final manifestation of corneal swelling of these
magnitudes.

7L20310-91

23

7L20291-91

24 Corneal Oedema: Folds and Black Lines:

Symptoms
CORNEAL OEDEMA
SYMPTOMS The majority of cases in which corneal oedema is
• Generally asymptomatic unless corneal detectable are asymptomatic. However, if the
cornea’s physiological requirements are not fulfilled,
swelling is significant
some type of discomfort will usually result (Mandell,
• Reduced vision: 1988). Those symptoms that are reported range
from relatively mild to barely detectable and are
- diffusive ‘spectacle’ blur more likely to be visual than any other type.
- haziness, haloes, coloured haloes Significant levels of oedema can result in reduced
vision and the patient may complain of blur, haloes
- little or no Rx change detectable
97200-55S.PPT
and/or haze during contact lens wear and with their
spectacles, for some time after contact lens
7L297200-55 removal. Often an assessment of their Contrast
26 IACLE Contact Lens Course Module 7: First Edition
Lecture 7.2: SCL Complications and Their Management

Sensitivity Function (CSF), or the use of a low-

contrast visual acuity chart, can reveal starkly the
extent of the visual perturbation.
Decreased visual acuity is the result of a loss of
corneal transparency, particularly if the corneal
epithelium is affected. This loss is due to a
swelling-induced decrease in the level of corneal
structural organization. While the mechanisms
responsible for the cornea’s normal transparency
have not been established clearly, Maurice’s
lattice/interference theory (1957, cited in Cotlier,
1975) offers a plausible explanation for much of
what can be observed. Francois and Rabaey
(1960, cited in Mandell, 1988) showed that when the
cornea swells, the diameter of the corneal collagen
fibrils remains the same but their separation
increases. This separation disturbs the regularity of
the fibrillar arrangement, and their normally helpful
interference behaviour is altered. This
disorganization results in a decrease in corneal
transparency.
Of greater clinical significance is the loss of
epithelial transparency that occurs with oedema.
Despite the lack of a layer thickness increase
(Bergmanson and Chu, 1982), the loss of epithelial
transparency is the greatest contributor to the level
of haze observed (Mandell, 1988). Oedema
adversely affects the epithelium’s barrier function
and fluid enters the epithelium from the anterior
surface (Bergmanson and Chu, 1982) and occupies
the space between the cells (Bergmanson, 1987).
Corneal thickness is maintained in the oedematous
state by cell shrinkage being compensated for by
fluid imbibition (Bergmanson and Chu, 1982).
What remains unclear is the relationship between
simple blur resulting from corneal oedema, and the
blur that can follow the removal of low Dk and
PMMA rigid lenses or low water toric SCLs with high
Rxs, i.e. spectacle blur. The latter blur has a
physical/topographical as well as physiological
aetiology beyond just oedema, and is probably less
diffusive in nature.
Mechanisms of Visual Loss
Corneal oedema is difficult to confirm using routine
techniques of visual assessment. A more reliable
method is to measure changes in the contrast
sensitivity function (Carney and Jacobs, 1984).
It is also possible for vision to remain normal (as
measured by visual acuity) despite marked corneal
swelling (Carney and Jacobs, 1984, and Lancon
and Miller, 1973, cited in Carney and Jacobs, 1984).
The aetiology (e.g. hypoxia or tonicity changes)
and/or location of the oedema (e.g. epithelial or
stromal) are also of importance with epithelial
oedema being the more debilitating (Carney and
Jacobs, 1984 citing Lancon and Miller, 1973, and
Zucker, 1966).
Despite the significant but small changes induced in
the contrast sensitivity function by corneal oedema,
it was found that the addition of a glare source

IACLE Contact Lens Course Module 7: First Edition 27

 Module 7: Contact Lens-Related Ocular Complications

would improve the sensitivity of the contrast tests.

Carney and Jacobs concluded that stromal
thickness changes were of minor importance and
that epithelial changes were more important.
However, they found that because of significantly
different visual outcomes, epithelial oedema caused
by osmotic factors was mechanistically different
from that caused by anoxia.
During contact lens wear, the wearer may notice the
onset of haloes or coloured haloes around lights
and/or, in cases of greater oedema, a general
haziness of vision (light diffusion in the cornea
resulting in reduced contrast).
Any visual symptoms induced by lens wear
disappear soon after lens removal, i.e. once access
to normal levels of oxygen is regained.
Overnight Swelling: Significance of Lens Wear
versus No Lens Wear and Lens Type
The overnight swelling of the normal cornea (no
lenses in either eye) has already been detailed. A
range of 3% to 4% is probably normative although
published figures range from 2.9% to 5.5%.
Fonn et al. (1999B) studied the overnight swelling
effects of high and low Dk SCLs as well as any
effects in the non-lens-wearing contralateral eye. In
the lens-wearing eye they found only 2.71% swelling
with a siloxane hydrogel and 8.66% with a 58%
conventional hydrogel lens. The contralateral eyes
that served as controls showed swellings that were
less than literature values. However, these values
depended on what lens was being worn in the other
eye, i.e. 1.44% while wearing the high Dk lens and
2.34% with the low Dk lens.
Fonn et al’s no-lens swelling data was 1% to 1.5%
less than literature figures for overnight swelling
without any lens wear in either eye. This appeared
to be related to an ‘overshoot’ by which a thinning
(recovery from oedema) cornea thinned about 1%
beyond baseline thickness. As they pointed out,
this finding had already been reported by O’Neal
and Polse (1985) and Sweeney and Holden (1987).
25 Corneal Oedema: General: Aetiology

CORNEAL OEDEMA Usually, regardless of magnitude, corneal oedema

AETIOLOGY is caused by a reduction in the amount of oxygen
• Normal eye closure (sleep) available at the anterior eye surface. Its most
• Anterior eye hypoxia common cause is normal eyelid closure as occurs
during sleep. Oxygen availability in the closed eye
• Hypotonicity of the tears
is covered in detail in Module 6, Lecture 6.1, Section
• Reduced tear film evaporation IV Effects of Hypoxia. Although this oedema
• Stromal pH changes occurs normally even without contact lens wear, the
• Reduced endothelial pump efficacy latter exacerbates the issue.
• Increased temperature under lenses As there are a number of possible contact lens wear
• Trauma 97200-56S.PPT
factors involved in corneal oedema, it is difficult to
establish the primary aetiology in many cases (see
7L297200-56 list of some possible causes in the slide opposite).
The most significant factor however, is the relative
hypoxia induced at the anterior corneal surface by
most conventional soft contact lenses. This effect is
exaggerated in most toric soft lenses due to the
28 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

26 latter’s greater overall thickness, and therefore their

lower oxygen transmissibility.
ENDOTHELIAL FOLDS The black lines seen with the slit-lamp represent a
AETIOLOGY
• Corneal hypoxia causes stromal swelling creasing and/or buckling of the posterior stroma,
Descemet’s membrane, and the endothelium. The
• Minimum of 8% corneal swelling required
stresses producing the buckling in the deeper
• Swelling directed posteriorly corneal layers are the result of the stroma being
- limbal limitations on lateral expansion pushed in a posterior direction by significant corneal
• Buckling of: oedema. The stresses, plus the restrictions on
- posterior stroma expansion imposed laterally on the cornea by the
sclera at the limbus, mean that the cornea must fold
- Descemet’s membrane
or buckle to accommodate its swollen self.
- endothelium 97200-77S.PPT
The level of anterior corneal hypoxia induced by the
7L297200-77 new siloxane hydrogels appears to be less than with
conventional hydrogels (Fonn et al., 1999B, Levy et
al., 2000, Sweeney et al., 2000). Overnight oedema
is also significantly less than with conventional
hydrogels and approximates that of no lens wear
(Fonn et al., 1999B, Sweeney, 1999).
Aetiologies not related to oedema must also be
considered. Examples include: tear evaporation
(O’Neal and Polse, 1985), and temperature under a
lens (Martin and Fatt, 1986, Sweeney, 1991).
27 Corneal Oedema, General: Management

CORNEAL OEDEMA The presence of folds indicates that the cornea is

MANAGEMENT under significant physiological stress and
intervention by the practitioner is required to
• Minimize contact lens effects:
improve the contact lens’ performance. An increase
- maximize lens Dk/t (priority) in the oxygen supply to the cornea needs to be
achieved if corneal oedema is to be minimized to
- optimize lens fit (less significant) acceptable levels.
The principal management strategy for dealing with
- fit siloxane hydrogels contact lens-induced corneal oedema is the
maximization of the oxygen available to the eye.
• Decrease lens wear This can be achieved by:
97200-57S.PPT

7L297200-57 x Optimizing the fitting characteristics of the

lenses (a less significant strategy), e.g. lens
movement.
28
x Increasing the oxygen transmissibility of the
ENDOTHELIAL FOLDS lenses supplied (a more significant strategy),
MANAGEMENT e.g. using a design that is as thin as
practicable.
• Intervention is mandatory
x Changing to a siloxane hydrogel (the most
• Significant increase in lens Dk/t needed effective strategy).
If fitting and oxygen supply are already optimized
• Very short wearing time
but corneal oedema remains a problem, the only
• Refit with siloxane hydrogels, or high-Dk
options remaining are:
x Reduce the wearing time to minimize the
RGP lenses
97200-78S.PPT adverse effects that ensue (unlikely to be
popular with a successful lens wearer, and
7L297200-78
relatively ineffective since the inadequate lens
performance is still experienced by the eyes
when the lens is worn).
x Switch to the superior physiology offered by
siloxane hydrogels and maintain the preferred
longer wearing times.
Previously, for some conventional SCL wearers, an
IACLE Contact Lens Course Module 7: First Edition 29
 Module 7: Contact Lens-Related Ocular Complications

RGP lens offered a better physiological environment

due to their inherently greater oxygen
transmissibility. However, the newer generation of
siloxane hydrogels has virtually eliminated this
advantage and probably now offer superior
transmissibility to current RGP lenses. The siloxane
hydrogel lenses offered currently only cover
spherical Rxs and it may be some time before
higher spherical powers, and stock toric Rxs,
become available. Therefore, this choice of lens
material is not available to all wearers.
II.B Epithelium: Microcystic Oedema

29 Microcystic Oedema: Introduction

MICROCYSTIC OEDEMA: Generally, microcystic oedema in not a contact
INTRODUCTION lens-related condition, rather it is usually secondary
to some other corneal or general ocular condition. It
• Generally not a CL-induced condition
is included here because of the potential for
• Usually secondary to other corneal confusion between it and contact lens-related
conditions microcysts.
The conditions associated with microcystic oedema
• Often confused with microcysts which
include:
are a CL issue
x Angle-closure glaucoma in nanophthalmos (an
• Vision may be impaired apparently normal eye with short axial length)
97200-230S.PPT
(Caronia et al., 1998).
7L297200-230 x Phacolytic glaucoma. May be accompanied by
stromal and Descemet’s folds (Lane et al.,
1988).
x Acute angle-closure glaucoma and the elevation
of IOP that follows (www.dr4eyes.com, 2000,
www.opt.pacificu.edu, 2000).
x Keratoconjunctivitis (Steensma, 2000)
x A toxic reaction to Rose Bengal (Terry, 2000,
personal communication).
The corneal disturbance is so severe in many of the
pathological conditions in which microcystic oedema
is secondary, that gonioscopy is rendered difficult or
impossible to perform. For related reasons, the
patient’s vision is also impaired.
30 Microcystic Oedema: Signs
MICROCYSTIC OEDEMA In this condition the onset is acute and literally
SIGNS hundreds of cysts (>200) may be scattered across
the central and mid-peripheral cornea.
• Hundreds of very small epithelial cysts Usually, the cysts are not induced by hypoxia, and
they can be differentiated from those that are by
• Larger than lens-related microcysts their larger size and more regular shape. However,
in high risk cases such as aphakia (e.g. using thick,
• Central and mid-peripheral low water lenses) and PMMA users (material Dk
virtually zero) hypoxia may be the cause or at least
a significant contributing factor. In such cases
97200-66S.PPT
differentiating microcysts by cause (size) may be
difficult unless the practitioner is experienced and
7L297200-66 can estimate their size adequately without any size
reference.

30 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

31

7L21169-95

32 Microcystic Oedema: Symptoms

MICROCYSTIC OEDEMA Symptoms associated with microcystic oedema are

SYMPTOMS more likely to be due to a coexisting condition rather
than microcystic oedema per se. The symptoms
• Symptoms are usually vague reported are likely to be those of mild to moderate
ocular irritation. Unless the primary condition
• Some ocular irritation may be reported produces obvious symptoms, the symptoms
expressed are usually vague depending on the
• Generally, not related to the cysts per se severity and the cause(s). The actual symptoms
are often difficult to establish with any certainty
• Decreased vision (disturbed epithelium) because toxic and/or inflammatory causes are
usually involved.
97200-67S.PPT

7L297200-67

33 Microcystic Oedema: Aetiology

MICROCYSTIC OEDEMA The cysts that develop in microcystic oedema are

AETIOLOGY often associated with an ocular inflammatory event
• Generally associated with corneal insult or an allergic reaction (Shiuey et al., 2000). Such
- toxicity: an event may involve a toxic reaction to a solution
– H2O2 such as Rose Bengal, or be associated with
– chlorhexidine significant physiological stress to the cornea in soft
– other chemicals contact lens extended wear (SCL EW).
- physiological stress: In the literature, microcystic oedema is confused
– acute hypoxia from thick SCL commonly with microcysts. Some authors have
– very low Dk/t lens used the term microcystic oedema to refer to the
• Part of an inflammatory episode extreme variation of corneal oedema that follows
97200-68S.PPT

the use of a thick, unmoving PMMA lenses

7L297200-68 (hypoxia-related), serious episodes of solution
sensitivity, and anterior uveitis.
Realistically, the use of PMMA lenses is no longer
justifiable and the response they induce is not really
inflammatory in nature. Few serious episodes of
solution sensitivity occur with modern lens care
products. These episodes are more likely to be
allergic than inflammatory in nature.

IACLE Contact Lens Course Module 7: First Edition 31

 Module 7: Contact Lens-Related Ocular Complications

34 Microcystic Oedema: Management

MICROCYSTIC OEDEMA In cases of microcystic oedema it is important to

MANAGEMENT ascertain the underlying aetiology of the epithelial
stress. If a lens care product is suspected,
• Consider cause of corneal insult identification should be by a logical process of
elimination. Once identified, suitable alternatives
- fitting characteristics
should be substituted. The lens fitting
- physiology characteristics and wearing schedule and/or mode
may require modification to minimize any remaining
• Reduce risk of toxicity
chronic physiological insult to the cornea.
- solutions If ocular pathology is implicated and severe enough,
97200-69S.PPT
the underlying condition needs to be treated before
lens wear continues. In some cases, lens wear can
7L297200-69 be continued after consultation with all the health
care providers involved in the case.
II.C Epithelium: Epithelial Microcysts

35 Epithelial Microcysts: Introduction

EPITHELIAL MICROCYSTS: Epithelial microcysts can occur in a variety of
INTRODUCTION corneal dystrophies (Humphreys et al., 1980), and
• Can occur in: in hypoxic, immunological, and infectious conditions
- dystrophies of the cornea. However, the aetiology may be
- inflammations
multifactorial (Stiegemeier, 2000).
- infections Observations of microcysts in contact lens wear
- chronic hypoxia were first reported by Brown and Lobascher (1975,
• Common, especially in SCL EW cited in Humphreys et al., 1980) and Ruben et al.
• Also occurs commonly in non-wearers (1976, cited in Efron, 1996).
• Low count regarded as ‘acceptable’
Incidence rate as high as 100% have been reported
97200-231S.PPT
in soft lens extended wear (Humphreys et al., 1980,
7L297200-231
Kenyon, 1986, Fonn and Holden, 1988, Soni and
Hathcoat, 1988). Lower figures have also been
reported, e.g. 41% (Zantos, 1981).
Microcysts can also be seen in non-lens wearers
but they are usually few in number, e.g. up to 5
(Holden et al., 1987). Their significance in non-
wearers remains unclear.
As microcysts are seen in non-lens wearers and
lens wearers alike, several authors have taken the
approach that low numbers are considered
acceptable and that some action, usually cessation
of lens wear, is required when the number of
microcysts exceeds a critical level. Suggested
critical levels are between 30 (Gottschalk, 1988)
and 50 (Zantos, 1984B).
36 Epithelial Microcysts: Signs

EPITHELIAL MICROCYSTS Using a slit-lamp and marginal retro-illumination,

SIGNS corneal epithelial microcysts are relatively easily
• Small, usually circular 'dots’, with relatively detected (Zantos, 1981). They appear as small (10
clearly defined borders - 50 µm, average 20 µm), usually circular (Efron,
- exhibit reversed illumination 1999), occasionally irregular, translucent, refractile
— ? higher n than surround ‘dots’ (after Zantos, 1983).
• Vary in number from a few to > 100 They are usually located in the central and
• Disclosed by fluorescein only when ‘breaking paracentral corneal regions and can be
out’ from the epithelial surface
differentiated from other dot-like corneal features
- surface disruptions appear as 'black dots' (e.g. endothelial bedewing) by virtue of their
– disrupted mucin layer location, i.e. epithelial as opposed to stromal or
97200-62S.PPT

deeper locations).
7L297200-62

32 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

37 Because they exhibit reversed illumination, i.e. the

illuminated (bright) half of the microcyst’s
DIVERGING CONVERGING appearance is on the opposite (reverse) side to the
REFRACTOR REFRACTOR (after Brown, 1971) slit-lamp’s illumination system, they are behaving as
x Observer
convex refractors (slide 37) meaning their refractive
index is higher than the surrounding medium, i.e.
the epithelium (after Brown, 1971).
x Transparent intra-corneal
object As long as the microcysts remain within the
x Background for marginal epithelium there is no accompanying sodium
retro-illumination
fluorescein staining (slide 38, marginal retro-
x Unreversed (U) and illumination, slide 39, indirect illumination).
U R reversed (R)
94058160.PR2
appearance If, and when, they break through the surface
epithelium, small black ‘dots’ become visible on the
7L294058160 corneal surface. These black areas represent
38 disruptions to the surface of the epithelium
(including the mucin layer) and appear as non-
staining areas of surface irregularity. Sometimes
this is referred to as ‘negative staining’, i.e. surface
perturbations exist which, somewhat paradoxically,
do not stain in the manner that usually follows
sodium fluorescein instillation (slide 40).

7L21566-96

IACLE Contact Lens Course Module 7: First Edition 33

 Module 7: Contact Lens-Related Ocular Complications

39

7L21169-95

40

7L20292-91

41 Microcysts: Observation

OBSERVING MICROCYSTS The refractile nature of epithelial microcysts

With slit-lamp: suggests retro-illumination as the technique of
choice. The most frequently recommended
• Set approx. 45° between slit and microscope
technique is marginal retro-illumination in which
• 1 to 2 mm wide slit to scan illumination to the observed area is split vertically
- 0.5 to 1 mm to observe between the retro-illuminated iris (relatively bright)
• 15X to 25X magnification to scan and the non-reflecting (dark) pupil.
- 30X to 40X to observe Details of the instrument set-up appear in the slide
• Use retro or marginal (pupil) retro-illumination opposite.
• Scan laterally to ascertain numbers Microcysts need to be differentiated from the larger
97200-201S.PPT
microcysts of microcystic oedema, as well as from
7L297200-201 epithelial vacuoles and bullae, and to a lesser extent
the mucin balls (see Section IV.I Mucin Balls) that
appear under siloxane hydrogel lenses in some
wearers.
While microcysts generally show reversed
illumination (slide 42), the other features listed show
unreversed illumination. (i.e. they have a lower
refractive index than their surround, slide 45), are
usually larger or much larger, appear more ‘bubble-
like’ (vacuoles and mucin balls) or hollow (vacuoles)
(after Holden and Sweeney, 1991). Punctate

34 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

42 staining, and mucin balls (slide 44) take up

fluorescein, microcysts do not.
To assist differential diagnosis, images of these
conditions are included here. These conditions
include:
x Microcystic oedema (slide 42).

7L2MICROCYST

43
x Mucin balls (white light) (slide 43).

7L2MBALL02

44
x Mucin balls (cobalt blue light) (slide 44)

7L2MBALLF02

IACLE Contact Lens Course Module 7: First Edition 35

 Module 7: Contact Lens-Related Ocular Complications

45 x Vacuoles (slide 45).

7L20483-95

46
x Bullae (slide 46).

7L2BULLK02

47
x Dimple veiling (slide 47).

7L20491-98

36 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

48 Epithelial Microcysts: Symptoms

EPITHELIAL MICROCYSTS Unless there are other ocular changes associated

SYMPTOMS with their formation, microcysts are usually
asymptomatic. As they are an important indicator of
• Asymptomatic, usually contact lens physiological performance, it is vital
that the practitioner looks for microcysts, especially
• May be associated with other ocular in the absence of patient symptoms.
Visual acuity is unaffected unless the number of
changes that do result in symptoms
microcysts approaches 200 (Efron, 1999). Zantos
and Holden (1978) reported one case in which
• Vision unaffected unless numerous visual acuity decreased by one line due to the
97200-63S.PPT
presence of a large number of microcysts.

7L297200-63

49 Epithelial Microcysts: Aetiology

MICROCYSTIC OEDEMA Microcysts are thought to be extracellular

AETIOLOGY accumulations of cellular debris derived from
• Generally associated with corneal insult necrotic (apoptotic), defective, or lysed deeper
- toxicity: epithelial cells, i.e. from the basal cell layer or its
– H2O2 adjacent layer (slide 50) (Zantos and Holden, 1978,
– chlorhexidine Zantos, 1983B, Henriquez, 1987, cited in Holden
– other chemicals and Sweeney, 1991, Madigan, 1989).
- physiological stress: More recently, Tuft and Luthert (1998) reported
– acute hypoxia from thick SCL extensive epithelial microcystic changes in four daily
– very low Dk/t lens wearers of SCLs. Histological analysis of a biopsy
• Part of an inflammatory episode from one case showed microcysts to contain
97200-68S.PPT

shrunken epithelial cells with small, condensed

7L297200-68 nuclei or fragments of nuclear material, often with
dark homogeneous eosinophilic cytoplasm. Further
analysis showed that a few cells had nuclei with
50
cleaved DNA. This latter finding may be in
agreement with speculation by Madigan (1989) that
‘distorted’ messages are conveyed to epithelial
daughter cells via altered RNA.
Circumstantial evidence suggests that the root
cause of microcysts is corneal hypoxia caused by
the relatively low oxygen transmissibility of
conventional soft contact lenses. This possibility is
supported by the observation that the greatest
number of microcysts is seen in extended wear.
Lens type appears also to have a role (slide 51),
because SCLs and RGP lenses of similar
transmissibility, worn on an EW basis, induce quite
different numbers of microcysts. Possible
7L2MICROCYSTHEN explanations of this difference include:
x The size of RGP lenses (less than the whole of
the cornea is covered).
x The RGP lens tear pump,
x The lesser pressure applied to the cornea by
RGP lenses compared with SCLs (Holden and
Sweeney, 1991).
More recently, Keay et al. (2000) showed that high
Dk/t siloxane hydrogel lenses produced few or no
microcysts during EW whereas low Dk/t hydrogel
lenses produced significant numbers (slide 52)
after more than a month of lens wear. Further, for
low Dk/t lenses, they showed a dose-response
relationship between length of lens wear (months)

IACLE Contact Lens Course Module 7: First Edition 37

 Module 7: Contact Lens-Related Ocular Complications

51 and the number of microcysts observed.

The number of microcysts observed in contact lens
MICROCYSTS vs LENS TYPE wearers varies considerably and they are believed
80 to be an indicator of the physiological performance
of the lenses worn (Kenyon et al., 1986), albeit with

Holden & Sweeney, 1991

a delayed onset of 2 to 3 months (Holden and
MICROCYSTS (#)

60
SCL (EW)
Sweeney, 1991 [slide 51], Keay et al., 2000 [slide
40 52]). This variation provides the practitioner with
evidence of how successful the lens is in meeting
RGP (EW)
20
the physiological demands of the cornea, especially
NO LENS its oxygen requirements.
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13
TIME (Months)
Prolonged mechanical pressure from contact lenses
on the epithelium has also been implicated in the
97200-258S.PPT

7L297200-258 aetiology of microcysts (Holden and Sweeney,

1991, Keay et al., 2000).

52
EPITHELIAL MICROCYSTS
AETIOLOGY:
60
EFFECT OF Dk/t
Keay et al., 2000

50
Microcysts

40
Low Dk/t
(Mean)

30

20

10
High Dk/t
0
Pre-Lens 1N 1Wk 1M 3M 6M 9M 12M
Extended wear
97200-280S.PPT

7L297200-280

53 Epithelial Microcysts: Management

EPITHELIAL MICROCYSTS Generally, discontinuation of lens wear in not
MANAGEMENT necessary when microcysts are detected.
• Careful monitoring The presence of microcysts in contact lens wear
- occur in non-lens wearers as well indicates that normal corneal physiology has been
• If < 10, no action is needed compromised. As they can occur in non- wearers in
• Increasing number warrants intervention small numbers, it has been suggested that if fewer
- increase lens Dk/t than ten microcysts are seen no action need be
- reduce wearing time taken.
• Rebound effect after lens discontinuation Greater numbers demand some form of intervention
• Lengthy time to resolve directed toward increasing the oxygen supply to the
97200-65S.PPT
cornea. Epithelial microcysts can be expected to be
7L297200-65
observed for as long as lenses of low Dk/t are worn.
Somewhat paradoxically, microcyst numbers are
widely reported to increase in number, sometimes
54 rapidly, following cessation of lens wear, i.e. they
exhibit a rebound effect, before eventually
EPITHELIAL MICROCYSTS disappearing (slide 54). Disappearance takes
AETIOLOGY: ‘REBOUND’
Keay et al., 2000 weeks or possibly months (Zantos, 1983A, Holden
Low Dk/t lens (6N EW) High Dk/t lens (30N EW)
et al., 1985, Gottschalk, 1988, Holden and
120
Sweeney, 1991, Keay et al., 2000).
Change

100
Microcysts

Rebound

80
This rebound in microcyst numbers is thought to be
60
a sign of epithelial reorganization, and the
40
restoration of the processes altered previously by
chronic hypoxic stress (and possibly mechanical
20

0
Pre-Lens
1M 3M 6M 9M 12M 1Wk 1M 3M pressure). Keay et al. showed the ability of siloxane
Extended wear
97200-278S.PPT
hydrogels to either produce few, if any, microcysts
when used as the lens of first choice, or decrease
7L297200-278 (after a rebound) the number of microcysts when

38 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

used as the solution to an episode of microcysts

induced by ‘lesser’ lenses.
Importantly, when managing a case of microcysts,
the practitioner should not be discouraged by
observation of the rebound effect when a lens
offering superior physiological performance is used
as part of the microcyst management strategy.
Instead, they should simply monitor the number of
microcysts to confirm their eventual decrease.
One study defined ‘recovery’ from microcysts as the
exhibition of fewer than 10 microcysts per eye
(Kenyon et al., 1986).
Tellingly, when siloxane hydrogels are worn under
normal circumstances, i.e. not during recovery from
a previous episode of microcysts induced by lesser
lenses, the incidence of microcysts is found to
approximate that of the spectacle-wearing
population.
II.D Stromal Thinning

55 Stromal Thinning: Signs and Symptoms

STROMAL THINNING Stromal thinning was first quantified by Holden et al.

SIGNS AND SYMPTOMS (1985) using experienced unilateral extended wear
contact lens wearers. Related effects were reported
as early as 1980 (Schoessler and Barr, 1980,
• Generally none Lebow and Plishka, 1980) but in the absence of
specific layer thicknesses (measures that are still
• Detected by pachometry difficult to ascertain) no meaningful conclusions
were possible at that time. Holden et al. 1985
reported a thinning of 11Pm over an approximately
5 year period, i.e. about 2 Pm per year of lens wear.
More recently, Liu and Pflugfelder (2000) reported
that long-term wear contact lens (–
97200-73S.PPT

x = 13.45 years
7L297200-73
for 64 eyes of 35 patients) reduced corneal
thickness by about 30-50Pm as well as increasing
56 corneal curvature and corneal surface irregularity.
These figures are comparable to the Holden et al.
STROMAL THINNING annual rate.
Difference in Stromal Thickness (Pm)

Holden et al., 1985)

20 Obviously, tissue loss cannot be sustained in the
(Lens eye – Control eye)

long term, but the time course of changes beyond

10
the 5 and 13.5 year periods reported here remains
True oedema

Apparent oedema

0
unknown. With the improvements in lens
Stromal thinning
physiological performance that have been made
–10 since most of these studies were carried out, e.g.
siloxane hydrogels, it is probable that the long-term
–20
0 10 20 30 40
outcomes from the use of previous generation
Time (Days) lenses will never be known.
97200-253S.PPT

There are no symptoms associated with a thinning

7L297200-253 of the stroma resulting from contact lens wear.
Such an event can only be detected with a
pachometer. Generally, pachometers are only
found in teaching institutions, contact lens research
clinics, and most refractive surgery suites. Since
pachometry is not a routine contact lens practice
procedure, the detection of stromal thinning is
unlikely except in contact lens research facilities.
Slide 56 shows the apparent corneal recovery in the
Holden et al. (1985) study. The first 33 days of
recovery following cessation of lens wear are
IACLE Contact Lens Course Module 7: First Edition 39
 Module 7: Contact Lens-Related Ocular Complications

shown. Since stromal thinning showed no apparent

recovery, the true extent of corneal oedema with
lens wear is masked. The apparent recovery of
corneal thickness is understated as a result.
57 Stromal Thinning: Aetiology

STROMAL THINNING Thinning of the stroma has been demonstrated to

AETIOLOGY occur in long-term, SCL, extended wear patients.
Whereas stromal thinning is regarded as a chronic
response to corneal oedema, stromal swelling is
• Chronic hypoxia with conventional SCL EW
regarded as an acute response. Stromal thinning is
a result of a compromise of the physiological
• Long-term oedema integrity of the cornea and is regarded as a patho-
physiological change resulting from lens wear over
• Loss of glycosaminoglycans from the stroma many years (after Efron, 1999).
In the Holden et al. (1985) study, no recovery of
97200-74S.PPT
stromal thinning was found. Interference with
stromal tissue synthesis involving keratocytes was
7L297200-74 given as the most likely explanation. Kangas et al.
(1988) showed that in the rabbit at least, corneal
oedema (induced by perfusion, not contact lenses)
resulted in a loss of stromal proteoglycans and an
uptake of water.
A second theory suggests that sustained elevated
levels of lactic acid associated with the oedema
caused by low transmissibility, conventional EW
hydrogel lenses, induces a chronic oedema that
may lead to the dissolution of polysaccharide
(glycosaminoglycans) ground substance in the
stroma (Efron, 1999).
No scarring or alterations in visual acuity has been
reported.
58 Stromal Thinning: Management

STROMAL THINNING The only management strategy available to the

MANAGEMENT practitioner is to prevent the occurrence of stromal
thinning by maximizing the oxygen supply to the
anterior cornea during SCL extended wear. The
alternative is the cessation of extended wear.
• Preventative
Conventional hydrogel lenses are unable to meet
the oxygen needs of the cornea and, in the long
• Lens with high DK/t for EW
term, can be expected to cause stromal thinning.
The newer generation of highly oxygen
transmissible soft contact lenses should eliminate
the primary cause of stromal thinning.
97200-75S.PPT

7L297200-75

40 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

II.E Endothelial Polymegethism

59 Endothelial Polymegethism: Introduction

The word polymegethism is a derivative of the
POLYMEGETHISM: INTRODUCTION Greek words for ‘many’ (poly) and ‘size’ (megethos)
• Literally, many (poly) sizes (megethos)
and literally means ‘many sizes’. It is used in the
context of a description (qualitative or quantitative)
• Endothelial mosaic contains cells of of the extent of the variation of the size of
significantly differing size endothelial cells within the one mosaic. The word
- some cells are smaller than normal was first derived by Rao et al. (1979).
- other cells are larger than normal The term pleomorphism also appears in the
• Age-related & CL-induced polymegethism literature. It refers to endothelial mosaics that
may be different exhibit higher numbers of non-hexagonal cells
97200-229S.PPT
(Doughty, 1990), i.e. changes in cell shape as well
as cell size. In polymegethism, the cell morphology
7L297200-229 is still essentially ‘normal’.
Doughty (1990) analysed the literature pertaining to
pleomorphism/polymegethism and concluded that
there was a difference between the appearance
changes induced by eye surgery and those induced
by contact lens wear, and that attempts to compare
the two situations were flawed.
Polymegethism has also been reported in a case of
mandibulofacial dysostosis (Nucci, 1990).
Nieuwendaal et al. (1994) showed that a
polymegethous or pleomorphic endothelium
resulting from contact lens wear (low Dk/t RGP
lenses) demonstrated a decreased control of
corneal hydration. Similarly, O’Neal et al. (1986)
showed a decreased endothelial pumping function
with increasing age.
Rao (1987) regards polymegethism as an index of
endothelial distress. He also suggested that the
polymegethous cornea had a lower functional
reserve and took longer to deswell (thin) after
surgery.
60 Endothelial Polymegethism: Signs

ENDOTHELIAL POLYMEGETHISM While a general assessment of the

SIGNS endothelium/endothelial mosaic can be made with a
• Variation in cell size slit-lamp at high magnification (30X or higher), a
detailed examination of the mosaic requires higher
- cell volume may also change
magnifications (60X or greater) not possible with
• Associated with normal slit-lamps. Because saccadic eye
- polymorphism movements make viewing difficult at higher
magnifications, the use of contacting microscopes
- increased polygonality
bring more than just optical benefits to the
• Requires careful slit-lamp assessment observation and photography of the endothelium.
• Slowly progressive Furthermore, the applanation of the cornea by a
97200-79S.PPT
contacting microscope objective makes the
7L297200-79 quantification of the mosaic easier by eliminating
the optical and mathematical complications of
dealing with a curved cornea.
Typically, very regular cells are observed in a young
eye, indicating a low level of polymegethism.
Significant variation in the size of the endothelial
cells can be observed as the level of polymegethism
increases. This occurs with increasing age, the
ongoing wear of contact lenses with low oxygen
transmissibilities, and follows some corneal surgical
IACLE Contact Lens Course Module 7: First Edition 41
 Module 7: Contact Lens-Related Ocular Complications

61 procedures involving significant corneal incisions,

i.e. corneal trauma.
A variation in endothelial cell size is associated with
alterations in cell shape, the shape of adjacent cells
and the regularity of the arrangement of the cells
within the mosaic (slide 61). Itoh et al. (1990)
showed that while contact lens wear increased
polymegethism, it did so without increasing mean
cell size, i.e. while some cells got smaller, others
enlarged to leave the average largely unaltered.
This assertion is compatible with an analysis by
Doughty (1990) who suggested that, in contact lens
wear, the endothelium exhibits a disproportionately
7L21665-91 higher number of smaller cells while also showing
isolated very large cells. Itoh et al. also showed that
polymegethism due to contact lens wear was
62 different from that resulting from increasing age,
and was seven times greater than the changes
attributable to old age.
Various methods of quantifying the level of
polymegethism are feasible including computer-
aided automated image analysis. However, the
costs and the complexity of the equipment required
are significant. A subjective rating scale has been
developed by the CCLRU (Sydney, Australia) as a
clinically valid, rapid and economic alternative to
image analysis (slide 62). The scale utilizes images
taken with a contacting specular microscope.
Bergmanson (1992) studied the endothelium of
7L20364-91
wearers and non-wearers using a scanning electron
microscope (SEM). He found that in contact lens
63 wearers the lateral cell walls were reoriented
obliquely. Further, he showed that although there
POLYMEGETHISM: (Bergmanson, 1992) was some detectable inter and intracellular oedema,
Posterior presentation as seen in specular reflection the cells were apparently normal otherwise,
including the appearance of the organelles.
Small Large
Interestingly, Bergmanson postulated that with this
Endothelial cells

wall reorientation it was possible for the cells to

equal volume

have a small or large presentation to the anterior

of

chamber, i.e. the specular microscope appearance

of the mosaic, while maintaining an equal and
Large normal cell volume. Thus polymegethous cells may
Small
Anterior endothelial surface (Descemet’s membrane side)
not vary in cell volume but only differ in their
(Not visible in specular reflection)
97200-236S.PPT
posterior surface presentation (slide 63).

7L297200-236

64 Endothelial Polymegethism: Symptoms

ENDOTHELIAL POLYMEGETHISM Polymegethism associated with contact lens wear is

SYMPTOMS a slowly progressive, asymptomatic condition.

• Asymptomatic

• May be associated with other ocular problems

97200-80S.PPT

7L297200-80

42 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

65 Endothelial Polymegethism: Aetiology

ENDOTHELIAL POLYMEGETHISM The primary cause of polymegethism in contact lens

AETIOLOGY wearer is chronic hypoxia. This has been shown to
occur in wearers of PMMA (hard) and soft contact
• Long-term lens wear lenses of low oxygen transmissibility.
(low transmissibility)
Hypoxia causes a lowering of stromal pH, i.e. an
• Chronic hypoxia acidic shift within the stroma, that may directly affect
the endothelial cells.
• pH change (acidosis?)
Furthermore, inhibited escape of CO2 from the
• Age cornea, and lactic acid accumulation within the
• Disease, surgery, trauma cornea, can alter the pH of the component layers of
97200-81S.PPT
the cornea. This means that hypoxia per se may
7L297200-81
not be the cause of polymegethism rather, it may be
only a contributing factor.
Schoessler and Orsborn (1987) and Kok et al.
(1992) postulated that, in the cases of complete
ptosis they observed, the polymegethism seen was
due to decreased levels of oxygen. This supports
the suggestion that corneal hypoxia and other
changes within the cornea, e.g. pH, pCO2, etc. are
causes of the polymegethism resulting from long-
term use of contact lenses.
The most common cause of endothelial
polymegethism in the general population is
increasing age.
66 Endothelial Polymegethism: Management

ENDOTHELIAL POLYMEGETHISM Prevention of polymegethism in contact lens wear is

MANAGEMENT best achieved by ensuring that the patient is fitted
with contact lens of high oxygen transmissibility.
• Preventative strategy
McLaughlin and Schoessler (1990) showed a small
- high Dk/t lenses but significant increase in cell density in lens
wearers who were changed to significantly higher
• Careful assessment with slit-lamp transmissibility lenses. No changes were found in
• Increase lens oxygen transmissibility polymegethism or pleomorphism as a result of such
changes.
• Minimal recovery expected Therefore it seems that once the condition occurs
97200-82S.PPT
there is little or no recovery to pre-lens wear levels,
7L297200-82
even if contact lens wear is discontinued or lenses
with a higher physiological performance are
introduced.
II.F Endothelial Bleb Response

67 Endothelial Blebs: Introduction

ENDOTHELIAL BLEB RESPONSE: Transient changes in the appearance of the
INTRODUCTION endothelium that followed the insertion of a contact
lens were first reported by Zantos (Zantos and
• Changes in the appearance of the Holden, 1977).
endothelial mosaic soon after lens insertion
Large individual variations in the magnitude of the
• Large individual variation endothelial bleb response have been observed
• Changes subside by one hour (Zantos and Holden, 1977, Vannas et al. 1979,
1981, 1984, Kamiya, 1980, Schoessler et al. 1982,
• Return in the evening in EW Williams, 1986). While the overall endothelial
• Adapts in EW response is apparently related to oxygen levels
97200-226S.PPT
and/or effects of varying oxygen levels, to date no
correlates of an individual’s endothelial
7L297200-226 responsiveness have been identified.

IACLE Contact Lens Course Module 7: First Edition 43

 Module 7: Contact Lens-Related Ocular Complications

68 Endothelial Blebs: Signs and Symptoms

The asymptomatic formation of endothelial blebs
produces a distinct and characteristic pattern in the
endothelial mosaic. Blebs appear as very small,
circumscribed, irregularly-shaped, black zones
obscuring the cellular mosaic when viewed with a
slit-lamp using specular reflection as the illumination
technique. The apparent separation of endothelial
cells can also increase. As can be seen in slides 68
and 69, individual blebs can occupy areas ranging
from one cell to perhaps five or six cells.
Blebs form within minutes (certainly within 10
minutes) of the application of a lens (especially if it
has a relatively low transmissibility) and the
response peaks after about 20 to 30 minutes (slide
70).
After peaking, the apparent response subsides at a
slower rate than it appeared. By about one hour the
response has almost disappeared, i.e. the response
is quite transient in nature.
Slide 70 also shows the time-course of the corneal
swelling induced by a contact lens (PMMA) plotted
against the endothelial response to the lens. As can
be seen, the paths taken are very different. The
corneal swelling in this example peaked at about
four hours (not shown) whereas the endothelial
response peaked between 20 and 25 minutes.
Daytime corneal swelling under a low
transmissibility contact lens usually peaks between
7L21433-96
four and six hours after insertion.
Clinically, the conspicuity of the endothelial
changes, their contrast, and perhaps their extent,
has been reported to vary according to the
instrument (usually a slit-lamp) used to observe the
changes (Williams, 1986). This is thought to be due
to the type of illumination system incorporated in the
instrument, i.e. Gullstrand or Köhler (a.k.a. Vogt)
systems. The Köhler system seems to provide the
‘better’ view. The working distance may also be a
factor, longer being ‘better’.
Endothelial blebs are difficult to see with a
contacting specular microscope. This may be due
to the corneal applanation that occurs with the
dipping-cone objective of such instruments.
Endothelial blebs should not be confused with
corneal guttata (a.k.a. Hassall-Henle bodies,
Hassall-Henle warts, Descemet’s warts) that are
often seen while examining the posterior cornea
(slide 71). In Fuch’s dystrophy, guttata appear
centrally initially, before spreading to the corneal
periphery (Westerhout, 1989). Central corneal
guttata at any age should be viewed with suspicion,
especially if contact lens wear is being
contemplated.
Guttata can be differentiated from blebs using the
following points:
x At least in the early stages of the attendant
condition, guttata are commonly described as
having a ‘beaten metal’ appearance and are not
44 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

69 necessarily black (compare slides 68 and 69

with slide 71).
x Guttata tend to appear to be concave (slides 71
and 72) while blebs appear to be convex (slides
68 and 69). For a diagrammatic explanation of
this concavity see slide 73.
x The area involved in the ‘depressions’ is usually
greater than a single cell (slide 72) and as the
condition progresses, a large percentage of the
area visible in specular reflection is ‘altered’ as
affected areas coalesce. This level of
endothelial involvement is rare in endothelial
blebs, even in the most responsive cases.
x Guttata are not transient, blebs are.

7L20926-91

70
ENDOTHELIAL RESPONSE:
PMMA LENS, OPEN EYE
Endothelial Response

14 Corneal Swelling
6
Corneal Swelling (%)

12
Endothelial Response (S/R)

10 5

8 4

6 3

4 2

2 1

0 0
0 60 120 180
TIME (Minutes)
97200-282S.PPT

7L297200-282

IACLE Contact Lens Course Module 7: First Edition 45

 Module 7: Contact Lens-Related Ocular Complications

71

7L20575-98

72

7L21886-93

73

POSTERIOR PERIPHERAL CORNEA

Incident light lost to observation
(appears black)

Stroma

Descemet's

H-H
Endothelium
H-H H-H

Endothelial Aqueous
Cell Thinned altered Humor
Displaced Endothelium over H-H
Endothelial Nuclei

H-H = Hassall-Henle Bodies (warts)

94071-23S.PPT

7L294071-23

46 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

74 Endothelial Blebs: Aetiology

ENDOTHELIAL BLEBS Initially, the bleb response was thought to be a

AETIOLOGY result of corneal hypoxia. Later, it was believed to
be due to pH changes in the cornea as a result of
• Contact lens wear
hypoxia. However, the bleb response can be
• pH change in stroma induced using gas mixtures containing normal levels
- carbonic acid of oxygen but significant levels of carbon dioxide
- lactic acid
(5% - 15%, the balance was nitrogen) (Williams,
1986). This supports pH as being a primary cause
- bidirectional ? of the endothelial alterations. Further evidence is
• Intra-cellular oedema supplied by Bonnano and Polse (1987B) who
• Altered cell shape measured the pH of the in vivo cornea during lens
97200-84S.PPT
wear using a technique based on non-invasive
7L297200-84 fluorophotometry (Bonnano and Polse, 1987A).
They demonstrated results similar to those found by
75 Williams (1986). These results showed a decrease
in pH (acidosis) resulting from lens wear and
ENDOTHELIAL BLEBS anoxia.
Incident light lost to observation
Incident light reflected (Irregular reflection, appears black) The application of a low oxygen transmissibility lens
(Specular reflection)
to an eye can cause an acidic pH shift in the stroma
Stroma

due to the formation of carbonic and lactic acids

Descemet's
from carbon dioxide accumulation (Bonnano and
Polse, 1987B), and anaerobic metabolism
Endothelium

respectively.
Endothelial
Aqueous
However, some evidence exists to support the view
Cell Oedematous Endothelial Cell
(Altered Reflection Properties) Humor that alterations per se to corneal pH (i.e. a shift in
97200-210S.PPT
either an acid, or a base direction) may be involved
7L297200-210 (Williams, 1986). Intra-cellular oedema resulting
from the pH alteration is thought to change the
shape of the cell, particularly its surface
76 configuration. This non-planar reflecting surface
exhibits altered reflectance properties and parts of
ENDOTHELIAL RESPONSE: the mosaic appear as black (non-reflecting) within
HYPOXIA / ANOXIA an otherwise normally reflecting endothelial cell
14
layer, slide 75).
O2 Concentrations
Endothelial Response (S/R)

12
Further, the bleb response to lower levels of hypoxia
0%
5%
10 10%

8
15%
21% peaks sooner and is lower in magnitude than that
6
with greater hypoxia (slide 76).
4
When contact lenses are worn on an EW basis, the
2
bleb response appears to be at a peak on
0
0 20 40 60 awakening and subsides rapidly, only to reappear
TIME (Minutes)
97200-211S.PPT
towards the end of a day for reasons that have not
been determined (slide 77). The response at eye
7L297200-211 opening the following morning was of a similar
magnitude to that of the night before, just prior to
the sleep period (slide 78).
77
Unlike most aspects of corneal behaviour, the bleb
ENDOTHELIAL BLEB RESPONSE: EW response appears to adapt to extended wear (see
25
slide 78) which shows a declining bleb response
25
over an 8-day study.
Bleb Response (S/R)

20
20

15
15
Day 1
10
10

55

00
-1.00
-1.00 1.00
1.00 3.00
3.00 5.00
5.00 7.00
7.00 9.00
9.00 11.00
11.00

Time (Hours)
97200-227S.PPT

7L297200-227

IACLE Contact Lens Course Module 7: First Edition 47

 Module 7: Contact Lens-Related Ocular Complications

78

BLEB RESPONSE: 8 DAYS WEAR

DAY
25 1
Sleep
Bleb Response (S/R)

2
Sleep

20

3
Sleep
15
4 Sleep
5

Sleep
10 6

Sleep
Sleep
7
5
8
0
-5 45 95 145 195
Time (Hours)
97200-228S.PPT

7L297200-228

79 Endothelial Blebs: Management

ENDOTHELIAL BLEBS The formation of blebs as a result of contact lens

MANAGEMENT wear is probably an indicator of corneal hypoxia.
The use of high oxygen transmissibility lenses
• Clinical significance is unclear minimizes the number of blebs that form after lens
insertion.
• Higher lens Dk/t minimizes:
The bleb response to siloxane hydrogels is reported
to be small but not necessarily zero (Sweeney,
- the number of blebs 2000, personal communication).

- the magnitude of the response

97200-85S.PPT

7L297200-85

II.G Epithelium: SLACH/Reduced Epithelial Adhesion

80 Reduced Epithelial Adhesion: Introduction

SLACH/REDUCED EPITHELIAL Alterations to the adhesion of the epithelium to the

ADHESION: INTRODUCTION basement membrane are very uncommon
regardless of the cause. Even less common are
• SCLs reduce the attachment of the
alterations due to contact lens wear. However, soft
epithelium to its basement membrane contact lenses have been shown to reduce the
(basal lamina) adhesion between the corneal epithelium and the
• Condition is unlikely to be detected in a basement membrane (basal lamina) (Madigan et
routine slit-lamp examination unless..... al., 1987).
• SLACH is likely to be detected because Normally, such a condition cannot be, and would not
of the accompanying loss of epithelium be, detected by a practitioner using a slit-lamp
97200-232S.PPT
unless a secondary condition such as the Soft Lens-
Associated Corneal Hypoxia (SLACH) syndrome is
7L297200-232 present. SLACH is the spontaneous loss of up to
40% of the epithelial surface resulting from hypoxia
(Wallace, 1985).
It is noteworthy that this condition is not only
extremely rare but is also only observed in EW of
conventional hydrogel lenses.

48 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

81 Reduced Epithelial Adhesion: Signs

REDUCED EPITHELIAL ADHESION The existence of SLACH syndrome is disclosed by

SIGNS the slit-lamp manifestation of the epithelial tissue
separated from the cornea (slides 82 and 83 due to
its weakened attachment (adhesion) to the
• Generally, none with a slit-lamp
underlying tissue.

• May manifest as 'SLACH' syndrome Bergmanson and Chu (1982) concluded that
contact lens-produced epithelial trauma was self-
limiting in even the most severe cases and
• Histological changes
permanent scar formation seldom resulted.

97200-58S.PPT

7L297200-58

82

7L23103-93

83

7L20578-98

84 Reduced Epithelial Adhesion: Symptoms

REDUCED EPITHELIAL ADHESION Although epithelial adhesion may be reduced, a

SYMPTOMS wearer will not experience any symptoms unless
there is a loss of epithelial tissue such as occurs in
cases of epithelial erosion and SLACH syndrome.

• Asymptomatic with lens in situ The exposed cornea produces symptoms of pain
and possibly photophobia. Somewhat
paradoxically, it is probable that the eye will be more
• Intense pain with 'SLACH' syndrome comfortable with a contact lens on rather than off
because of the lens’ bandage effect. The exposure
of the inner cornea to the tears and atmosphere, i.e.
97200-59S.PPT
the breakdown of the epithelium’s barrier function, is
the root cause of the symptoms. The epithelium is
7L297200-59 extensively innervated with sensory nerves that
service all epithelial levels. While nerves are more
IACLE Contact Lens Course Module 7: First Edition 49
 Module 7: Contact Lens-Related Ocular Complications

numerous at the basal wing cell layer, some reach

to within one or two cell layers of the tear film
(Hamano and Kaufman, 1987). Once these nerve
fibres are exposed and/or damaged, the sensation
of pain is almost inevitable. Even relatively minor
damage can produce severe pain, i.e. there may not
be a proportional relationship between sensation
and apparent trauma.
85 Reduced Epithelial Adhesion: Aetiology

REDUCED EPITHELIAL ADHESION

Primarily, the cause of reduced epithelial adhesion
AETIOLOGY in soft contact lens wear is hypoxia (Madigan et al.,
1987).
• Hypoxia
• Decreased hemidesmosome density Hemidesmosomes, a type of adhesion or bond
between cells and their basement membrane
• Decrease in number of cell layers
involving cytoplasmic tonofilaments, provide
- no apparent epithelial oedema attachment of the basal layers of the epithelium to
• Development of cuboidal rather than columnar its basement membrane (basal lamina) (Hogan et
basal cells al., 1971).
- anchoring fibrils apparently unaltered
Madigan and Holden (1992) demonstrated that the
97200-60S.PPT
wearing of low-transmissibility contact lenses
7L297200-60 resulted in a significant reduction in the number of
hemidesmosomes per unit area. Interestingly, they
found no obvious epithelial oedema. Other changes
to the epithelium’s microstructure included a
decrease in the number of cell layers and the
appearance of cuboidal rather than columnar basal
cells. No alteration to the appearance of the
anchoring fibrils was observed.
These effects are more prominent in conventional
hydrogel extended wear due to the prolonged and
greater corneal hypoxia, and are less likely in RGP
and siloxane hydrogel extended wear.
86 Reduced Epithelial Adhesion: Management
Prevention of corneal hypoxia in contact lens wear
REDUCED EPITHELIAL ADHESION is the only strategy for managing the effects of
MANAGEMENT
reduced epithelial adhesion successfully. The use
of highly oxygen transmissible soft lenses, including
• Preventative siloxane hydrogels, or RGP contact lenses for
extended wear, will minimize or eliminate the risk of
reduced adhesion.
• High Dk/t lens

97200-61S.PPT

7L297200-61

50 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

II.H Corneal Exhaustion Syndrome (CES)

87 Corneal Exhaustion Syndrome: Introduction

CORNEAL EXHAUSTION SYNDROME: This is a very rare condition and is included here
INTRODUCTION largely for historical completeness.
• Result of long-term wear of lenses with Commonly, the initial manifestation of Corneal
no, or low, O2 transmissibility Exhaustion Syndrome (CES) is an intolerance of
- PMMA (most likely) contact lens wear that develops suddenly. Usually,
many years of PMMA lens wear are involved but
- low water, toric SCLs CES with high Rx spherical and toric soft lenses
- low water, high BVP spherical SCLs (very thick, low water content) have also been
• Sudden development of lens intolerance reported.
• All layers of the cornea affected Korb (1961) was the first to use the term ‘corneal
97200-225S.PPT
exhaustion’ to describe intolerance of hard (PMMA)
7L297200-225
contact lenses. Similar cases were subsequently
reported by Abrams et al. (1980, cited in Sweeney,
1992), Abrams and Schmakel (1981), and Pence
(1988). The name ‘CES’ was first applied to this
condition by Holden and Sweeney (1988).
88 Corneal Exhaustion Syndrome: Signs

CORNEAL EXHAUSTION SYNDROME This syndrome affects all layers of the cornea albeit
SIGNS some indirectly.
• Altered/irregular refraction Posterior corneal changes include distortion of the
• Distorted keratometer mires endothelial mosaic and moderate to severe
• Acute oedema polymegethism.
• Posterior stromal haze/opacities In the longer term, the stroma develops a hazy
appearance and the endothelial mosaic looses its
• Endothelial changes
normal surface properties of smoothness and
- polymegethism regularity, i.e. it becomes ‘bumpy’ and exhibits
- distortion/bumpiness polymegethism (see Section II.E Endothelial
97200-86S.PPT
Polymegethism).
7L297200-86

89 Corneal Exhaustion Syndrome: Symptoms

In CES, the wearer develops a loss of tolerance to
CORNEAL EXHAUSTION SYNDROME
their contact lenses, the onset of which is relatively
SYMPTOMS
sudden. At best, a decrease in wearing time is
reported, at worst, complete intolerance may be
• Reduced lens comfort
reported.

• Decreased wearing time

Symptoms include ocular discomfort, a reduction in
vision quality, and photophobia (after Sweeney,
1992).
• Blurred or fluctuating vision

97200-87S.PPT

7L297200-87

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 Module 7: Contact Lens-Related Ocular Complications

90 Corneal Exhaustion Syndrome: Aetiology

CORNEAL EXHAUSTION SYNDROME CES is a complex condition in which the signs

AETIOLOGY suggest the physiological limits of the cornea have
been exceeded.
• Long term wear of low Dk/t lenses Attention has been focused on the endothelium
(e.g. Kobari et al., 1990). Sweeney (1992)
• Chronic hypoxia
assessed the swelling response of several CES
• Acidosis patients experimentally to low or moderate
transmissibility contact lenses and found the
• Endothelial function is compromised response to be rapid and excessive. She
concluded that CES was probably a result of
97200-88S.PPT
endothelial dysfunction brought on by long-term
hypoxia and corneal acidosis. The resulting
7L297200-88 compromise in corneal hydration regulation leads to
excessive corneal oedema, subsequent contact
lens intolerance, and irregularities of refraction and
keratometry.
91 Corneal Exhaustion Syndrome: Management

CORNEAL EXHAUSTION SYNDROME Prevention of CES is achieved by using contact

MANAGEMENT lenses with high oxygen transmissibility. Refitting
the wearer is mandatory to enable them to continue
• High Dk/t lens to prevent occurrence lens use. If CES occurs with SCL wear, the best
option may be to refit with siloxane hydrogels, or
switch to RGP lenses.
• Refit with lenses of much higher Dk/t :
Some CES cases in reports by Pence (1988) and
- siloxane hydrogels Sweeney (1992) were fitted with higher
transmissibility lenses (rigid or soft) that were
- RGPs
successful initially. However, the transmissibilities
97200-89S.PPT
of lenses available at that time were not especially
high and these cases returned some 5 years (4-6)
7L297200-89 after refitting, with a repeat of CES, i.e. the problem-
solving lenses eventually became incapable of
satisfying the cornea’s requirements. This suggests
a declining capability of the cornea to maintain
control of hydration. Higher transmissibility lenses
usually resolved the issue for several more years.
The final outcomes for these wearers is unknown.
The general use of better performing lenses, and
the recent availability of very high transmissibility
lenses, means practitioners are no longer limited in
the magnitude of the improvements in lens
physiological performance they can offer CES
cases. Further, the almost universal abandonment
of the use of low transmissibility lenses in general
contact lens practice has meant the virtual
elimination of this condition.

52 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

II.I Corneal Vascularization

92 Corneal Vascularization: Introduction

CORNEAL VASCULARIZATION: Corneal vascularization is also termed
INTRODUCTION neovascularization, meaning literally ‘new blood
• Sometimes called neovascularization (new vessels’. Before new blood vessels become
blood vessels) apparent, or existing vessel appear to carry more
blood than previously, it is probable that significant
• Vessels observed are often not ‘new’
limbal redness was a chronic attendant feature of
• All lenses make limbal vasculature more lens wear, i.e. chronic limbal blood vessel dilation
obvious, RGP lenses and siloxane hydrogels may be a precursor to true neovascularization
produce the least obvious alterations (McMonnies et al., 1982).
• Need to distinguish between ‘new’ vessels
and filled ghost vessels
97200-224S.PPT

7L297200-224

93 Corneal Vascularization: Signs

CORNEAL VASCULARIZATION The earliest signs of neovascularization are usually

SIGNS spike-like, or branching, fine vessels emanating
from the normal limbal vasculature.
• Early signs are vessel spikes
A major issue is the difficulty of differentiating filled
• Branching capillaries from limbal arcade
limbal vessels that otherwise normally exist as
- episcleral vessels ghost vessels, and vessels that are vascularizing
(anterior ciliary artery) previously avascular corneal regions (limbal
transitional zone or cornea proper). McMonnies et
• Anterior or deep vessels
al. (1982) present definitions of vascularization (new
- level of stimulating pathology vessels in an avascular corneal region) and
97200-90S.PPT
neovascularization (new vessel growth in a
previously vascularized region). In would seem that
7L297200-90 their definitions are not widely used in the literature
and both terms appear to be used interchangeably.
94 Compounding the confusion surrounding
‘neovascularization’ is the anatomy of the
CORNEAL VASCULARIZATION vasculature of the anterior eye. The limbal arteries
SIGNS are derived from the conjunctival vessels that arise
from the episcleral branches of the anterior ciliary
• Limbal versus clear corneal involvement
artery. The conjunctival vessels form the superficial
• Transudate from limbal capillaries marginal plexus of the cornea. From the plexus
arise vessels that form the peripheral corneal
• Lipid deposits from deep vessels arcade (the forward extension) while others run
posteriorly to supply the perilimbal conjunctiva (after
• Ghost vessels Hogan et al., 1971, slide 95 is a meridional view of
the relevant anatomy).
97200-92S.PPT
Limbal vessel engorgement involves all the limbal
7L297200-92 and perilimbal vasculature because they are part of
the same ‘system’. A frontal view of the limbal
vasculature as well as the lymphatic system
appears as slide 64 in Module 1, Lecture 1.1.
Anatomically, the transition from conjunctiva to
cornea is usually smooth and gradual. The limbus
should not be thought of as a structural entity
(Hogan et al., 1971) but rather a zone of transition,
without a clear beginning or end. The anatomist’s
‘divisions’ appear in slide 95. As can be seen, the
demarcations are not axial but are oblique. An
encroachment of 1-3 mm into the cornea
encompasses most literature values for what
constitute ‘neovascularization’ (based on data
summarized in Efron, 1999).

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 Module 7: Contact Lens-Related Ocular Complications

95 McMonnies et al. (1982) found that soft lens

wearers showed greater limbal injection than did
ANTERIOR EYE VASCULATURE rigid lens wearers, the latter being indistinguishable
Limbo-scleral junction Corneo-limbal junction
ginal
from that of non-wearers. Further, they found the
cial Mar
Conjunctival Superfi
response to soft lenses to be similar to that when

Cornea
Plexus
Vessels

Ca
na
l
limbal capillaries fill with blood under the influence
Anterior Ciliary ’s

Artery hle
m
m
of vasodilating agents (in their study, ocular
Sc
Episcleral s Vein
pharmaceuticals).
Branch eou
Aqu

Iris
Arteries Major Holden et al. (1986) studied unilateral soft contact
Veins
Perforating
Branch
Simplified diagram
lens wearers and found that all lens-wearing eyes
Ciliary
Processes after Hogan et al.,
1971
showed more conjunctival hyperaemia and greater
Major
Arterial limbal vessel penetration (by some 0.5 mm) that did
Circle
97200-202S.PPT
the non-wearing eye.
7L297200-202 New vessels encroaching into the cornea may be
96 observed at any level. The depth at which they
penetrate from the limbus is usually dictated by the
underlying cause of the vascularization. Generally,
the deeper the new vessels are located, the greater
is the physiological compromise, i.e. the more
physiologically stressful the ‘cause’.
Vascularization of the cornea must be adequately
described and documented by the practitioner. The
key aspects of the documentation are the extent to
which the vessels encroach beyond the limbal
transition zone into the clear cornea, and their depth
(z-axis) within the cornea. Each of the corneal
quadrants should be assessed and described
independently.
7L21238-92
It is important to distinguish between dilation of the
existing blood vessels within the limbal zone (slide
97 96) and the growth of new vessels beyond the
corneo-limbal transition zone into the clear corneal
CORNEAL VASCULARIZATION tissue that is not normally vascularized (slides 98 to
SIGNS
100). Slide 98 shows a pannus-like formation of
• Description
blood vessels that was seen in some wearers of
• Documentation early soft lenses (thick, low water). As in this slide,
- extent of penetration most were superficial in nature (after Ruben, 1978).
- location Vascularization can be described as:
- depth x Intralimbal
- severity
x Corneal
• Assessment by quadrant
97200-91S.PPT The limbal capillaries are very fine and at times a
transudate may appear surrounding the tips of
7L297200-91
some of the vessels (slide 99). In direct retro-
illumination, this fluid is often visible as a ‘halo’
98 around the vessel, especially during periods of
anterior segment inflammation. A deposit of lipid
within the corneal stroma may occur in some cases.
Such manifestations are usually adjacent to blood
vessels and may become a permanent or semi-
permanent corneal feature.
While haemorrhages of corneal vessels (slide 101
shows a resolving intracorneal haemorrhage) are
rare, cases were reported by Laroche and
Campbell, 1987 (haemorrhage at Bowman’s layer),
Yeoh et al., 1989 (deep stromal haemorrhage),
Cavallerano and Weiner, 1990 (a diabetic aphake
with intrastromal haemorrhaging), Cavallerano,
7L21116-99 1990 (no apparent cause), and Donnenfeld et al.,
1991 (deep stromal haemorrhages). The latter
54 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

99 found that most involved deep stromal

neovascularization that developed insidiously,
usually without acute symptoms. Most, but not all,
cases involve aphakic (therefore post-surgical)
eyes. The risk in cases of deep stromal
neovascularization even without haemorrhage was
found to be that of visual loss caused by lipids that
had leaked from the new vessels (Rozenman et al.,
1989).
McMonnies (1983) claims that established blood
vessels do not regress when the stimulus is
removed, rather they remain as ghost vessels with
the potential to become active carriers of blood
within a short period of time.
In general, neovascularization is a sign of chronic
corneal hypoxia (and the resulting oedema), while
deep stromal vascularization is a sign of serious
hypoxia or anoxia.

7L2NEOVASC

100

7L20557-98

101

7L21003-91

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 Module 7: Contact Lens-Related Ocular Complications

102 Corneal Vascularization: Symptoms

Vascularization of the cornea occurs in the absence
CORNEAL VASCULARIZATION
SYMPTOMS
of symptoms (McMonnies, 1983). Generally, there
is no reason why SCL wearers who have
vascularization should be symptomatic as it is
• Asymptomatic usually due to chronic hypoxia (see earlier in this
lecture). For this reason it is important to assess
• Vascularization may accompany the peripheral cornea of contact lens wearers at
every after-care visit.
painful anterior segment disease
In some severe conditions such as a chemical burn
to the cornea, the process of vascularization can
97200-93S.PPT
occur very quickly and can be accompanied by
significant symptoms. This contrasts with the slow,
7L297200-93 painless process that occurs in susceptible contact
lens wearers.
103 Corneal Vascularization: Aetiology

CORNEAL VASCULARIZATION The potential causes of corneal vascularization are

POSSIBLE AETIOLOGIES numerous.
• Vaso-proliferative stimuli include: Corneal oxygen requirements vary between
- angiogenic factors (existing vessels) individuals. As an individual’s response to contact
- tight-fitting lenses lens wear cannot be predicted, the need for a
- lactic acid build-up meticulous examination of the external eye during
- oedema (not in isolation) the course of lens wear cannot be over
- inflammatory mediators emphasized.
- trauma/disease
- keratocytes and inflammatory cells Lens-induced corneal vascularization is often
- neural control related to the hypoxia caused by the inadequate
97200-94S.PPT
oxygen transmissibility of conventional hydrogel
7L297200-94
lenses. Typically, the growth of vessels into the
cornea occurs after some period of time and
moderate levels can develop within six months of
104 EW (Dumbleton et al., 1998). The length of this
latent period is dictated by a number of factors
CORNEAL VASCULARIZATION including:
AETIOLOGY
x Wearing schedule.
• Individual susceptibility
x Lens oxygen transmissibility.
• Long-term contact lens-induced hypoxia x Individual variability.
In a study of monkeys wearing EW hydrogel lenses,
- more common in extended wear
Madigan et al. (1990) found deep stromal
• Latent period vascularization accompanied by keratocytes,
extravascular leukocytes including macrophages,
97200-95S.PPT
lymphocytes and, less commonly, neutrophils. They
postulated that apart from hypoxia, another possible
7L297200-95 cause is the release of a macrophage angiogenic
factor, i.e. a factor that encourages and facilitates
the growth and travel of new blood vessels.
Summary:
x Metabolic Theory:
– Hypoxia: Hypoxia is considered to be the
predominant cause but the actual
mechanisms by which it affects vasculature
are unknown.
– Lactic Acid: A known result of hypoxia. Tight
fitting lenses may aid the accumulation of
lactic acid in the cornea by constricting
venous drainage from the anterior eye.
– Oedema: Usually a precursor of
56 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

neovascularization but no mechanism has

been suggested.
– Stromal softening: The result of corneal
oedema in which the normally compact
stroma eventually provides less resistance to
the proliferation and passage of new blood
vessels or the extension of the existing ones.
x Angiogenic Theory: See above, or Madigan et
al., 1990).
x Angiogenic Suppression Theory: A factor
postulated to be present in the normal cornea
suppresses division and migration of vascular
cells. Anything that interferes with such
suppression will result in vascular proliferation.
x Neural Control Theory: The vasculature is
controlled by corneal neurology and interference
with these processes by contact lenses may
result in neovascularization.
The mere presence of a lens is not a factor because
siloxane hydrogel (flexible) lenses did not result in
episodes of vascularization or limbal redness
(Papas et al., 1997, Dumbleton et al., 1998).
No single theory can explain all observations
associated with neovascularization but no unified
theory has been accepted to date.
105 Corneal Vascularization: Management
The key to successful management of ‘corneal
CORNEAL VASCULARIZATION
MANAGEMENT vascularization’ is the early detection of vessel
spikes or buds, and the extension of vessels within
• Acceptable level of vessel growth the limbal region. Such vessel changes should not
be permitted to progress to vascularization beyond
- budding
the corneo-limbal transition zone. Careful
- limbal or clear cornea monitoring is required because ghost vessels fill
rapidly.
• Optimize lens fitting
Problems with lens fit should be either resolved or
• Increase lens Dk/t optimized, and oxygen transmissibility increased to
97200-96S.PPT
better meet the corneal oxygen demand.
7L297200-96 Corneal pannus that developed in SCL (and PMMA)
wearers was reported to have been reversed
successfully by refitting with RGP lenses by Chan
106 and Weissman (1996).
Even with the best hydrogel lenses, oxygen supply
CORNEAL VASCULARIZATION
MANAGEMENT
to the cornea is insufficient for some wearers.
Therefore, in these cases it is prudent to
• Change lens solutions recommend the use of RGP lenses that avoid the
• Patient education and follow-up limbal area altogether, or the newer siloxane
hydrogels that can better meet the needs of most
• Optimize fitting characteristics corneas. Modifying the wear mode or wearing
times may also be required.
• Decrease wearing time
If an adverse response to a lens care product is
• Refit with siloxane hydrogel or
suspected of being a contributing factor, the cause
RGP lenses should be investigated by a process of elimination of
97200-97S.PPT

potential causes. Once the cause has been

7L297200-97 determined, a suitable substitute should be
prescribed.

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 Module 7: Contact Lens-Related Ocular Complications

II.J Corneal Oedema-Induced Refractive Changes

107 Corneal Oedema-Induced Refractive Changes:
Introduction
OEDEMA-INDUCED REFRACTIVE
Although the physiological effects of CLs may be of
CHANGES: INTRODUCTION
greater concern, it is imprudent to ignore any effects
• Often neglected aspect of CL practice as lenses may have on vision and/or refraction. These
‘physiology’ issues are pursued changes may be simple refractive changes
(resulting in refractive blur) that are correctable, or
• Changes are usually small with SCLs
‘spectacle blur’-type changes (non-refractive blur)
- spectacle blur uncommon that do not respond to correction by lenses.
• Changes are usually myopic Generally, the incidence of SCL-induced refractive
• Changes are usually slow (weeks, months)
changes have been low (usually a myopic shift)
97200-259S.PPT
(e.g. Knoll et al., 1970, Masnick, 1971, Sarver,
1973, Gasson, 1989, Lowther and Tomlinson, 1979,
7L297200-259 Lowther, 1994).
EW is more likely to cause greater refractive
changes over time than DW of similar lenses, and
usually take weeks or months to develop to the
stage of clinical significance (Lowther, 1994).
Changes are more likely to be induced by thick, low
water, toric, or high-Rx lenses, i.e. lenses of low
Dk/t.
108 Corneal Oedema-Induced Refractive Changes:
Signs
OEDEMA-INDUCED REFRACTIVE
CHANGES: SIGNS Apart from the signs of corneal oedema (covered
• Corneal oedema
earlier in this section), the only other sign(s) of
oedema/hypoxia may be an altered subjective
• Decreased acuity on testing
refraction and/or reduced (i.e. less than pre-fitting)
• Usually, corneal curvature also altered
visual acuity, with, and especially without, contact
- may be steeper or flatter
lenses.
- meridians of one eye can change in
opposite directions The refractive state should be ascertained
- eccentricity may also be altered immediately after lens removal (Lowther, 1994). No
• Correlation between changes in curvature apparent reason for any reduction may be obvious,
and Rx often poor e.g. the lenses may be in good condition. If the pre-
97200-260S.PPT

lens wear spectacle Rx is known, any alteration to

7L297200-260 the refractive state is determined easily. If pre-lens
fitting data is unavailable, the presenting acuity and
refraction data must be interpreted.
109
Hazlett (1969), Bailey and Carney, (1972, 1973),
OEDEMA-INDUCED REFRACTIVE and Hill (1975), found that lens-induced corneal
CHANGES: SIGNS thickness increases are not usually accompanied by
Refractive changes (greater in EW):
• Determine after lens removal significant changes in corneal curvature.
• Maximum spherical change <–0.50D (<0.1mm) Furthermore, despite corneal swellings of up to
- hyperopic shifts have been reported 8.3%, the curvature changes that did occur
• Maximum cylindrical change <0.33D (<0.06mm)
- flattening initially, steepening eventually
correlated poorly with changes in refraction ( Bailey
• Irregular changes uncommon and Carney, 1972, 1973, Hill, 1976, Saks, 1979).
• Over-Rx should agree with change measured A summary of changes reported with SCLs follow:
after lens removal
• Recovery may be:
x Increases in myopia of up to 0.50D mostly
- rapid after lens removal
- nil 97200-261S.PPT
occurring in the first few days, and certainly
within the first month, e.g. Harris et al. (1975),
7L297200-261 Hill (1975), Barnett and Rengstorff (1977),
Rengstorff and Nilsson (1985), Dumbleton et al.
(1999), and Fonn et al. (2002).
x Some studies, e.g. Harris et al. (1975), Hill
(1976), and Miller et al. (1980) reported a
significant correlation between corneal
steepening and the increase in myopia found,
58 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

110 while others, e.g. Hill (1975), Barnett and

Rengstorff (1977), Tomlinson (1979), and
‘MYOPIC’ SHIFT: EFFECT OF Dk Høvding (1983B), did not. Significantly, any
after Fig. 4, of Dumbleton et al., 1999
myopic shift found was also found to correlate
+0.10D
with an increase in corneal thickness
measured. Some refer to this as

EW
0
Rx SHIFT (dioptres)

Low-Dk EW

k
myopia/myopic creep, e.g. Marohn and Henry

h-D
–0.10D

Hig
–0.20D Low-Dk DW (1994).
–0.30D x Harris et al. (1975) and Hill (1976) noted an
–0.40D increase in with-the-rule corneal toricity that
persisted. This does not necessarily equate to
–0.50D
0 3 6 9 0 3 an increase in manifest WTR ocular
TIME (months)
97200-309S.PPT astigmatism because of the poor correlation
between curvature and refractive changes.
7L297200-309
x Initial flattening, and subsequent steepening
(<0.50D), was reported by Grosvenor (1975),
Barnett and Rengstorff (1979), and Høvding
(1983).
x Dumbleton et al. (1999) reported a myopic shift
in low-Dk, SCL, myopic EW of 0.30D that did
not occur in a similar group of subjects wearing
high-Dk, siloxane hydrogel lenses. Any
recovery that followed switches from low-Dk
EW to low-Dk DW, and finally to high-Dk EW
was studied in a subset of the subjects. A
recovery of 0.37D was found from the nine
month shift of –0.25 for this subset (max. about
0.45D at six months) (slide 110).
x Sweeney (2000) reported that long-term,
disposable SCL wearers who were refitted with
siloxane hydrogel lenses, showed a reduction
in myopia of about 0.25D after 12 months of
siloxane hydrogel lens wear.
Before one concludes that a change in myopia in
the longer term (years) is contact lens-induced, the
findings of Ellingsen et al. (1997) warrant
consideration. They concluded that a population of
normal, uncomplicated, adult, non-contact lens-
wearing myopes should be considered a separate
sub-group of the general population. This group’s
Rx changes per decade were reported to be:
x 20s: –0.60D.
x 30s: –0.39D.
x 40s: –0.29D.
x 50s: +0.28D.
x 60s: +0.41D.
Given that the majority of contact lens wearers are
myopes, it would seem that only changes on
average beyond those suggested by Ellingsen’s
group should be considered as true ‘alterations’ in
refractive status.
If the presence of spectacle blur is suspected this
also needs to be confirmed (see Corneal Oedema-
Induced Refractive Changes: Management) as a
mixture of refractive change and spectacle blur is
possible. If lens wear is discontinued, or the wearer
is refitted with siloxane hydrogels, and myopia

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 Module 7: Contact Lens-Related Ocular Complications

decreases subsequently, it is reasonable to assume

that the increase in myopia was lens induced.
111 Corneal Oedema-Induced Refractive Changes:
Symptoms
OEDEMA-INDUCED REFRACTIVE
CHANGES: SYMPTOMS The most obvious symptom is reduced acuity when
contact lenses are worn. Reduced VA is also
• Reduced vision: reported with spectacles of the same effective
correction.
- diffusive blur
Usually, small decrements in visual acuity are not
- refractive blur reported. Instead, they are ‘discovered’ during an
• Often, none – change is uncovered after-care visit that is either routine, or not vision-
related. Any change in mean refractive error with
during a consultation or after-care visit
SCLs is likely to be small (0.25-0.30D, but the range
97200-262S.PPT
can be as much as 1.50D) unless the lenses have a
low Dk, i.e. thick, low water, toric or high Rx lenses.
7L297200-262 However, McLennan (1988) reported manifest
corneal astigmatism induced by the use of thick
toric, and high-Rx spherical, SCLs. Schornack
(2001) also reported corneal warpage in a SCL
wearer.
The effects of oedema on vision depend on its
aetiology (e.g. hypoxia or tonicity changes) and/or
location (e.g. epithelial [more debilitating] or
stromal) (see discussion earlier in this section, and
Carney and Jacobs, 1984).
To help differentiate refractive blur, i.e. blur due to
uncorrected astigmatism, under or over-correction
of spherical ametropia, or a change in refractive
error induced by lens wear, from other types of blur,
i.e. hypoxic or hypo/hypertonic, a simple pin-hole
test is probably all that is required. If the pin-hole
acuity is better than the normal acuity, then a
refractive ‘error’ is very likely. However, diffractive
blur could also occur.
112 Corneal Oedema-Induced Refractive Changes:
Aetiology
OEDEMA-INDUCED REFRACTIVE Support for an oedema aetiology
CHANGES: AETIOLOGY
• Poor lens physiological performance x The lack of a consistent relationship between
- corneal hypoxia changes in corneal curvature and any
- greater with thick lenses (low Dk/t & n rigidity) concurrent refractive state meridionally, or
• Uneven corneal swelling: overall (see Corneal Oedema-Induced
- different local Dk/ts under lens Refractive Changes: Signs) suggests that the
- lens design factors refractive changes involve more than just the
- differing BVPs
anterior corneal surface (Rengstorff, 1971,
• Corneal ‘softening’
Barnett and Rengstorff, 1977, Bier and Lowther,
- corneal molding (individual characteristic)
97200-263S.PPT 1977B). Other possible explanations include
changes to: posterior corneal curvature, corneal
7L297200-263
thickness, corneal refractive index, and anterior
chamber depth.
x Short-term studies show complete reversal of
SCL-induced myopic changes when refitted with
siloxane hydrogel lenses (high Dk/t) (Dumbleton
et al., 1999, Sweeney, 2000). As these
reversals involved the use of more rigid (cf.
conventional hydrogels) siloxane hydrogel
lenses, it seems unlikely that corneal shape was
a significant factor either in the original changes,
or in their reversal.

60 IACLE Contact Lens Course Module 7: First Edition

Lecture 7.2: SCL Complications and Their Management

x Any changes that did not reverse completely

may not be exhibiting an induced change at all
(see Ellingsen et al. 1997), or may have been
experiencing a mixture of induced and other
changes.
x Harris et al. (1975), Saks (1979), Dumbleton et
al. (1999), and Sweeney (2000) postulated that
the myopic shift they found was due to contact
lens-induced hypoxia interfering with corneal
metabolism. Importantly, Dumbleton et al.
(1999) reported that the myopic changes they
found in their low-Dk EW cases, showed a
myopic shift early in the trial rather than later.
This suggests an oedema-based aetiology
rather than a molding one because the latter is
more likely to be dose dependent (duration of
exposure) (Høvding, 1983B).
x The reversibility of EW-induced myopia and the
fact that the same lenses worn on a DW basis
do not induce myopia, support the oedema
theory (hypoxia-induced corneal swelling) over
the alternative molding theory.
Support for a molding aetiology
x Hill (1976B) and Bradley and Schoessler (1979)
found that thicker lenses (0.1 to 0.2 mm as
opposed to 0.06 mm), changed corneal
curvature or manifest refraction significantly.
This suggests a mechanical factor (e.g. lens
rigidity) is implicated in changes in refraction.
Grosvenor (1975) postulated that the changes
he found were due to widespread (whole of the
cornea) oedema, mechanical pressure
(molding, especially in steeper fits), and
possibly tightening of the lens due to
dehydration in situ.
x Carney (1975) and Larke (1985) conceded that
while most topographical changes were due to
non-uniformly distributed corneal thickness
changes and/or mechanical molding, there were
few such changes associated with most lens-
induced corneal swelling. Non-uniform corneal
swelling is mainly the result of the varying local
Dk/ts that exist under lenses, especially those
with refractive power. The physiological basis
of this swelling unevenness was confirmed by
Carney (1975B) who demonstrated that a 100%
oxygen atmosphere in front of a contact lens
virtually eliminated all corneal swelling in all
corneal locations.
x Complicating the topographical swelling issue is
the peripheral ‘anchoring’ of the cornea by the
sclera and the limits this places on perilimbal
corneal swelling, (see Bonanno and Polse,
1985, and Bonanno et al., 1986).
Regardless of the foregoing, the aetiology of these
changes remains unclear. On balance, the
probable cause is corneal oedema even if it is
subclinical. However, it is reasonable to assert that
the root cause of corneal change is hypoxia.

IACLE Contact Lens Course Module 7: First Edition 61

 Module 7: Contact Lens-Related Ocular Complications

113 Corneal Oedema-Induced Refractive Changes:

Management
OEDEMA-INDUCED REFRACTIVE
Hill (1976B) and Saks (1979) advised practitioners
CHANGES: MANAGEMENT
• Try to determine if Rx change is lens-induced
not to assume myopic shifts occurring during
successful contact lens wear in the relatively short
• Refit with lenses with superior physiological
characteristics term (weeks and months) were ‘normal’. They
- use thinner lenses suggested that those showing an increase in
- fit siloxane hydrogels from the start myopia be refitted with lenses offering superior
- use lenses with lower rigidity physiology, and they be monitored carefully
• Monitor eyes exhibiting change more closely subsequently.
• Treat larger than acceptable changes more It is necessary to established that any myopic shift
seriously (set limits for what is ‘acceptable’) is due to the lens(es) (more likely in EW).
97200-264S.PPT

Depending on their magnitude, reversal of lens-

7L297200-264 induced refractive changes can take months
following cessation of lens wear. If reversal occurs
quickly, the wearer should be refitted with siloxane
hydrogels especially if EW or CW is desired.
Should the VA decrease correlate poorly with the
over-Rx, or the end point of a spectacle refraction
after lens removal be ambiguous, i.e. VA not as
expected, pinhole aperture does not improve VA,
etc., spectacle blur is confirmed. However, true
spectacle blur usually subsides after either lens
removal, and/or a sleep period without lenses. If
this is not the case, corneal changes and/or
refractive changes have occurred, necessitating
further investigation.

62 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

III Inflammation and Infection

III.A Effects: Ocular Discomfort

114 Lens-Induced Ocular Discomfort: Introduction

OCULAR DISCOMFORT: Most conditions affecting the eye disclose their
INTRODUCTION presence by induced ocular discomfort.
• Probably the most common contact
lens-induced condition
• May be accompanied by redness and
corneal staining
• Must consider the possibility that it is not
contact lens related
• Various descriptions may be used
• Descriptions may be misleading
97200-223S.PPT

7L297200-223

115 Lens-Induced Ocular Discomfort: Signs

The most common sign associated with ocular
DISCOMFORT
SIGNS discomfort is an apparent increase in the redness
(see next topic) of the eye. Typically, this is
• Bulbar and/or palpebral hyperaemia of the bulbar and/or palpebral
conjunctival redness conjunctiva with the other areas, e.g. ciliary and
episcleral, affected in more serious conditions, or
• Staining (with sodium when the uvea is involved.
fluorescein, Rose Bengal,
In some cases, the presence of significant sodium
Lissamine Green) fluorescein staining (or staining by another agent) of
the anterior eye’s surface may also be a feature
• May be none
97200-98S.PPT
(after Lowther, 1993).
7L297200-98 The lens per se should also be considered when
signs are being assessed as lens signs (see slide
116 opposite) may also provide valuable
116 information. These signs are more likely to be
observed in cases reporting discomfort and/or
DISCOMFORT dryness. Detection of these signs may play a role in
LENS SIGNS determining or confirming the cause of the
• Surface drying symptoms reported. Loss of tear film lubrication
(dry lens surface) and/or lack of a smooth surface
(surface deposits) will decrease comfort and
• Surface deposits
probably increase traction between lid and lens,
leading to increased blink-induced lens movement.
• Excessive lens movement
Should the wearer have a ‘dry eye’, the drying of the
lens surface and/or the accumulation of deposited
• Defect or damage tear debris on the lens surface are a logical sequel
97200-247S.PPT
with negative wearer comfort ramifications.
7L297200-247

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 Module 7: Contact Lens-Related Ocular Complications

117 Lens-Induced Ocular Discomfort: Symptoms

At some stage most contact lens wearers
DISCOMFORT
SYMPTOMS
experience some degree of discomfort while
wearing lenses. The discomfort reported can range
from very mild to somewhat painful. The response
• Mild to painful to uncomfortable lenses has been studied by
Chalmers et al. (1995). They found that 57% of
• Vague to specific wearers (study size, n=2,200) continued wearing
lenses, 42% removed their lenses, 37% rinsed their
- can indicate cause eyes with saline, and only 21% contacted their
contact lens practitioner.
97200-99S.PPT
While it is logical to implicate contact lenses should
a wearer present with discomfort, it is prudent to
7L297200-99 remember that the discomfort may not be related to
contact lenses.
Discomfort is a difficult entity to describe and the
veracity of patient responses often depends on their
verbal communications skills.
Both open (reply can be descriptive) and closed
(reply can only be a yes or a no, or one of two or
more alternatives presented by the practitioner)
probing (questioning) should be used when
elucidating the wearer’s history and investigating
their complaint. Nothing the practitioner says
should deter the wearer, intentionally or otherwise,
from volunteering any type of information.
Questions should also elicit information that the
wearer has either forgotten or not associated with
the clinical issues at hand (this section after Covey
and Munro, 1999).
Covey and Munro (1999) suggest the following
questions be included:
x When does the discomfort occur? On lens
insertion, on lens removal, during work, in the
evening, using a computer, etc.
x What type of discomfort is it? Itching, grittiness,
dryness, foreign body sensation, stinging,
burning, painful.
x How severe is the discomfort? Mild, moderate,
severe.
x How long does the discomfort last? Seconds,
minutes, hours, as long as lens is on eye.
x Does the discomfort resolve, and if so, what
makes it better? Lens removal, lens insertion,
in-eye comfort drops, turning-off the air-
conditioner, removing, cleaning, and reinserting
the lens.
Additional questions could be added:
x One eye or both eyes?
x If both eyes are involved are they:
– affected equally?
– affected at the same time?
– affected for the same time?
– made better by the same factor(s)?
– made better equally rapidly?

64 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

If a wearer has been knowingly non-compliant, it is

probable that they will avoid ‘incriminating’
themselves in the aetiology of the problem(s) they
present (after McMonnies, 1989).
Although careful questioning is time consuming, the
temptation to ‘cut corners’ should be resisted, as the
costs to both the wearer and practitioner are
118 potentially high.
DISCOMFORT The most likely symptoms to be reported in
SYMPTOMS association with discomfort are presented in slide
• Dryness 118.
• Itchiness Sometimes the level of discomfort described by the
patient can help determine the underlying cause of
• Grittiness (scratchiness) the problem. However, in many cases discomfort is
• Watery described in very vague terms that may be of little
diagnostic value. Worse, the relationship between
• Stinging/burning the severity of the pain reported and the apparent
• Pain cause is not direct (or can even be inverse) and can
97200-248S.PPT therefore mislead.
7L297200-248 Prevention or resolution of ocular discomfort is
important to contact lens wear in general, and RGP
lens wear in particular, because 18% of RGP
discontinuations are due to comfort issues (Holden,
1990). Conventional hydrogel lenses are not
discontinued as frequently because of discomfort
but significantly, some 20% - 50% of SCL wearers
report discomfort and dryness (Fonn et al., 1999)
although the figure could be as high as 75% (see
Brennan and Efron [1989] below).
In a study of 199 self-identified contact lens failures,
Schlanger (1993) reported that 72% claimed their
failure was due to comfort issues. After refitting,
Schlanger claimed 82% (of all 199 failures) returned
119 to successful contact lens wear.
Pritchard et al. (1999) surveyed a large number of
CONTACT LENS DROPOUTS
Surveys Returned
from: Pritchard et al., 1999 contact lens wearers with specific reference to
n = 1,444 4,415 questionnaires
16 practices, Quebec, Canada temporary or permanent abandonment of lens wear
34% Dropouts 66% CL Wearers
(slide 119). They found that, of the wearers that
n = 488 n = 956
had discontinued wear, 49% had been refitted at
least once for discomfort. They also found that the
22% Permanent 1% Unknown 77% Resumed CLs
n = 105 n=5 n = 378 primary reasons for abandoning lens wear were
discomfort, dryness, and red eyes.
48% Dropouts 2% Unknown 50% Continued CLs
n = 10 n = 187
Brennan and Efron (1989) studied 104 HEMA lens
n = 181

35% Permanent 3% Unknown 62% Resumed CLs wearers and found dryness was reported more
n = 63 n = 15
97200-249S.PPT
n = 113
frequently than scratchiness or wateriness. In their
study only 25% of subjects reported never noticing
7L297200-249 symptoms of ‘dryness’. Significantly, they also
found that users of oral contraceptives were more
likely to report symptoms of scratchiness and
dryness than non-users. Symptoms of dryness
were also reported more frequently by wearers of
older lenses (>6 mth).
Low relative humidity (RH), as occurs in particular
climates or air-conditioned environments, can
contribute to symptoms of dryness/discomfort. A
survey by Orsborn and Robboy (1989) found
greater dryness problems resulting in reduced
wearing times in a land-bound US state (low RH)
than in a coastal state (high RH).

IACLE Contact Lens Course Module 7: First Edition 65

 Module 7: Contact Lens-Related Ocular Complications

Peyton et al. (1989) reported dryness symptoms

after 3 months (as well as a 27% incidence of
epithelial staining) in one-third of contact lens
wearers who were using a vasoconstrictor
(preservative: benzalkonium chloride) daily.
Itchiness was described as a hallmark of allergic
changes (lens and non-lens related) by Covey and
Munro (1999). While possibly unilateral, it is more
commonly presented bilaterally especially in the
more severe cases. Symptoms are usually only
experienced while lenses are worn and they may
increase in severity during the wearing period.
Upper lid changes (CLPC) may occur and the
severity of the symptoms generally gets worse over
time. Wearers may report increased lens
awareness and mild foreign body sensations
emanating from the altered upper lid. Paradoxically,
the itchiness may increase immediately after lens
removal and then subside. Patient complaints may
include:
x Reduced wearing time.
x Loose lens feelings.
x Occasional blurry vision.
x Increased lid/lash encrustation and discharge
on awakening.
x Stringy discharge.
Grittiness (scratchiness, foreign body sensation)
usually only occurs when a lens is on the eye. The
lens itself is the most probable cause. Less
disturbing levels may accompany lens insertion or
may become apparent after a period of lens wear.
Mild or more severe sensations are most likely to be
due to lens defects and are usually accompanied by
obvious redness, and tearing/watery eyes (Covey
and Munro, 1999). Symptoms that persist beyond
lens wear may not be caused by the lens either at
all or only partially.
If paradoxical symptoms are reported, i.e.
symptoms only appear after lens removal, then an
epithelial defect should be suspected. The lack of
symptoms during lens wear can be explained by the
lens’ bandage effect.
Wateriness of the eyes (other than as an adaptive
symptom which is ignored here) can result in
blurred vision, alterations to lens fit, increased lens
mobility, and even tear overflow (epiphora). Lens
defects, infective keratitis, sterile keratitis, and acute
toxicity are possible causes (Munro and Covey,
1998).
Stinging is most probably caused by a sensitivity to,
or inappropriate use of, lens care products. Onset
is usually at or soon after insertion of a lens carrying
variable amounts of lens care product on and in the
lens. While the incidence of such reactions is now
low due to the evolution of these products over
some 50 years, the possibility should never be
ignored.
Other environmental factors such as chemical and
66 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

industrial pollutants, or household products such as

hair care products and cosmetics, also warrant
consideration when investigating possible causes.
Pain is a nebulous symptom when the presentation
is mild and the tolerance to it varies with individuals
and possibly by sex (females are probably more
tolerant). The most likely causes are the presence
of a foreign body trapped under the lens and
inflicting significant corneal damage, or microbial
keratitis (MK). The pain associated with the latter is
likely to be accompanied by photophobia,
mucopurulent discharge, excess tearing, unilateral
redness, and possibly a disturbance of vision
depending on the location of the lesion, i.e. in, near,
or beyond the visual paraxial zone (after Covey and
Munro, 1999).
Except in wearers of very thin, high water lenses in
which pervaporation is a known problem, the cause
of the dryness/discomfort remains unclear. The
symptoms correlate poorly with lens hydration and
BUT with the exception of Lowther’s 1993 study that
showed a significant decrease in BUT and
lactoferrin levels, and increased fluorescein staining
in symptomatic SCL wearers.
120 Lens-Induced Ocular Discomfort: Aetiology
Frequently, the aetiology of ocular discomfort is
DISCOMFORT
AETIOLOGY
multifactorial in origin. This makes it difficult to
determine the cause of any discomfort. A wide
• Multiple aetiologies range of physical, physiological, and psychological
factors need to be considered during history taking.
- physical
All of the causes shown in the slides opposite
- physiological
should produce a spontaneous response that the
- psychological patient expresses as discomfort or, if the condition
is severe, as pain. This is much more likely if the
• Careful questioning of the patient cornea is involved rather than the conjunctiva.
97200-100S.PPT
Acute:
7L297200-100 Acute discomfort /irritation is more likely to be
perceived as localized. In most instances, the
causes will produce corneal/conjunctival damage
121 resulting in cell loss and exposure of superficial
nerve fibres as the triggering mechanism.
ACUTE DISCOMFORT Sometimes the discomfort is worse when the lens is
AETIOLOGY
• Mechanical removed because the lens acted as a bandage
- foreign body (debris trapped under lens) while on the eye.
- ocular surface damage
• Toxicity
- solution mediated
• Lens defect
- surface
- edge
• Edge: shape & thickness
• Lens fit (too tight, too loose)
• Infection/inflammation
97200-283S.PPT

7L297200-283

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 Module 7: Contact Lens-Related Ocular Complications

122 Chronic:
The causes of chronic discomfort/irritation are
CHRONIC DISCOMFORT usually multifactorial as listed in the slides opposite.
AETIOLOGY What makes discomfort so difficult to understand is
• Drying of the lens front surface that patients can express the symptoms in a
number of ways, e.g. as dryness, grittiness, burning,
• Drying of the exposed conjunctiva itching, etc. Usually, the symptoms become worse
• Depletion of the post-lens tear film
towards the end of the day/evening and many
patients will report reduced wearing time.
• Reduced lubricity of the lens front surface Although many causes have been listed, it appears
• Tightening of the lens fit
that if contact lenses were adequately permeable to
97200-284S.PPT
oxygen a number of factors contributing to
discomfort would be eliminated. Adequate
7L297300-284 permeability would reduce corneal hypoxia,
eliminate conjunctival hyperaemia, and help sustain
a normal tear film, i.e. one not carrying inflammatory
123 or other cells, and metabolic by-products, thereby
minimizing friction at both lens surfaces.
CHRONIC DISCOMFORT
AETIOLOGY After evaluating 50 SCL wearers, Bruce et al. (1995)
• Front & back surface deposits postulated that the exposed bulbar conjunctiva,
rather than the interaction between the anterior lens
• n lens movement surface and the tarsal conjunctivae or tear film
• Limbal/conjunctival hyperaemia instability, was the source of soft lens discomfort.
Importantly, they also found that comfortable lens
• Hypoxia & retention of metabolic by-products
wear allowed more than 50% greater wearing time.
• Hypersensitivity to preserved solutions
A less likely cause is indoor air quality, e.g. Sick
• Altered conjunctival sensitivity Building Syndrome (SBS). In one study of 12 public
97200-285S.PPT
buildings and their 877 occupants, 29% reported
7L297200-285 ocular discomfort (contact lens wearers were not
identified and studied specifically) (Backman and
Haghighat, 1999).
Another possible cause is Meibomian Gland
Dysfunction (see Section III.E Meibomian Gland
Dysfunction (MGD)). The hyposecretion of lipids
can cause ocular discomfort as well as ocular
surface abnormalities (Shimazaki et al., 1995).
124 Lens-Induced Ocular Discomfort: Management
DISCOMFORT Management of ocular discomfort in contact lens
MANAGEMENT wearers is more difficult when no obvious cause of
• Can be difficult to alleviate the discomfort can be determined. While it is
• Optimize lens: always prudent to consider the possibility that the
- fitting discomfort in not contact lens induced, such a
- care question is more relevant when no apparent cause
- replacement schedule is found despite a comprehensive investigation.
• Change: Ignoring the possibility that the discomfort is caused
- material (to higher or lower water content) by something else may mislead the practitioner and
- change lens design result in a fruitless, time-consuming investigation.
• Use dehydration-resistant lens
97200-101S.PPT
Clear-cut causes such as defective lens edges, lens
deposits, tight lens fits, or solution toxicity are easily
7L297200-101 dealt with and should bring about almost immediate
relief from symptoms.
In other cases the practitioner’s skill in relating the
patient’s symptoms to subtle signs, or interpreting
the symptoms on their own, dictate the course of
management.
If the cause of discomfort is not found and changing
lenses, lens design, or lens care fails to resolve the
discomfort satisfactorily, the practitioner essentially

68 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

has two choices. Either seek the opinion of, or refer

to, a learned colleague, or consider the patient to be
unsuccessful.
While success rates of 100% are virtually
impossible to achieve, the vast majority of problems
can be resolved satisfactorily and in a timely
manner.
Significantly, McMonnies (1987) found that 36% of
after-care remediation involved non-technical
aspects of lens fitting, e.g. patient education, re-
education, advice and counselling.
The use of lubricants or different lens care products
may help. If removing and rinsing the lenses before
reinsertion helps alleviate the discomfort this
suggests a tear volume problem may be in play
(see Lecture 7.4).
III.B Effects: Ocular Hyperaemia

125 Ocular Redness: Introduction

Like baseline levels of conjunctival redness in non-
OCULAR REDNESS: INTRODUCTION wearers, the degree of ocular redness observed in
• Subject to individual variation contact lens wearers is subject to individual
• Pre-lens wear assessment is essential
variation. Because of this it is important to establish
the baseline level of redness for each patient prior
• Need to assess: to the commencement of lens wear.
- location of redness
Ocular redness is relatively common in SCL
- extent of redness wearers. Vajdic et al. (1999) reported that redness
- depth of vessels involved occurred often or constantly in 16% of SCL wearers.
- type (bulbar, tarsal, limbal) Abnormal ocular redness can present in a variety of
97200-222S.PPT
forms each of which can assist potentially in
7L297200-222
determining the underlying cause. Three primary
factors that must be evaluated are the:
x Location of the redness.
x Extent of the redness.
x Depth of the vessels involved.
126 Ocular Redness: Signs
Ocular redness is more likely to be detected in the 3
OCULAR REDNESS
SIGNS & 9 o’clock ‘triangles’ (after Munro and Covey,
1998) (see slide 127) bound by the canthi (as the
• Location may be:
apices) and the corneal limbus (as the bases). The
- localized upper and lower lid margins act as the sides of the
- sector ‘triangles’. These are also the most exposed parts
of the eye.
- diffuse
An exception is redness resulting from a foreign
- bulbar and/or limbal
body (FB), in which case the redness is usually
• Deep and/or superficial vessels greatest (at least initially) in the quadrant of the FB
97200-102S.PPT
itself. Usually, FB-induced redness is accompanied
by acute symptoms of discomfort.
7L297200-102
Edge defects, or other imperfections, can be
expected to cause limbal and bulbar redness (slide
132) and staining in a matching arcuate pattern
(slide 133), assuming that the lens is rotating on the
eye.
Deeper episcleral vessels are unlikely to be involved
in contact lens-induced redness (see slide 128)
unless there is an attendant or concurrent uveitis,

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 Module 7: Contact Lens-Related Ocular Complications

127 (acute onset), or the mechanical irritation is

moderate to severe (see slides 135 and 136 that
show engorgement of deeper conjunctival and
episcleral blood vessels) (after Munro and Covey,
1998).
With an acute toxic response, severe limbal and
bulbar redness will be seen, along with diffuse
corneal staining. Generally, a delayed
hypersensitivity response will have slightly lower
levels of redness and staining.
If the aetiology is allergic in nature, i.e. a reaction to
an antigen on, or in, a lens, e.g. denatured tear
proteins, redness is most commonly first noticed in
7L21117-99 the upper palpebral conjunctiva with little or no
128 alteration in bulbar redness.
Eventually, the palpebral conjunctiva will exhibit
papillary changes accompanied by mucoid floaters
in the tear film, and probably increased lens
deposition.
If no action is taken to remove the cause, the
papillary changes may become so voluminous that
the position, shape and even the mobility (ptosis) of
the upper lid may be affected.
Redness, tearing and swollen lids will invariably
accompany infections of the eye. Initially,
Acanthamoeba infections may only show limbal and
7L20302-94
bulbar redness adjacent to the region of infection,
but ultimately this develops into circumlimbal
conjunctival redness (after Efron, 1999).
129 Objective measurement of ocular (limbal and
conjunctival) redness using image analysis
techniques has been reported by Willingham et al.
(1995), Guillon and Shah (1996), Papas (2000), and
Simpson (2000).
Ocular redness can take on many appearances.
Some examples are included here. A classification
of the types of redness may include:
x Tarsal (slide 128).
x Limbal
– sectoral, e.g. nasal (slides 129, 130)
7L20535-94 – circumferential (slide 131).
x Bulbar, superficial
130
– sectoral (slide 134)
– global (slide 135).
x Bulbar, deep/episcleral (slides 135,136).

7L20953-25

70 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

131

7L2 RED CIRCUM

132

7L2 RED LENS EDGE

133

7L2 STAIN LENS EDGE

134

7L22655-93

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 Module 7: Contact Lens-Related Ocular Complications

135

7L20310-98

136

7L20418-97

137 Ocular Redness: Symptoms

The eye can show an increased level of redness in
OCULAR REDNESS
SYMPTOMS
the absence of symptoms. Conversely, when the
eye is severely red the patient may complain of a
• Asymptomatic to a hot/burning sensation hot, burning sensation. A wide range of symptoms
may be presented between these two extremes.
• Typical symptoms include:
The symptoms expressed by patients are usually
- irritation related directly to the stimulus, e.g. mechanical,
- dryness toxic, allergic, and infective, and not the hyperaemia
that accompanies each of the causes. However,
- lens intolerance hyperaemia is a sign of inflammation that in itself
97200-103S.PPT
can cause a burning or hot, uncomfortable, dry eye.

7L297200-103

138 Ocular Redness: Aetiology

In most cases of increased ocular redness, more
OCULAR REDNESS
AETIOLOGY than one causative factor is involved. This is
because almost all entities/events that can affect
• Multifactorial the eye adversely induce an accompanying ocular
redness.
• Lens effects on:
Many such issues can be contact lens-related. The
- tear film
practitioner must carefully evaluate a wide range of
potential causes to effectively diagnose and
- blinking manage the condition.
Munro and Covey’s (1998) categorization of ocular
97200-104S.PPT
redness associated with contact lens wear is
7L297200-104
presented in slide 139. Many of these conditions
will be dealt with as separate entities elsewhere in
this lecture.

72 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

139 A summary of each of these possible aetiologies

follows (some after Efron, 1999):
OCULAR REDNESS x Tear deficiency. A significant contributing factor
AETIOLOGY in the development of ocular redness in many
after Munro & Covey, 1998
• Tear deficiency
cases is ocular and/or lens surface dehydration.
• Mechanical (physical)
• Toxicity/solution incompatibility x Mechanical (physical). This may be a subtle
• CLPC
effect related to the lens surface quality or a
particular design feature, e.g. peripheral back
• Allergy
surface shape, or an effect of an obvious
• Infective keratitis problem such as a large edge defect. Lens-
• ‘Sterile’ keratitis caused trauma can lead to mast cell
• Hypoxia 97200-286S.PPT
degranulation that results in histamine release
locally and a vasodilation subsequently.
7L297200-286
x Toxicity/solution incompatibility. An ocular
redness reaction may be induced, often
acutely, by exposure to the active ingredients,
preservatives, enzymes, and other chemical
entities in lens care products. The
physicochemical properties of solutions can
also be a factor, especially their pH and
osmolality. If either of these factors is outside
the tolerance of the tissues of the anterior eye,
increased redness, and often tearing, can be
expected.
x Contact Lens-associated Papillary Conjunctivitis
(CLPC). Detailed separately in Section III.D:
CLPC.
x Allergy. Antigens stimulating ocular redness
may be:
– environmental (probably seasonal)
– lens care product ingredients
– lens deposits.
x Infective keratitis (microbial keratitis or MK).
Detailed separately in this lecture in Section III.H
Microbial Keratitis. This condition may
also be accompanied by excessive lacrimation.
x ‘Sterile’ keratitis. This category may include:
sterile infiltrative keratitis, Contact Lens-induced
Acute Red Eye (CLARE), Culture-Negative
Peripheral Ulcer (CNPU), and Asymptomatic
Infiltrates (AI). These are dealt with separately
under their own headings in this lecture (Section
III.I CLARE, Section III.J CLPU & CNPU, and
Section III.F Corneal Infiltrates. These
condition are also often accompanied by
excessive lacrimation.
x Hypoxia (already dealt with in Module 6,
Lectures 6.1 to 6.3) is a possible cause of
ocular redness. However, many modern
lenses, while not necessarily providing for all the
cornea’s needs, will not induce obvious
redness. Serious oxygen deprivation can result
in limbal redness, blood vessel engorgement, or
even neovascularization (dealt with earlier in
this lecture). Severe cases can produce
Superficial Punctate Keratitis (SPK) [Note: To
some, SPK can mean SP Keratitis (implying

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 Module 7: Contact Lens-Related Ocular Complications

with infiltrates) or SP Keratopathy (no

infiltrates). To many, the terms are used
interchangeably. In these modules, SPK is
used to imply simple staining. Specific names
are applied to conditions that involve infiltrates,
e.g. Infiltrative Keratitis (IK)]. Papas et al.
(1997, 1998) have shown that high oxygen
transmissibility SCLs do not induce limbal
hyperaemia and that there is an inverse
relationship between lens transmissibility and
limbal hyperaemia.
140 Ocular Redness: Management
If the practitioner is able to isolate the cause of
OCULAR REDNESS
MANAGEMENT
ocular redness, steps can be undertaken to
minimize the problem. If they are lens or lens care
• Based on cause that needs to be
product related, the solution to the problem is
eliminated, or at least reduced obvious. If the condition is infective, a course of
• Individual basis antibiotics or referral for such a course may be
required. If Acanthamoeba is suspected, urgent
• Minimize dehydration of: referral is essential because even with early
- ocular surface intervention, a positive outcome cannot be
guaranteed.
- lens surface
97200-105S.PPT
Tear deficiencies may be amenable to treatment.
However, many treatments only provide temporary
7L297200-105 relief and do not address the underlying
condition(s).
If hypoxia is suspected, lenses of higher
transmissibility are required. These include RGP, or
siloxane hydrogel lenses (see du Toit et al., 2001).
III.C Endothelial Bedewing

141 Endothelial Bedewing: Introduction

ENDOTHELIAL BEDEWING: Endothelial bedewing is a rare condition.
INTRODUCTION It is more likely to be observed with an inflammatory
• A rare condition response either with or without contact lens wear.
• Marginal retro-illumination & 25-40X mag. In a study of idiopathic corneal anomalies in non-
contact lens-wearing subjects, Hickson and Papas
• Appearance is dynamic, i.e. it changes from one (1997) found 20% of 70 subjects showed
examination to the next endothelial bedewing. When followed for a month,
quite dramatic changes in the pattern of bedewing
• Can be seen in up to 20% of non-wearers (Hickson were noted, with a tendency for the pattern to
and Papas, 1997) ‘scatter’ somewhat.
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142 Endothelial Bedewing: Signs

Typically, bedewing presents with a relatively orderly
ENDOTHELIAL BEDEWING
SIGNS
arrangement of white cells clustered in a confined
• Cluster of cells columnar area in the inferior region of the
endothelium. The cells are best observed with a
- variable number slit-lamp using the technique of marginal retro-
illumination at magnifications of 25X to 40X (slide
- inferior region
143 and 144).
- vertical orientation
Deposits on the posterior surface of the
• Posterior endothelial surface (i.e. endothelium are relatively uncommon. The most
anterior chamber interface)
common deposits are keratic precipitates (kp) that
97200-106S.PPT
might be idiopathic and are usually regarded as
benign or the result of an anterior uveal
7L297200-106 inflammatory event that is usually accompanied by

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 Lecture 7.2: SCL Complications and Their Management

143 aqueous flare.

Duke-Elder (1965) claims that the state of the
endothelium reflects accurately the presence of
uveal inflammation, and any precipitates are usually
preceded by endothelial bedewing. Further, the
source of cellular and fibrinous exudate was
attributable to the ciliary body (Duke-Elder citing
Fuchs) or the iris (citing Baas). Duke-Elder citing
Parsons claimed that kp were almost always
preceded by oedematous and inflammatory events.
Fresh kp are usually grey-white and unpigmented
whereas those that have existed for some time may
be pigmented (Duke-Elder, 1965).
7L22872-93 McMonnies and Zantos (1979) reported endothelial
bedewing in three cases in which contact lens
(PMMA and high water SCL) intolerance was a
144 common feature. All cases were long-term,
successful lens wearers until the time of
presentation with bedewing.
Accompanying signs may include conjunctival
injection, epithelial erosion, epithelial oedema, and
decreased corneal transparency.
Usually the condition is bilateral. The white
(inflammatory) cells shown in slide 144 are probably
leucocytes, because of their refractive properties.
The vertical orientation of endothelial deposition
probably results from the direction of convection
currents in the anterior chamber (iris is warmer,
aqueous rises in front of the iris and falls down the
back of the endothelium with an essentially vertically
directed flow).
Zantos and Holden (1981) presented a case report
7L22871-93 of a wearer (SCL, EW) suffering an episode of
Contact Lens-induced Acute Red Eye (CLARE) who
also demonstrated endothelial bedewing.
Accompanying signs included diffuse corneal
infiltrates, acute inflammation, and guttate changes
in the endothelium. The latter proved to be
transient.
145 Endothelial Bedewing: Symptoms
Endothelium bedewing per se is typically an
ENDOTHELIAL BEDEWING
SYMPTOMS
asymptomatic condition. If symptoms are present
they generally relate to a concurrent ocular
• Usually, asymptomatic inflammation with or without contact lens wear.
In contact lens-related bedewing, other symptoms
• Possible accompanying symptoms of
may include a fogging or blurring of vision, or
ocular inflammation stinging eyes. Usually, when these or similar
symptoms are reported, endothelial bedewing is
• Decreased tolerance to lens wear unlikely to be seen in the vast majority of cases.

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146 Endothelial Bedewing: Aetiology

As the main reports of bedewing are quite dated, it
ENDOTHELIAL BEDEWING
AETIOLOGY
has been suggested that endothelial bedewing was
a response to earlier lenses of comparatively low
physiological performance and that the
• Mild or severe inflammatory response phenomenon is probably less common now (after
Efron, 1999).
- idiopathic, or..... While this may be true, the performance of
conventional lenses in higher Rxs (spheres, and
- lens-induced especially torics) is not significantly different to that
of the lenses used at the time of the initial reports.
97200-108S.PPT
This means that bedewing is still a possibility and it
is prudent to look for signs of bedewing even in the
7L297200-108 absence of accompanying symptoms. McMonnies
and Zantos (1979) reported seeing two cases of
endothelial bedewing in successful contact lens
wearers who remained successful despite the
bedewing.
The presence of white inflammatory cells indicates
that the eye is undergoing an inflammatory event
within the anterior segment. The condition can
develop independent of lens wear but it is more
likely to be a response to contaminated lenses,
preserved solutions, or entrapped debris.
While the cause is usually unknown, poor lens
physiological performance would appear to be
implicated as a contributing factor, at least in the
earlier reports.
147 Endothelial Bedewing: Management
When endothelial bedewing is present without any
ENDOTHELIAL BEDEWING
MANAGEMENT
symptoms the best course of management is to
allow the condition to resolve of its own accord and
• Treat signs of inflammation
monitor the progress of the condition. Resolution
may depend on the individual, the aetiology, and the
severity of the condition.
• Improve physiological performance of lens
The literature also suggests that if there is any
underlying inflammation (indicated by hyperaemia
• Days to weeks for cells to disappear for example), or lens fitting characteristics are not
optimal, it is prudent to evaluate ways in which the
97200-109S.PPT
overall lens performance/physiology can be
improved. Preserved solutions, or contaminated
7L297200-109 lenses, that may cause the reaction should also be
changed.
III.D CLPC

148 Contact Lens-Induced Papillary Conjunctivitis

(CLPC): Introduction
CONTACT LENS-INDUCED
PAPILLARY CONJUNCTIVITIS The initial report of soft contact lens-induced
palpebral conjunctival changes was made by Spring
• CLPC or earlier, Giant Papillary
Conjunctivitis (GPC)
(1974). A similar report was made by Koetting and
Boyd (1976). However, Kennedy (1968) reported a
• Mainly a result of SCL wear case whose description matches that normally given
• Usually bilateral to CLPC but which resulted from PMMA lenses
• Incidence: 0.8% and 12% worn on a daily basis. In some reports, the
appearance of the condition was described as being
• Onset: 2 months to 14 years
‘cobblestone-like’, an apt description of CLPC.
• Induced by RGP lenses less commonly
97200-220S.PPT
The changes Spring observed in many of his
contact lens patients, especially those wearing soft
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Lecture 7.2: SCL Complications and Their Management

lens, were later referred to as Giant Papillary

Conjunctivitis or simply GPC. However, because
the papillae are usually not truly ‘giant’ (i.e. greater
than say 1 mm in diameter), and the appearance of
the palpebral conjunctiva can be somewhat variable
in this condition, the use of CLPC has become the
accepted name more recently. CLPC is sometimes
used to describe a milder form (diameter as small
as 0.3 mm) of Giant Papillary Conjunctivitis (GPC).
The condition is usually bilateral but can be
unilateral or markedly asymmetrical (Palmisano et
al., 1993).
Although the incidence rate has not been
established with certainty, rates have appeared in
the literature ranging from 0.8% to 12% depending
on lens type, mode of wear, and the study cited (see
summary in Dart, 1986 and Rao et al., 1996). In a
prospective study of 330 EW lens wearers,
Sankaridurg et al. (1999) found that CLPC
accounted for only 10.9% of adverse events (137
events in the first 13 months). By contrast,
infiltrative events accounted for 76.6% of adverse
events. The highest figure of 12% was reported by
Kenyon et al. (1986) in EW.
The time to develop may range between two
months and 14 years (Mackie and Wright cited in
Dart, 1986).
The incidence of CLPC appears to have decreased
over the last 20 years. This is probably because
lenses are now thinner, lens materials and
manufacturing technologies have evolved, lens care
products are simpler and less allergenic, and
disposable lenses dominate the soft lens market.
Some authors, e.g. Molinari (1981), Mathers and
Billborough (1992), Gutgesell et al. (1982), and
Martin et al. (1992) have suggested that Meibomian
Gland Dysfunction (MGD) may be more common
with CLPC. More recently however, Molinari and
Stanek (2000) showed that there was no
association between MGD and CLPC within the
context of modern contact lens practice.
While soft lenses have proved to be more inducive
of CLPC (Dart, 1986, Alemany and Redal, 1991),
RGP lenses can also produce the condition
(Douglas et al., 1988, Grant et al., 1989, Alemany
and Redal, 1991, Roth, 1991) as can ocular
prostheses (Srinivasan et al., 1979, Dart, 1986),
extruded scleral buckles (Robin et al., 1987),
cyanoacrylate surgical glue (Carlson and
Wilhelmus, 1987), and raised corneal deposits of
keratin and calcium (Dunn et al., 1990).
Interestingly, Douglas et al. found that the lower the
Dk of the RGP material used, the sooner did CLPC
occur.

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149 Contact Lens-Induced Papillary Conjunctivitis

(CLPC): Signs
CONTACT LENS PAPILLARY
CONJUNCTIVITIS One of the first signs of this condition is often
SIGNS excessive lens deposition. Once such an
• Enlarged papillae observation is made, the conjunctiva of the upper lid
• Roughened appearance should be examined carefully for signs of
(irregular specular reflection) conjunctival hypertrophy. It is for reasons such as
• Palpebral redness this that the upper and lower palpebral conjunctivae
should be examined routinely at every after-care
• Tissue oedema visit.
• Precursor to Giant Papillary Conjunctivitis
Once CLPC is found, the cornea and superior
(GPC)
97200-110S.PPT
limbus should be examined for staining,
hyperaemia, corneal infiltrates, and excessive tear
7L297200-110 mucus (Efron, 1999).
For purposes of comparison, the normal everted
150 upper lid is shown in slide 150. CLPC (slide 151),
which usually starts in the tarsal zone of the
conjunctiva (the zone between the marginal and
orbital conjunctivae overlying the tarsal plate, see
slide 152), alters the normally smooth conjunctival
tissue and is usually accompanied by ocular
discomfort and increased mucus production. CLPC
is least likely to be found in the marginal zone
(adjacent to the lid margins). CLPC results in a
roughened, cobblestone appearance that is easily
seen using a slit-lamp. The extent of the alterations
to the palpebral surface is best assessed using the
technique of specular reflection. The addition of
7L22622-93 fluorescein may also help assess the extent of the
induced changes in both white and cobalt-blue light
since the fluorescein pools in the ‘valleys’ between
151 papillae (slide 153) and stains the apices of the
papillae when the disease is active. This pooling
delineates the width (diameter of the base) of
papillae and assists in determining their height as
well. The extent of the condition is usually
asymmetric but seldom unilateral.
As the condition progresses, the papillae enlarge
and the level of palpebral conjunctival redness
increases. This hyperaemia may take the form of a
central tuft of blood vessels as well as vessels at
the base of the papilla. The vasculature has been
described as glomerular-like.
In more advanced cases, the palpebral conjunctiva
7L22018-95
may also appear oedematous. In this oedematous
state the palpebral conjunctiva, especially the
152 papillae, acquires a milky translucency, and the
papillary vasculature looses its definition due to the
CONJUNCTIVA: ZONES/AREAS translucency of the overlying tissue.
Fornix
Flat discoid scars may also be detectable in the
Orbital

Bulbar
upper tarsal conjunctiva as evidence of previous
Limbal
episodes of CLPC (Dart, 1986).
Tear fluid
Slide 154 shows a mild case of CLPC. When
Tarsal

Cornea

Tarsal plate CLOSED EYE

(tarsus)
examining the palpebral conjunctivae with a slit-
Marginal
lamp, it is useful to note the quality of the specular
Marginal Limbal reflection from the conjunctival surface (see slide
Tarsal
Bulbar 154).
Orbital

97200-289S.PPT
Fornix
Slide 155 shows a mild case (upper image) and a
severe case (lower image) of CLPC. Note that in
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 Lecture 7.2: SCL Complications and Their Management

153 the lower image (severe) the vasculature is

somewhat obscured by the papillae.

7L22543-93

154

7L20694-96

155

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 Module 7: Contact Lens-Related Ocular Complications

156 Slide 156 shows the attendant redness that can

accompany CLPC, and how the grade of redness
may not mirror the size of the papillae, e.g. the
upper image shows only mild redness while the
lower image shows severe reddening despite the
levels of CLPC being similar in both pictures.
Clinically, a recurring difficulty is differentiating
papillary (papillae, slide 158) changes from follicular
(follicles) changes (after Efron, 1999). Key points
detailing each of these entities are presented in
slides 157 and 159 respectively. Slide 160 presents
follicles in the upper eyelid while slide 161 shows
follicles in the lower lid (their more common
location). As noted in slide 159, follicles have a
predilection for a location towards the outer canthus
(see slide 160 and 161).
A key factor in any differentiation is a case history.
If the papillae are the result of an episode of vernal
conjunctivitis unrelated to lens wear, the papillae my
be extremely large, i.e. the opposite to the
statements of size that appear in slides 157 and 159
(i.e. that follicles are normally larger). The presence
of a number of extremely large papillae in vernal
conjunctivitis can result in distortions of the lids and
sometimes the inability to close the eyes
completely.
In summary, follicles are usually viral in origin, i.e.
not usually contact lens-related, are larger, pale,
located towards the outer canthus, usually in the
7L20887-92
lower lid, and are uncommon in the ‘normal’
conjunctiva. Papillae are usually smaller, vascular,
157 normally allergic in origin, and can appear in the
‘normal’ conjunctiva. Contact lenses may be factor
PAPILLAE in their aetiology.
CHARACTERISTICS
• Raised, cobblestone-like
• Walls perpendicular to tarsal plate
• Occurs in allergic diseases
• Vessels at base & as central vascular tuft
• Associated with allergy/allergic response
• Eventually, apex may appear as a white point
• Mainly inflammatory cells
• 0.3 – 0.9 mm diameter
• May be accompanied by strands of mucus
• Seen in the normal conjunctiva
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158

7L20958-91

159
FOLLICLES
CHARACTERISTICS
• Usually NOT CL-related
• Often in viral/chlamydial disease
• Pyramidal or rounded rice grain shape
• Pale, translucent (milky-white, greyish-white)
• Most, but not all, are avascular
• 0.2 – 2 mm diameter
• Usually, inferior, palpebral conjunctiva
- adjacent to the outer canthi
• Subepithelial lymphoid tissue
• Overlying conjunctiva usually normal
97200-288S.PPT

7L297200-288

160

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161 Several grading scales of CLPC (and other ocular

parameters) exist. Most notable are the CCLRU
Grading Scale (sponsored by J&J Vision Products,
Inc.) and the Efron Grading Scale (sponsored by
Hydron Ltd.).
Slides 162 to 165 reproduce the CCLRU Grading
Scale’s four levels of lid roughness as seen with the
aid of instilled sodium fluorescein, light via a cobalt
blue exciter filter, and the camera equipped with a
yellow barrier filter.
Skotnitsky et al. (2000) found that baseline tarsal
roughness, EW, tarsal and conjunctival hyperaemia,
lens tightness, and lack of patency of Meibomian
7L21352-96
gland orifices during EW, are more likely to be seen
in cases of manifest CLPC.
162

7L2CLPC 1

163

7L2CLPC 2

164

7L2CLPC 3

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165

7L2CLPC 4

166 Contact Lens-Induced Papillary Conjunctivitis:

Symptoms
CONTACT LENS PAPILLARY
CONJUNCTIVITIS Typically, very mild forms of CLPC are
SYMPTOMS
• Most likely asymptomatic in early stages asymptomatic. Unfortunately, if symptoms are mild,
• In moderate/advanced stages: wearers will often assume that the symptoms they
- increased lens awareness experience are just the normal sensations contact
- increased lens movement lens wearers experience. This often results in
- increased mucus affecting: inaction on the part of the wearer.
– drying of lens surface
– lens deposits If the condition advances, the wearer will become
– decreased or fluctuating vision more aware of the lens due to its greater mobility on
- itching the eye. Irritation of the palpebral tissue generally
- lens intolerance
97200-111S.PPT
results in greater mucus production that can cause
increased lens deposits. The lens deposits may
7L297200-111 reduce the quality of vision (Dart, 1986) as well as
enhance the influence the lids have on lens
movement. Itching in the early stages may be
limited to only following lens removal but later may
also be experienced while wearing the lenses.
However, Dart (1986) states that the release of
inflammatory mediators from the conjunctiva is the
primary cause of any discomfort and discharge.
The other causes are secondary effects, e.g. lens
movement, lens deposits, etc.
As the condition develops, the discharge increases,
as does the rate of lens deposition and the resulting
blurred vision. Lids sticking together in the
mornings, itching while the lenses are in situ, and
itching that worsens following lens removal are
more likely to occur in the advanced stages of
CLPC. However, the correlation between signs and
symptoms is variable and frequently poor (after
Dart, 1986). Discomfort and fluctuating vision are
likely to ensue.

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167 Contact Lens-Induced Papillary Conjunctivitis:

Aetiology
CONTACT LENS PAPILLARY
CONJUNCTIVITIS CLPC is a complex, locally mediated,
AETIOLOGY hypersensitivity and traumatic response occurring in
• Lens front surface deposits
contact lens wearers, users of ocular prostheses,
and those with exposed ends of Nylon™ corneal
sutures (Reynolds, 1978, Dart, 1986).
- mechanical irritation
After the allergy/inflammatory aetiology, the next
- immune response most likely contributor to CLPC is mechanical
interaction between the contact lens front surface
- drying of lens surface and the palpebral conjunctival tissue. This
97200-112S.PPT
mechanical effect is greater when the lens has a
high level of surface deposits. The deposits can
7L297200-112 also act as an antigenic component in an ocular
immune system response.
However, it has been shown that there is no direct
correlation between the amount of protein in or on a
lens and CLPC (Grant et al., 1989, 1989B). While
the use of disposable lenses has reduced the
incidence of CLPC, they has certainly not eliminated
CLPC (see Grant et al., 1989, 1989B, and Rao et
al., 1996).
A mechanical contribution to the aetiology is further
supported by findings of CLPC in cases involving
exposed sutures, and the greater incidence in
wearers of thick or poorly finished contact lenses.
Dart (1986) found CLPC sufferers were more likely
to have atopic conditions such as hay fever,
eczema, and asthma. Furthermore, he found that
those with such conditions often had more problems
with CLPC than those who did not suffer from such
conditions.
Evidence supporting the importance of
hypersensitivity in CLPC includes the frequent
presence of eosinophils, basophils, lymphocytes,
mast cells, and plasma cells in the conjunctiva.
These are also seen in Vernal KeratoConjunctivitis
(VKC) (Dart, 1986). The itching and hyperaemia
can be explained by the presence of mast cells and
the inflammatory mediators they release including
histamine. Furthermore, a mast cell stabilizer with
or without an antihistamine, is effective in cases of
CLPC. An association between CLPC and atopy
was found by Soni and Hathcoat (1988).
168 Contact Lens-Induced Papillary Conjunctivitis:
Management
CONTACT LENS PAPILLARY
CONJUNCTIVITIS CLPC is a condition that has the capacity to limit
MANAGEMENT severely the ability of the eye to tolerate contact lens
wear in the longer-term.
• Modify lens wear
Once CLPC has developed, lens wear must cease
• Change lens design until the eye’s inflammatory condition has resolved.
• Frequent lens replacement Depending on the severity of the condition, drug
therapy for conjunctival inflammation can be
• Optimize lens care and maintenance initiated. Traditionally, topical steroids have been
reserved for severe inflammations because
97200-113S.PPT
prolonged use of topical steroids has the potential
7L297200-113 risks of raising intraocular pressure, corneal
infection, and cataract formation. NSAIDs (Non-

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 Lecture 7.2: SCL Complications and Their Management

169 Steroidal Anti-Inflammatory Drugs) have also been

used in vernal conjunctivitis (Marren, 1998). Other
CONTACT LENS PAPILLARY drugs, e.g. cromolyn sodium, (an anti-allergy drug,
CONJUNCTIVITIS preferably preservative-free) (Meisler et al., 1982,
MANAGEMENT
Donshik et al. (1984), stabilize mast cell
• RGP lenses membranes thereby preventing the release of
histamines and other biochemical mediators. This
• Pharmacological therapy therapy can be continued at maintenance levels
once lens wear is reinitiated. Combination drug
• Patient education therapy (e.g. an anti-histamine combined with a
mast cell stabilizer) also seems to be useful for the
• Complete resolution is unlikely symptomatic relief of GPC (CLPC) (Trocme, 1996).
97200-114S.PPT Alternatives to sodium cromoglycate have been
studied, e.g. Suprofen™ (Wood et al., 1988),
7L297200-114
loteprednol etabonate 0.5% (Howes and Asbell,
1995), and Livostin™ and Patanol (Marren, 1998).
However, Dart (1986) estimated that about 80% of
cases can be resolved without resorting to topical
drug treatment.
Essentially, the preferred method of managing and
resolving CLPC is preventative. This involves the
use of disposable lenses (Coursaux et al., 1990,
Taylor, 2000), disposed of daily if possible with, or
without, a reduction in contact lens wear. The
added benefit of using daily disposable lenses is the
complete avoidance of lens care products and the
preservatives and other chemical entities therein.
In some cases, patients may be refitted with RGP
lenses but this necessitates adaptation to the
lenses, something some patients are unable to do.
Refitting patients who have already ceased lens
wear has been found to be less successful.
III.E Meibomian Gland Dysfunction (MGD)

170 Meibomian Gland Dysfunction (MGD):

Introduction
MEIBOMIAN GLAND DYSFUNCTION:
INTRODUCTION Ong (1996) defines MGD as a bilateral, non-
• Bilateral inflammatory clinical condition where there is a
change in the lipid appearance from a normally
• Non-inflammatory
clear state to a viscous and cloudy appearance,
• Meibomian gland fluid changes from without any clinically observable Meibomian gland
clear & free-flowing to cloudy & viscous abnormalities.
• Tested by expression of gland contents
To ascertain the appearance of the gland’s
• Condition is very relevant to CL wear secretions they must be expressed by finger
• Should not be confused with blepharitis pressure applied to the lids (the lower lid is more
97200-219S.PPT
accessible and is therefore a suitable starting point).
7L297200-219 MGD:
x Increases tear film osmolarity.
x Produces keratoconjunctivitis sicca (KCS) (see
Lecture 7.4 of this module).
x Decreased goblet cell density.
x Decreased corneal epithelial glycogen levels.
x Epithelial abnormalities.
x Rose Bengal staining ( this section after
Gilbard and Rossi, 1994).
Hom et al. (1990) provide a simpler definition of
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 Module 7: Contact Lens-Related Ocular Complications

MGD, i.e. a cloudy or absent Meibomian gland

secretion upon repeated expression of the lower lid.
Marren (1994) used a similar criterion to evaluate
the presence of MGD, i.e. the number of lower lid
glands expressing freely when pressed gently.
The Meibomian glands are long, well developed
sebaceous glands of holocrine origin (Ong and
Larke (1990) (i.e. a gland in which secretion occurs
by the total disintegration of cells) located in both
the upper (average 25 longer glands) and lower
(average 20 glands) lids within the tarsal plates.
The glands are arranged as parallel glands with
their orifices located between the leading and
trailing edges of the lid margins. Their side walls
consist of a series of sebum-secreting saccules
(alveoli or acini) that empty into the central duct that
ultimately empties to the anterior eye via the lid
margin orifices (Warwick, 1976). The epithelium
lining the ducts and orifices are keratinized (Jester
et al., 1981) and it will be shown that this is relevant
to an understanding of duct and orifice blockage.
More recently Mansour et al. (1988) described
valve-like projections at the outlet end of the acini
that separate individual acini as well as help prevent
regurgitation of their contents. A possible role in
assisting the containment of local inflammatory
processes was also postulated.
Not all Meibomian glands function simultaneously
(Norn, 1980, cited in Norn, 1985).
The secretion from Meibomian glands has been
termed meibum by some workers (e.g. Nicolaides et
al., 1981) to distinguish it from sebum from ordinary
sebaceous glands.
As was shown in the CLPC section of this lecture,
Meibomian Gland Dysfunction (MGD) has
significant ramifications for contact lens wearers
and practitioners alike. Because of the overlap of
occurrence between CLPC/GPC and MGD
(Gutgesell et al., 1982, Martin et al., 1992, Mathers
and Billborough, 1992) it is prudent to investigate
the Meibomian ‘system’ should CLPC be diagnosed.
Mathers and Billborough’s study investigated the
number of partially or completely missing
Meibomian glands using a technique of
transcutaneous infrared photography (they used the
term ‘gland dropout’ to describe the apparent lack of
gland tissue in the resulting photographs). Robin et
al. (1982 and 1985) used a technique of in vivo
transillumination biomicroscopy and photography to
study the Meibomian glands and MGD. They found
that all MGD sufferers had morphological
abnormalities of their Meibomian glands with
varying degrees of glandular distortion.
Further, there is some overlap between two
potentially confusing conditions, MGD and
blepharitis (an inflammatory condition not covered in
this lecture) because they both involve abnormal
Meibomian gland secretions. While neither
condition is the result of the use of contact lenses,

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 Lecture 7.2: SCL Complications and Their Management

the practitioner may be required to distinguish

between them should either present in the
consulting room. To add to the confusion, Martin et
al. (1992) used the term Meibomian gland
dysfunction blepharitis when referring to MGD.
Some degree of MGD is relatively common in both
contact lens wearers, and non-lens wearers
reporting ocular discomfort (Shimazaki et al., 1995).
Ong and Larke (1990) found 30% of contact lens
wearers develop some degree of MGD after 6
months of lens wear whereas only 20% of non-lens
wearers have a similar problem. This figure
confirms Larke’s (1985) figure. However, in a later
paper (Ong, 1996), a figure of 49% in lens wearers
and 39% of non-wearers was quoted for MGD but
statistically, it could not be shown that wearers
presented with MGD more often than non-wearers.
Hom et al. (1990) published a similar figure of
38.9%.
Regardless of the data used, it is apparent that a
very significant number of contact lens wearers (and
non-wearers alike) have some degree of MGD and
that it is unlikely that contact lens wear is a
causative factor.
Ong and Larke found a tendency for males to be
more commonly affected than females although
only equality was shown statistically. Lens type was
not a factor in the incidence rate. Despite the
altered appearance of the secretions of abnormal
and normal glands, their composition was found to
be indetectably different. However, Ong and Larke
did find that the melting point of the abnormal
gland’s fluid was some 3°C higher than that of the
normal fluid. Interestingly, none of the subjects in
their study exhibited inflamed lid margins or
abnormal gland appearances (viewed
transcutaneously).
171 Meibomian Gland Dysfunction (MGD): Signs

MEIBOMIAN GLAND DISEASE In MGD, plugs of waxy or cheese-like material can

SIGNS block the lipid-producing Meibomian glands (slide
• Often bilateral 172). The number of glands involved may range
• Numerous blocked Meibomian glands
- cheese-like material
from a few in mild cases, to the majority in a severe
- pouting of gland orifices manifestation of the disease.
• Cloudy gland secretion when expressed Since the glands are visible as yellow streaks
• Roughened lid margins
• Tear film abnormalities through the palpebral conjunctiva (Warwick, 1976) it
- lipid deficiency is sometimes possible to see the affected gland(s)
- rapid break-up even when there is no gland swelling to alter the
- frothing local topography. However, ‘pouting’ (protrusion) of
• Corneal staining
97200-119S.PPT
the orifices (slide 173) or inflammatory signs, or
both, does not always accompany stagnation or
7L297200-119 accumulation within the gland ducts, making the
condition easy to miss (Henriquez and Korb, 1981).
The lid margins are typically red and roughened and
the tear film abnormalities will normally be apparent
because of the reduced availability of lipids. The
tear lipid layer is the outer anti-evaporative layer and
is some 0.1 Pm thick. Another function of the lipid
component of tears is its role in preventing tear
spillage and overflow beyond the outer lid margins.
While most of the tear’s lipids are secreted by the
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 Module 7: Contact Lens-Related Ocular Complications

172 Meibomian glands, some are contributed by the

Glands of Zeis. (For more details on the lipid layer
see Module 1, Lecture 1.1, Section II.B Tears).
Because of lipid component deficiency (anti-
evaporative function compromised), signs of MGD
include shortened Tear Break Up Times (TBUT),
tear film instability (see Bron and Mengher, 1987),
contact lens intolerance, and lens deposits.
Shimazaki et al. (1995) found that Schirmer tear test
results indicated tear production was significantly
increased in cases of MGD (non-lens wearers)
which is contrary to other reports. They postulated
that this may be a compensation for the abnormality
7L20342-98 of the ocular surface or a result of increased reflex
tearing. It is possible that the increased evaporation
rate may also be a factor, although intuitively, this
173 would be expected to lower tear availability.
Tear foaming may be present in MGD cases even in
asymptomatic eyes (Korb and Henriquez, 1980,
Efron, 1999). The same authors also suggest
gentle, moderate, and forceful expression
(sustained if necessary) of inspissated (thickened or
dense) secretions as a way of differentiating the
degree of blockage and the type of secretion
trapped within. From the cross-section of the
expelled material it is also possible to estimate the
shape and patency of any restriction or blockage,
e.g. circular, thin circular, ribbon-like, etc. Efron
(1999) postulates that tear foaming or frothing may
7L20314-97 be the result of a lowering of the surface tension of
the film in the absence or reduction of its lipid
component.
It is also possible that corneal staining will be
observed (Marren, 1994, Shimazaki et al., 1995)
although sequential instillation of fluorescein may be
required (Korb and Henriquez, 1980).
On manual expression of Meibomian gland
secretions, the lipids from dysfunctional glands tend
to be more ‘waxy’ in appearance (Ong and Larke,
1990).
While no similar report involving contact lens
wearers was found, English and Nutting (1981, cited
in Gutgesell et al., 1982) reported the presence of
members of the arachnid family (mites Demodex
sp., especially D. folliculorum and brevis) in
Meibomian glands.
174 Meibomian Gland Disease: Symptoms

MEIBOMIAN GLAND DISEASE The most common symptom in MGD is ocular

SYMPTOMS irritation or a feeling of dryness, itchiness, and
contact lens intolerance. More severe cases may
• Dry eye sensations
complain of a burning sensation on the eye,
• Generally worse in the morning stinging, foreign body sensations, and apparent
ocular redness. Typically, the symptoms are worse
• Mild irritation to burning/stinging in the hours after waking.
Also of concern to patients with MGD is the
• Contact lens intolerance
increased level of redness along the lower lid
• Concerns about eye/lid appearance margin and of the bulbar conjunctiva.
97200-120S.PPT
Sufferers may also complain of ocular dryness and
7L297200-120
lens intolerance (Henriquez and Korb, 1981).
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 Lecture 7.2: SCL Complications and Their Management

MGD is a major cause of ocular surface

abnormalities and ocular discomfort even in non-
lens wearers (Shimazaki et al., 1995).
175 Meibomian Gland Disease: Aetiology
The underlying issues in MGD are not well
MEIBOMIAN GLAND DISEASE
AETIOLOGY understood. Cytological studies indicate that MGD
is due to the obstruction of the Meibomian gland
• Orifice blockage orifices by desquamated epithelial cells that tend to
aggregate in keratotic clusters. The blockage of
- keratinization of Meibomian gland epithelia gland secretion alters the gland’s contribution of
lipids to the tear film.
- secondary bacterial infection
A further problem may follow should the bacteria
• Sebaceous glad dysfunction (general) present proliferate in the aggregated cells and
release further bacteria and their toxic products into
• Age
the precorneal tear film (after Henriquez and Korb,
97200-121S.PPT
1981). Keratin protein concentrations up to 10%
7L297200-121 greater than normal have been reported in the
secretions of abnormal Meibomian glands by Ong et
al., (1991). They agreed with the postulations of
other authors that this increase may be due to
hyperkeratinization or abnormalities of the
keratinizing process of the Meibomian gland duct
epithelium (e.g. Jester et al., 1981). This, along
with increases in cellular debris within the lumen of
the outlet duct, would be compatible with the
findings that keratinized cells are the primary cause
of duct and orifice blockage. Secondary bacterial
action may follow.
Robin et al. (1986) suggested that SCL deposits
may be associated with MGD.
Eye rubbing had been thought to play a part in MGD
but an investigation of this association failed to
show a correlation (Marren, 1994).
Another possible cause is generalized sebaceous
gland dysfunction that affects both sebaceous and
specialized sebaceous glands (e.g. Meibonian
glands) (McCulley and Sciallis, 1983).
Using rabbits, Gilbard et al. (1989) closed the
Meibomian gland orifices surgically and showed that
tear film osmolarity increased (because of
increased tear evaporation) and ocular surface
abnormalities resulted. This clearly demonstrated
the importance of its secretory products.
Furthermore, goblet cell density and corneal
epithelial glycogen levels declined over the 20 week
period following closure.
Previously, Meibomian gland disease or dysfunction
was thought to be primarily due to Staphylococcal
sp. infection (Thygeson, 1937, and Allen, 1937,
cited in Gutgesell et al., 1982). However, current
thinking has little to do with infection as the primary
cause of MGD.
One other significant factor is advancing age, i.e.
the incidence of MGD increases with age (Hom et
al., 1990). Pascucci et al., (1988) studied age-
related changes in the Meibomian glands and found
that aging resulted in the loss of the ‘plumpness’ of
the glands seen in the young, a generalized loss of
acini, and a widening of the central duct. The gland
width also decreases with age.
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176 Meibomian Gland Disease: Management

MEIBOMIAN GLAND DISEASE In most cases, the condition becomes chronic

MANAGEMENT without adequate intervention and treatment.
• Hot and cold compresses
Lens wear can continue as long as the wearer is
• Lid scrubs and massage: tolerant of the sensations that motivated them to
- with baby shampoo consult their contact lens practitioner in the first
instance. Initial treatment of MGD is directed
- with special lid care products
toward loosening the plugged material at the orifice
- without any other product and deeper within the gland by repeated application
• Oral tetracycline of hot compresses (Ong, 1996B) and the use of
digital massage (Rengstorff, 1980).
• Antibiotics and steroids
97200-122S.PPT
Use of oral tetracycline (or similar) is capable of
7L297200-122 improving the lipid quality within the Meibomian
gland.
The most common and least expensive treatment is
lid scrubs performed with cotton buds (cotton tips)
and a baby shampoo (or other shampoo known not
to sting should it enter the eye inadvertently).
Another solution is to use special-purpose lid scrub
formulae available from several manufacturers in
most world markets. Detailed descriptions of lid
scrub procedures are presented in Farkas et al.
(1986), Caffery (1994A, 1994B), Townsend (1997).
A simpler technique to clean the lid margins was
recommended by Farris who prefers to use a cotton
bud (or cotton swab) wound tightly. The surfactant
properties of shampoos were cited as a reason to
avoid their use because of the tear film alterations
they can cause.
Korb and Greiner (1994) studied MGD management
in non-lens wearers using a combination of office-
based treatment (six-weekly expression of all
glands using finger pressure to the front of the lid
and a cotton bud from behind under topical
anaesthetic), and daily, self-administered treatment
(hot compresses to the lower lid for two minutes and
eyelid scrubbing with baby shampoo and cotton
buds).
All subjects showed improvements in Meibomian
gland function and a decrease in the number of
glands exhibiting solidified meibum. The thickness
of the lipid layer, measured by thin-film interference,
was increased by the procedures in the study and
symptomatic relief was reported by all subjects, i.e.
increased comfort and/or decreased dry eye
symptoms.
Hot and cold compresses are also recommended
on a daily basis, especially in the early stages of the
condition (Henriquez and Korb, 1981). These not
only increase blood flow to the area but also heat-
soften Meibomian gland secretions in situ, the gland
ducts and orifices. This procedure along with
manual expression assists in dislodging orifice
plugs already formed and already blocking gland
secretion.
Hom et al. (1990) recommend that Meibomian
gland expression be incorporated as a routine
testing procedure, especially if the eyes are
suspected of being dry or borderline dry. Gland

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 Lecture 7.2: SCL Complications and Their Management

expression has been shown to be effective (Paugh

et al., 1990).
A complication of managing MGD is the potential for
confusion between MGD-related tear abnormalities
and other causes of tear abnormalities, e.g. dry eye.
Tests such as the Phenol Red Thread Test (PRTT),
Schirmer strips, or other tests of tear volume may
be required. Should the volume of the aqueous
component appear to be adequate, MGD should be
suspected (Efron, 1999).
In more severe cases, the application of antibiotics,
anti-inflammatories, and corticosteroids may be
warranted, although such an approach was found to
be unjustified and was not supported by Gutgesell
et al. (1982).
Without treatment, the prognosis for MGD sufferers
is relatively poor. With attention to lid hygiene, lens
condition, and possibly hot and cold compresses
with lid massage, the effects of the MGD may be
reduced but probably not eliminated. Lens wear
can be resumed or continued successfully in the
majority of cases. Overall the prognosis is good.
III.F Corneal Infiltrates

177 Corneal Infiltrates: Introduction

CORNEAL INFILTRATES: Corneal infiltration induced by contact lens wear
INTRODUCTION have been reported in the literature for some time
• A relatively common CL-induced condition (Bernstein and Kemp, 1975, cited in Yeung and
Weismann, 1998, Zantos and Holden, 1977,
• Also seen in 1% of non-lens wearers Ruben, 1978).
• May be epithelial, sub-epithelial or stromal
Lens-induced infiltrates may be in the epithelium,
• Usually, the overlying epithelium is intact sub-epithelial, or within the stroma.
• Believed to be discrete collections of
Once lens wear ceases and treatment is initiated, it
inflammatory cells
takes one to two weeks for the infiltrates to
• May be ‘sterile’ or infected disappear completely (Zantos and Holden, 1978).
97200-218S.PPT

Usually, the epithelium overlying infiltrates remains

7L297200-218 intact (Gottschalk, 1988), although others have
found significant percentages of infiltrates with
overlying epithelial defects (Bates et al., 1989, Mertz
et al. 1990).
The incidence of infiltrates ranges from 1.6% to
16.6% (Fleischman, 1979, Josephson and Caffery,
1979, Hamano et al., 1985, Kenyon et al., 1986,
Cutter et al., 1996, Fonn et al., 1997, Hickson and
Papas, 1997), and is known to be higher in EW than
DW, and lower in daily disposables (Suchecki et al.,
2000).
The prevalence of infiltrates in the non-wearing
population has been shown to be about 1% and this
needs to be accounted for when considering
presumed contact lens-related infiltrative events
(Sweeney et al., 1996).
Infiltrates are believed to be discrete collections of
inflammatory cells (Josephson and Caffrey, 1979).
They believe that in the early stages of infiltrative
events, the infiltrates are predominantly
PolyMorphoNuclear (PMN or PMNs) leucocytes
(particularly neutrophils), while in the later stages

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macrophages and lymphocytes are more likely to be

found.
Infiltrates may be ‘sterile’ or infected (Stein et al.,
1988). The term ‘sterile’ is common in the literature
on infiltrates. By convention it is used to describe
infiltrative corneal conditions from which cultures
are taken but whose cultures fail to reveal any
causative micro-organisms. Infiltrates may also be
microbial in origin. Ring-shaped infiltrates are
usually indicative of several systemic diseases
(Shovlin, 1989B) and will not be dealt with here.
Bates et al. (1989) used ‘sterile’ for infiltrates that
are non-progressive, of uncertain pathogenesis, and
that may be sterile.
The terms infiltrate and ulcer have been used
interchangeably in the literature to the point of
confusion. For example, the central infiltrate
described in the following paragraph might well be
defined as an ulcer.
Infiltrates that are central, have accompanying pain,
discharge, significant overlying epithelial staining,
and an anterior chamber reaction are suggestive of
infection (Stein et al., 1988, Bates et al., 1989). The
acronym PEDAL has been used to list these
features in an infection:
x Pain.
178
x Epithelial defect.
CORNEAL INFILTRATES x Discharge.
TERMINOLOGY
x Anterior chamber involvement.
• IK – Infiltrative Keratitis
x Location (especially if central).
Infections need to be distinguished from ‘sterile’
• AIK – Asymptomatic Infiltrative Keratitis infiltrative conditions, a distinction that can be
difficult to make (Bates et al., 1989). Stein et al.
(1988) found sterile infiltrates to be smaller, multiple
• AI – Asymptomatic Infiltrates
or arcuate, without significant pain, epithelial
97200-290S.PPT staining, or anterior chamber reaction.
7L297200-290 The three main corneal infiltrative conditions are
presented in slide 178.
179 Corneal Infiltrates: Signs

CORNEAL INFILTRATES With a slit-lamp, focal infiltrates can be observed

SIGNS with bright white light and medium magnification,
• May be focal, arcuate, or diffuse against a dark background. Steps should be taken
• Hazy, greyish-white (0.5 mm to 2 mm)
to ensure that light does not reflect directly from the
iris unless retro-illumination is intended. The latter
- tiny circular to ‘wooly’ appearance technique is probably unsuited to more subtle
• Location conditions such as early AI.
- epithelial Slides 179 and 180 present the generalized signs of
- subepithelial infiltrates while slide 182, 185, and 188 detail the
- stromal signs of IK, AIK, and AI respectively. Diagrammatic
97200-123S.PPT
representations of these conditions appear as slides
184, 187, and 190 respectively.
7L297200-123
Infiltrates can be difficult to see when located near
the limbus, especially if they are diffuse (slides 183,
and 186). The affected areas of the cornea will
exhibit an ‘orange peel’ appearance when viewed in
retro-illumination (after Grant et al., 1990) (slide

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 Lecture 7.2: SCL Complications and Their Management

180 191, cf. slide 183 using direct, focal illumination).

Corneal infiltrates have a wide-range of
CORNEAL INFILTRATES appearances (see examples opposite) but most
SIGNS
commonly appear as a greyish-white opacity (after
• Accumulation of:
Gottschalk, 1988). When sub-epithelial, they may
- PMN leucocytes look more like a greyish-white stromal haze which
can be seen with the naked eye if large enough
– principally, neutrophils
(Josephson and Caffrey, 1979).
- macrophages Infiltrates are usually described in terms of their:
- lymphocytes x Shape (focal, diffuse, arcuate).
• Unilateral or bilateral (more common) x Size (small if <1 mm, large >2 mm).
97200-124S.PPT

x Overlying corneal staining (none, punctate,

7L297200-124
coalesced, etc.).
x Number.
181
x Location within the cornea (peripheral – within 2
CORNEAL INFILTRATES mm of the limbus, central, or paracentral).
SIGNS
(After Stein et al., 1988, and Bates et al., 1999).
Accompanying signs Infiltrates are more likely to be found in the corneal
periphery (Gordon and Kracher, 1985, Bates et al.,
• None to severely red, discharging eye 1989). The main reason for this peripheral location
of infiltrates is because of the vascular proximity of
• Eye can be white and quiet
the limbus (Mondino, 1988).
• Overlying epithelial staining (half of cases) Differential diagnosis of infiltrative conditions from
Epidemic KeratoConjunctivitis (EKC) may be
97200-125S.PPT required. Slides 192 and 193 show cases of EKC.
The number, size and distribution of the lesions in
7L297200-125
EKC are unlike those in any infiltrative condition.
By way of a summary, a composite image of the
182 common forms of infiltrates is presented as slide
194.
INFILTRATIVE KERATITIS (IK)
SIGNS from CCLRU/LVPEI’s Guide to Infiltrative Conditions

• Peripheral, to mid-peripheral
• Mild to moderate diffuse infiltration, and/or
small, focal infiltrate, possibly multiple
• In anterior stroma (sub-epithelial)
• Usually no observable corneal oedema
• Slight to moderate staining
• No anterior chamber reaction
• Moderate limbal redness
• Can be bilateral
97200-291S.PPT

7L297200-291

183

7L22663-93

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 Module 7: Contact Lens-Related Ocular Complications

184

7L2SANK-IK

185
ASYMPTOMATIC INFILTRATIVE
KERATITIS (AIK): SIGNS
• Peripheral from CCLRU/LVPEI’s Guide to Infiltrative Conditions

• Small, focal infiltrates (up to 0.4 mm) and/or

mild to moderate diffuse infiltration
• In anterior stroma (sub-epithelial)
• Usually no observable corneal oedema
• Often punctate staining
• No anterior chamber reaction
• Mild to moderate limbal redness
• Can be bilateral
97200-293S.PPT

7L297200-293

186

7L2 INFIL MID-PERI

187

7L2SANK-AIK

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 Lecture 7.2: SCL Complications and Their Management

188
ASYMPTOMATIC INFILTRATES (AI)
SIGNS from CCLRU/LVPEI’s Guide to Infiltrative Conditions

• Commonly peripheral, but can be anywhere

• Very small, focal infiltrate, usually solitary
(0.2 mm), and/or mild, diffuse infiltration
• In anterior stroma (sub-epithelial)
• Usually no observable corneal oedema
• No staining
• No anterior chamber reaction
• No limbal redness
• Can be bilateral
97200-292S.PPT

7L297200-292

189

7L2 INFIL PERI

190

7L2SANK-AI

191

7L20499-94 RETRO

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192

7L2 EKC-1

193

7L2 EKC-2

194

7L297200-297.JPG

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 Lecture 7.2: SCL Complications and Their Management

195 Corneal Infiltrates: Symptoms

CORNEAL INFILTRATES A wide range of symptoms can be associated with

SYMPTOMS corneal infiltrates.
• Range from asymptomatic to painful
The main ones reported are: redness, photophobia,
• Lens can ‘mask’ the problem (bandage pain, and a foreign body sensation (Cutter et al.,
effect)
1996). It is possible for infiltrates to be present in
• Dictated by cause the cornea in the absence of symptoms, e.g.
• Typically: Asymptomatic Infiltrates (AI) (Sankaridurg et al.,
- foreign body sensation 1999B).
- photophobia
- lacrimation
97200-126S.PPT

7L297200-126

196 Corneal Infiltrates: Aetiology

The presence of infiltrates in the cornea indicates
CORNEAL INFILTRATES that the ocular defence system has been activated.
AETIOLOGY The causes of this activation in the cornea are
• Bacterial presence numerous (see slides opposite). Inflammatory
mediators, including histamine, alter the
permeability of the venules and small veins by
• Tight lens
altering the ‘tight gaps’ between the vascular
endothelial cells, allowing neutrophils (and later
• Eye closure with lens macrophages and lymphocytes) to pass into the
extravascular space (the perilimbal cornea), and
• Mechanical trauma move (chemotactically, along the corneal lamellae
97200-294S.PPT
[Basu and Minta, 1976, cited in Silbert, 2000]) to the
7L297200-294 inflammatory site. Once an inflammatory cell has
traversed the vascular endothelial barrier, the gap
closes. This process is without apparent detriment
197 to the endothelial cells involved (visit
http://medweb.bham.ac.uk, 2002, and peruse slide
CORNEAL INFILTRATES 198).
AETIOLOGY Immunologically, the cornea is ‘privileged’ by virtue
• Hypersensitivity of its essentially avascular nature, and the absence
of Langerhans cells (dendritic cells that enter the
• Hypoxia cornea on a massive scale [Jager, 2001] from the
• Lens deposits conjunctiva epithelium following the initiation of an
immunological response). Langerhans cells bind to
• Hygiene antigens and eventually present the antigen to the
local lymph node, thereby sensitizing the host to the
• Inadequate disinfection
antigen [Chandler and Gillette, 1983]) (Suzuki et al.,
97200-295S.PPT
2000, McMenamin, 2002).
7L297200-295 The chemotactic stimuli to the release of leucocytes
are numerous and the literature provides general
agreement on the stimuli most likely to be involved,
198
although the actual mechanism(s) are not well
CORNEAL INFILTRATES: SCHEMATIC understood. However, Sankaridurg et al. (2000)
di ato
rs have shown that, in guinea pigs at least, SCL EW
me
Neutrophil
Macrophage
ma
tor
y induces the migration of Langerhans cells (ATPase-
lam
Lymphocyte
I nf
positive dendritic cells) into the central cornea.
Extravasated
INFILTRATE
neutrophils They thought this may play a role in the
pathophysiology of some adverse events in contact
CORNEA

Venule lens wear.

Limbal vasculature
Extended wear is associated with a higher incidence
Neutrophils of infiltrates and the main factors implicated in this
Arteriole
Vascular endothelium wear modality are eye closure and the entrapment
97200-298S.PPT of debris under the lens (Crook, 1985). Trapped
debris may include bacteria (predominantly Gram
7L297200-298
–ve bacteria) and any toxins they have released, as

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 Module 7: Contact Lens-Related Ocular Complications

well as cellular debris. During prolonged eye

closure, the tear film aqueous is depleted,
effectively tightening the lens and preventing the
escape of debris and metabolic by-products from
under it. Tight lids and/or tight lenses have been
implicated in the aetiology of infiltrative events
(Zantos, 1984, Horowitz et al., 1985, Shovlin,
1989A).
Hypoxia is the inevitable outcome of the use of
traditional hydrogels for EW and has been
suggested as an aetiological factor (Stein et al.,
1988). Under hypoxic circumstances, blood
vessels, especially limbal blood vessels, dilate
thereby enabling the escape of inflammatory cells
(Josephson and Caffery, 1979, Pavilack et al.,
1992, Efron, 1999) (see slide 198).
While mechanical insult to the cornea will not
necessarily result in an inflammatory response
(Holden and Swarbrick, 1989), the latter is more
likely when soiled SCLs harbouring bacteria (and
other pathogens) are worn (Modino, 1988, Stein et
al., 1988, Bates et al., 1989, Baleriola-Lucus et al.,
1991, Mondino et al., 1991, Holland et al., 1991,
Willcox et al., 1995, Sankaridurg et al., 1999A).
Potentially, lenses soiled by contaminants
transferred from the hands (adsorbed or absorbed
into the lens matrix) can cause a sensitivity reaction
(Tripathi et al., 1978, 1994B, Vajdic et al., 1995).
Such personal hygiene issues have also been cited
as a cause of infiltrates (Bates et al., 1989).
Examples are:
x Case contamination resulting in poor
disinfection.
x The use of lens care products whose efficacy is
inadequate.
x Deficient cleaning procedures (or no cleaning
procedures at all) leaving high levels of
bacterial contamination
(After Tripathi et al., 1978, Stapleton et al., 1997).
Similarly, care solutions and eye drops used in
conjunction with lenses can often result in infiltrates
(Josephson and Caffrey, 1979, Mondino and
Groden, 1980, Bates et al., 1989, Hood, 1994,
Townsend, 1998). Because of the adverse reaction
rates (including infiltrates), disinfection/preservation
by traditional chemicals such as thimerosal and the
chlorhexidines has all but ceased. These reactions
may have been exacerbated by the use of old and
deposited lenses (Holden and Swarbrick, 1989,
Tripathi et al., 1994B) as these preservatives can
bind to the deposits (Tripathi et al., 1988, Stapleton
et al., 1997).
Schein et al. (1989) and Cutter et al. (1996) found
that smoking (in both former and current smokers)
was associated with increases in the incidence of
infiltrates.
Lens wearers who have experienced a Contact
Lens-induced Acute Red Eye (see Section III.I

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 Lecture 7.2: SCL Complications and Their Management

CLARE) are four times more likely to have a

recurrence of infiltrative keratitis than would a
neophyte wearer (CCLRU data cited in Holden,
1989). Holden postulated that CL-induced
inflammation may sensitize the cornea, leaving it
more susceptible to later adverse episodes.
Despite the hopes held for them, disposable lenses
did not eliminate infiltrative events, as became
obvious soon after their release (Parker and Wong,
1989, Serdahl et al., 1989, Stapleton et al., 1992,
Boswall et al., 1993, Poggio and Abelson, 1993, and
Hamano et al., 1994)
It is also possible for infiltrates to form in the cornea
in the absence of any other signs, i.e. they are
apparently idiopathic.
199 Corneal Infiltrates: Management

CORNEAL INFILTRATES The initial management of infiltrates is to

MANAGEMENT discontinue lens wear and to commence the most
appropriate therapy as dictated by each case.
• Dictated by:
Lens wear must not recommence until the cornea is
- signs and symptoms
clear. This may take months in some cases. Milder
- underlying cause manifestations usually resolve much sooner, i.e.
- lens-related one to two weeks (Zantos and Holden, 1977).
- non-lens related The most significant confounding factor in deciding
on a management strategy is whether epithelial
- risk of infection
staining is associated with the underlying infiltrate.
97200-128S.PPT
Such cases involve an increased risk of corneal
7L297200-128
infection and must be managed in a way that
reduces the risk. Typically, prophylactic antibiotics
are prescribed.
200 Stromal infiltrates with overlying epithelial defects
CORNEAL INFILTRATES should be regarded as potential cases of microbial
MANAGEMENT keratitis until proved otherwise (Schein et al., 1985).
• Accompanying staining requires intervention The use of antibiotics is not widely supported in the
literature (see Townsend, 1994) and usually
- lens wear discontinuation
cessation alone (until the cornea is clear), is
- monitoring sufficient.
- antibiotic prophylaxis ? If an episode of CLARE has been experienced by a
lens wearer before, it is advisable that a thorough
• Resolution (clear cornea) necessary before high-magnification examination of the corneas be
lens wear continued undertaken at each routine after-care visit because
97200-129S.PPT
of the increased likelihood of infiltrative events
7L297200-129
subsequently.
201 Recurrence rates as high as 25% have been
reported.
CORNEAL INFILTRATES
MANAGEMENT For treatment purposes, a differential diagnosis is
• Risk of recurrence important.
• Need to reduce risk If the condition is viral and severe, or severe from
- isolate cause lens-related factors, treatment with a steroid, an
- change lenses, solutions, care routine antibiotic-steroid combination, or an NSAID (Non-
- change wear schedule Steroidal, Anti Inflammatory Drug), has been
- patient re-education suggested.
• Refit with daily disposables, siloxane For milder conditions without corneal staining, lens
hydrogels, or RGPs
abstinence with artificial tears, ocular
• Use preservative-free products
97200-130S.PPT decongestants, antihistamines (topical and oral),
and/or cold compresses have been suggested
7L297200-130
(Silbert, 2000).

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 Module 7: Contact Lens-Related Ocular Complications

To minimize the risks of recurrence, ensure the eye

is quiet and the infiltrates have resolved completely
before stressing the cornea again.
Logically, the lens wear modality of choice is daily
disposable because it eliminates spoilage, deposits,
and preserved solutions.
III.G Corneal Abrasions/Erosions

202 Corneal Abrasion/Erosion: Introduction

CORNEAL ABRASIONS/EROSIONS Although contact lenses can abrade the corneal
INTRODUCTION epithelium and result in damage to it, most corneal
• Most are not contact lens wear related abrasions are not contact lens-related (Brown and
Bron, 1976, Frucht-Pery et al., 1991). However,
• Those apparently related are often only Hood and Sadiq (1995) reported that 19.7% of
contact lens-related casualty department
indirectly so, e.g. finger /fingernail-induced
admissions were for corneal abrasions. Often,
trauma at insertion/removal abrasions that occur during contact lens wear are
caused indirectly by:
• Corneal abrasions may be treated with
x The effects of fingers or fingernails (the ‘vast
bandage CLs
97200-216S.PPT
majority’ according to Weene, 1985).
7L297200-216 x Epithelial trauma during the insertion or removal
process.
x The result of eye rubbing while the lenses are
being worn.
203 Corneal Abrasion/Erosion: Signs
Abrasion damage can be disclosed readily with a
CORNEAL ABRASION/EROSION
vital stain. However, mild abrasions can often be
SIGNS
seen with a slit-lamp and white light (slide 204).
• Dense, localized staining with fluorescein Usually, retro-illumination (208), or marginal retro-
illumination (slide 207), will demonstrate the optical
• Bulbar redness extent of any corneal damage, regardless of how
subtle the defect may appear initially. A narrow
• Lacrimation optic section is required to assess the depth of an
abrasion usually with the addition of a stain, e.g.
• Stromal infiltrates possible sodium fluorescein. If the abrasion is deep, a
subepithelial spreading of instilled fluorescein can
97200-131S.PPT
result in a fluorescein ‘halo’ appearing around
7L297200-131 (under actually) the abraded area (slide 207).
Several aspects of an abrasion need to be
evaluated. Aspects include:
204
x The extent (size).
x The presentation of the damaged area’s surface
(punctate, diffuse, dimple, coalesced, dense,
continuous).
x The depth (superficial, moderate, deep, e.g. the
full depth of the epithelium, stromal).
x The shape (circular, linear, random).
x The general location (superior, central, inferior,
nasal, temporal).
x The relative location (limbal, perilimbal,
7L20563-94 peripheral, mid-peripheral, paracentral, central).
x Any relevant observations that imparts to others
an understanding of the lesion, or that may
assist in tracking changes over time.
Some common staining patterns resulting from
100 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

205 corneal abrasions are presented diagrammatically

in slides 209 and 210. Slides 205 and 206 show
SCL-related and eyelash-caused staining
respectively. Obviously, no SCL wear was involved
in the latter.
Signs associated with corneal abrasions include:
x Significant bulbar redness. When observed
with the naked eye, the location and pattern of
bulbar conjunctival hyperaemia often discloses
the affected quadrant.
x Profuse watery discharge.
x Stromal infiltrates. These may accompany a
7L21595-95 stromal inflammatory event resulting from a
corneal abrasion. Infiltrates, along with tissue
necrosis, are indications of an infective process
206 (Wallace, 1985B).

7L20012-10

207

7L20732-95

208

7L20220-91

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 Module 7: Contact Lens-Related Ocular Complications

209
Corneal Abrasions
Staining Patterns
Linear, random
(paracentral to perilimbal)
(FB)
Coalesced
light, medium, dense,
& continuous
(mid-peripheral No abrasion
& peripheral)

Spiral
(central Fine, continuous
& paracentral) (mid-peripheral
(trapped FB) to peripheral)
(finger, clothing, etc.)

Medium, continuous Linear

(mid-peripheral (mid-peripheral
to peripheral) 97200-299S.PPT
to peripheral)
(finger, clothing, etc.) (lens removal)

7L297200-299

210
Corneal Abrasions
Staining Patterns
Random Arcuate
(mid-peripheral) (perilimbal)

Diffuse
Continuous fine, medium & dense
(mid-peripheral) (central, mid-peripheral,
& peripheral)

Dimple Fine, punctate

(paracentral (mid-peripheral
& mid-peripheral) to peripheral)

Dense, punctate Punctate

(mid-peripheral (mid-peripheral
to peripheral) 97200-300S.PPT to peripheral)

7L297200-300

211 Corneal Abrasion/Erosion: Symptoms

Typically, a corneal abrasion is associated with
CORNEAL ABRASION/EROSION
significant symptoms including (Wallace, 1985B):
SYMPTOMS
• Mild to severe pain x Ocular pain.
x Watery eyes.
• Photophobia
x Photophobia.

• Lens’ bandage effect may mask The symptoms manifested often depend on the
severity of the abrasion and may be masked by the
symptoms until lens removal continued presence of a contact lens.
97200-132S.PPT
Once the lens is removed, and its bandage effect
lost, the intensity of the symptoms usually
7L297200-132 increases. Deeper lesions, coalesced areas of
staining, or more widespread epithelial damage can
be expected to produce more severe symptoms.
However, an objective assessment of the extent of
an abrasion should override patient symptoms
because the later are not always proportionate, i.e.
significant epithelial damage may not be
accompanied by significant symptoms while
apparently minor damage may result in severe
symptoms.

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 Lecture 7.2: SCL Complications and Their Management

212 Corneal Abrasion/Erosion: Aetiology

The most common cause of an abrasion is an
CORNEAL ABRASION/EROSION
external (to the lens-eye system) mechanical insult
AETIOLOGY
to the epithelium. The most common ‘weapon’ is
• Mechanical aetiology is most common
the fingernail (Brown and Bron, 1976). Such an
- fingernails/fingers
assault can result in a significant disorganization of
- trapped foreign body the superficial epithelium’s regular cellular
- lens defect arrangement and the tight junctions between
adjacent epithelial cells.
• Significant abrasion leads to disorganization
A range of possibilities needs to be considered
of epithelium’s regular cellular arrangement
when trying to determine the exact cause of an
97200-133S.PPT
abrasion. Likely factors include:

7L297200-133 x Trapped foreign body.

x Lens deposit (especially if located on the
posterior surface, usually an uncommon
occurrence).
x Damaged lens surface.
x Lens edge defect (relatively common with thin-
edged lenses).
x Lens tear, including a tear or fracture within the
lens proper, or at the lens edge.
The epithelial repair process is detailed
schematically in Module 1, Lecture 1.1, slide 152.
213 Corneal Abrasion/Erosion: Management
The three goals of treatment of corneal abrasions
CORNEAL ABRASION/EROSION
(regardless of aetiology) are to:
MANAGEMENT
• Prevent secondary infection x Prevent secondary infection.
- prophylactic antibiotics x Speed the healing process.
• Monitor patient closely x Reduce patient discomfort (Wallace, 1985B).
• If infiltrates detected - treat as MK The major risk associated with an abrasion of the
• Avoid corticosteroids
cornea is secondary infection.

• Bandage soft contact lens

In moderate to severe episodes, the prudent course
97200-134S.PPT
is to provide, or arrange for the administration of,
prophylactic antibiotics, i.e. treat as if the condition
7L297200-134 was either an infection, or could develop into one.
Udell et al. (1987) advised that if the abrasion is
‘clean’, culturing of lenses, lens case, cornea and
solutions are not needed unless poor lens hygiene
is suspected (or known). Defects with infiltrates
should be treated as microbial keratitis (MK). Udell
et al. also advised strongly against the use of topical
corticosteroids.
Clemons et al. (1987) advised against the use of
pressure patching in patients with corneal abrasions
because of the significant risk of developing a
Pseudomonas ulcer.
Corneal abrasions only rarely result in a stromal
inflammatory response if treated within the first 24
hours (Wallace, 1985B). Most contact lens-
associated abrasions are even less likely to result in
involvement of the stroma.
Occasionally, the fear is expressed that diagnostic
products such as sodium fluorescein and Rose
Bengal may alter the time course of epithelial
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 Module 7: Contact Lens-Related Ocular Complications

healing. Gómez et al. (1991) found that in rabbits at

least, fluorescein appeared to promote healing while
Rose Bengal tended to retard healing of abraded
epithelia. Corneal abrasions usually heal in several
days without further symptoms (Weene, 1985) and
most are not followed by recurrent erosions unless
the corneas are already abnormal (Brown and Bron,
1976).
The use of a bandage SCL with a high Dk/t may be
applicable in some cases to decrease the pain
experienced, and to promote epithelial wound
healing even though the eye remains open and the
blink mechanism functional.
The contact lens practitioner should try to ascertain
the true cause of any corneal abrasion before
concluding that the lenses themselves are to blame.
Non-contact lens causes include plant or vegetable
matter (e.g. plant parts, tree limbs, vines, etc.) with
an attendant risk of subsequent fungal infection
(Wallace, 1985B).
Differential diagnosis requires a thorough
examination of the eye and lens for possible defects
or foreign bodies. Appearances similar to an
abrasion have been mimicked by either toxic or
hypersensitivity reactions to lens care products
(Margulies and Mannis, 1983).
III.H Microbial Keratitis (MK)

214 Microbial Keratitis: Introduction

MICROBIAL KERATITIS (MK): The term microbial keratitis, and the abbreviation
INTRODUCTION MK, is not accepted universally. To some, MK
means marginal keratitis of which a CLPU (Contact
• Relatively uncommon but.....
Lens-induced Peripheral Ulcer, see Section III.J
• Most serious CL condition known CLPU & CNPU) is believed to be an example.
• CLs are the most likely cause of MK What is referred to here as microbial keratitis can
• EW increases the risk of MK be referred to by others as bacterial keratitis, viral
• Risk: EW: 2% DW: 0.07% (Fonn et al, 1997) keratitis, Acanthamoeba keratitis, etc. to match the
• Many alternative names are in use aetiology (see the alternative names in slide 215).
- MK or CL-MK used in this lecture Eye infections related to soft contact lens use were
97200-215S.PPT
reported soon after SCLs were introduced (Anon.,
1972, cited in Kirn, 1987, Tragakis et al., 1973, cited
7L297200-215 in Brown et al., 1974, and Brown et al., 1974). More
reports appeared following the introduction of
Extended Wear (EW) (Zantos and Holden, 1978,
Sjöstrand et al., 1981, Adams et al., 1983).
Microbial keratitis (MK) is an inflammation of
corneal tissue due to the direct effect of infection by
a microbial agent, i.e. bacteria, viruses, fungi or
protozoa. However, MK may not necessarily be
ulcerative (ulcers are treated separately later in this
lecture), i.e. involving a breakdown or breach of the
ocular surface.
In countries with a significant contact lens-wearing
population, contact lenses are the most likely cause
of all corneal infections. A contact lens wearer has
an 80X risk of corneal infection compared with that
of a healthy non-wearer. Using the lenses on an
extended wear (EW) basis increases the risk by a
further 3X to 8X. Despite these numbers, the risk

104 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

even in EW is ‘small’ (this section after Dart, 1999).

A summary of MK events per 10,000 wearers per
year from Poggio et al. (1989), Benjamin (1992),
Nilsson and Montan (1994) follows.
Poggio Benjamin* N&M
D SCL EW 10
C SCL EW 20.9 88 13.3
D SCL DW 2.16
C SCL DW 4.1 2.17
RGP DW 4 1.48
RGP EW 42
D = Disposable C = Conventional (non-disposable)
* Benjamin, 1991 extrapolates to ‘patients’ rather
than ‘eyes’ whereas Benjamin, 1992 uses ‘%’ only.
No comprehensive figures are available yet on the
complication rates for the newer siloxane hydrogel
lenses.
215 Alternative Names:
Alternative names have been used in the literature
MICROBIAL KERATITIS for MK (see slide 215) and some others are listed
SOME ALTERNATIVE NAMES below according to a scheme based on Efron
• Microbial infiltrative keratitis (1999).
• Infectious keratitis x Microbial Infiltrative keratitis (MIK).
• Corneal infection
• Corneal ulcer*
x Contact Lens–Microbial Keratitis (CL-MK). MK
or MIK believed to be caused directly or
• Bacterial keratitis*
indirectly by contact lenses, or contact lens
• Bacterial ulcer*
wear.
* not necessarily an accurate description
97200-203S.PPT
x Contact Lens-Microbial Infiltrative Keratitis (CL-
MIK.
7L297200-203
Hereafter, the term microbial keratitis, or its
abbreviation MK or CL-MK as appropriate, will be
used in this lecture.
216 Microbial Keratitis: Signs
MK is characterized by:
x Disruption of the corneal epithelium associated
with suppuration of the underlying corneal
stroma (slide 218).
x Bulbar redness.
x A watery or muco-purulent discharge.
x Ulcerative keratitis.
x Acute inflammation, usually with localized loss
of stroma with new white spots (infiltrates)
(Campbell, 1987), usually greater than 1 mm in
7L2SANK-MK
diameter (Munro and Covey, 1999) (slide 219).
x Localized epithelial and stromal oedema.
x In severe cases, hypopyon may develop along
with aqueous flare in the anterior chamber.
Keratic precipitates (kp) may follow.
x Sodium fluorescein stains the lesion rapidly and
the underlying stroma will also stain, giving rise
to the possibility of a halo of stain as the
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 Module 7: Contact Lens-Related Ocular Complications

217 fluorescein spreads beneath Bowman’s layer

(after Grant et al., 1990).
MICROBIAL KERATITIS x The stroma may exhibit striae and/or folds in
SIGNS
• Severe redness advanced, or severe, cases.
• Discharge
- watery x The patient may be sensitive to light.
- muco-purulent
• Inflammation x A reduction in vision is likely if the infection is
• Ulcer with oedema/infiltrates ? severe and/or located at or near the centre of
• Dendritiform epithelial defect (Acanthamoeba) the cornea. Any excessive tearing that results
• Ring of lesions (Acanthamoeba) will also disturb vision, but more variably.
• Infiltrate with feathery margins (fungus)
• May have anterior chamber reaction, hypopyon x In some cases, conjunctival chemosis and
• Lid oedema
97200-135S.PPT
upper eyelid oedema with associated mild to
moderate ptosis may also be seen (Munro and
7L297200-135 Covey, 1999).

218

7L21322-95

219

7L20513-99

220

7L2 ACANTH-EARLIEST

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 Lecture 7.2: SCL Complications and Their Management

221 One of the most serious and difficult to treat

infections is that caused by Acanthamoeba sp. (see
slide series 220-223 courtesy of Dr K McClellan,
Sydney, Australia). Typically, an inflammatory
response around the corneal nerves can be seen.
The earliest signs are characteristically a mottled
dendritic (branching, tree-like) epithelial defect that
looks somewhat like ocular herpes. It can also look
like disciform keratitis with singular or multiple
nummular (coin-like) infiltrates. Once the ring form
shows (slide 221), the diagnosis of Acanthamoeba
keratitis is made easier (McCulley et al., 1995).
Slide 222 also shows the surface disturbance
caused by the infection, i.e. the rough surface and
7L2ACANTH-EARLY
the dull and irregular specular reflection.
222 Moore et al. (1985) also described the presence of
keratic precipitates, a mild anterior chamber
reaction, central epithelial bullae, and superior
nodular scleritis.
If a fungus is the cause of MK, the appearance
includes corneal infiltrates with irregular, feathery
margins, or satellite lesions. The anterior chamber
may also show white cells (Foroozan et al., 2000).

7L2 ACANTH-HI-MAG

223

7L2 ACANTH-LATER

224 Corneal Infection: Symptoms

MICROBIAL KERATITIS Symptoms associated with corneal infection can

SYMPTOMS range from mild to very severe. In the early phases
of the condition, the patient may complain of a
• May be mild irritation to severe pain foreign body sensation and a strong desire to
• Foreign body sensation remove their contact lenses. If lens removal does
not provide at least some relief reasonably rapidly,
• Excessive tearing/discharge then MK should be suspected as the cause of the
symptoms.
• Redness
Possible complaints include:
• Decreased corneal sensitivity
x Excessive tearing.
97200-136S.PPT

x Vision disturbance/loss.
7L297200-136
x Eye redness.
x Swollen lids.

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 Module 7: Contact Lens-Related Ocular Complications

x Reddened lid margins.

x Discharge from the eye, either clear or turbid.
x In advanced stages, corneal infections are
typically very painful conditions. Early stages
are usually relatively comfortable.
Atypically, Acanthamoeba keratitis is usually quite
painful even in the early stages (McCulley et al.,
1995). This may assist in a differential diagnosis of
herpes conditions that typically are not particularly
painful in the early phases, despite having similar
signs.
Acanthamoeba keratitis may also have decreased
corneal sensation associated with it in later stages
(Moore et al., 1985). However, this does not mean
that the condition is pain-free.
225 Corneal Infection: Aetiology

MICROBIAL KERATITIS As the wearing of contact lenses introduces multiple

AETIOLOGY risk factors, the aetiology of MK associated with
• More common in EW (closed eye) contact lens wear is almost certainly multi-factorial.
MK of the cornea is most frequently associated with
• Hypoxia
SCL EW and Pseudomonas aeruginosa (P.
• Bacterial adherence esp. Gram aeruginosa) (Aswad et al., 1990, and Townsend,
negative P. aeruginosa
2000) although fungi, viruses, and protozoa may
• Can be viruses, fungi, or protozoa also cause the disease. Risk factors other than EW
• Protection against disinfection afforded include:
organisms by their own biofilm
x Corneal hypoxia.
97200-137S.PPT
x Overwear.
7L297200-137 x Non-compliance.
x Hygiene/personal hygiene issues.
226
In a mixed population of RGP and SCL wearers,
MICROBIAL KERATITIS Roth (1990) found the following attributions in 88
AETIOLOGY wearers with a corneal infection:
• Organisms in stagnant PLTF
x 70 due to Pseudomonas sp.
• Lens deposits
• Acquired resistance to lens care products x 5 to Pneumococci sp.
• Non-compliance x 4 to Pyocyaneus sp.
- no surfactant cleaner
- no rub and rinse step x 1 to Acanthamoeba sp.
• Low safety margin disinfectants x 3 to Candida sp.
• Some lens materials more deposit prone
x 5 remained unknown (or were called ‘sterile’).
97200-138S.PPT

The use of contact lenses for extended periods of

7L297200-138
overnight wear may make the cornea more
susceptible to infection due to chronic epithelial
hypoxia, an abnormal epithelial mucin layer, and the
increased numbers of organisms present on the
anterior ocular surface.
P. aeruginosa is specifically associated with
cosmetic SCL usage for reasons that are still not
clear (Schein et al., 1989B). Corneal infections
associated with contact lens wear should be
presumed to be caused by the Gram-negative
bacteria P. aeruginosa until proved otherwise
(Weissman, 1996).
However, Alfonso et al. (1986) found that 78% of
contact lens-associated ulcers were caused by
108 IACLE Contact Lens Course Module 7: First Edition
Lecture 7.2: SCL Complications and Their Management

Gram-negative bacteria, 14% by Gram-positive

bacteria and 3% by fungal organisms. Interestingly,
non-lens associated ulcers revealed figures of 45%,
28% and 24% respectively, suggesting that CLs
alter the susceptibility of the anterior eye to
particular classes of bacteria.
Fungi are a possible but improbable cause of MK
unless the patient’s history suggests otherwise.
However, recently (Tanure et al. cited in Foroozan
et al., 2000) reported that 30% of fungal infections
seen in one institution were now associated with
contact lens usage. Their probable cause is usually
eye trauma by vegetable matter especially tree
branches flicking into and abrading an eye, or
encounters with plant material in the garden (after
Nixon, 1998). Practitioners need to recognize that
many ‘convenience’ lens care products have a
relatively poor anti-fungal performance (after Lowe
et al., 1992).
Two cases of non-Acanthamoeba amoebic keratitis
associated with contact lenses have also been
reported (Aitken et al., 1996, who also cited
Kennedy et al., 1995). Lack of storage case
hygiene was blamed.
The ‘mechanics’ of corneal infection and the factors
controlling anterior eye susceptibility to a pathogen
are still not well understood. Originally, it was
thought that an intact epithelium provided an
impenetrable barrier to all microbial forms
(DiGaetano et al., 1986, Dart and Seal, 1988,
Fleiszig, 1990) but this has been shown to be untrue
(Fleiszig et al., 1998).
Another possible contributing factor is the ability of
organisms to attach themselves to either a contact
lens surface (with or without deposits, DiGaetano et
al., 1986, Duran et al., 1987, Aswad et al., 1990),
the lens storage case, or the corneal or conjunctival
epithelium. However, these studies failed to explain
the particular connection between P. aeruginosa
and contact lens wear (Aswad et al., 1990).
Similarly, Dart and Badenoch (1986) showed that
Staphylococcus aureus (S. aureus) adhered to all
lens types, including used lenses, much more than
P. aeruginosa. This suggests that adherence per
se cannot explain the preponderance of P.
aeruginosa-MK in CL-MK.
With regard to P. aeruginosa infection:
x Fleiszig et al. (1992) showed that P. aeruginosa
had enhanced adherence to epithelial cells in
users of EW SCLs.
x Boles et al. (1990) showed that P. aeruginosa
can colonize SCLs in vivo, especially during eye
closure.
x Dart and Seal, 1988 postulated that delayed
access to PMNs afforded the cornea because it
is avascular, may also assist the infection of the
cornea by P. aeruginosa specifically.
x Cheng (1999) found a substantial number of
contact lens wearers lacked detectable IgA
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 Module 7: Contact Lens-Related Ocular Complications

antibodies to P. aeruginosa.
Regardless of the foregoing, the mere presence of
infectious organisms cannot explain corneal
infection (Solomon et al., 1994).
Dart (1999) summarized the current thinking on the
aetiology of MK. He presented the following:
x Bacterial adherence to the lens surface.
x Formation of a bacterial glycocalyx on the lens
and in the storage case.
x Resistance of organisms to the components in
lens care products.
x Inadequate compliance with recommended
wear and care regimens.
x Reduced corneal resistance to infection
resulting, at least partially, from the effects of
hypoxia.
x Stagnation of the tear film under the lens.
x Deposits on the lens surface.
x The effects of the contact lens on the closed-
eye environment.
To this list could be added the following from Efron
et al. (1991):
x Omission of surfactant cleaning.
x Omission of the rub and rinse step.
x Use of disinfectant with marginal efficacy.
x Use of a lens type that attracts, and rapidly
deposits, protein.
The role of the tears and the tear film in infection
are explored more fully in Lecture 7.4 of this
module.
Rabinovitch et al. (1987) reported that contact lens-
associated ulceration was also seasonal (highest in
summer). Katz et al. (1997) reported a similar
finding for ulcerative keratitis (non-contact lens
related) (i.e. highest in summer and autumn).
227 Corneal Infection: Management

MICROBIAL KERATITIS When a corneal infection occurs in a contact lens

MANAGEMENT wearer, it is prudent to assume it is microbial in
• Cease lens wear origin (Schein et al., 1994) until proved otherwise.
• Should it be treated as an emergency? Once the existence of a corneal infection is
• Experienced anterior eye professional required suspected, all lens wear should cease and an
• Cultures or swabs of: ophthalmological opinion sought. Any infiltrates with
- eye (lesion) overlying epithelial defects, and all epithelial lesions
- lens case should be treated as potential infections, or even an
- solutions ocular emergency until proved to be otherwise (after
Gottschalk, 1988, Grant et al., 1990, Nixon, 1998).
• Dictated by causal organism and severity
97200-139S.PPT
Mismanagement of MK cases, including no
7L297200-139 management at all, can have devastating, long-term
effects on visual capacity. The loss of an eye is a
realistic possibility and the loss of both eyes has
been reported (Chalupa et al., 1987).
When considering contact lens-associated eye

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 Lecture 7.2: SCL Complications and Their Management

228 infections, it is necessary to take an all-

encompassing approach. Factors to be considered
MICROBIAL KERATITIS include:
MANAGEMENT
• Antibiotics x The eye and its state of health.

• No steroids until infection controlled x Lens type and their condition.

• No patching x Mode of lens wear.

• Monitoring until resolved

x Lens case and its condition/contamination
status.
• Delay resumption of lens wear
x Lens care products and their efficacies.
• Change lens type and/or wear mode ?
97200-140S.PPT
x Personal hygiene.

7L297200-140
x The level of wearer compliance with practitioner
instructions, especially in relation to lens care
product usage.
One reason for this approach is the frequency with
which the same organism responsible for an
episode of MK can be recovered from the lens case
and/or the lens care solutions used by the patient
(Golden et al. 1971, Cooper and Constable, 1977,
Lebow and Plishka, 1980, Wilson et al., 1981,
Adams et al., 1983, Moore et al., 1985, Mondino et
al., 1986, Wilson and Ahearn, 1986, Chalupa et al.,
1987, Bottone et al., 1992). However, significant
(52%) lens case contamination, and contamination
of lens care solutions (13%) in asymptomatic
contact lens wearers (Donzis et al., 1987) suggests
strongly that contamination per se is not sufficient to
cause an episode of MK.
To help limit any condition’s progress, wearers
should be counselled generally from the first
consultation: ‘If in doubt, take them out’. Such a
message should also be reinforced at each
subsequent opportunity.
Usually, the type of organism causing the infection is
determined by microbiological analysis (culturing
biopsy material recovered from the infected cornea
or, at the very least, the taking of a swab from the
adjacent fornix). This is followed by the application
of the most efficacious therapeutic agent available,
often intensively.
Once therapy is commenced, the patient must be
monitored closely. Should the initial regimen prove
to be unsatisfactory, an alternative treatment must
be initiated promptly. Under these circumstances it
is often necessary to re-evaluate the original
diagnosis and/or identification of the supposed
causative organism with a view to confirming or
revising the original conclusion. This occurs when
Acanthamoeba is not suspected initially, but
confirmed subsequently, largely as a result of the
failure of the initial treatment(s).
A return to contact lens wear must be considered on
a case-by-case basis. The type of lenses and
wearing schedule should be carefully reviewed to
ensure that the risk of further corneal infection is
minimized.
There is general agreement in the literature as to the
undesirability of applying steroids to contact lens-
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 Module 7: Contact Lens-Related Ocular Complications

associated epithelial defects, including that caused

by Acanthamoeba keratitis (Brown et al., 1974,
Chalupa et al., 1987, McCulley et al., 1995,
Weissman, 1996). The adverse effect of steroids on
corneal healing is probably due to their
immunosuppressive effects, the negative effects on
epithelial metabolism, and the rate of re-
epithelialization.
Unless and until infection is ruled out via culturing,
no eye patching should be undertaken. However,
the efficacy of patching has been challenged (e.g.
Harkins, 1996, Arbour et al., 1997).
Finally, there are the issues of patient compliance.
In many reports, including those related to
Acanthamoeba keratitis, the recurring theme of non-
compliance, some bordering on gross irresponsibility
(e.g. Heidemann et al., 1990, Aitken et al., 1996), is
presented. If lens care is attempted, it is often with
unapproved or inappropriate products including
home-made saline using the combination of tap
water and salt tablets (Wilson et al., 1981).
Unless the wearer is complying with practitioner
instructions to at least the minimum level compatible
with safety, there will always be an increased risk of
complications with contact lens wear. It has been
shown that even with full compliance the risk
associated with wearing contact lenses is not zero
(e.g. Killingsworth and Stern, 1989). Any factor
adding to this risk must be addressed.
If an episode of CL-MK occurs in EW, it is probably
prudent to switch the wearer to DW once the
resolution of the problem is confirmed.
If the wearer is a regular gardener, advice on
suitable eye protection should be given to reduce
the risk of a fungal infection.
Regardless of the factor(s) involved in the disease
originally, it would seem prudent to revise carefully
the lens type, wear mode, lens care product choice,
and all compliance issues in order to reduce the
possibility of a recurrence of MK.
III.I CLARE

229 Contact Lens-induced Acute Red Eye (CLARE):

Introduction
CLARE: INTRODUCTION CLARE is an acute inflammatory response
• An acute inflammatory response usually associated almost always with SCL EW (Holden et
associated with SCL EW al., 1996). It is also known as Acute Red Eye
• Sudden onset, usually early AM (ARE), Contact Lens-Associated Red Eye (CLARE),
or sometimes simply red eye (in contact lens
• Presentation is dramatic
wearers).
• 5% - 30% incidence in SCL EW, 4% in
disposable SCL EW Some characteristics of CLARE follow:
• More likely in first 3 months of lens wear x An acute and dramatic presentation of a
• More common in female wearers reddened contact lens-wearing eye.
97200-214S.PPT

x Usually unilateral but can be bilateral.

7L297200-214
x Redness readily apparent over the whole of the
bulbar conjunctiva (360°).
x Spectacular in appearance, tending to

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 Lecture 7.2: SCL Complications and Their Management

exaggerate the ‘seriousness’ of the condition.

– this leads the wearer to remove lenses
immediately and seek professional help
promptly.
x Onset is frequently in the early hours of the
morning. CLARE has been called ‘3 AM
syndrome’ to mirror the experience of many
CLARE patients.
x Depends on lens type, care regimen and lens
replacement frequency.
x Is more likely to be experienced within the first
three months of lens wear.
x Sankaridurg et al. (1999) reported 12.3 CLARE
events per 100 wearers per annum based on
data from 102 wearers during the first 13
months of EW using disposable hydrogel
lenses.
x In EW the time between lens
removals/replacements was a factor in the
incidence of CLARE (Crook, 1985).
x Has a much greater incidence in females
(Crook, 1985).
x Is seasonal. New cases of CLARE rose to
7.41% in late winter (Soni and Hathcoat, 1988).
x The highest figure reported is 41% in non-
replaced lenses (Zantos, 1984).
230 Contact Lens-induced Acute Red Eye (CLARE):
Signs
CLARE signs include:
x Significant ocular redness involving limbal and
conjunctival vessels (slide 232).
x A watery discharge that may border on the
profuse (slide 232).
x A slit-lamp examination usually reveals the
presence of either focal stromal infiltrates (slide
233) or widespread diffuse stromal infiltrates
accompanied by isolated, dense, or focal areas
of infiltration.
7L2SANK-CLARE
– the infiltrates are usually within 2-3 mm of the
limbus (because of their vascular origin, and
231 the avascular nature of the cornea).
CLARE x Central corneal oedema may also be observable
SIGNS (Munro and Covey, 1999).
• Moderate to severe ocular redness
x The limbus is also frequently oedematous
- may have 360° conjunctival redness (Williams, 1978).
• Diffuse infiltrates (2-3 mm from limbus) x Epithelial staining is rarely seen and if present is
generally minimal, e.g. mild micropunctate
- may also have focal zones of infiltrates
staining at worst.
• Minimal or no staining
x Sodium fluorescein pooling, as opposed to
• Lacrimation, often profuse staining, may be observed in cases in which
97200-141S.PPT
debris has been trapped under a lens leading to
7L297200-141
epithelial indentation. Pooling occurs in the
indentation.

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 Module 7: Contact Lens-Related Ocular Complications

232 x Increased mucus (Koetting and Boyd, 1978).

x Decreased lens tolerance (Koetting and Boyd,
1978).
x CLPC (Koetting and Boyd, 1978).

7L20142-91

233

7L20413-96

234 Contact Lens-induced Acute Red Eye (CLARE):

Symptoms
CLARE
SYMPTOMS In cases of CLARE:
• Patient woken (often early AM) by a x The patient is either woken from sleep by a
painful eye
painful eye or eyes, or immediately after waking,
they note the presence of pain.
• Photophobia x Tearing.
• Lacrimation x The pain may be moderate to severe (Holden et
al., 1996).
• Ocular irritation
x Mild to moderate light sensitivity is always
97200-142S.PPT
associated with CLARE.
7L297200-142
x Eye irritation, in addition to the pain, may also be
reported.
235 Contact Lens-induced Acute Red Eye (CLARE):
Aetiology
CLARE
AETIOLOGY By definition CLARE is a complication associated
• Extended wear (closed-eye hypoxia) with extended wear of contact lenses.
• Lens binding overnight The following summary of aetiological factors follows
- entrapped debris & deposits that presented by Grant et al. (1990):
• Gram-negative bacteria x A toxic response to cellular debris trapped
• Sensitivity to lens care products beneath a relatively immobile lens.
• Debilitated general health x Trauma, or physical/anatomical ramifications of
• Some seasonal variation a poorly fitting, or inadequately moving, lens.
97200-143S.PPT
There can be little justification for such a
situation being allowed to continue.
7L297200-143
x Bacterial contamination. This is an area still
114 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

under investigation with mounting evidence

supporting the claim. The most likely cause is
the action of Gram-negative bacterial toxins that
initiate an immune or an inflammatory response
in the eye during sleep. Gram-negative bacteria
(P. aeruginosa, P. putida and Serratia
marcescens) have been isolated in significantly
greater quantities from CLARE cases than from
other conditions in which organism culturing was
undertaken. However, it is probable that the
biggest single source of lens contamination is
still the wearer’s hands.
x An allergic/toxic response to long-term exposure
to lens care systems and their preservatives.
This is now less of a problem with modern, more
compatible, and less toxic lens care
components. Lens care products have also
been shown to be a possible source of lens/eye
contaminants, especially bulk, unpreserved
saline solutions (Sweeney et al., 1992).
x Residues of manufacturing processes remaining
in and on lenses. With highly automated and
tightly-controlled lens production, especially as
used for modern disposable lenses, this would
now seem to be an unlikely cause.
x Tear protein accumulation on and in lenses.
x The general health of the lens wearer, especially
episodes of colds, influenza, or general debility.
An important association in many cases is with
the patient’s poor general health during the
day(s) leading up to the CLARE event. This
suggests the immune system may be
compromised, thereby allowing the bacterial
toxins to produce a response greater than might
otherwise have been.
x Seasonal variation of CLARE has also been
reported with the condition being more likely to
occur in winter (Koetting and Boyd, 1978, Soni
and Hathcoat, 1988). Koetting and Boyd
concluded that a sensitivity to airborne allergens
and bacteria was unlikely to be the cause of
CLARE given its seasonality, but that household
moulds, dust, or even reduced indoor humidity
from home heating, may be implicated.
236 Contact Lens-induced Acute Red Eye (CLARE):
Management
CLARE
MANGEMENT The majority of CLARE events are self-limiting in
nature. Their management follows a conservative
• Temporary discontinuation of wear
and logical path including:
• Palliative therapy
x Immediate lens removal (mandatory). This
- saline rinse (sterile) usually leads to a complete resolution of the
- lubrication symptoms.
• Regular lens replacement x Monitoring the accompanying infiltrates carefully
• Low toxicity lens care products
as these usually take 2-3 weeks to disappear
but can take up to 3 months (Grant et al., 1990,
97200-144S.PPT
Holden et al., 1996). If the sensitivity to light
7L297200-144 causes difficulties when using a slit-lamp, a drop
of local anaesthetic may alleviate the problem

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 Module 7: Contact Lens-Related Ocular Complications

237 (Grant et al., 1990).

x Confirm that any epithelial staining healed
CLARE quickly and ascertain that there is no residual
MANGEMENT
corneal or conjunctival staining before restarting
• Monitor recovery
lens wear. Recurrence of CLARE is likely in up
- complete resolution of infiltrates
to 50% of lens wearers who resume EW after
- about 1-3 weeks
‘resolution’ of the initial episode (Sweeney et al.,
• Re-start with DW initially
1993).
• Caution with continued EW
- optimize fitting x Rule out the possibility of MK by confirming that
- change lens type there are no infiltrates with overlying epithelial
- change lens care products defects.
• Monitor for recurrence
97200-145S.PPT x Usually, there is no need for therapeutic
7L297200-145
intervention (Grant et al., 1990). However, in
rare cases the use of antibiotics for prophylaxis
may be required.
x Recommence lens wear with new lenses worn
on a daily wear basis. Consideration should be
given to the availability of lenses with better
designs, physiological performance, physical
properties, etc.
x Any return to extended wear must be delayed
until a full recovery is achieved. Close
monitoring of resumed EW is required because
the likelihood of a recurrence of CLARE in EW
is high (Koetting and Boyd, 1978, Grant et al.,
1990), and multiple recurrences are possible
(Sweeney et al., 1993).
x Patient education is vital to ensure that the risk
is minimized. If recurrence becomes an issue it
is possible that contact lens wear may have to
be stopped, perhaps permanently.
Palliative measures include:
x Frequent use of saline to soothe and lubricate
the eye and to remove tear debris.
x Cold compresses to reduce the inflammation.
x Artificial tears.
III.J CLPU & CNPU

238 Contact Lens-induced Peripheral Ulcers (CLPU)

and Culture-Negative Peripheral Ulcers (CNPU):
CLPU/CNPU: INTRODUCTION Introduction
• Corneal ulceration may not be CL-related According to some sources that are not contact
• CLs are the most ‘important’ risk factor lens-specific, e.g. Kanski’s Clinical Ophthalmology,
• Defined as: what are called CLPUs here are referred to as
‘ulceration of the corneal epithelium with
underlying inflammation of the corneal variants of marginal keratitis. Increasingly, the
stroma’ contact lens literature is moving towards being more
• Corneal scrapes are culture-negative specific about contact lens-related conditions and
- if not, condition is a microbial keratitis the CLPU terminology is used here.
• Condition is inflammatory
• Ulcer usually located peripherally Contact Lens-induced Peripheral Ulcers (CLPUs) or
97200-213S.PPT
Culture-Negative Peripheral Ulcers (CNPUs) are so-
called ‘sterile’ or ‘culture-negative’ corneal ulcers.
7L297200-213
Other terms used include peripheral sterile infiltrated
ulcers, contact lens-associated sterile ulcers, etc.
The use of the term ‘sterile’ in this context should be
viewed as an indication of a failure to culture a
causative organism rather than a claim that there is

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Lecture 7.2: SCL Complications and Their Management

no organism involved in the aetiology of the ulcer

(see III.J CLPU & CNPU: Aetiology).
Although not necessarily a direct consequence of
being ‘sterile’, CLPU/CNPUs are generally less
serious than MK (Grant et al., 1998), generally
induce less severe pain, less redness, and are
accompanied by little or no inflammatory response
in the anterior chamber.
The literature suggests that between 17.2% and
60% of contact lens-associated ulcers are ‘sterile’
and usually do not constitute a serious threat to the
visual welfare of the wearer experiencing such an
episode (Alfonso et al., 1986, Donnenfeld et al.,
1986, Rabinovitch et al., 1987, Campbell, 1987,
Cohen et al., 1987, Momose et al., 1989, Cohen et
al., 1991, Laibson et al., 1993, Goyal et al., 1994,
Cohen et al., 1996).
In a 45-month study of SCL EW, Sweeney et al.
(1993) showed than, unlike CLARE, CNPU did not
recur during the study. They also showed that the
average time to the first occurrence was about two
years but could be as little as 3-4 months.
A significant number of cases go unreported. RGPs
produce fewer ulcers, and uncontrolled EW produce
the most (70X) (Roth, 1990).
The incidence of CLPU/CNPU is difficult to ascertain
because of the overriding concern for the infectious
form of ulceration. Sankaridurg et al. (1999)
estimated an ‘event’ incidence of 13.6% per patient
year. For SCL EW, Grant et al. (1998) gave figures
of:
x 2.9% per patient year for conventional lenses.
x 2.0% per patient year for disposable lenses.
x 1.6% per patient year for intermittent EW.
x <0.5% per patient year for DW.
The advent of disposable lenses did not decrease
the incidence of ulcers as much as anticipated
(Dunn et al., 1989, Kent et al., 1989, Goyal et al.,
1994). To the contrary, disposable lenses have
been associated with higher incidences of corneal
complications including ulcers (Mondino et al., 1986,
Dart et al., 1991, MacRae et al., 1991). However,
the reasons for these counter-intuitive findings
remain unclear although much longer wearing times
have been used to explain this ‘anomaly’, if in fact it
is an anomaly (after Grant et al., 1998).

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239 CLPU and CNPU: Signs

CLPU/CNPU In cases of CLPU/CNPU the typical signs are:

SIGNS x CLPU/CNPUs usually present singly as small,
• Small, single, circular focal infiltrate circular, very dense sub-epithelial focal infiltrates
- halo of diffuse infiltration (slides 241 and 242) in the mid-periphery of the
cornea up to 2 mm in diameter (Grant et al.,
• Usually peripheral, not central
1998) but more commonly 0.5 to 1.5 mm (Goyal
• Located in anterior stroma et al., 1994 found 77% were d1.00 mm). The
• Overlying epithelium breached infiltrate is surrounded by diffuse infiltrative
• Redness (local and general) material in the anterior stroma. The infiltrates
come from the stromal and limbal blood vessels
• Tearing
97200-146S.PPT (Campbell, 1987).
7L297200-146 x The affected eye is usually very red.
x A watery discharge is present.
240 x Usually, an evaluation with sodium fluorescein
indicates that the overlying epithelium is
compromised.
x In some cases, a full-thickness excavation of the
epithelium can be seen.
x Bowman’s layer remains intact (CCLRU/LVPEI
Guide to Infiltrative Conditions, 1999).
x The ulcers tend to be self-limiting (Grant et al.,
1998), and usually have no anterior chamber
involvement.
x There is usually a clear band or zone between
7L2CLPU.TIF peripheral infiltrates/ulcers and the limbus
(slides 241 and 242). This is thought to be a
result of the ability of the limbal vasculature to
241 deal with infiltrative material close to itself, but
not material further away (after Fisch, 1990).
x If sodium fluorescein is instilled into the eye, a
fluorescein halo may often be seen around the
ulcer (slides 243 and 244) as the fluorescein
traverses the defective epithelium and then
spreads into the subepithelial and anterior
stromal zones.
To differentiate ‘sterile’ from infected infiltrates, the
following was presented by Stein et al. (1988).
Compared to infected conditions, sterile infiltrates
are:
7L20391-98 x Usually smaller.
242 x Multiple or arcuate.
x Without significant pain.
x Without epithelial staining.
x Without anterior chamber involvement.

7L20918-9

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 Lecture 7.2: SCL Complications and Their Management

243

7L20288-91

244

7L200419-00

245 CLPU and CNPU: Symptoms

In general a CLPU/CNPU is associated with:
CLPU/CNPU
SYMPTOMS x Significant to severe ocular pain. However, it is
• Asymptomatic to severe pain possible for CLPU cases to have only mild
symptoms or in some cases, no symptoms at all
• Foreign body sensation due to the bandage effect of a SCL worn on an
extended wear basis (after Fisch, 1990).
• Photophobia
x Symptoms are generally less severe than those
• Decreased corneal sensitivity experienced in ulcerative keratitis (MK).
x Sensitivity to light.
• May report a preceding condition
97200-147S.PPT
x Decreased corneal sensitivity.
7L297200-147
If vision is reduced, either the severity of the
condition is greater than initial impressions may
suggest or the ulcer is located closer to the visual
axis. The location and the extent of ocular redness
may also indicate the location, and to a lesser extent
the severity of the ulcer.
Some cases may have had a preceding
Staphylococcal blepharoconjunctivitis. Typically,
such ulcers start as a superficial stromal infiltrate,
with an intact overlying epithelium that breaks down
subsequently (Fisch, 1990).
In addition to the signs observed, a detailed history
is essential to the differential diagnosis of MK versus
CLPU/CNPU. Careful questioning as to recent
corneal trauma is necessary, e.g. botanical material
entering or abrading the eye in a garden, a foreign
body entering the eye, etc., to ascertain the
likelihood of the complaint and symptoms being due
to MK rather than CLPU/CNPU.

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246 CLPU and CNPU: Aetiology

Ulcerative keratitis is normally defined as an
CONTACT LENS PERIPHERAL ULCER
inflammation of corneal tissue characterized in
AETIOLOGY
whole or in part by significant epithelial compromise
• Bacterial toxins
with epithelial and/or stromal infiltrates and possible
- Staphylococcus sp.
stromal ‘melting’. Ulcerative keratitis was defined by
- Corynebacterium sp. Erie et al. (1993) as ‘ulceration of the corneal
• Culture-negative epithelium with underlying inflammation of the
• Interaction of lens & epithelial surfaces corneal stroma’.
• Scarring due to post-inflammatory
cicatrization Ulcerative keratitis may not necessarily be microbial
• Seasonal factor may apply
in origin. Generally, the word ‘ulcer’ means any
97200-148S.PPT
break in the continuity of the epithelium covering a
surface, especially with a defined ‘crater’.
7L297200-148
The most likely cause of a CLPU/CNPU is bacterial
toxins affecting anterior corneal tissue. Importantly,
studies indicate that if the Gram-positive bacteria
Staphylococcus sp. and Corynebacterium sp. are
present in greater than normal numbers, wearers
are more likely to experience a CLPU/CNPU.
Staphylococcus is also the same genus that causes
non-lens related corneal ulcers (Baum and
Boruchoff, 1986).
Risk factors for CLPU/CNPU are:
x SCL EW (Hassman and Sugar, 1983, Adams et
al., 1983, Weissman et al., 1984, Baum and
Boruchoff, 1986, Donnenfeld et al., 1986, Cohen
et al., 1987, Poggio et al., 1989, Poggio et al.,
1989, Schein et al., 1989, MacRae et al., 1991).
Schein et al. (1989) suggested that the risk of
ulcerative keratitis in SCL EW is 10 to 15 times
greater than in DW. Willcox et al. (1995) go so
far as to state that CNPU occurs only in SCL
EW.
x A cornea predisposed to ulceration by being
compromised in some way beforehand (after
Tripathi et al., 1994).
x Diabetes (Adams et al., 1983).
x Aphakia (Adams et al., 1983).
Schultz et al. (1997) found that purified
lipopolysaccharide derived from either P. aeruginosa
and S. marcescens can cause CLARE and corneal
ulcers in the absence of live bacteria. However, it is
impossible to claim that micro-organisms are not
implicated in such ulcers.
Willcox et al. (1995) found that CNPU-associated
lenses were contaminated with species of Gram-
positive Staphylococcus or Corynebacterium or
species of Gram-negative Pseudomonas, Moraxella
or Serratia bacteria. Following an analysis of their
data, Willcox et al. found that when lenses harbour
high levels of Gram-positive bacteria, wearers are
more likely to develop CNPU than other wearers.
Fisch (1990) suggested an antigen/antibody reaction
to Staphylococcus sp. as a probable cause of
CLPU/CNPU.
The post-inflammatory scarring that may remain is
due to corneal tissue cicatrization.

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 Lecture 7.2: SCL Complications and Their Management

CLPU/CNPUs have been reported in wearers of

siloxane hydrogels (e.g. Holden et al. (2000). This
suggests that hypoxia per se is not a key aetiological
factor.
Rabinovitch et al. (1987) did suggest non-
compliance may be a factor. However, patient
compliance is apparently not a key factor in
CLPU/CNPU because Cohen et al. (1987) only
found 15% of ulcer cases were non-compliant
wearers.
Seasonal factors have also been confirmed by
Rabinovitch et al. (1987) who showed that corneal
ulcers are more likely in summer.
Current thinking leans towards the involvement of
epithelial trauma caused by the interaction between
the lens and corneal epithelium which, along with
bacterial contamination, appear necessary to
produce CLPU/CNPU (Holden et al., 2000).
247 CLPU and CNPU: Management

CONTACT LENS PERIPHERAL ULCER x All contact lens wear should cease and
MANAGEMENT treatment be instigated immediately. Generally,
the ‘sterile’ nature of the CNPU ensures that the
• Discontinue lens wear immediately initial stage of the healing response is rapid.
• Generally, healing is rapid x It is prudent to treat all ulcers as cases of
• Monitor carefully for first 24 hrs
microbial keratitis (MK) until proved otherwise
(after Goyal et al., 1991) because of the
• Prophylaxis potentially serious consequences of an early
misdiagnosis, especially if Pseudomonal. Early
• Resolves with scarring
intervention is essential to a good prognosis,
97200-149S.PPT visual loss minimization, and the avoidance of
the possibility of a penetrating keratoplasty (after
7L297200-149
Kenyon and John, 1994).
x Careful monitoring in the early stages is required
in all cases. Several authors emphasize the
desirability of patients reporting earlier (small
ulcers) rather than later (larger, deeper, more
developed ulcers) (Cohen et al., 1987, Derick et
al., 1989). Pain is a useful indicator of progress
of the disease. If a substantial reduction on the
second day is reported, it is likely that the
infiltration of the affected area will resolve. If the
pain gets worse it is likely that the ulcer is
infective (bacterial) and the causative organism
is not in check (after Campbell, 1987).
x Assess the degree of epithelial staining.
Generally, in cases where the epithelium is
compromised, the use of a prophylactic
antibiotic is recommended. However, antibiotics
in cases of a simple CNPU are probably of little
use (see McLaughlin et al., 1989). Recovery of
epithelial integrity may occur very rapidly.
However, the signs of inflammation such as
stromal infiltrates may take many days to
resolve completely.
x The sub-epithelial region corresponding to the
location of the dense focal infiltrate resolves with
a circular scar that is less opaque in the centre
producing a ‘doughnut’ appearance (see slide

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242 under CLPU and CNPU: Signs). If the

scar is central or paracentral, vision may be
adversely affected (Tripathi et al., 1994).
x A motivated wearer can resume contact lens
wear once the ulcer scar is healed and the
anterior eye is apparently normal. However, if
there are indications of dry eye, exposure
keratitis, or any dystrophy or abnormality of the
eye surface or cornea, the risk of recurrence
can be expected to be higher (after Campbell,
1987).
x Compliance with lens care instructions and
caution about lens care product ‘use by’ and
‘discard after’ dates and times is also necessary
if the number of preventable cases of
CLPU/CNPU is to be reduced.
x If CLPU/CNPU was apparently secondary to a
staphylococcal infection of the lids, lid hygiene
measures may be useful (after Fisch, 1990).
III.K Corneal Scarring

248 Corneal Scarring: Introduction

Corneal scarring may or may not be associated with
CORNEAL SCARRING contact lens wear. If traumatic in origin, it is
• May not be associated with contact probable that it is not contact lens-related as the
lenses latter affords the cornea some (SCL), or significant
• Contact lenses offer the cornea some (RGP), impact protection (see Module 9, Lecture
protection against 9.3, Section II.B Mechanical Hazards).
- impact
A complication to the healing process occurs when
- splash
astigmatism is induced by scar tissue formation in
- vapour (often a delay only) the cornea. The resulting glare, the optical
• Accurate baseline assessment essential irregularity, and any opacity remaining, all affect
97200-212S.PPT
vision, especially when located centrally or
paracentrally.
7L297200-212
Some scarring heals almost completely while other
instances heal little, or very slowly (after Kilp et al.,
1982), sometimes with the induction of ‘fairly
marked’ astigmatism (Conway and Wagdi, 1983).
249 Corneal Scarring: Signs

CORNEAL SCARRING The shape and location of a scar depends primarily

SIGNS on:
• Depends on cause x The cause.
- trauma x The severity of the original problem.
- infection/infiltration x The depth to which the cornea is affected (e.g.
• Circular scars are most common slide 250 shows anterior chamber, and probably
crystalline lens, involvement).
- anterior stroma
The regularity of the resulting lesion and any effect it
- usually less than 1mm diameter
may have on corneal topography depends on the
97200-150S.PPT
initial cause:
7L297200-150 x It can be irregular if traumatic.
x More regular if infective.
x Spread relatively widely if it is due to poor
physiological performance, pervaporation
desiccation, or toxicity/hypersensitivity.
Corneal scars are observed commonly when

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 Lecture 7.2: SCL Complications and Their Management

250 examining the external eye with a slit-lamp. Small

circular scars located at the sub-epithelial level are
easily observed with direct focal illumination and
medium to high magnification (slide 251). However,
in some cases the actual extent of the scar may be
more apparent. In this circumstance, retro-
illumination (direct, indirect, or marginal) will be
required to reveal the full extent (slides 251 and
252), and the optical effect of any such defect.
Sclerotic scatter may reveal very subtle scars,
especially if they are very diffuse or involve relatively
large areas.
Barr et al. (1996) described a photo-documentation
7L21775-93 system for recording and evaluating corneal scars.
Their results led them to suggest that the system
developed was suited to, and valid for, use in multi-
251 centre studies

7L21592-95

252

7L2324-98

253 Corneal Scarring: Symptoms

CORNEAL SCARRING In the vast majority of cases of corneal scarring the

SYMPTOMS patient is unaware of their presence. Furthermore,
most are unable to provide any relevant history, i.e.
• Many are asymptomatic the patient has no symptoms at presentation and no
recollection of symptoms that might explain the
- no history of ocular problem current appearance of their eye.

- bandage effect of soft lens

Should a scar be caused by infiltrative or
inflammatory mechanisms, it is probable that, while
• Pain associated with trauma the lenses are worn, their bandage effect helps the
patient remain asymptomatic. This possibility needs
97200-151S.PPT
to be explored at each after-care visit in case a
subclinical condition exists with no symptoms to
7L297200-151 ‘disclose’ its presence.
As most scars are a later/late manifestation of a
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 Module 7: Contact Lens-Related Ocular Complications

healing or adaptation process, it is likely that the

original condition that caused the scar produced
more symptoms than the scar per se.
Unless central or paracentral corneal areas are
involved, the vision is unlikely to be affected.
If the scar is big enough to be visible to the naked
eye (wearer, or observer), then a cosmetic issue
exists and the wearer may complain about their
appearance.
254 Corneal Scarring: Aetiology

CORNEAL SCARRING The fundamental corneal tissue changes that result

AETIOLOGY in scarring are essentially a disruption of the regular
stromal lamellar structure. Traumatic penetrating
• Penetrating injury injury to the cornea always results in scar tissue due
to the damage to Bowman’s layer of the anterior
- damage to Bowman's layer
stroma.
- disruption of stromal lamellae Inflammation of the anterior stroma, such as occurs
• Severe infiltrative response in CLPU, is capable of forming a permanent scar
(see slide 242 under CLPU/CNPU). Similarly, a MK
• Infection infection can also result in scarring, an
97200-152S.PPT
Acanthamoeba infection probably being an extreme
example.
7L297200-152
A major cause of corneal scarring in contact lens
practice is keratoconus. This, and related matters,
are dealt with separately in Module 8, Lecture 8.1:
Keratoconus).
Ruben (1975) attributed some corneal scarring to
lens forces acting for protracted periods of time on
the cornea. Scarring as deep as the anterior stroma
was attributed to these zones of localized pressure.
However, such pressures are routinely applied
during orthokeratology procedures with special rigid
lenses, usually without any adverse outcome.
Weissman et al. (1986) reported the case of an
aphakic lens wearer with a ‘mulberry’ lens deposit,
colonized by micro-organisms that damaged the
cornea. A small corneal scar eventuated with no
permanent visual impairment.
255 Corneal Scarring: Management

CORNEAL SCARRING The most obvious management strategy is to avoid

MANAGEMENT the causes of corneal scarring, or to reduce
• Dictated by size and location exposure to the risk factors for scarring.
- central versus peripheral Most cases of corneal scarring require no
management other than educating the patient about
- irregular topography
the presence of the scar. Should the scar be of
• Usually no ill effects significant size, or unacceptable cosmetically or
• Consider risk of recurrent erosion topographically, it is probable that PTK (Photo
• Don't recommence contact lens wear Therapeutic Keratectomy) may offer at least a partial
too soon solution.
97200-153S.PPT
In some cases with a traumatic aetiology, the long-
7L297200-153
term risk is that the epithelium may be susceptible to
recurrent erosion of the affected area. As
prevention is better than cure, the use of safety
eyeware when appropriate should eliminate most
potential traumatic threats to the eye.
If the scarring is a result of active inflammation
associated with contact lens wear, the practitioner

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Lecture 7.2: SCL Complications and Their Management

must ensure that the cornea has recovered fully,

prior to recommencement of lens wear. This allows
the epithelium to attach firmly to the basal lamina
(basement membrane), reducing the chance of a
corneal erosion occurring later.
Dada et al. (1975) reported high success rates using
rigid contact lenses in cases of scarred corneas.
Kok et al. (1991) suggested the use of highly oxygen
permeable, aspheric RGP contact lenses as one
way of obviating the need for corneal surgery in
severe cases. Horner et al. (1991), and Kanpolat
and Çiftçi (1995) made a similar recommendation in
the case of post-traumatic scarred corneas,
especially following perforating injuries.
In most cases, once the cause of corneal scarring is
identified and eliminated, and the healing process is
complete, it is probable that contact lenses are also
the solution to any subsequent vision problems. In
some cases the type of lens may need to be
changed, e.g. RGP or siloxane hydrogel lenses may
be required by a wearer who used SCLs originally.

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 Module 7: Contact Lens-Related Ocular Complications

IV Lens and Lens Fit-Related Complications

IV.A Lens Fitting Problems

256 Lens Fitting Problems: Signs

As the quality and characteristics of an SCL fit are
FITTING PROBLEMS
SIGNS
important to the maintenance of anterior eye health,
a careful assessment of lens fitting characteristics is
• Decentration important. Adequate but not excessive lens
• Corneal coverage movement is a key factor in successful lens
- inadequate performance, ocular physiology, and comfort.
- limbal exposure The primary lens fitting factors are:
• Movement on blinking x Centration.
- limited x Tightness.
- excessive
x Movement.
97200-191S.PPT

Poor centration (slides 260 and 261) results in

7L297200-191 inadequate or variable coverage of the limbus that
may produce epithelial fluorescein staining. In
extreme cases of decentration involving little or no
257 lens movement despite blinking, the lens may indent
FITTING PROBLEMS the cornea (less likely) and/or conjunctiva (more
SIGNS likely). This indentation is best seen with a slit-lamp
• Lag on eye movement using tangential illumination at low magnification (7X
- horizontal gaze – 10X) (slide 262).
- vertical gaze After lens removal, and the instillation of sodium
• Tightness fluorescein dye, indentation is disclosed by
- push up test fluorescein-stained tears pooling in the depression,
and/or the staining of the indentation’s perimeter
- excessive
due to epithelial damage caused by the heavy
- loose, inadequate
bearing of the lens edge (slide 263). Any lens
- recentration speed movement is likely to increase the size of the areas
disclosed.
97200-192S.PPT

7L297200-192 Lens tightness is assessed most validly by the lower

lid push-up test. Excessive tightness restricts the
removal of debris from the post-lens tear layer by
258 frustrating post-lens tear film circulation and may
FITTING PROBLEMS also produce limbal and bulbar redness,
SIGNS compression of the blood vessels, and in extreme
• Retinoscopy reflex cases, vessel closure leading to cessation of blood
- central shadow (steep) flow. The latter shows as a blood column that
- peripheral distortion (flat) appears to stop at the pressure point, usually the
• Over refraction lens edge, i.e. arteries appear beyond the lens edge
- variable and cease at or near the lens edge while veins
• Keratometer mires appear under the lens, stop at or near the lens edge,
- irregular and are not visible beyond the lens.
- improve on blinking (steep) Perilimbal conjunctival indentation is another
- change on blinking (flat) possible sign of a tight lens fit (slide 262).
97200-194S.PPT

Reduced or no lens movement may be indicated by

7L297200-194
a build-up of ocular debris in the post-lens tear film,
and circumferential conjunctival redness that may be
accompanied by the signs of lens tightness
presented previously.
SCL fitting issues are covered in some detail in
Module 2, Lecture 3.2: Spherical SCL Fitting and
the Effects of Parameter Changes.
A lens that is too loose can be seen to either move
excessively, or decentre significantly with, or without
movement on blinking.
A lens that is excessively flat may exhibit edge
fluting (wavy lens edge) as it endeavours to ‘fit’ its
126 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

259 actual circumference into its on-eye size (soft lens

conformance results in a steeper lens shape, and a
FITTING PROBLEMS smaller circumference).
SIGNS A lens that is very loose may not stay on the eye.
• Edge stand-off
Rather, it may be dislodged from the eye by a blink
- flat fit
because of edge stand-off or edge fluting interacting
- inside-out lens
with the lid margins, especially of the lower lid.
• Ocular changes
- redness Excessive lens movement may also be disclosed by
- staining fluorescein staining of the area traversed by the lens
— cornea edge, especially if the area affected is not covered
— conjunctiva by the lid all or most of the time. Interestingly, these
- palpebral conjunctiva same wearers typically do not encounter problems
97200-193S.PPT when no lenses are worn at all, i.e. total corneal
exposure in those areas not normally covered by the
7L297200-193
lids except during a normal blink.
260
Other clinical signs that are the result of an ill-fitting
lens are presented in slides 256 to 259.

7L20930-93

261

7L20086-99

262

7L2SCL INDENT

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263

7L23093-93

264 Lens Fitting Problems: Symptoms

FITTING PROBLEMS A wide range of symptoms may be associated with

SYMPTOMS poor SCL fitting characteristics. Most commonly the
• Poor or variable vision patient complains of:
• Discomfort x Decreased lens comfort.
• Decreased tolerance to lens wear
x Unstable/variable vision.
- reduced wearing time
- early onset of symptoms x Reduced wearing time.
• Lost lens x Lens loss from the eye for no apparent reason.
• Uneasiness about lens staying on the eye
x The lens feeling as though it is ‘loose’, ‘mobile’,
• Comfort not a reliable indicator of fit
97200-155S.PPT
‘unsettled’, or likely to come out of the eye. The
wearer expresses feelings of insecurity about
7L297200-155 retention of their lens(es) on their eye.
These symptoms may occur from the insertion of
lenses, after the lenses have been worn for some
time (hours), or they may start after the lenses have
been worn successfully for a period (days, week,
months). The delay before onset of symptoms is
important in helping the practitioner determine the
likely cause of the problem.
SCL comfort is rarely a reliable guide to matters of
lens fit at any time.
Practitioners also need to be aware of the initial
false, transient comfort that accompanies a tight,
unmoving lens. It should never be assumed that a
lens that is unmoving at delivery will become mobile
later.
265 Lens Fitting Problems: Aetiology

FITTING PROBLEMS A fitting problem (other than during trial fitting or

AETIOLOGY equilibration phases) may be the result of:
• Inappropriate lens parameters x Inappropriate BOZR (wrong selection, or
- poor selection inaccurate fabrication).
• Limited lens choice
x Inappropriate TD (wrong selection, or inaccurate
- stock (compromise too great)
fabrication).
• Change in parameters over time
• Lens spoilage x Lens design different from that of trial lens.
• Manufacturer’s tolerances too lax x Material physical properties different from those
• Simple errors/labelling errors of the trial lens, i.e. different material.
97200-156S.PPT

x Significantly different lens centre thickness (tc)

7L297200-156
from that of trial lens.
x Faulty lens material (unlikely).

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Lecture 7.2: SCL Complications and Their Management

x Mislabelling of lens package (increasingly rare

as levels of production automation increase).
x Forced compromise (see below).
x Failure of Quality Assurance (during
manufacture) and/or Quality Control (after
manufacture but before dispatch).
Because a wide variety of SCL materials and lens
designs/parameters are only available as stock
lenses in predetermined combinations, the
combination a practitioner believes will address a
wearer’s fitting problem may not be available, e.g.
only a relatively limited range of fitting parameters is
available currently in siloxane hydrogel materials.
The use of stock lenses often requires a
compromise in lens fit and/or physiological
performance. This may mean that not all patients
can be fitted optimally, or even satisfactorily.
Even when a ‘suitable’ choice is available, it is
possible for the lens selected initially to prove to be
unacceptable ultimately. This situation may arise
because of an error of judgment, a misinterpretation
of trial lens behaviour, or simply an error (e.g. a
transcription or clerical error).
The cause(s) of corneal and conjunctival staining in
areas left exposed by a decentred, or excessively
moving lens remain unclear. The contribution of the
lens-induced disruption to the pre-lens tear film is
explored further in Lecture 7.4: Diagnosis and
Management of Dry Eye in Contact Lens Wear.
It is also possible for the fitting characteristics of an
SCL to change over time. This may be a material-
dependent phenomenon, or may be due to
increasing lens spoilage (deposits). Increased
traction between the lids and a soiled lens may
increase the apparent lens movement, giving the
appearance of an altered fit. A new lens would
probably emulate the original fit seen at lens delivery
assuming no other key factor(s) have changed in the
interim.
Despite its initial comfort, the adverse physiological
ramifications of an unmoving lens soon become
apparent. These ramifications include hindered
removal of tear debris, reduced corneal oxygenation
especially with conventional hydrogels, and
discomfort including stinging and burning
sensations, usually within 90 minutes of lens
insertion. These factors explain many of the
symptoms reported.

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 Module 7: Contact Lens-Related Ocular Complications

266 Management of Lens Fitting Problems

FITTING PROBLEMS The key to successful soft contact lens wear is the
MANAGEMENT selection of an optimum fitting lens for each patient.
• After-care evaluation To ensure that the quality of fit is maintained, regular
• Refitting as required after-care visits, including an evaluation of the lens
- change parameters/material fit, are necessary.
- stock lens with a compromise? If the initial choice of parameters, design, or material
- choose alternative lens of the lenses ordered proves to be inadequate or
- custom design inappropriate, a revision and reorder at the first
• Change manufacturers after-care is required. If the obvious combination of
• Revise office systems to trap fitting factors is not possible because the lenses
errors prescribed originally were stock lenses, either a
97200-157S.PPT

compromise is required, or a different lens

7L297200-157 type/series needs to be trialled.
If custom lenses were used, appropriate changes
(see Lecture 3.2) to the TD, BOZD, tc, or material
are required.
If lens spoilage proves to be an issue, a more
deposit-resistant material is required, or the lens
replacement interval shortened. If the interval is
already short, daily disposables may be a solution.
Simple errors (e.g. transcription or clerical) are
suggestive of inadequate systems of checks and
balances in the practice office. If errors occur too
frequently, steps may be required, or systems put in
place, to double-check or have another party cross-
check the orders leaving the practice once the order
is reconciled with the patient clinic record.
Should the evidence suggest loose tolerances
applied by the manufacturer, consideration should
be given to finding an alternative source of lenses.
IV.B SEALs

267 Superior Epithelial Arcuate Lesions:

Introduction
SEALs
A Superior Epithelial Arcuate Lesion (SEAL) is a
• Superior Epithelial Arcuate Lesion (SEAL)
contact lens-induced epithelial defect that is usually
• Alternative names: located in the superior corneal periphery, arcuate,
- epithelial splitting or splits resembles a split in the corneal epithelium, and may
- Soft Lens Arcuate Keratopathy (SLAK) be unilateral (more commonly) or bilateral.
- superior arcuate keratopathy The alternative names used for this condition are
- soft lens-induced superior arcuate listed in the slide opposite.
keratopathy SEALs is not a recent phenomenon, slide 269 is
- tight-lens syndrome dated 1974-06-13 and the earlier term ‘epithelial
97200-255S.PPT
splitting’ was used to describe the condition shown.
7L297200-255 The incidence of arcuate staining with the early spin-
cast HEMA lenses may have been as high as 46%
with 10% being moderate to heavy (Kline and
DeLuca, 1975, Part 2), or as low as 1.8% to 5.4%
(Knoll and Clements, 1972).
‘Smile’ staining (or inferior arcuate corneal staining)
as reported by Zadnik and Mutti (1985), is now
accepted as being a separate entity to SEALs and
will be dealt with separately in this lecture. Although
it is possible for an inferior epithelial arcuate lesion
of the type to be dealt with here to occur, it is
uncommon.

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268 Hine (1987) reported:

SEALs x 14% of a group of 150 presbyopes developed

SEALs either:
• Observed soon after SCLs introduced (1970s)
– unilaterally (81%)
• Incidence rates vary:
- range reported: 1.8% to 10% – or bilaterally (19%).
- mostly unilateral (80% versus 20%) x 8% of all soft lens wearers in a retrospective
study had SEALs.
• Inferior variant is uncommon
• Depth can be full epithelial thickness
x An inferiorly located variant in some wearers.

• Male presbyopes more susceptible x The lesions to be within 2 mm of either the

97200-256S.PPT
superior or inferior limbus.

7L297200-256 x 8 of the 20 SEALs cases had developed full

epithelial thickness split within two months of
269 wear.
x Male presbyopes are more likely to exhibit
SEALs.

7L22565-93

270 Superior Epithelial Arcuate Lesions: Signs

The signs of SEALs include (some variation is
possible):
x A white, arcuate lesion, 2 to 5 mm long, 0.5 mm
wide with slightly roughened or thickened
irregular edges (Malinovsky et al., 1989) usually
between 10 and 2 o’clock, i.e. the area normally
covered by the eyelids.
x An arcuate area of stippled fluorescein staining
that varies in degree.
x The staining areas are usually close to, and
parallel with, the limbus.
7L2SEAL-G.TIF
x The degree of stippling tended to taper off
towards the limbus (Wechsler, 1977).
271
x In the more severe, or the more advanced
SEALs cases, the staining areas coalesce.
TYPICAL SIGNS
x In advanced cases, the coalescence is more
• Split-like arcuate lesion
widespread and the damage deeper than just
• Parallel to limbus the epithelium.
• 1-3 mm inside limbus x A subepithelial opacity may also be present
(Horowitz et al., 1985).
• 10 o’clock to 2 o’clock location
x Limbal capillary loops and the paralimbal
• 0.5 mm wide, 2-5 mm long conjunctival vessels became engorged and
• In area under upper lid injected locally (Wechsler, 1977).
97200-205S.PPT

x Diffuse stromal infiltrates in the affected areas

7L297200-205 may be seen.
x However, Hine (1987) and Malinovsky et al.

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272 (1989) found no signs of inflammation, limbal

injection, or infiltrates in cases of SEALs.
SEALs
SIGNS cont’d
x The lids are usually normal although Horowitz et
• May start as arcuate area of staining al. (1985) found them to be ‘tight’ (greater lid
• Can involve full epithelial thickness tonus) in SEALs cases.
• Lesion often has irregular edges x Fluorescein staining is apparent in almost all
• Little or no local injection or inflammation cases but the lesion does not stain with Rose
Bengal (Malinovsky et al., 1989).
• ‘Tight’ eyelids a common factor
• Usually, unilateral x 70% of SEALs cases also had an accompanying
arcuate area of punctate staining (Hine, 1987)
• Stains with fluorescein but not Rose Bengal (slides 275 to 277 have some staining
97200-206S.PPT surrounding the arcuate lesion itself).
7L297200-206 Hine described two types of epithelial split, the line
split and the band split. The line split developed in
stages progressing from an initial arcuate punctate
273 stain (slide 273) to a coalesced stained area forming
a full epithelial split with a jagged configuration (slide
276 [white light], a larger lesion slide 277 [blue light
and fluorescein] ). The band lesion is a 0.5 mm
wide staining area (slides 274 and 275) of constant
depth. It is usually closer to the limbus and does not
have a jagged outline. Hine also observed a
superficial, non-progressive, inferior, arcuate
staining that she believed was a simple mechanical
effect.
Generally, there are no other signs accompanying
SEALs, e.g. CLPC and, usually, the bulbar
conjunctiva is not injected (Horowitz et al., 1985).
7L20031.5

274

7L20953-25

275

7L20145-87BB

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 Lecture 7.2: SCL Complications and Their Management

276

7L20065.22

277

7L20392-93

278 Superior Epithelial Arcuate Lesions: Symptoms

SEALs Hine (1987) reported that most SEALs cases remain

SYMPTOMS asymptomatic. This is probably the case as long as
• Typically, asymptomatic if epithelium intact the epithelium remains intact (Horowitz et al., 1985).
• Some may report: In symptomatic cases the complaints may include:
- discomfort/irritation x In severe cases:
- dryness – discomfort (mild to severe)
- scratchiness
– eye irritation (mild, see Jalbert et al., 2001)
- burning
– dryness
• Pain is less likely
97200-207S.PPT – sandy or scratchy sensations
7L297200-207 – itchiness
– mild photophobia
– burning and redness (Kline and DeLuca,
1977).
x Pain may be experienced but is less likely
because the affected superior peripheral cornea
is less sensitive than the central zone
specifically, and the horizontal zones generally
(after Wechsler, 1977).
x Reduced vision quality caused by lens
decentration:
– symptom relief may be reported when
decentred lenses are recentred manually.
– visual symptoms may return once the lens
returns to its preferred (decentred) position.

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 Module 7: Contact Lens-Related Ocular Complications

x Symptom severity may increase with increased

wearing time during the day (Wechsler, 1977).
x Foreign body or dry eye sensations may be
elicited by direct and detailed questioning
(Malinovsky et al., 1989).
279 Superior Epithelial Arcuate Lesions: Aetiology

SEALs
There is still not a consensus on the aetiology of
SEALs.
AETIOLOGY
• Mechanical The following summarizes the aetiologies proposed
• Desiccation (?) in the literature:
• Hypoxia
Mechanical/Bearing Aetiologies
• Young & Mirejovsky hypothesis
- pressure point due to incomplete x Kline et al. (1979) described staining patterns
conformance by relatively ‘rigid’ lens with soft lenses. Although they dealt with pitting
• Decentration (?) and arcuate staining separately, essentially, they
• Physiology (??) attributed them to mechanical factors. It is
• Combinations of the above possible that the condition they described in their
97200-208S.PPT
papers is a manifestation of the same basic
7L297200-208 condition created by disparate lens designs. A
mechanical aetiology was also accepted by
Koetting (1974), and generally alluded to by
280 Ruben (1975).
SEALs x Somewhat paradoxically, Josephson (1978B)
Young & Mirejovsky’s Hypothesis (1993) found little success with the thinning, polishing,
flattening, or junction blending of SCLs.
Soft lens CONFORMS
However, all these alterations could be
Anterior eye construed as assuming a mechanical aetiology
Limbus
(see Josephson’s physiological theories under
Soft lens RESISTS conformance
(too rigid)
Physiological Aetiologies below).
x Also paradoxically, while assuming a
Pressure point, (SEAL location)
physiological aetiology, Josephson did observe
Soft lens FORCED to conform partially
by lid forces, compromise that most SEALs cases had tight or low-
flattened ‘S’ shape
97200-204S.PPT
positioned upper eyelids, an observation
consistent with a physical/mechanical aetiology.
7L297200-204
The same observation regarding tight lids was
also made by Horowitz et al. (1985) and Holden
et al. (2001).
x Young and Mirejovsky (1993) postulated that
SEALs is caused by mechanical trauma due to
inadequate lens flexure (higher Young’s
Modulus of Elasticity). This inflexibility,
combined with the presence and pressure of the
upper eyelids, results in mechanical damage
(slide 280 presents their theory
diagrammatically). The authors claim that the
condition occurs with all types of soft lenses,
designs, materials and manufacturing
processes. Local pressure on the post-lens tear
film and the subsequent thinning, results in
abnormally high mechanical forces particularly
frictional forces, on the cornea, especially during
lens movement. Abnormalities of the tear film,
particularly the post-lens tear film may also
affect the likelihood, or severity of SEALs
occurrences. This theory is further supported by
the slightly higher incidence of SEALs in wearers
of siloxane hydrogels, lenses known to be more
rigid than conventional hydrogels (after Nilsson,
2000, and Holden et al., 2001). Nilsson gave
the SEAL rate as <0.5%. The location of the
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Lecture 7.2: SCL Complications and Their Management

arcuate lesion in siloxane hydrogels tends to be

either closer to the limbus, or further into the
cornea compared with SEALs that occur with
conventional hydrogels (Sankaridurg, 2000 –
personal communication).
x O’Hare et al. (2000) and Holden et al., 2001
concluded that SEALs were due to ‘sheer’ forces
that led to a disruptive interaction between lens
and ocular surfaces when using high Dk EW
siloxane hydrogel lenses. Further, they also
concluded SEALs were more likely in wearers
with poor lens wettability and tighter lens fits.
However, the occurrence of SEALs in these high
Dk/t lenses suggest that hypoxia has little or no
role in their aetiology.
Physiological Aetiologies
x Wechsler (1977) suggested that lenses
decentred superiorly (or superior nasally or
superior temporally) could result in arcuate
staining that was rarely seen in inferiorly
decentred lenses. He suggested that arcuate
staining was the result of interruption of the lipid
or mucous layers of the tears.
x Josephson (1978A) found SEALs could be
induced by most of the lenses commonly
available at that time with the arcuate lesion
appearing between the 10:30 and 1:30 clock
positions some 2 to 3 mm in from the limbus.
His solution at the time was the use of
fenestrations, adding to his postulation of a
physiological basis. He felt that in most cases
the cause was not mechanical. With ‘nothing to
loose’ an existing troublesome lens was
fenestrated and a SEALs problem was resolved.
Fenestrations were successful in other wearers
except those using bifocal and toric, i.e. thicker,
lenses.
Arguably this finding conflicts with a
physiological aetiology and could support, albeit
weakly, a mechanical theory based on the fact
that fenestrations weaken a lens (in the sense
that they decrease its rigidity). The use of
thinner lenses as they became available solved
more problem cases because, it was thought, of
their higher physiological performance.
However, their decreased mechanical
stimulation may also have contributed to their
lower problem rate.
x Malinovsky et al. (1989) supported both theories
and presented hypoxia, mechanical factors, or a
combination of these as the likely causes.
x Also of probable significance is the fact that the
superior cornea (the most common location of
SEALs) is covered by the upper eyelid most of
the time. This means that, physiologically, its
conditions are related to the closed-eye
situation, albeit not as oxygen deprived.
x Dehydration and desiccation (pervaporation
staining) have also been put forward as
possible contributing factors.

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x Holden et al. (2001) also implicate gender

(more common in males), age, and poor tear
film quality in the aetiology of SEALs.
The exact aetiology still remains unclear. However,
it is almost certainly a combination of the factors
covered in the foregoing with an emphasis on the
mechanical factors. Currently, Young and
Mirejovsky’s theory has probably the broadest
support among interested parties.
281 Superior Epithelial Arcuate Lesions:
Management
SEALs
MANAGEMENT
Lens wear should be stopped immediately.
• Cease lens wear immediately The risks of SEALs remaining untreated include:
- risk of infection, scarring and x Infection changing the condition into a case of
neovascularization
MK. The risk of infection is real because the
• Wait 3 to 7 days
epithelium’s barrier function is breached by the
• Continue with:
lesion, i.e. the arcuate lesion constitutes a
- same lenses
- new lenses, same specifications
potential portal of entry for micro-organisms.
- new lenses, different specifications x Scar formation. Scar formation normally only
• Prescribe RGP lenses follows damage sustained by Bowman’s layer.
97200-209S.PPT
Most damage to the corneal epithelium is
7L297200-209 usually repaired promptly, efficiently, and
without scarring.
x Neovascularization (after Wechsler, 1977 and
Horowitz et al., 1985). Neovascularization is
usually a response to either the assault on
corneal integrity a SEAL constitutes, or hypoxia
(after Wechsler, 1977).
Hine (1987) reported that in half of the cases in her
study SEALs was resolved by altering:
x The lens factor (different parameters,
materials, thicknesses, designs).
x Lens care regimen.
x Wearing time.
x Ceasing lens wear for at least a week resolved
some 37% of SEALs cases. Generally,
continuation of lens wear with the same lenses
was successful in only 50% of cases, i.e. 50%
recurred when no changes to the lenses were
made.
x Some 13% of SEALs cases recurred no matter
what steps were taken to resolve the problem.
Gerry (1995) suggested lens wear be discontinued
for 3 to 7 days before attempting to return the
wearer to contact lenses. He also suggested that
SEALs was less common in disposable lenses.
This may be due to their generally lower rigidity,
attributable to either their thin designs, higher water
materials, or manufacturing processes, e.g. molded,
wet-molded, spin-cast, etc.
Regardless of the steps taken to resolve all the
issues involved, SEALs recurrence has been
reported to be as high as 33%.
If no hydrogel lens proves to be satisfactory, RGP
lenses should be considered as an alternative.

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 Lecture 7.2: SCL Complications and Their Management

IV.C ‘Smile’ (Inferior Arcuate Epithelial) & Desiccation Staining

282 ‘Smile’ & Desiccation Staining: Introduction

Inferior arcuate staining was reported by Knoll et al.
‘SMILE’ STAINING: INTRODUCTION (1971), Kline and De Luca (1977), and Zadnik and
• Staining in the inferior cornea Mutti (1985).
• Pattern similar to ‘smiling face’ They reported:
• Severity subject to individual variation
x Staining that was larger and deeper than so-
• Worst with high water, ultrathin SCLs called ‘punctate’ staining.
Smile Smile Desiccation x Arcuate lesions were located within 3 to 4 mm
of the limbus.
More central
x In some cases, the staining was still apparent
97200-238S.PPT
some 15 hours after lens wear ceased.
7L297200-238 x A trend towards lenses of lower BVP being
implicated in more cases.
x Zadnik and Mutti (1985) described the staining
pattern as being ‘smile shaped’. They attributed
the staining to a combination of metabolic
disturbance and desiccation (pervaporation
staining). The fit, centration, wetting, and other
clinical attributes of the lens fit were reported to
be normal.
x The problem is more common when very thin
hydrogel lenses are worn, especially in
environments of low relative humidity (Holden et
al., 1986, Zantos et al., 1986, McNally et al.,
1987, Orsborn and Zantos, 1988).
x These early findings are the main reason that
very thin, high water contact lenses are not
widely available, or used.
x Onset of staining following lens insertion has
been reported as two hours (Holden et al.,
1986, Guillon et al., 1990), and four hours
(Orsborn and Zantos, 1988).
x Zantos et al. (1986) found 11% of thin, high
water lens wearers exhibited coalescent central
staining, or even epithelial erosion while
Orsborn and Zantos (1988) put the incidence of
desiccation staining (pervaporation) at one in
three wearers of thin high water lenses. They
also suggested that abnormal or deficient
precorneal tear films may predispose lens
wearers to pervaporation problems. However,
Little and Bruce (1995) found no evidence to
support this finding.
x Interestingly, there is no suggestion in any
studies that these same wearers have a
problem when not wearing contact lenses.
x Smile and pervaporation staining are less likely
in hyperopia because of the greater lens centre
thicknesses.

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 Module 7: Contact Lens-Related Ocular Complications

283 ‘Smile’ & Desiccation Staining: Signs

x Typically, the dominant sign is punctate sodium
‘SMILE’ STAINING: SIGNS fluorescein staining limited to the inferior
• Punctate staining in the inferior quadrant corneal quadrant (slide 284, courtesy of Assoc
• Staining may coalesce Prof. L. Jones, UWaterloo, Canada).
• Stained area isolated from the limbus x Generally, the shape of the staining area tends
• Severity ranges from diffuse to severe to be arcuate, especially when there is
• Severe cases may also have lighter significant coalescence of staining ‘islands’.
staining superiorly x The area involved tends to be parallel to, but
• Staining area (the ‘mouth’) may vary isolated from, the limbus.
from small to almost semi-circular
97200-237S.PPT x Occasionally, higher levels of staining in the
inferior quadrant may be accompanied by
7L297200-237
diffuse punctate staining in the superior
quadrant (Little and Bruce, 1995).
284 Because of their similarity, smile and desiccation
(pervaporation) staining need to be differentiated.
x Pervaporation staining per se tends to be
more central or paracentral but it is not clear
whether these conditions are manifestations of
the same, related, or overlapping conditions.
Compounding the issue of differentiation is the
numerical dominance of minus lenses
(myopia) that are thinner centrally. Slide 285
is suggestive of both smile and paracentral
staining (the two horizontal flash reflections
should be ignored).
x In severe cases, coalescence of the staining
7L2LJ001005 areas may be seen and, if wear continues, the
condition can progress to a full-thickness
epithelial erosion (Holden et al., 1986).
285
x Individual variation in the severity of the
staining was reported by several authors, e.g.
Holden et al., 1986, Guillon et al., 1990
(compare slides 284 and 286).
x Holden et al. (1986) and McNally et al. (1987)
reported a trend that suggested that higher
water content lenses produced:
– earlier onset of staining
– more severe staining
– greater numbers of wearers exhibiting
staining.
7L31029-99 x Limbal redness may also be seen (Holden et
al., 1986).
x Generally, SCL-induced corneal staining is
more common in the vertical quadrants than
the horizontal quadrants (Guillon et al., 1990).
x Inferior (smile) and superior arcuate staining
were reported by McNally et al. (1987) in areas
adjacent to the normal position of the upper
and lower lid margins, when lenses with
parallel surfaces were worn. They also
reported significant stromal fluorescein
penetration despite the apparently superficial
nature of the staining.
x In lenses replaced infrequently, any lens
138 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

286 deposits seen in the mid-periphery are

suggestive of incomplete blinking. A band
(non-rotating lenses, e.g. toric), or ring
(rotating lenses e.g. spherical) deposits are
formed by the ‘gap’ between the lids at
maximum lid closure, albeit incomplete. This
clue should be noted, and greater attention
paid to the inferior quadrant of the cornea
when examining it for signs of desiccation,
and/or mechanically-induced epithelial effects.

7L21835-92

287 ‘Smile’ & Desiccation Staining: Symptoms

Most cases of either smile or desiccation staining
‘SMILE’ STAINING: SYMPTOMS are asymptomatic.
• Most are asymptomatic
Zantos et al. (1986) reported discomfort in wearers
Symptoms reported include: exhibiting corneal staining resulting from thin, high
water lenses used in low relative humidity office
• Dryness
environments. They also reported such staining and
• Itchiness
discomfort were reversible rapidly (often <2 hours,
• Grittiness
[90 minutes, McNally et al., 1987]) simply by
• Lens awareness increasing the ambient humidity significantly (e.g.
30% to 80%). Somewhat surprisingly, they found a
Usually, pain is not reported poor correlation between discomfort and the severity
97200-240S.PPT

of staining.
7L297200-240
Symptoms in their and other studies included:
x Dryness.
x Itchiness.
x Grittiness.
x Burning.
x Lens awareness.
x Pin-prick sensation (McNally et al., 1987)
No pain was reported even when dense staining
was detected (McNally et al., 1987) but pain was
reported, along with a burning sensation, by Holden
et al. (1986).
288 ‘Smile’ & Desiccation Staining: Aetiology
The most common explanations offered for smile
‘SMILE’ STAINING: AETIOLOGY staining are:
• Pervaporation leads to:
- depletion of the aqueous phase of the
x Mechanical/physical.
post-lens tear film x Pervaporation. Following a study of ultrathin,
- desiccation of corneal epithelium high water SCLs worn for two hours, Little and
- lens adherence (?) Bruce (1995) concluded that depletion of the
• Potentially, corneal area not covered by aqueous component of the post-lens tear film
the upper eyelid can be affected by pervaporation is a contributing factor to both
• Desiccated area stains with sodium inferior arcuate staining and lens adherence.
fluorescein The damage revealed by staining is due to
97200-239S.PPT
epithelial desiccation.
7L297200-239 x Efron et al. (1986) and Bruce and Little (1995)
confirmed that the front surface of ultrathin
SCLs was relatively less hydrated, suggesting
a loss of water content to the atmosphere.
Subsequently, water from the posterior lens
IACLE Contact Lens Course Module 7: First Edition 139
 Module 7: Contact Lens-Related Ocular Complications

flows forward along the hydration gradient

created by anterior water loss. The posterior
lens draws water from the post-lens tear film
and ultimately, the anterior cornea. The
desiccated corneal epithelium stains with
sodium fluorescein, revealing both the area
affected, and the severity of the water loss.
x Because of staining differences between
powered and parallel-surface lenses, McNally
et al. (1987) suggested that pervaporation is
not solely responsible for the staining detected.
Two possibilities they considered were:
– a localized temporary lens adherence.
Any subsequent lens movement that
broke the adhesion may explain the
staining observed. The authors were not
very supportive of this, their own
suggestion.
– the thinner pre-lens tear film at the apices
of the upper and lower tear prisms may
have led to greater pervaporation loss
from the post-lens tear film via these
thinned zones. However, Little and Bruce
(1995) found no supporting evidence for
this suggestion.
x Despite using lenses of different thickness (0.08
– 0.12 mm), Guillon et al. (1990) found no
difference in the staining patterns that resulted.
x The foregoing points suggests that desiccation
staining would seem to be explicable by
pervaporation while ‘smile’ staining is not
completely explained by it.
Possible additional mechanisms include:
x Mechanical/physical (see SEALs in this lecture).
Guillon et al. (1990) argued against mechanical
factors because lens fit had not been an issue.
However, to take an extreme example, few
cases of SEALs have been attributed to
unacceptable lens fits. Therefore, it seems
possible that an adverse corneal response can
be induced mechanically, and mechanical
factors in smile staining cannot be excluded.
x Hypoxia-induced epithelial fragility.
x Lipid layer thinning resulting in instability of the
pre-lens tear film (see Lecture 7.4, this module).
x Incomplete blinking. Collins et al. (1989) found
significantly decreased lens hydration in the
inferior half of lenses worn by incomplete
blinkers, along with smile-like staining of the
underlying cornea. They also noted that the
lowest upper eyelid position during a blink
corresponds approximately to the location of the
greatest junction thickness of a minus lens,
thereby contributing to inferior quadrant
mechanical pressures on the cornea. The only
hyperope in their incomplete blinking group also
exhibited staining similar to that shown by the
myopes.

140 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

x Meibomian Gland Dysfunction (MGD) has also

been implicated in inferior arcuate staining
(Craig and McGhee, 1999).
x The relative humidity of the environment in
which the lenses are used should also be
considered when investigating corneal staining
of almost any type.
x Whether hypoxia contributes to these conditions
is not clear.
289 ‘Smile’ & Desiccation Staining: Management
The factors that may decrease the problems of
‘SMILE’ STAINING: MANAGEMENT ‘smile’ staining and/or desiccation staining are:
• Try to ascertain fundamental cause(s)
x Alterations to lens thickness, lens design,
• If pervaporation:
and/or lens material (myopia assumed):
- increase centre thickness
– increase lens thickness to reduce
- lower water content pervaporation of water
- alter lens design, e.g. FOZD
– alter lens design to redistribute lens
- some combination of the above thickness, e.g. find a balance between
• If stock lens, try another lens series or a FOZD (reduce) and centre thickness
different manufacturer
97200-241S.PPT
(increase) to reduce pervaporation with a
minimal decrease in Dk/t.
7L297200-241
– lower material water content along with a
decrease in lens centre thickness. A
pervaporation decrease may be affected
with little or no decrease in Dk/t.
– If a lid pressure-mediated staining is
suspected, regional (junctional) lens
thicknesses need to be reduced. This is
achieved by reducing the FOZD, lowering
the water content to increase the refractive
index of the lens material (to thin the lens),
or doing both.
x If a hyperope shows smile staining, the
thickness of the lens ‘skirt’, or the junction
thickness at the edge of the optic zone may
need to be increased. Central staining is less
likely to be seen.
x Where little or no lens factor options exist, e.g.
when stock lenses are in use, all a practitioner
can do is try an alternative lens series that has
a different water content or centre thickness. It
is not possible to alter the FOZD in such
circumstances.

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 Module 7: Contact Lens-Related Ocular Complications

IV.D Solution Sensitivity

IV.D.I Solution Sensitivity: General

290 Signs of Solution Sensitivity

SOLUTION SENSITIVITY The use of contact lens care and maintenance

SIGNS products may provoke either a hypersensitivity, or a
toxicity response in some wearers (see below for a
• Ocular redness differentiation).
• Infiltrates Typically, a hypersensitivity may include a mild to
moderate inflammatory response with:
• Palpebral conjunctival follicles
x Increased ocular redness.
• Coarse punctate staining
x Corneal infiltrates.
• Mild superior pannus
x Staining.
97200-162S.PPT

x Follicles in the palpebral conjunctiva, especially

7L297200-162 of the upper lids.
A superior corneal vascular pannus may be present
in more advanced cases.
An episode of toxicity is a local chemical effect that
is concentration dependent. An episode of toxicity
does not have infiltrates (the immune system is not
involved, at least initially), and is accompanied by
stinging and staining. A hypersensitivity is more
serious because it involves the immune system
291 Solution Sensitivity: Symptoms

SOLUTION SENSITIVITY An ocular hypersensitivity response often provokes

SYMPTOMS symptoms such as:

• Itchy eye(s) x Itchiness.

x Irritation.
• Irritation
x Lacrimation (usually present).
- foreign body sensation
x Photophobia (in more severe cases).
• Lacrimation

• Photophobia
97200-163S.PPT

7L297200-163

292 Solution Sensitivity: Aetiology

SOLUTION SENSITIVITY Most solutions used for the care and maintenance of
AETIOLOGY contact lenses contain preservatives that have the
• Accumulation of preservatives from lens
potential to induce a hypersensitivity response in
some individuals. Repeated exposure of the lenses
care products, especially storage solutions to the solutions during routine cleaning, rinsing, and
storage/disinfection can result in a build-up of the
• Delayed hypersensitivity to the preservative(s) within the lenses. Subsequently, the
wearer’s corneas are exposed to the lenses which
preservatives in lens care products then release the preservative slowly but for
prolonged periods.
• Predisposition to sensitivities
97200-164S.PPT
As most preservatives are not natural chemical
entities, they cannot be recognized or dealt with by
7L297200-164 the eye’s normal defences. Potentially, this
prolonged exposure can cause an adverse response
(see Module 6, Lecture 6.5 for details of ocular
defence mechanisms).
Some wearers are predisposed to developing
sensitivities to chemical entities they may encounter
142 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

in their daily lives. Prescribing preservative-free lens

care products, or daily disposable lenses, are
obvious courses of action for such patients.
293 Solution Sensitivity: Management

SOLUTION SENSITIVITY x Initially, temporary discontinuation of lens wear.

MANAGEMENT x In mild to moderate cases, the anterior ocular
surface recovers quickly, as long as all
exposure to the offending preservative or
• Discontinue lens wear temporarily solution component ceases.
x Re-exposure to the offending solution
• Change lens solutions (preservative)
component is likely to produce an immediate
ocular response, probably at least as severe as
any previous reaction. Therefore, any further
exposure to the component must be prevented.
97200-165S.PPT

x If possible, the component needs to be

7L297200-165
identified. As this is not usually done in routine
contact lens practice, e.g. a skin patch-test of
specific solution components, an alternative
lens care product using a basic chemistry
different from the problem product is required.
x Assume that the main preservative(s) is the
likely cause of the sensitivity response.
Therefore any new product to be introduced
should not contain, at the very least, any of the
same preservatives as the rejected product.
x If these steps prove unsuccessful, assume that
another solution component other than the
preservative is the problem. The avoidance of
such solution excipients requires a more
detailed knowledge of lens care products, i.e. a
knowledge of what is in the problem product, as
well as what other products do and do not
contain the same constituents.
x Alternatively, a hydrogen peroxide system, a
low toxicity product, or a preservative-free
system could be considered.
x Despite often valiant attempts to purge the
offending chemistry from the wearer’s used
lenses, such steps are rarely successful.
Therefore, it is prudent to avoid reusing the old
lenses.
x Having selected an alternative care product,
start the new lens care product with new lenses
to avoid confusing the effects of the new
solution, and the reuse of used lenses that
probably contain residues of the previous
chemistry.
x If the problem proves to be intractable, consider
daily disposables which have the advantage of
not requiring a lens care regimen.

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 Module 7: Contact Lens-Related Ocular Complications

IV.D.II Solution Sensitivity: SLK

294 Superior Limbic Kerato-Conjunctivitis (SLK):

Signs
LENS-ASSOCIATED SUPERIOR
LIMBIC KERATO-CONJUNCTIVITIS As this condition’s name implies, its signs are
SIGNS localized to the superior quadrant of the eye.
• Typically bilateral Alternative names include: vascularized limbal
• Superior bulbar and limbal hyperaemia keratitis (VLK), superior limbic keratitis (also SLK).
• Apron of redundant folds of bulbar Usually, the logical abbreviation SLKC is not used.
conjunctiva at superior limbus
Contact lens-associated SLK is a very rare,
• Conjunctival chemosis
multifactorial condition. Little data has been
• Infiltrates (grey)
published on its incidence. Stapleton et al. (1992)
• Sub-epithelial haze showed only 5 superior limbic keratopathies
• SCL wearer occurred in a sample of 1,104 lens-related disorders
97200-48S.PPT

at a major UK eye hospital.

7L297200-48
Signs of CL-related SLK include (some of this
section after Sendele et al., 1983):
295
x Associated with hydrogel contact lens wearers
LENS-ASSOCIATED SUPERIOR (Sendele et al., 1983, Abel et al., 1985).
LIMBIC KERATO-CONJUNCTIVITIS
SIGNS x Appears as a monocular condition with an
irregular, pitted, superior quadrant limbal
• Corneal and conjunctival staining
conjunctiva. However, it is usually actually
- fluorescein/Rose Bengal
bilateral, but unequally so (Grant et al., 1990)
• Limbal hypertrophy
• Palpebral response x Bulbar conjunctival injection more intense in the
- papillae/redness superior limbal area.
• Signs remain well after cessation of wear x Cytological changes in conjunctival tissue.
• Differential diagnosis – SLK of Theodore These may appear as:
97200-49S.PPT
– fleshy grey thickenings of the superior limbal
7L297200-49 and corneal epithelium (slide 296, note the
irregularity of the specular reflection)
– a superior vascular pannus (called a
296
micropannus by some authors), often with
redundant folds over the superior limbus
– a gelatinous superior limbal hypertrophy as
reported in three of four cases by Stenson
(1983).
x Moderate punctate epithelial staining in the
upper half of the cornea on the affected side,
demonstrating significant corneal and
conjunctival tissue disorganization. Sodium
fluorescein and Rose Bengal staining are
usually detectable (slide 297).
x Some staining may be seen in the other eye.
7L20659-92
x Fine subepithelial opacities (grey according to
Fuerst et al., 1983) may be seen in the upper
half of the affected cornea (Miller et al., 1982).
Sendele et al. (1983) reported:
– intercellular oedema
– pseudoepitheliomatous hyperplasia
– acute and chronic inflammation
– a decrease in goblet cell numbers.
x Lid eversion reveals upper palpebral
conjunctival involvement. Fine papillary
changes accompany moderate redness of the

144 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

297 palpebral conjunctiva.

x Uncommonly, filamentary keratitis.
Contact lens-related SLK must be differentiated
from Theodore’s SLK, a condition that is not contact
lens related.
To aid the differential diagnosis of these two
conditions, the following points apply to contact lens-
associated SLK.
x It does not recur.
x Its resolution is slow but usually complete
(Sendele et al., 1983).
7L20892-94 x It is uncommon among elderly females.
However females are more susceptible
(Stenson, 1983, Hickson and Papas, 1997).
x It is not associated with a thyroid condition.
x Lid and limbal abnormalities tend to be less
severe.
x Filaments are not seen usually seen in the tear
film but are possible (Stenson, 1983).
x Cessation of lens wear produces significant
improvements (however, idiopathic cases do not
improve significantly).
Onset of CL-related SLK after commencement of
lens wear has been reported as being from 10
weeks to 25 months (Miller et al., 1982), five months
to three years (Stenson, 1983), or six months to
eight years (Fuerst et al., 1983).
298 Superior Limbic Kerato-Conjunctivitis:
Symptoms
LENS-ASSOCIATED SUPERIOR
LIMBIC KERATO-CONJUNCTIVITIS Wearer symptoms include:
SYMPTOMS x Substantially reduced wearer tolerance of
• Increased lens awareness contact lenses. Usually, the patient is unable to
achieve even modest wearing times due to the
• Burning, itching, photophobia rapid onset of a burning and/or itching sensation
after lens insertion.
• Mild discharge
x Pain.
• Vision may be affected slightly
x Foreign-body sensations.
97200-50S.PPT
x Photophobia.
7L297200-50
x Mucoid discharge.
x Decreased blink rate (Stenson, 1983).
x Blepharospasms (Modino et al., 1982, Miller et
al., 1982).

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 Module 7: Contact Lens-Related Ocular Complications

299 Superior Limbic Kerato-Conjunctivitis: Aetiology

LENS-ASSOCIATED SUPERIOR It has been suggested that the aetiology of SLK is

LIMBIC KERATO-CONJUNCTIVITIS multifactorial (Grant et al., 1990) and may involve
AETIOLOGY several risk factors. The possible causes of SLK
• Multifactorial are reported to include:

• Solution preservative sensitivity x Mechanical/physical factors resulting from the

presence of a contact lens, particularly its
• Mechanical irritation by lens edges, and complicated by its physical
properties. Further, Stein et al. (1995)
- lens fit implicated improper fit with a large diameter,
loose fit, and/or eccentric ride as possible
- lens deposits
97200-51S.PPT
factors.
7L297200-51 x Solution sensitivity/toxicity. This was more likely
when thimerosal was used as a preservative
(Sendele et al., 1983). While an association
with the latter has not been proved (see Fuerst
et al., 1983 and Miller et al., 1982) it is the most
likely cause.
Significantly, Miller et al. found that changing to
preservative-free saline, thermal disinfection,
and/or solutions of lower toxicity allowed most
cases to resume contact lens wear. This was
interpreted to mean that contact lens-related
cases were a case of toxicity rather than
sensitivity. However, significantly, Fuerst et al.
found contact lens-associated SLK in three
patients who used preservative-free lens care
regimens.
x Hypoxia.
300 Superior Limbic Kerato-Conjunctivitis:
Management
LENS-ASSOCIATED SUPERIOR
LIMBIC KERATO-CONJUNCTIVITIS When contact lens wear is the apparent cause of
MANAGEMENT SLK, lens wear must be discontinued for a period of
time to allow the ocular tissue to recover.
• Distinguish from SLK of Theodore
Resolution is complete when there is an absence of
• Discontinue lens wear corneal staining, no apparent conjunctival defects,
• Monitor recovery and no micropannus. However, even after the
• Lubrication
anterior eye has recovered, some areas of punctate
corneal epithelial loss may persist.
• Change lens design/lens fit
If the cause was attributed to physical/mechanical
97200-52S.PPT
factors and SCLs are still preferred, appropriate
7L297200-52 alterations to lens fit, design, materials, or type
should be made. However, refitting with an RGP is
always an alternative and may be the better option
301 regardless of personal preferrences.

LENS-ASSOCIATED SUPERIOR Regular use of ocular lubricants/artificial tears is

LIMBIC KERATO-CONJUNCTIVITIS recommended during the initial stages of treatment
MANAGEMENT (Sendele et al., 1983).
• Fit RGP lenses (probably the best option) In some cases of SLK, the use of mild
corticosteroids may be indicated to reduce the level
• Use alternative solutions
of inflammation and speed the recovery process.
- preservative-free The recovery times appearing in the literature range
- different preservatives from two to four months (Miller et al. (1982), to 15
months (Fuerst et al., 1983).
• Steroid therapy
97200-53S.PPT
This condition is now rare in contact lens practice
because of the decrease in lens deposits (a result of
7L297200-53 the widespread use of disposable lenses), and

146 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

improvements in lens care products. Thimerosal in

particular, is no longer used and those constituents
used currently have been chosen for their low
toxicity, and low allergenicity.
IV.E Non-Compliance

302 Patient Non-Compliance: Introduction

Patient non-compliance with practitioner instructions
PATIENT NON-COMPLIANCE is very common in most aspects of health care.
INTRODUCTION
Contact lens usage is no exception and non-
• Non-compliance is common in health care
compliance may affect one or more of the following
• Contact lenses are no exception aspects of contact lens practice:
• Main aspects include:
x Physical lens care procedures.
- lens care procedures
x Incorrect use of solutions.
- lens care products
- lens wear schedules
x Incorrect choice of solutions including the use of
products that are not prescribed, or are
- lens replacement schedules unapproved.
97200-303S.PPT

7L297200-303 x Failure to heed solution expiry dates and

discard-after periods.
x Wear schedule, especially misapplication of
lens type, e.g. using a DW lens for EW, or
sleeping in DW lenses.
x Lens replacement schedule.
Compliance generally is presented in more detail in
Lecture 7.3 of this module.
303 Patient Non-Compliance: Signs
PATIENT NON-COMPLIANCE Signs associated with non-compliance are
SIGNS numerous. Typically, the signs are the direct or
• Specific to type of non-compliance indirect adverse effects of:
• Lens related
- deposits x Inappropriate or non-existent lens care.
- discoloration
- altered physical properties x Inappropriate lens care products on lenses
- shape distortion
• Ocular x The use and effects of mistreated lenses on
- redness (eyeball and lids) the cornea and anterior eye.
- epithelial staining
- corneal oedema x The use of old, soiled lenses.
- papillae (follicles if toxicity an issue)
97200-166S.PPT
x The wearing of lenses for excessive periods of
time.
7L297200-166
Some of these signs are presented in the slide
opposite.
304

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305 Patient Non-Compliance: Symptoms

PATIENT NON-COMPLIANCE Patient non-compliance often results in a reduction

SYMPTOMS in lens performance, on-eye comfort, and/or ocular
health.
This may manifest itself as:
• Decreased lens tolerance
x Poor vision, should the level of lens surface
deposits increase, and/or lens movement and
• May be irritation, itching, etc centration be affected adversely.
x Decreased lens tolerance.
x Reduced wearing time.
97200-167S.PPT

x Ocular irritation.
7L297200-167
x Ocular redness (as noted by the wearer).
306 Patient Non-Compliance: Aetiology

PATIENT NON-COMPLIANCE It is rare for a patient to deliberately set out to

AETIOLOGY disregard, or not comply with the practitioner’s
• Little or no contact lens education instructions regarding their contact lenses and
contact lens wear.
• Lack of information reinforcement
The most common causes of non-compliance are:
• Poor/no after-care scheduling
x No instruction provided (practitioner).
• Failure to appreciate their own role in
x Inadequate education (practitioner).
successful contact lens wear
x Failure to understand (wearer).
• Human nature
97200-168S.PPT
x Misinterpretation of instructions given (wearer).

7L297200-168 x Failure to provide written/illustrated support

material (practitioner).
x ‘Cutting corners’ (wearer).
x Attempts to save money (wearer).
x Laziness (wearer).
x Failure to impart (practitioner), or accept
(wearer) the importance of compliance to ocular
health, and contact lens-wear success.
307 Patient Non-Compliance: Management
Significant amounts of time and effort must be
PATIENT NON-COMPLIANCE expended on patient education at the
MANAGEMENT
commencement of contact lens wear. Good habits
• Careful questioning and observation should be demonstrated by the practitioner from the
very first contact with a prospective contact lens
• After-care evaluation wearer.
With regard to compliance and lens hygiene issues,
• Strong emphasis on patient education the wearer should be informed by the practitioner of
what they (the practitioner) are doing during office
• Discontinuation from lens wear procedures, e.g. hand washing, lens inspection,
care and maintenance procedures, etc.
97200-169S.PPT

Once the initial educational steps are complete,

7L297200-169 continued reinforcement is required at each
subsequent exposure, e.g. routine and unscheduled
after-care visits, to ensure that the patient remains
aware of the need to comply with the instructions
issued, if ocular health and safety are to be
maintained.
After-care visits provide the ideal opportunity for the
practitioner to act as patient educator and to monitor
the wearer’s progress. Failure to do this often
148 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

results in the patient lapsing into bad habits and

poor practices.
For their own safety, a patient who continues to
disregard instructions should be encouraged to
discontinue lens wear.
As this is unacceptable to most patients, most will
elect to continue wearing lenses until such time as
the difficulties induced produce practical problems
for continued wear.
A prudent practitioner documents the exact nature of
the instructions provided (including printed matter
supplied), the non-compliance detected, and the
steps taken to rectify the situation. Probably, the
patient should be informed that records of this
nature exist (see Module 10, Lecture 10.4:
Standards of Practice).
IV.F Lens Case Contamination

308 Lens Case Contamination: Signs

LENS CASE CONTAMINATION A case may become discolored with age, and dirt
SIGNS can often be seen in the threads of the lids (growth
of micro-organisms, especially the dark fungii) and
• Dirty lens case the knurling on the outside of the lids (finger-borne
contaminants) (slide 309).
• Discoloured appearance
Cultures taken from the inside surfaces of the case,
• Association with corneal inflammation
and samples of solutions remaining in the case, may
be positive for residing organisms.
and infection
The eyes of the wearer may also show signs of
infection, inflammation, redness, papillae, etc.
97200-170S.PPT

7L297200-170

309

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310 Lens Case Contamination: Symptoms

LENS CASE CONTAMINATION Debris and micro-organisms from a dirty lens case
SYMPTOMS can be transferred to the eye via the lens upon
insertion. Lens insertion may be accompanied by a
• Ocular irritation sharp corneal irritation, stinging, general discomfort,
or a slowly increasing lens awareness that may be
• Infection associated with:
accompanied by increasing ocular redness. Profuse
- pain tearing and perhaps a sensitivity to light may also
accompany the foregoing.
- lacrimation
Should the presence of micro-organisms cause an
- photophobia ocular inflammatory reaction or, in some cases, an
97200-171S.PPT
ocular infection (MK), the severity of the symptoms
may be dictated by the degree of inflammation
7L297200-171 and/or infection.
311 Lens Case Contamination: Aetiology

LENS CASE CONTAMINATION The main causes of lens case contamination are:
CAUSE x The use of poor, or no, hygiene practices by the
wearer.
• Poor hygiene
x Inadequate or no case care.
• Neglect
x Infrequent or non-existent case replacement.
• Infrequent replacement Ultimately, these factors result in a build-up of dirt
and other contaminants inside and outside the lens
• Biofilm formation case, and the increased likelihood of a biofilm
forming inside the case.
97200-172S.PPT

Cases that are not replaced regularly can become

7L297200-172 contaminated and are a potential harbour for
disinfectant-resistant bacteria.
As an adaptation to their circumstances that
includes the challenge of regular exposure to
antimicrobials (some compliance is assumed in
such a statement), some micro-organisms produce
protective biofilms that can line the inside of lens
storage cases. This biofilm can be difficult to
eliminate completely, even when regular brushing,
boiling, etc. is undertaken to disrupt the film’s
continuity and kill the micro-organisms residing in,
and protected by, the film.
312 Lens Case Contamination: Management

LENS CASE CONTAMINATION The best ways of preventing case contamination

MANAGENT and an excessive build-up of case contaminants is:
x Compliance with case-care instructions.
• Patient education
x Regular case replacement.
• Routine case cleaning To these ends, many lens care products are now
supplied with disposable lens cases. As the solution
• Regular case replacement
volumes often target approximately one month of
normal usage, this means many wearers can
replace their cases approximately monthly. In the
97200-173S.PPT
absence of such case bundling, it is desirable that
cases be replaced about every three months.
7L297200-173
Where this rate is not feasible, steps need to be
taken to reduce the possibility of case contamination
once usage is commenced. Even if the case is to
be replaced regularly, some of these same steps are
prudent, preventative care applicable to all cases,
regardless of the replacement frequency.

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 Lecture 7.2: SCL Complications and Their Management

Daily case rinsing with very hot tap water followed by

air-drying (upside down) is generally sufficient to
keep the case in good order in the short term.
Weekly, it is desirable that the case be brushed
inside with a stiff toothbrush reserved for the
purpose, i.e. not a toothbrush that has seen service
in its original intended role. This step, which is
intended to disrupt and brush away any biofilm lining
the walls, should be followed by a thorough rinsing in
very hot water, and finally an air-drying upside-down
as before.
Many of the plastic cases used currently cannot be
boiled because they deform, and/or melt at or near
100°C. If safe lens storage is to continue, the cases
must be discarded regularly.
Theoretically, lower temperatures can disinfect (as
opposed to sterilize) lens cases. However, the
difficulty of defining and maintaining a suitable lower
temperature (say maintaining the lens at 70 - 80°C
for at least 5 minutes) has far too many attendant
risks in the hands of the unscientific and should not
be suggested.
IV.G Lens Deposits: Front

313 Lens Deposits: Signs

LENS DEPOSITS Soft contact lenses attract and/or bind surface

SIGNS deposits within minutes of their placement on the
• Front and back surface build-up
anterior eye. The appearance of the resulting
deposits can take many forms and the practitioner
- irregular specular reflection will often find it difficult to determine the exact nature
- allow lens to dehydrate of any deposit detected.

- move lens to differentiate deposits from debris When deposits are laid down they usually result in:

• Palpebral conjunctival inflammation x An irregular specular reflection from the lens

surface (slide 314).
• Corneal staining
97200-174S.PPT

7L297200-174

314

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315
x Discrete or diffuse deposits on the lens (slide
315).

7L21119-99

316
x A lessening of the brightness of any reflections
from the lens front surface (slide 316) as seen
through a slit-lamp.

7L20917-92

317
If a lipid deposit is present, a fingerprint-like
appearance may be seen (slide 317).

7L21618-95

318
If the deposits are denatured tear proteins, e.g.
lysozyme (slide 318), it is likely that eventually an
allergic reaction will occur as the eye’s immune
system refuses to accept the tear proteins as
belonging to ‘self’. This reaction may show as:
x Generalized bulbar and palpebral redness.
x Limbal vessel engorgement.
x Excess tearing.
x Possibly corneal infiltrates.
If a protein film was to peel and flake there are
physical ramifications for the anterior eye as well.
7L21964-91
These include staining issues such as abrasions of
the palpebral and bulbar conjunctiva, and loss of
152 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.2: SCL Complications and Their Management

319 epithelial coverage.

Deposits can cause a mechanical insult to both the
bulbar and palpebral conjunctivae. The presence of
such insults may be disclosed by epithelial staining
(slide 319), or upper lid inflammation (CLPC).

7L20629-97

320 Lens Deposits: Symptoms

LENS DEPOSITS Usually, symptom severity correlates well with the

SYMPTOMS magnitude of the deposition on the lens surface.
Commonly, lens wear simply becomes less
• Discomfort comfortable. Any vision reduction may be the
reason given by a contact lens wearer for seeking a
consultation. The symptoms include:
• Lens awareness
x Discomfort.
• Reduced vision x Lens intolerance.
x Eye redness.
97200-175S.PPT
x Tearing.
7L297200-175
x Mucus or ‘sleep’ being detected, especially on
awakening.
x Reduced vision if the deposits are significant.
x Pain and irritation if a peeling/flaking deposit is
present.
321 Lens Deposits: Aetiology
Material that deposits on the surface of a SCL may
LENS DEPOSITS
AETIOLOGY come from a number of sources. Most commonly
the deposits originate in the ocular tear film, or in the
• Interaction between: environment external to the eye including the
- lens material wearer’s fingers.
Most SCL materials have an affinity for tear film
- tear film/ocular surface
constituents such as:
- environment x Protein.
• Proteins denature when attached to the lens x Lipid.
97200-176S.PPT
x Mucin.

7L297200-176
Protein deposits have a tendency to denature once
they are attached to the lens surface. This is less of
a problem now that thermal disinfection is
uncommon. The build-up of deposits on the lens
can irritate the eye and cause an increase in the
mucous secretions that act to defend the eye and
envelop the offending object. These secretions may
add to the level of deposits and so a ‘vicious circle’
is established.
The role of a biofilm laid down by a colonizing micro-
organism in lens deposits remains unclear.
However, it is probable that any adherent film may
assist the deposition of some other lens
contaminants.
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322 Management of Lens Deposits

LENS DEPOSITS SCL deposits are best managed by the appropriate

MANAGEMENT use of optimal care and maintenance products, and
regular lens replacement. Management begins with
• Optimize care and maintenance the initial episode of patient education before lens
- solutions
issue, and continues for as long as the wearer is
under practitioner care.
- regimen In most cases it is not possible to maintain a SCL in
an ideal clean condition no matter how thorough the
• Frequent lens replacement
patient’s cleaning technique. Recognition of this fact
- daily disposal resulted in the development and acceptance of
97200-177S.PPT
frequent replacement of SCLs for both daily and
extended wear. Daily disposal of SCLs takes such a
7L297200-177 paradigm to its logical extreme.
IV.H Lens Deposits: Back

323 Back-Surface Debris: Signs

BACK SURFACE DEBRIS An accumulation of loose debris (slide 324) behind a

SIGNS SCL is a common occurrence due to the relatively
• Loose debris trapped by the lens close fitting relationship between the lens and the
- tear film components
anterior eye.
- cellular Most of the debris originates from the tear film. It
may also include epithelial cells (sloughed-off from
- foreign material
the cornea and conjunctiva) and foreign matter from
• Mucin balls the atmosphere and external environment generally.
- fluorescein pooling from indentation Usually, the debris seen are not adherent, or are
• Corneal staining readily removed by daily lens cleaning. By moving
97200-178S.PPT
the lens in situ, e.g. performing a lower-lid push-up
7L297200-178
test, lens-bound deposits can be differentiated from
other deposits by virtue of their movement with the
324 lens.
Mucin balls (slide 326) are observed frequently in
extended wear of SCLs, especially siloxane
hydrogels, but may also appear in daily wearers.
They are detailed in the next section.
Back surface debris may also cause some mild
punctate epithelial staining (slide 325).

7L20059-99

325

7L20054-99

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326

7L23040-93

327 Back-Surface Debris: Symptoms

BACK SURFACE DEBRIS Debris behind a SCL usually does not cause any
SYMPTOMS symptoms. If there is a substantial accumulation of
debris and, most likely, associated surface deposits,
the wearer may complain of slight irritation during
• Usually asymptomatic lens wear. It is almost impossible to attribute such
symptoms directly to the debris alone. Rather, they
• Mild irritation probably reflect the general condition of the lens.

97200-179S.PPT

7L297200-179

328 Back-Surface Debris: Aetiology

BACK SURFACE DEBRIS Removal of debris from behind a SCL depends on

AETIOLOGY lens movement over the surface of the eye under
the influence of a blink. Since limited tear exchange
is the norm under a SCL, the debris removal
• Lack of tear exchange process is slowed or hindered depending on the
lens-cornea fitting relationship, and the back
peripheral lens design and its topographical
• Occlusive nature of soft lens fits relationship to the anterior eye.
The relatively occlusive nature of a characteristic
SCL fit ensures that some of the debris remains
97200-180S.PPT
trapped. This may contribute to the appearance of
‘deposits’ on the lens back surface which may
7L297200-180 actually be either loosely adherent accumulated
debris, or simply trapped debris in apposition to the
back surface of the lens.
329 Back-Surface Debris: Management

BACK SURFACE DEBRIS In most cases, the presence of debris in the post-
MANAGEMENT lens tear film of daily SCL wearers is of no
consequence. In extended wear, the debris may
• Consequences are usually minor contribute to inflammatory events such as CLARE,
especially if the debris is cellular in origin.
• May contribute to inflammatory events
If the amount of debris is excessive, the practitioner
• Assess lens tightness and movement must assess carefully the lens fitting characteristics.
A lens that is too tight and/or demonstrating limited
• Refit if required movement with a blink should be refitted to optimize
these factors, and to enhance tear exchange
97200-181S.PPT
between the post-lens tear film and the anterior eye
tear film beyond the lens.
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IV.I Mucin Balls

330 Mucin Balls: Signs

MUCIN BALLS: SIGNS Mucin balls are not lens deposits, and are not
Sweeney, 2000 ‘complications’ in the usual sense of the word used
• Seen within minutes of lens insertion in this lecture. They are however, a ‘sequel to’, or a
• Size, and numbers, n with n wearing ‘consequence of’, wearing contact lenses. They are
time included here for completeness more than any other
• Tend to be patient-specific reason.
• Seen in both adapted and unadapted Mucin balls are seen most commonly, but not
wearers exclusively (some hydrogel lenses have also
• 25% exhibit t10 mucin balls induced mucin balls, Fleming et al., 1994), in
• 8% have >35 mucin balls wearers of current generation siloxane hydrogel
97200-312S.PPT
lenses.
7L297200-312 The main signs are presented in the slides opposite.
Images of mucin balls appear as slides 326 and 332
331 (in retro-illumination, lens on), 333 (direct
illumination, lens on), and 334 (with sodium
MUCIN BALLS: SIGNS fluorescein stain, lens off).
Sweeney, 2000
• Round, 10-50 Pm in size Mucin balls absorb sodium fluorescein but not Rose
• Clarity varies, smaller (10-20 Pm) usually Bengal.
translucent, larger (20-50 Pm) tend to be
opalescent The presence of the balls results in matching
• May be scattered or clumped, usually in indentations in the epithelial surface (a situation
superior quadrant, along upper lid resting
position similar to the dimple veiling that occurs under rigid
• Trapped/attached to corneal surface, leaving lenses). These indentations cradle the mucin balls
indentations (when fluorescein filled o a closely, explaining, at least partially, their immobility.
dimple veiling-like appearance)
• Do not move with the lens The full extent of the indentations is revealed only
97200-313S.PPT after lens removal and the instillation of fluorescein
7L297200-313
as the indentations fill with fluorescein-stained tears.
True epithelial ‘staining’ is not seen, confirming that
332 the indentations do not affect the epithelial surface
cell membranes adversely. This suggests that the
effects are physical rather than pathophysiological.
A higher incidence is reported in:
x Wearers with steeper corneas.
x Those who do not use rewetting drops.
x Those who use their lenses for 30-day EW
rather than 7-day (or shorter) EW (Jones and
Dumbleton, 2002).

7L20850-02

333

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334

7L20321-98

335 Mucin Balls: Symptoms

Lens wearers in whom mucin balls are present
MUCIN BALLS: SYMPTOMS remain totally symptomless even when the number
of mucin balls is large (Sweeney, 2000).
Somewhat surprisingly, vision also remains
• Usually, none unaffected even if numerous mucin balls are present
- not even when >100 mucin balls over the centre of the cornea, i.e. within the eye’s
entrance pupil. To all intents and purposes, the
present wearer remains completely unaware of the presence
of mucin balls.
The absence of any apparent effect on vision
97200-314S.PPT
probably due to their refractive index differing little
7L97200-314 from the surrounding tear fluid (i.e. little optical
effect), and their small size.
336 Mucin Balls: Aetiology
MUCIN BALLS: AETIOLOGY The mechanism governing the formation,
enlargement, and proliferation of mucin balls is still
• Postulated to be a combination of: poorly understood. The current thinking on the
- high squeeze pressures (action of lens & subject is included in the slide opposite.
lids) While the physical properties of siloxane hydrogels
- high surface friction (?) (lens o mucin) are apparently central to the causation of mucin
balls, some coatings trialled during the development
- disturbed mucin layer o fragments (?) of one siloxane hydrogel lens series did alter the
- fragments sphericalize (rolling, surface number of mucin balls observed (Sweeney, 2000).
tension, other factors ?) This suggests that, in addition to the underlying
97200-315S.PPT
material’s physical properties, especially its elastic
modulus, surface properties may be implicated in
7L97200-315 their aetiology.

337
MUCIN BALLS: AETIOLOGY

• Lens surface properties can affect ball

numbers
- ? Modulus of Elasticity is not the only
factor ?
• Assay shows balls to be mucin with tear
proteins
- little lipid content
97200-317S.PPT

7L97200-317

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338 Mucin Balls: Management

MUCIN BALLS: MANAGEMENT No adverse sequlae have been attributed to the

• To inform or not to inform? presence of mucin balls. Furthermore, neither their
• Mucin balls viewed negatively by practitioners numbers nor their sizes have been correlated with
- try alternative lenses, fits, wear regimens, any other outcome of lens wear, adverse or
siloxane hydrogel materials otherwise.
- reduce wear to minimum practicable
• Ignore their presence (?) Lens removal, and/or subsequent blinking, dislodges
• Monitor the evolution of existing products the mucin balls and the indentations resolve rapidly.
• Monitor new product releases Although it has been suggested that alternative lens
• As a last resort, refit with conventional lenses designs, lens fits, lens wear regimens, or lens
- monitor for mucin balls (often patient-specific) materials may decrease or eliminate the occurrence
- reduce wear times (poorer physiology)
97200-316S.PPT
of mucin balls (Fleming et al., 1994) this has yet to
be demonstrated conclusively.
7L97200-316
Generally, the lens fit should be checked to confirm
it is optimum. If an alternative lens type is available
it could be trialled.
Philosophically, no practitioner is ever happy with
lens-induced changes, no matter how benign they
are known to be. It is arguable whether the wearer
should even be informed of the presence of mucin
balls because considerable effort will then be
needed to allay the ‘fears’ that such a revelation will
inevitably raise.
The wearer should be advised to wear their lenses
the minimum time practicable and if/as alternative
high physiology lenses (siloxane hydrogel and other
technologies) are released, their induction of mucin
balls can be explored on a case by case basis.

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 Lecture 7.2: SCL Complications and Their Management

V Vision Problems
V.A Vision Problems: General

339 Vision Problems: Introduction

VISION PROBLEMS It is probable that, after discomfort/dryness, and

• Reasonably frequent symptom but redness, the most likely motivator of consultations is
less so than discomfort/dryness, and decreased, or altered vision.
redness However, it is unwise to treat vision problems in
• Establish cause, or association isolation, i.e. simply as a vision problem, because
they may be secondary to other, potentially more
• Record vision data: serious, underlying causes, e.g. a developing central
- at fitting visit or paracentral ulcer.
- on delivery The importance of accurate recordings of vision with
- at all subsequent visits and without contact lenses at fitting (baseline),
97200-254S.PPT
delivery, and after-care visits, cannot be over
7L297200-254 emphasized. Without this data, it is impossible to
ascertain accurately, changes in vision that may
have occurred with contact lens wear. From a legal
standpoint, a practitioner’s only defence will probably
come from their clinical records. Usually,
procedures or data not recorded are assumed to
have not been carried out, or never existed.
340 Vision Problems: Signs

VISION PROBLEMS Decreased visual performance with contact lenses

SIGNS may present in many ways. Characteristics of visual
loss include:
• Decreased habitual vision
x Degree (severity).
- high contrast
- low contrast x Constancy (stable or fluctuating).
- distance and/or near x Onset (immediate or delayed).
• Decreased contrast sensitivity x Occurrence (during lens wear only, or persists
• Unilateral or bilateral
after lens removal).
97200-182S.PPT
x Factors associated with the vision loss.
7L297200-182 A number of vision assessment methods are
available. These include:
x Most commonly, a high-contrast Snellen-type
341
letter chart, or its equivalent, e.g. symbols,
illiterate Es, etc. (slide 341)
x A low-contrast chart (slide 342). An assessment
of contrast sensitivity provides another method of
testing visual performance. Generally, corneal
oedema-altered vision is due to a decreased
contrast sensitivity (Cox, 2001 personal
communication).
x Sine wave gratings (slide 343) to assess the eye’s
resolution (in cycles per degree of angular
subtense at the eye).

7L20373-91
x Halometry, i.e. the qualitative and quantitative
assessment of haloes. Halometry is used to
assess the visual outcomes of alterations to the
corneal epithelium.
Aided acuity will reveal any change in vision since
dispensing, or at any other stage in the
supply/wearing process.
Blink rate should also be assessed. SCL wearers
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 Module 7: Contact Lens-Related Ocular Complications

342 modify (increase) their blink rate to maintain stable

vision (Carney and Hill, 1984, Pointer, 1988, Cox,
2001 personal communication). Cox also reported
that SCL wearers are likely to report this blink-rate
adaptation as being one of ‘poor visual
performance’. This may be due to:
x Lens surface dryness from surface deposits
(lipids, proteins, etc.).
x Eye conditions affecting the tear film.
x Lens age.
x Altered refractive error.

7L20341-95
If lens parameters are altered, especially BVP and
BOZR, it is prudent to assess any likely effect the
changes may have on vision.
343
SINE WAVE GRATINGS

97200-310S.PPT

7L297200-310

344 Vision Problems: Symptoms

VISION PROBLEMS Regardless of the cause, the patient will usually
SYMPTOMS report symptoms such as those listed in the slide
• Blurred or variable vision opposite.
• Problems with binocular vision
• Poorer vision at night
These symptoms are more likely to be due to the
• Glare lens itself (its physical condition, or optical function),
• Haze than the eye (as a result of lens wear). The more
• Fluctuations of the foregoing complicated the prescription, e.g. toric, bifocal,
• Asthenopia Progressive Addition Lens (PAL), the more likely are
• Alteration(s) symptoms.
- during lens wear
- after lens wear
97200-183S.PPT

7L297200-183

345 Vision Problems: Aetiology

VISION PROBLEMS Generally, SCL vision problems are due mainly to

AETIOLOGY either instability of the pre-lens tear film (covered in
• Blur may be: detail in Lecture 7.4), or lens front surface distortions
- refractive (Cox, 2001 personal communication). The latter is
- diffusive more likely with very thin lenses, lenses fitted too
flat/steep, or when both factors are combined. In
• Incorrect BVP
the case of tear film instability, the greater the
• Poor fitting
instability, the greater the visual disturbance. This
• Surface deposits disturbance may be a combination of decreased
• Myopic creep vision and a loss of contrast sensitivity.
- extended wear
97200-184S.PPT
Another contributing factor is spherical aberration,
the largest monochromatic aberration of contact
7L297200-184 lenses (Westheimer, 1961). However, in vitro levels
of spherical aberration overstate the in vivo levels.
e.g. they are slightly less for plus lenses and
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 Lecture 7.2: SCL Complications and Their Management

reduced by 50% for minus powers (Cox, 2001

personal communication).
A wide range of other possibilities need to be
considered when trying to determine the cause of
vision-related problems with SCLs.
These include:
x True, as opposed to induced, changes in the
refractive error over time, especially in the long
term.
x Corneal hypoxia induced changes in refractive
error (see Section II.J Corneal Oedema-
Induced Refractive Changes).
x Incorrect lens back vertex power (prescribing
error).
x Swapped lenses (wearer error).
x Surface deposits (see previous section) and
wettability problems (inherent or induced).
x Inadequate lens fitting characteristics
(prescribing error, or lens changes during use).
346 Vision Problems: Management

VISION PROBLEMS During history taking, the patient’s symptoms need

MANAGEMENT careful analysis and the findings related to visual
• Optimize lens fit acuity need to be assessed.
• Accurate over-refraction A full sphero-cylindrical over-refraction is an
appropriate starting point for the determination of the
• Adjust spherical and/or cylindrical best method of managing vision-related problems
power as indicated with SCLs.
If lens factors are suspected, the lens fit should be
• Change lens material
optimized (avoiding a fit that is too flat/steep) and
• Lens care issues lens thickness considered (avoiding ultrathin lenses
97200-185S.PPT
if necessary). The obvious answer to both these
7L297200-185 issues are siloxane hydrogels because of their
relative rigidity (less likely to conform to the anterior
eye irregularly) and their high oxygen transmissibility
(thickness is less of an issue).
Other issues such as lens surface deposits must be
considered. If deposits are excessive, the patient
must be counselled on how to improve their lens
care and maintenance procedures, and to replace
their lenses more frequently.
In the longer-term, the following should reduce
contact lens-induced vision problems further:
x Better lens designs to optimize the lens-cornea
fitting relationship to reduce the likelihood of
lens distortion.
x Stable toric lenses with appropriate optics.
x Better surface properties, e.g. more wettable,
less deposit prone, with longer BUTs.
x High lens transmissibilities that are equal to or
better than current siloxane hydrogels.

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 Module 7: Contact Lens-Related Ocular Complications

V.B Lens/Corneal Wrinkling

347 Lens/Corneal Wrinkling: Signs

LENS WRINKLING In rare circumstances, the shape of the cornea, the

SIGNS lens itself, or both can become distorted during lens
wear. Often, the cornea remains altered for some
• Corrugated central or mid-peripheral lens area time after lens removal.
The most distinctive sign of SCL wrinkling is a
corrugation of the lens centre (usually) that is best
• Does not change with a blink
viewed with tangential lighting, or specular reflection.
The corneal wrinkling (slides 348 [white light]) that
• Lens wrinkling can cause corneal wrinkling
often occurs under such a lens can be viewed after
lens removal using instilled sodium fluorescein.
97200-158S.PPT

7L297200-158

348

7L20817-93

349
A series of approximately parallel lines of fluorescein
pooling in the indentations (slide 349 [with sodium
fluorescein]) corresponding to the lens corrugations
(valleys) can be seen on the cornea.
Central epithelial folds from mid-water, high minus
SCLs with subtle to significant vision reduction were
reported by Quinn (1982), Lowe and Brennan
(1987), Daniels et al. (1994), Cox (1995), and Giese
(1997). All showed rapid recovery.

7L23275-93

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 Lecture 7.2: SCL Complications and Their Management

350 An even less common condition is that of peripheral

lens and/or corneal wrinkling first reported by Snyder
(1998). Slide 350 is of a similar case and shows the
cornea without a lens (courtesy of Mr D Pye, UNSW,
Sydney).

7L2WRINKFLUO

351
Corneal wrinkling must also be differentiated from
the Fischer-Schweitzer epithelial mosaic, the sodium
fluorescein pattern (not true staining) that follows
forceful trans-lid corneal massage of a normal
cornea when testing for integrity of the corneal
surface (slide 351).

7L23135-93

352 Lens/Corneal Wrinkling: Symptoms

LENS WRINKLING The induced corneal distortions reduce visual acuity

SYMPTOMS by amounts that may range from undetectable
(Snyder, 1998) to ‘extremely painful’ (Efron, 1999).
• Severe vision reduction if wrinkling is in The rate of onset of such changes range from
minutes after lens application, e.g. Lowe and
the pupil zone Brennan (1987), Cox (1995), to months, e.g. Quinn
(1982). When the lens is removed, the vision often
• Onset may be rapid (minutes) to months remains distorted for some time and only returns to
normal gradually as the corneal shape recovers.
• Recovery: ‘prompt’ to ‘hours after’
In some cases, a ‘dose-response’ relationship
97200-159S.PPT
appears to exist in that recovery seems to be related
to the length of the exposure to the stimulus (Lowe
7L297200-159 and Brennan, 1987). Usually there are few, or no
(Giese, 1997), symptoms associated with SCL
wrinkling. If symptoms are reported they are likely to
be some discomfort or ocular irritation, and/or
haloes (Daniels et al., 1994).

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 Module 7: Contact Lens-Related Ocular Complications

353 Lens/Corneal Wrinkling: Aetiology

LENS WRINKLING In most SCL wrinkling cases, a similar combination

AETIOLOGY (Minus Lenses) of factors appear to contribute to the condition.
Typically, the patient is wearing a lens that is:
Usually a combination of factors:
x Of high minus-power.
• High minus BVP
x Of low to mid-water content.
• Low water material
x Ultra-thin.
• Ultra-thin central lens design
This combination results in a lens with an extremely
• Thick mid-peripheral zone
thin centre surrounded by a relatively thick mid-
• Lid forces on blinking periphery. In some cases, the lid forces during the
97200-160S.PPT
blink are sufficient to cause the thin central area of
7L297200-160 the lens to buckle, forming the corrugations that are
easily seen with a slit-lamp.
Conversely, in the less common scenario involving a
354 plus lens, the thinnest zone (except for the extreme
LENS WRINKLING edge) is located just outside the optic zone and the
AETIOLOGY (Plus Lenses) lens and corneal buckling occurs in the periphery of
the cornea rather than the centre. The thin, wrinkled
• Usually a combination of factors: lens zone is subject to the greatest rate of thickness
change (measured radially) and is suggestive of a
- higher plus BVP central rotational component (torque) that is resisted
by the lens periphery (lens a relatively tight fit?).
- low water material
Ruben (1975) attributes some lens wrinkling effects
- thin peripheral lens design
to the rucking (wrinkling, ridging, or creasing) of the
- lid forces on blinking lens edges and the effect this has on ‘loose
97200-265S.PPT
epithelium’.
7L297200-265 Findings of corneal alterations are consistent with
the detailed work done by Bowman et al. (1978) who
confirmed that just lid pressure alone acting on the
cornea while the eyes are fixating at near, can affect
corneal topography to the extent of inducing
monocular diplopia.
355 Lens/Corneal Wrinkling: Management

LENS WRINKLING Management of lens wrinkling usually involves

MANAGEMENT refitting the patient with a lens that can withstand the
• Change lens design lid forces acting on it during a blink.
- higher water content In minus lenses, a thicker central zone may be
required and this can be achieved in conventional
- thicker design hydrogels by increasing the centre thickness of low
water lenses, or by using a high-water (HWC) lens
• Consider a more rigid material
(greater thickness). In some cases, simply
- siloxane hydrogel changing the lens material may provide the change
in lens physical properties required. Siloxane
• Consider RGP lenses hydrogels are unlikely to exhibit the phenomenon
97200-161S.PPT

because of their higher Modulus of Rigidity.

7L297200-161
Increasing the lens material’s water content probably
also applies to wrinkling from plus lenses because a
different (increased) junctional thickness will result.

164 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.2: SCL Complications and Their Management

V.C Vision Problems: Changes in Refraction

356 Changes In Refraction: Signs

CHANGES IN REFRACTION Changes in refraction may be real or induced.
SIGNS: WITH & WITHOUT LENSES Those induced by corneal hypoxia are detailed
• Decreased VA earlier in this lecture (see Section II.K).
• Does over-Rx (with) or ‘best’ Rx (without):
- improve VA (to baseline, < baseline) An over-Rx, and a refraction without contact lenses,
- fail to improve VA must be re-determined and the result compared with
• If YES, refraction has altered those recorded earlier (at fitting, last after-care, or
- myopic creep
- lens-induced change (regular) original Rx).
- true change in Rx
• If NO, other issues involved: Changes in refraction also occur if the corneal
- change in corneal topography (irregular) topography has changed or been altered by lenses.
- distorted lens
- poor lens condition (e.g. deposits) This can be determined by either keratometry, or
97200-186S.PPT
preferably, by keratoscopy (or videokeratoscopy).
7L297200-186

357 Changes In Refraction: Symptoms

CHANGES IN REFRACTION Typically, if a shift in refractive error occurs during

SYMPTOMS contact lens wear, the patient may complain of a
• Blurred vision
change in visual performance with the lenses and/or
visual discomfort while wearing them.
- distance
Reported blurring of vision can be at any distance,
- intermediate and may also be accompanied by headaches and/or
- near eyestrain. Binocular vision problems are possible
but less likely.
- all distances
If the changes are either a slight decrease in
• Asthenopia myopia, or a small increase in hyperopia, and the
97200-187S.PPT
wearer’s accommodative amplitude is adequate, it is
7L297200-187
probable that no change in vision will be reported.
358 Changes In Refraction: Aetiology

CHANGES IN REFRACTION Refractive changes during contact lens wear may

AETIOLOGY occur as part of the normal ocular development or
• Natural growth/development aging process. Such changes may not involve the
• Normal age changes cornea. In some cases the alteration to refraction
• Onset of presbyopia
may be related to physical (topographical) changes
in the cornea brought about by:
• Lens-induced
- chronic hypoxia x Applied lid pressure during a disease process,
- bearing pressure e.g. a hordeolum. This is more likely to induce
• Irregular astigmatism astigmatism.
• Onset of keratoconus x A tight fitting lens.
97200-188S.PPT

x Chronic hypoxia from low oxygen transmissibility

7L297200-188 SCLs.
359 Changes In Refraction: Management

CHANGES IN REFRACTION Normal age-related changes in the refractive error

MANAGEMENT are managed by up-dating contact lens BVPs.
• Accurate refraction Regular after-care visits ensure that any small
change in refraction are corrected promptly, and any
• Assess VA carefully untoward changes are addressed appropriately.
• Adjust lens BVP If the fitting characteristics are suboptimal, the
- sphere, cyl, axis practitioner must alter the lens parameters, or
change lens type, to overcome the problems.
• Optimize fitting
If manifest astigmatism has increased, possible
• Use high Dk/t material causes should be investigated. If nothing untoward
97200-189S.PPT
is found, the BVP of the lens requires alteration.
7L297200-189
Obviously, if a cause is found, it needs to be treated
or removed, and the issue(s) resolved before lens

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 Module 7: Contact Lens-Related Ocular Complications

wear continues, or any changes to the lens are

ordered.
If the VA with toric lenses is poor or fluctuating, the
underlying reasons need to be identified. If the
orientation of a lens is different from that exhibited at
fitting, the reason(s) should be sought, and the
suitability of the particular design to the patients eye
questioned. Mislocation maybe due to a
manufacturing error, the Rx, the design, or some
combination of these (see Module 3, Lecture 3.6 for
details). Possible outcomes are:
x A remake with the same Rx.
x A change of Rx especially of axis.
x A change of design.
x A switch to RGP lenses.
x Abandonment of lens wear.
If corneal physiology is compromised, a lens with
higher oxygen transmissibility (Dk/t) is necessary.
Siloxane hydrogels are a solution to this problem,
and have already been shown to have less effect on
the refractive state (Dumbleton et al., 1999).
Because corneal diseases such as keratoconus,
pellucid marginal degeneration, dystrophies, etc.,
can develop, the practitioner should ensure that the
VA is correctable to baseline level. If this is not the
case, or the refraction end-point is unclear, further
investigation of the cornea is warranted.
V.D Vision Problems: Residual Refractive Error

360 Residual Refractive Error: Introduction

RESIDUAL REFRACTIVE ERROR (RRE)

As the name suggests, residual refractive error
INTRODUCTION (RRE) is any error that remains uncorrected when
• Refractive error remaining with primary vision the primary form of vision correction is worn, i.e.
correction in place current spectacles, or contact lenses.
- errors & omissions excluded Residual errors due to mistakes, or omissions, are
• May be spherical and/or cylindrical ignored here as these are not complications per se.
• Corneal or ‘internal’ cause(s) Although astigmatism is usually the main type of
- regular or irregular residual error, other, more subtle errors exist
• Other: disease, senile changes because the eye, as a biological entity, is not
- retinal, lenticular, etc necessarily spherical, or sphero-cylindrical in shape.
97200-266S.PPT
This may mean a correction is only approximate
7L297200-266 when common lens forms are used.
In extreme cases, e.g. irregular astigmatism, or
decentred ocular optical components, normal VA
may not be achievable with SCLs. Some of these
cases may be correctable by RGP or scleral lenses,
while for others, no lens type may be ideal.

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 Lecture 7.2: SCL Complications and Their Management

361 Residual Refractive Error: Signs

The principal sign of residual refractive error is
RESIDUAL REFRACTIVE ERROR lower than expected visual acuity that does not
SIGNS respond to normal prescription alterations.
• VA less than expected
Should a pinhole aperture improve vision quality, the
• VA not responsive to Rx changes
aetiology of any reduced vision is, at least partially,
• Pinhole may improve VA but….
refractive in origin.
- problem may not be all refractive
- required Rx may be impossible to Although residual refractive errors range from the
determine subtle to the obvious, generally their magnitude is
- Rx changes may be to no avail mirrored by the amount vision is reduced.
• Usually, reduced VA mirrors RRE magnitude
97200-267S.PPT

7L297200-267

362 Residual Refractive Error: Symptoms

Usually, the wearer complains about their vision
RESIDUAL REFRACTIVE ERROR quality. However, when assessed on a high-
SYMPTOMS contrast letter chart, their acuity is often good to
• Sub-optimal vision very good. Unless a low-contrast chart is also used,
little evidence supporting the wearer’s claims will be
- apparent at trial fitting
found.
- apparent at dispensing
Residual refractive error is usually apparent sooner
- apparent once wear commences
rather than later, and seldom ‘gets better with time’,
- does not improve with time the forlorn hope of many wearers and clinicians
• Even small reductions can be symptomatic when such problems are encountered
97200-268S.PPT
unexpectedly.

7L297200-268
Reduced vision will usually be reported if an
astigmatic RRE exceeds the wearer’s astigmatic
tolerance (usually about 0.50D – 0.75D, unless the
axes are nearly vertical or horizontal). Wiggins et
al. (1992) found that, although VA was affected little
by small amounts of uncorrected residual
astigmatism, ignoring it resulted in visual
discomfort.
363 Residual Refractive Error: Aetiology
Probably, residual refractive error is an anatomical
RESIDUAL REFRACTIVE ERROR issue related to shape, rather than refractive index,
AETIOLOGY variations.
• Degree of lens conformance (to cornea)
Astigmatic RRE may be either internal, or due to the
• Usually, anatomical
degree of lens warping, flexing, or conformance that
- if astigmatic, usually Against-the-Rule occurs (after McMonnies, 1972). The orientation of
• If toric, lens orientation may vary with fixation residual astigmatism is predominantly Against-the-
distance, esp. at near distances Rule (Grosvenor, 1963, Grosvenor et al., 1988,
• RRE may not be sphero-cylindrical
Dunne et al., 1994, Keller et al., 1996), a fact
enshrined in Javal’s Rule (of 1890).
- ? full correction is difficult or impossible
97200-269S.PPT
An often overlooked difficulty with toric SCLs is lens
7L297200-269 rotation modulated by fixation distance, an effect
that is usually more marked at near. At near, lenses
often exhibit so-called nasal rotation, i.e. R
anticlockwise, L clockwise, because the lower lid
margin’s orientation varies with the direction of gaze
and/or state of convergence. Little can be done to
eliminate this effect entirely because it is largely an
anatomical issue and depends on fixation distance.

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364 Residual Refractive Error: Management

Should an astigmatic residual error be detected, a
RESIDUAL REFRACTIVE ERROR compromise using either the spherical correction
MANAGEMENT that provides the best vision (best vision sphere), or
• Do spectacles or CLs provide best VA? the best sphero-cylindrical correction, is the only
• Supply best correction possible possible answer.
• If toric SCL orientation varies:
In those RREs that common lens forms do not
- try another design (thinner?)
correct fully, a similar approach can be taken, i.e.
- alter head position/body posture
the sphere (or sphero-cylinder) that delivers the best
- optimize Rx for preferred distance
vision.
• Complete solution unlikely
- compromises are probably required If the problem is variable toric orientation at near,
97200-270S.PPT
trialling alternative lens designs may reduce the
7L297200-270
problem, but elimination is unlikely. Altering head
tilt to vary lens-lid interaction may be of some
assistance but this may lead other postural
problems. If lens usage is primarily at one distance,
e.g. a computer screen, the Rx should be optimized
for this distance, and the wearer informed of the
limitations this imposes.
Ultimately, all that can be provided is a compromise
that requires an understanding of the cause(s) and
that should be explained fully to the patient before
ordering lenses.
V.E Vision Problems: Poor Optical Quality

365 Poor Optical Quality: Introduction

No amount of clinical skill, or complex design can
POOR OPTICAL QUALITY overcome either faulty manufacture, or a wearer’s
INTRODUCTION mistreatment of a lens to the point that its optical
May be: performance is degraded.
• A fabrication defect Fortunately, poor optical quality resulting from
defective manufacturing is less likely with the newer,
• The result of wearer mistreatment computerized, wet-molding, volume production
• Apparent from the outset, or.....
techniques used, especially when combined with
automated lens verification.
• May become apparent later
97200-271S.PPT

7L297200-271

366 Poor Optical Quality: Signs

Clinically, a wearer will exhibit reduced vision that is
POOR OPTICAL QUALITY
SIGNS
not improved by an over-Rx. A pinhole aperture will
• Reduced vision: probably not improve vision significantly either,
although if there is little or no diffusive component to
- over-Rx has no effect
the degradation, vision may be improved slightly,
- over-Rx has minimal effect suggesting a ‘refractive’ cause. Attempts to pursue
- pinhole aperture improves (refractive/shape) this ‘refractive’ cause will usually prove fruitless
- pinhole has no effect (diffusive)
because the over-Rx will not be spherical or sphero-
cylindrical, rather it is more likely to be irregular.
- pinhole o some improvement (mixed aetiology) Often the wearer’s complaint can be corroborated
• Retinoscopy with & without contact lenses by an abnormal retinoscopic reflex while the lens is
97200-272S.PPT
on the eye but which disappears once the contact
7L297200-272 lens is removed.
Lens Inspection:
x Confirm the clarity of the lens material and the
quality of its surfaces, looking for scratches,
abrasions, or incompletely polished surfaces.
Polishing defects may appear as greyish or

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 Lecture 7.2: SCL Complications and Their Management

367 ‘frosted’ areas that are isolated, or that cover

much or all of the lens surface. Inspect the
POOR OPTICAL QUALITY surfaces closely using high magnification, or
SIGNS specular reflection. Look for ‘burns’ and surface
• Lens inspection: anomalies such as ‘orange peel’ effects.
- clear, translucent, frosted, opaque Inspect the very centre of any lathed surface
- polishing defect(s) looking for a protruding nipple or cone that
- surface regularity, shape defect(s) indicates a failure of the lathe set-up. The
- inclusions
- striae central location of such a defect can have an
- bubbles adverse effect on vision.
- deposits x ‘Candling’ (holding the lens at arm’s length and
- optical quality (assess focimeter image)
observing a regular pattern such as an insect
97200-273S.PPT screen, or blinds through the lens, may reveal
7L297200-273
refractile irregularities.
x If the lens appears to be ‘clear’, and no local
refractile irregularity is detected, a shape
368 anomaly should be suspected. Preferably, the
lens should be suspended in normal saline, and
its surface shape assessed.
x Generally, both surfaces should be inspected
with a stereo microscope at moderate to high
magnification using direct illumination (using an
epi-illuminator), and retro-illumination (using a
sub-stage mirror or diffuser).
Testing Optical Quality:
x Testing the optical quality of SCLs in vitro is
difficult. One suggested technique is to blot the
lens and assess the target quality in a focimeter
(lensometer) fitted preferably with a ‘circle of
dots’ target (Bier and Lowther, 1977).
7L20222-02
x Wet-cell assessment can mask, or decrease
369 dramatically, the optical effects of many lens
defects, and is unsuitable for subtle defects.
While not strictly an optical quality matter, lens
deposits (slide 368) can exacerbate optical quality
issues, and reduce VA. They can also decrease
lens wettability (slide 369), or tear film stability, both
of which can affect the lens’ ‘optical’ performance.

7L20073-99

370 Poor Optical Quality: Symptoms

POOR OPTICAL QUALITY Reduced vision is probably the most obvious
SYMPTOMS symptom to be reported.
• Reduced vision:
If a suspect lens is exchanged for a new, identical
- from the outset ?
lens, and VA is restored to baseline levels, the lens
- delayed onset ?
is confirmed as the cause.
• Does anything improve vision?
- narrowing interpalpebral aperture Other considerations include:
- cleaning and rinsing x Poor vision experienced from the outset is
- use of protein remover suggestive of manufacturing and/or shape
- in-eye lubricating/hydrating drops regularity problems.
- switching to a new, identical lens
97200-274S.PPT
x Vision problems occurring later, are suggestive
7L297200-274
of reduced surface quality, or some other

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 Module 7: Contact Lens-Related Ocular Complications

change in the lens.

x Usually, attempts by the wearer to improve VA
prove fruitless, e.g. squinting (stenopaeic slit),
careful lens cleaning, in-eye
lubricating/hydrating drops, etc.
x If the cause is diffusive (deposits or surface
abrasions), the wearer may report a hazing of
vision, or obvious haloes (uncoloured), or flare
around objects.
371 Poor Optical Quality: Aetiology
The likely causes include:
POOR OPTICAL QUALITY
AETIOLOGY x Optical:
• Optical:
– manufacturing defects
- manufacturing
– ‘nipple’ at lens centre
- surface distortion – molding defect, e.g. bubbles at
- incorrect surface shape lens surface, or within the lens
material
- material defects
– decentred front surface optics
- striae, bubbles, other inhomogenieties
97200-275S.PPT – if lathed, ‘burnt’ surfaces, or
remnants of lathe marks
7L297200-275
– ‘orange peel’ surface

372 – foreign matter inclusions.

– surface distortion
POOR OPTICAL QUALITY – heat disinfection/heat disinfection in
AETIOLOGY inappropriate solution
• Diffusive:
– heat disinfection of unsuitable lens
- deposits
– denaturation of protein deposits
- surface scratches/abrasions forming a thick distorting film.
- chemical surface damage – incorrect/inappropriate surface shape
- incompletely polished surfaces – material defect giving irregular lens/lens
- molding, mold-release defects surface hydration
97200-276S.PPT

– striae, other material inhomogenieties.

7L297200-276
x Diffusive:
– surface deposits
– surface scratches/ abrasions
– chemical damage to the surface
– incompletely polished front surface
– heat damage from over polishing
– molding, or mold-release defects.

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 Lecture 7.2: SCL Complications and Their Management

373 Poor Optical Quality: Management

Almost invariably, lens replacement is the only
POOR OPTICAL QUALITY option. If vision restoration in still incomplete, ocular
MANAGEMENT
reasons for the decrease must also be sought. If a
• Usually, lens replacement required distorted lens was involved, the cornea’s shape may
• Try a ‘good’ lens to confirm lens is the cause have been altered (see cornea/lens wrinkling earlier
in this section) and the vision degradation may be a
- if vision still reduced:
compound issue, rather than one having a single
– consider ocular cause(s) cause.
– errors or omissions No attempt should be made to restore the lens to
• Keep ‘used’ lenses out of supply chain
usefulness as this is never successful. Importantly,
97200-277S.PPT
the introduction of used (worn) lenses into a
laboratory should be prohibited because of the
7L297200-277 potential for introducing ocular diseases (and other
pathologies) into the broader contact lens supply
chain.

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Zantos SG (1984B). Management of corneal infiltrates in extended-wear contact lens patients. ICLC.
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Zantos SG et al. (1986). Studies on corneal staining with thin hydrogel contact lenses. J BCLA. 9(2):
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Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

Unit 7.3
(4 Hours)

Lecture 7.3: Rigid Gas Permeable

Contact Lens Complications
and Their Management

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 Module 7: Contact Lens-Related Ocular Complications

Course Overview

Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and

Their Management
I Introduce RGP Contact Lens Complications
II Detail complications related to:
x Staining
x Hypoxia and corneal oedema
x Inflammation and infection
x Lens and lens fit
x Hypersensitivity and allergy
x Solution toxicity
x Ocular discomfort
x Reduced vision

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Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

Lecture 7.3
(4 Hours)

Rigid Gas Permeable Contact Lens

Complications and Their Management

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 Module 7: Contact Lens-Related Ocular Complications

Table of Contents

I RGP Contact Lens Complications: Introduction................................................195

II Inflammation and Staining-Related Complications ..........................................196
II.A Ocular Redness..............................................................................................196
II.B CLPC ..............................................................................................................200
II.C 3 & 9 O’Clock Staining....................................................................................204
II.D Corneal Dellen................................................................................................209
II.E Corneal Ulceration ..........................................................................................211
II.F Corneal Staining .............................................................................................213
II.G Conjunctival Staining......................................................................................220
II.H Vascularized Limbal Keratitis (VLK) ...............................................................222
III Oedema and Hypoxia-Related Complications..................................................227
III.A Corneal Oedema ...........................................................................................227
III.B Corneal Vascularization.................................................................................231
IV Mechanical and Pressure-Related Complications...........................................234
IV.A Lens Adherence ............................................................................................234
IV.B Corneal Warpage ..........................................................................................238
IV.C Corneal Shape Changes...............................................................................248
IV.D Ptosis ............................................................................................................253
IV.E Discomfort .....................................................................................................256
V Vision Complications ..........................................................................................264
VI Lens and Fitting-Related Complications ..........................................................276
VI.A Blink-Related Problems.................................................................................276
VI.B Fitting Problems ............................................................................................280
VI.C Lens Flexure .................................................................................................285
VI.D Lens Warpage...............................................................................................290
VI.E Wearer Non-Compliance...............................................................................293
References................................................................................................................300

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I RGP Contact Lens Complications: Introduction

1 RGP Contact Lens Complications: Introduction
In the interests of completeness and efficiency, this
lecture is designed to complement Lecture 7.2: Soft
Contact Lens Complications and Their
RIGID GAS PERMEABLE Management in this module. Some subjects are
described more fully in 7.2 and the discussions in
CONTACT LENS
this lecture are intended to be complementary
COMPLICATIONS AND rather than comprehensive. Many of the
THEIR MANAGEMENT illustrations used in each lecture are equally
applicable to both rigid and soft lenses.
Obviously, there are some topics that are rigid
lens/RGP-lens specific and these are treated in
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7L397300-1
The volume of literature relevant to rigid lenses is
smaller than that pertaining to soft lenses for two
possible reasons. The extent of complications is
generally considered to be smaller (although doubt
exists, e.g. see Fonn et al., 1995), and the market
size is much smaller.
RGP lenses offer significant physiological benefits
some of which are matched only by siloxane
hydrogel lenses. These, combined with a lower
reported complication rate, make RGP contact
lenses a safe vision correction option.
According to Terry et al. (1989), RGP EW
complications, although low, may include the
following:
x Corneal ulceration.
x Corneal erosion.
x Corneal distortion following lens adherence
after overnight lens wear.
x CLARE.
x CLPC.
Terry et al. also report that, as in SCL EW, the more
serious complications are likely to occur in EW
especially if the patient ignores the early warning
signs such as increased redness and lens irritation.
The simple concept of ‘if in doubt take them out’
should be emphasized.
‘See well, look good, feel good’ is appropriate
advice for patients to monitor their eyes upon
awakening each day.

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II Inflammation and Staining-Related Complications

II.A Ocular Redness
2 Ocular Redness: Introduction
Ocular redness is an important baseline
OCULAR REDNESS: INTRODUCTION assessment that should be recorded/documented
• A baseline assessment is important
before any lens fitting is undertaken. If the patient
• A good history is essential is already a lens wearer, the practitioner can only
• If lens wear has already commenced undertake a monitoring and recording role, unless
practitioner can only play a monitoring role lens wear has ceased temporarily.
• Consider: A good history is an appropriate starting point.
- lens type Baseline data takes on even greater importance in
those prospective wearers who have inherently
- lens care products used redder eyes before any lenses are used.
- environment Information sought should include:
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7L397300-138
x The type(s) of lens(es) worn.
x The lens care products used.
x The environment in which the lenses are used.
x Visual acuity provided by the lenses.
x Slit-lamp examination results.
x An assessment of pupil responses.
x A thorough history.
This information will assist the formulation of a plan
to resolve the problems presented (after Munro and
Covey, 1998). For a more comprehensive
introduction to ocular redness and its probable
causes, see Lecture 7.2, Section III.B Effects:
Ocular Hyperaemia in this module.
3 Ocular Redness: Signs
Typically, any increase in the level of ocular
OCULAR REDNESS redness associated with RGP contact lens wear
SIGNS occurs in the nasal and temporal quadrants (slide 4)
extending from the paralimbal regions to the
• Increase in vascular response
canthus (Munro and Covey, 1998). In many cases
• Typically in the nasal and there is an accompanying corneal and/or
conjunctival staining pattern.
temporal quadrants
Redness is often rated on a 5-point scale as
• May be associated staining follows:
0 Absent.
97300-2S.PPT 1 Very slight.
7L397300-2
2 Slight.
3 Moderate (slide 4).
4 Severe (slide 5).
4 Redness can be further qualified by location (by
description or using analogue clock positions),
sector (quadrant), and extent. Comments about the
depth of the anterior eye involved also apply, e.g.
superficial conjunctival, deep conjunctival, or
episcleral (unlikely).
If the condition is allowed to persist for an extended
period, conjunctival degeneration may ensue
leading to a dellen formation in the corneal
periphery. Other signs may include:
x Reduced or irregular tear prism.
x Excessive tear debris.
7L3990-91
x Dulled specular reflection from the bulbar

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5 conjunctiva.
x Conjunctival staining (depending on the cause
of the redness).
x Excessive or blocked Meibomian gland
secretion.
x Rose Bengal staining.
x Reduced tear Break Up Time (BUT).

Redness may be unilateral (slide 6) or bilateral.

7L30146-90

7L30143-96
7 Ocular Redness: Symptoms
Often a mild increase in ocular redness is not
OCULAR REDNESS associated with any symptoms. A greater level of
SYMPTOMS redness is likely to be accompanied by symptoms
shown in the slide opposite.
• Often asymptomatic Should the symptoms reported worsen after lens
removal, a corneal lesion should be suspected.
• Associated condition may Worsening symptoms suggest the lens has been
cause discomfort behaving as a bandage and decreasing the severity
of, or hiding the effect of, a corneal problem. This
situation is more likely to occur when the
epithelium’s integrity has been compromised.
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7L397300-3

8
OCULAR REDNESS
ACCOMPANYING SYMPTOMS
• Irritation
• Dryness (tear problem?)
• Itchiness
• Grittiness (tear problem?)
• Burning (tear problem?)
• Stinging on insertion (physical or chemical
cause?)
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9
OCULAR REDNESS
ACCOMPANYING SYMPTOMS
• Reduced lens tolerance (toxicity or allergy?)
• Tearing (inflammatory event?)
• Mild photophobia (inflammatory event?)
• Pain & discomfort (suspect MK esp. if with
mucopurulent discharge)
• Decreased vision (central/paracentral
lesion?)
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7L397300-191
10 Ocular Redness: Aetiology
OCULAR REDNESS Frequently, the cause of increased ocular redness
AETIOLOGY is multifactorial which makes diagnosis difficult.
• Multiple causes
This is just one reason why a comprehensive
• Most common are: patient history is required.
- 3 & 9 o’clock staining
Acute or chronic conditions that are commonly
- pinguecula irritation associated with increased redness include:
- pterygium irritation
x 3 & 9 staining - chronic staining resulting in an
- dry eye/lens
increased vascular response in the nasal and
• Solution preservatives temporal quadrants.
• Acute or chronic
97300-4S.PPT
x Pinguecula irritation - from peripheral
7L397300-4 desiccation of cornea/conjunctiva.
x Pterygium irritation – mechanical insult of this
11 degeneration’s leading edge by the edge of a
mobile lens can lead to redness, irritation, and
OCULAR REDNESS possibly, further stimulation of the pterygium.
AETIOLOGY: ACUTE or CHRONIC? While an advanced pterygium is a
• Acute: contraindication for RGP lenses, prohibition of
- more likely to be physical RGP lens wear is probably extreme. In some
- chemical cases, acceptance may depend on the
- pathological/infectious cosmetic issue of apparent eye redness.
• Chronic: x Corneal oedema.
- more likely to be physiological
- low-grade mechanical
x Dryness – a dry ocular and/or lens surface is
- a developing solution sensitivity
often a cause of increased redness. This may
97300-176S.PPT
be due to factors such as Meibomian Gland
Dysfunction (MGD) (see Lecture 7.2, Section
7L397300-176 III.E Meibomian Gland Dysfunction (MGD)).
x Preservative sensitivity – lens care and
maintenance solutions used by the patient may
irritate the eyes and cause inflammation. This
is less likely in RGP lenses because of their
lower absorption capacity.
x Microbial keratitis (MK) – the cornea’s defence
mechanisms are delivered largely via the
vasculature, particularly the limbal vasculature,
and the tears. Vasodilation accompanies the
response and assists in the delivery of
leukocytes to the corneal periphery via the
limbal vasculature. Tears and blinking also play
a role (see non-specific host defences detailed
in Module 6, Lecture 6.5: Ocular Host Defence
Systems and Contact Lens Wear).

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x Ulceration – see Section II.E Corneal

Ulceration in this lecture. The redness may be
severe.
Whether the condition is chronic or acute can be
established from a thorough history. Aetiological
information that may assist in their differentiation is
presented in the slide opposite.
12 Ocular Redness: Management
The possibility that a serious eye condition such as
OCULAR REDNESS
MANAGEMENT microbial keratitis may be the cause of ocular
• Dictated by the cause redness needs to be explored fully.
Regardless of whether the redness is acute or
• Minimize staining or mechanical effects chronic, management relates largely to controlling
• Optimize: or eliminating the cause or causes.
Issues that need to be addressed include:
- solutions
x Elimination of 3 & 9 o’clock staining (see
- care and maintenance procedures Section II.C 3 & 9 O’Clock Staining in this
• Treat any tear film problem lecture).
97300-5S.PPT
x Alter the lens care products used in favour of
7L397300-5 preservative-free or low-toxicity preservative
products.
x Use tear supplements for eye dryness.
x Recommend lid scrubbing and warm
compresses for cases of Meibomian Gland
Dysfunction (MGD).
x Address physical and physiological issues.
– oxygen transmissibility
– damaged lens
– foreign body
– chemical irritant (source?)
– finger-borne?
– infection (hygiene, compliance?)
– inspect/swab lens case
– lens design.
Dry eye and marginally dry eye cases are more
difficult to manage because of the lack of diagnostic
certainty (see Lecture 7.4 for more details).
It is prudent to alter only one variable at a time, i.e.
a process of elimination.
The possibility that the problems reported are not
contact lens-related must be considered, especially
when a condition is confirmed but no apparent
cause is found.

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II.B CLPC
13 Contact Lens-Induced Papillary Conjunctivitis:
Introduction
CONTACT LENS-INDUCED PAPILLARY
CONJUNCTIVITIS (CLPC): While now regarded as primarily a condition
INTRODUCTION affecting SCL wearers, this condition was first
observed in wearers of plastic (presumably PMMA)
• Multi-factorial
ocular prostheses (Thygeson, 1978, cited in Mackie
• Immunological inflammatory condition of and Wright, 1978). Thygeson called it
the superior tarsal conjunctiva ‘pseudovernal conjunctivitis’ because of its likeness
• Mechanical irritation a factor to that vernal conjunctivitis. It has also been called
‘Spring’s catarrh’ after Spring (1974) who first
• SCLs > RGP lenses
reported it in relation to SCL wear and because of
• Superior lid > inferior lid its similarity to a mild form of spring catarrh.
97300-140S.PPT

Korb (1978, cited in Mackie and Wright, 1978)

7L297300-140 reported a 7% incidence in rigid lens wearers over a
5 year period.
Mackie and Wright (1978) point out that papillary
changes in the lid margin zone of the upper lid are
relatively common even in non-contact lens
wearers. Allansmith et al. (1977) concluded that
CLPC sufferers were no more likely to have an
atopic condition than those without signs of CLPC.
CLPC is a multi-factorial condition. It is an
immunological inflammatory disease of the superior
(usually) and inferior (rarely) tarsal conjunctivae
associated with lens deposits, sutures, prostheses,
corneal glue, or any persistent mechanical irritation
of the conjunctiva. It is much more a SCL issue
than an RGP lens issue (Korb et al., 1980).
14 Contact Lens-Induced Papillary Conjunctivitis:
Signs
CLPC
SIGNS In CLPC, the normally smooth palpebral
• Redness conjunctival tissue takes on a roughened
appearance that is easily seen with the slit-lamp in
• Roughness of the palpebral conjunctiva specular reflection. The papillae enlarge and the
- papillary level of redness increases. In more advanced
- follicular (usually not CL-related)
cases, the palpebral conjunctiva may appear
oedematous (appears more translucent or more
• Typically starts near the lid margin greyish-white than normal).
• Ptosis with chronic, giant, widespread papillae
Judging severity is easier if fluorescein is instilled,
97300-6S.PPT and a yellow barrier filter used in the observation
system to enhance contrast (slide 20).
7L397300-6
CLPC describes the condition that is now
considered a mild form of giant papillary
15 conjunctivitis (GPC), i.e. these conditions are
essentially the same and vary in degree only (see
CLPC Lecture 7.2, Section III.D CLPC in this module for
SIGNS historic information on the names). In RGP lens
• Lens fitting change wear, the onset of CLPC occurs most commonly
near the lid margin. This is in contrast to the
- increased movement condition associated with SCL wear in which the lid
changes occur first in the region adjacent to the lid
- higher riding fold (on lid eversion).
• Surface deposits/surface drying As the lid surface roughens the lens fitting
characteristics may alter. Often the average
• Excess mucus position moves higher (the influence of the upper
97300-125S.PPT
lid), decentration is greater, and the amount of lens
7L397300-125 movement on blinking increases.
Increased lens surface deposition of mucus is also
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16 a feature of CLPC.
Mackie and Wright (1978) noted that CLPC papillae
do not extend into the superior fornix (they do in
chlamydial infections). They also noted the
development of transient ‘white heads’ in larger
papillae that disappeared at some later stage.
Some flat papillae were also reportedly seen in
some patients. Surprisingly, Mackie and Wright
found unilateral ptosis in four of the 29 cases they
monitored with seemingly no relationship to the
severity of the CLPC. Generally, no relationship
was found between CLPC signs and CLPC
symptoms.
Sometimes confusion exists between CLPC and
7L3077-99
follicles. Differential diagnostic information is
presented in slides 17 and 18.
17
PAPILLAE OR FOLLICLES?
Papillae Follicles
• Seen in CL wear, and • Usually, not CL related
normals
• Cobblestone-like, • Translucent, pale,
hyperaemic, with central elevated, round rice-grain
vascular tuft, ‘white points’ shaped, usually avascular
may be seen centrally
• Diameter: 0.3 - 0.9 mm • Diameter: 0.2 - 2 mm
• Superior palpebral • Inferior palpebral
conjunctiva near lateral conjunctiva near lateral
canthus
canthus
97300-187S.PPT

7L397300-187

18
PAPILLAE OR FOLLICLES?
Papillae Follicles
• Allergic reaction/allergy • Often viral infection
(e.g. viral
conjunctivitis)
• Chronic • Not as chronic
• Seen in normal • Not seen in normal
conjunctiva conjunctiva
• Mainly inflammatory • Local aggregation of
cells lymphocytes
• n mucus strands • No n mucus strands
97300-192S.PPT

7L397300-192

19

7L3628-97
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20

7L32543-93
21 Contact Lens-Induced Papillary Conjunctivitis:
Symptoms
CLPC Very mild forms of CLPC are typically
SYMPTOMS asymptomatic. If the condition advances, the
wearer becomes more aware of the lens due to its
• Lens awareness
greater on-eye mobility.
• Decreased wearing time The patient may complain of an itchy sensation and
may also report a decrease in the period for which
• Itchiness the lenses remain comfortable to wear.
Mackie and Wright (1978) report four common
• p vision symptoms.
97300-7S.PPT x The predominant symptom is a discharge from
the eye. Initially the discharge is simply an
7L397300-7
increase in the quantity of morning ‘sleep’ but
this can increase to stringy mucus once the
22 lenses are worn. Eventually, the symptoms
may include eyelids being stuck together on
CLPC: COMMON SYMPTOMS awakening.
Mackie & Wright, 1978 x Itching (probably). In its extreme form some
sufferers may even describe the sensation as
• Discharge from the eye
painful. Itching often starts after lens removal.
This can lead to vigorous eye rubbing.
• Itching (probably)
x Blurred/fluctuating vision. This may be due to
• Blurred/fluctuating vision fine milky deposits or large white blobs of
loosely adherent mucus on the dry lens
• n on-eye lens movement surfaces.
x Increased on-eye lens movement. This is due
97300-193S.PPT

to the increased traction between lens (usually

7L397300-193 deposited) and lids. In extreme cases, lid
attachment may be observed.
23 Contact Lens-Induced Papillary Conjunctivitis:
Aetiology
CLPC
AETIOLOGY The most likely causes of CLPC are the mechanical
• Lens deposits interaction between the contact lens front surface
and the palpebral conjunctival tissue, and allergy.
- mucoprotein Any mechanical effect is greater when the lens has
• Mechanical action a higher level of surface deposits. Deposits may
- lid movement also act as an antigen and the eye’s immune
- lens edge system responds to the ‘foreign’ material
appropriately.
• Exacerbate pre-existing problem
At biopsy, Mackie and Wright (1978) found
- previous SCL wearer ? hyperplasia of the epithelium with many
97300-8S.PPT

‘downgrowths’ into the stroma, occasional inclusion

7L397300-8 cysts containing goblet cells, and eosinophilic
infiltration of the epithelium and stroma. Goblet cell

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and basophil numbers were also higher than

normal. They concluded that CLPC was an allergic
reaction.
The fact that CLPC associated with RGP lenses
usually starts in the region near the lid margin
suggests that the lens edge may interact with the
palpebral conjunctiva. This implicates the edge
clearance, the edge design, or the finish of the lens.
Some patients wearing SCLs who experience
CLPC are switched to RGP lenses. In these cases,
the RGP wear has not caused the CLPC but often
exacerbates the problem, i.e. RGP lenses may not
be the solution to an SCL-initiated CLPC case.
24 Contact Lens-Induced Papillary Conjunctivitis:
Management
CLPC
MANAGEMENT CLPC is a condition that all practitioners and lens
• Minimize wear, or discontinue temporarily wearers must be aware of because, in the long-
term, it has the capacity to severely limit the ability
• Determine cause if possible and modify
of the eye to tolerate contact lenses.
- replace lens, or polish lenses completely
In most cases, it is a preventable, lens-related
- deposits/care and maintenance
condition. Preventing CLPC requires the
- edge shape (apex position) optimization of lens material, care and
- thinner overall lens design maintenance, wearing schedule and frequency of
- overwear (DW or EW) lens replacement. Discontinuation is an option but
97300-9S.PPT such an extreme move is seldom required, or
7L397300-9
justified. Mackie and Wright (1978) found that if
lens wear ceased, it took more than a week for the
staining they observed at the apex of the papillae to
25
disappear.
CLPC
Lenses should be thin, well finished, thin-edged
MANAGEMENT
• Therapeutic with an apex biased towards the posterior surface
and fabricated in a higher Dk material. Lenses
- mast cell stabilizer should be replaced regularly, and lens care
- combination stabilizer & antihistamine
systems used should be preservative-free or be
known to have low toxicity. Preservative-free care
- histamine blocker or daily disposable lenses (currently, SCLs only)
may be the answer to continuing lens care-related
- mild steroid
problems or, in some cases, wearer compliance
• Lens replacement schedule problems.
97300-126S.PPT

If a lens harbours denatured protein, it should be

7L397300-126
either replaced or resurfaced completely (polished).
If a wet lens surface cannot be maintained, frequent
use of an in-eye lubricant during lens wear should
be considered.
Regardless of the treatment given it seems that
rapid resolution cannot be expected and
improvements over one to four months are a more
realistic expectation.
The use of Opticrom® (2% cromolyn sodium)
appears frequently in the historic literature.
However, its use is now less common and subject
to local availability and/or regulations/restrictions.
More commonly, a mast cell stabilizer such as
lodoxamide, a combination mast cell stabilizer and
antihistamine such as olopatadine, or histamine
blockers such as levocabastine are now employed.
Other, less conventional, treatments exist. Molinari
and Rengstorff (1988) used aqueous drops of

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 Module 7: Contact Lens-Related Ocular Complications

Vitamin A in SCL CLPC cases. Cold compresses,

topical steroids, and mast cell stabilizers have also
been used. Mackie and Wright (1978) reported that
systemic tetracycline rendered some wearers
asymptomatic for 6 to 12 months.
In some cases, a switch from SCLs to RGP lenses
resolved CLPC.
Patient education at the commencement of lens
wear is a vital step in CLPC prevention.
II.C 3 & 9 O’Clock Staining
26 Three & Nine O’clock Staining: Introduction
3 & 9 O’CLOCK STAINING The rigid lens-associated staining pattern known as
INTRODUCTION 3 & 9 o’clock staining has been known for many
• Described by Mackie, 1966
years. Papers as far back as 1966 (Mackie, 1966)
have detailed the clinical appearance of the
• Individual susceptibility condition with PMMA lenses. According to Mackie
• Some delay before condition arises there appears to be a threshold of wearing time that
• May develop into two more serious is subject to significant individual variation, after
forms: which 3 & 9 o’clock staining may appear in
- without infiltrates susceptible wearers. He found that after the
condition appeared, it could develop at any time
- with infiltrates into one of two more serious forms. The first form
97300-141S.PPT
has no accompanying infiltrates while the second
7L397300-141 form does. In a later paper, Mackie (1971)
describes the first form as being a dellen or dellen-
like and the latter as being pterygium-like. In
extreme cases corneal erosions and even
ulceration can follow 3 & 9 o’clock staining
(Bursinger et al., 1989).
This condition has a number of alternative names.
These include:
x Peripheral desiccation staining.
x Peripheral corneal desiccation (PCD).
x Peripheral corneal staining.
x Juxtaposition staining.
x Confluent erosions.
Solomon (1986) asserted that the use of the term ‘3
& 9 o’clock staining’ is a misnomer as the areas
involved are often more extensive than 3 & 9
o’clock suggest.
3 & 9 o’clock staining has been described as the
being one of the most persistent RGP lens after-
care problems (Kerr, 1988). It is also more
prevalent in RGP EW than in DW (Henry et al.,
1990).
Estimates of its incidence in the literature range
between 1% and 85% (Mackie, 1966, Barabas,
1967, cited in Golding, 1990, Henry et al., 1987,
Lowther and Paramor, 1982, Schneider, 1988, and
Barr and Testa, 1994). In Schneider’s study, 15%
of wearers were so severely affected that
intervention was required, and fully 38% of all RGP
lens wear discontinuations were due to 3 & 9
o’clock staining.
A rare but more serious complication of rigid lens
wear is the development of a pseudopterygium as a
sequel to chronic 3 & 9 o’clock staining. Whereas a
pterygium is a degenerative and hyperplastic
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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

condition in which the conjunctiva invades the

cornea, pseudopterygium is an inflammatory
adherence of conjunctival tissue to the cornea that
has a pterygium-like appearance (Golding, 1990).
However, pseudopterygium may not be a contact
lens related condition.
27 Three & Nine O’clock Staining: Signs
3 & 9 O'CLOCK STAINING Typically, staining occurs as an arcuate band on the
SIGNS peripheral cornea between 3 and 5 o’clock and 7
• Invariably, bilateral and 9 o’clock. The staining occurs in the area not
• Nasal & temporal areas affected covered by the lens, which is why it is sometimes
referred to as ‘exposure’ staining. Usually, the
• Increases over time staining is present both nasally and temporally
• Peripheral staining (slide 29), and bilaterally, although not necessarily
equally advanced. Conjunctival hyperaemia
- punctate to patches
localized to the horizontal axis (slide 30) will always
- outline follows lens edge (i.e. accompany the staining (slide 31) (Businger et al.,
the inner edge is arcuate) 1989).
97300-14S.PPT

Mackie’s original description follows: The first sign

7L397300-14
is punctate or granular fluorescein staining in the 3
and 9 o’clock zones, usually accompanied by local
28 ciliary injection. No clear area exists between the
3 & 9 O'CLOCK STAINING staining and the sclera and it is usually present in
SIGNS all the corresponding zones if it is present in one
• Bulbar redness zone. The staining may worsen at any time,
- nasal and temporal developing more serious lesions that appear to be
- tufts of vessels of two types.
• Advanced cases The first type has a 2-3 mm diameter fluorescein-
- dellen staining facet adjacent to the sclera but no
- erosion/ulceration infiltrates. It perhaps looks more serious than it is.
- vascularization Cessation of lens wear usually results in a
- scarring resolution in two to three days, leaving little or no
97300-15S.PPT trace of its existence.
7L397300-15 The second type is an infiltrated lesion that affects
both the stroma and epithelium. The affected tissue
29 is elevated above the corneal surface, and may
subsequently ulcerate and become vascularized.
This form takes longer to resolve (weeks) and
leaves a permanent scar. Mackie concluded that
the second, and more serious form, may simply be
a later stage of the first.
Mackie also observed that wearers with pinguecula
were more prone to 3 and 9 o’clock staining. This
may be because the pinguecula’s elevated profile
increases the lid’s bridging of the affected areas.
As the level of staining becomes more pronounced,
associated signs such as increased ocular redness
and dellen are more likely to be observed. Severe
7L33&9DF
cases may result in corneal ulceration, and
vascularization.
Slides 29 and 31 provide some indication of the
‘averaged’ lens position.
If a pseudopterygium is present it usually appears
as either a nasal or temporal vascularized lesion
encompassing the paralimbal, limbal and peripheral
corneal regions (Golding, 1990). Local conjunctival
and limbal vessel hyperaemia indicates the areas
affected. The apex of the elevated tissue may not
be vascularized, and punctate staining with sodium
fluorescein may be observed in the surrounding
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30 tissue (part of the area affected by the preceding 3

& 9 o’clock staining condition).

7L31700-94

31

7L30014-93
32 Three & Nine O’clock Staining: Symptoms
Mild forms of 3 & 9 o'clock staining may be
3 & 9 O'CLOCK STAINING
asymptomatic. Most complaints centre on the
SYMPTOMS
• Often asymptomatic if mild hyperaemic appearance of the eyes. Pain is almost
never reported.
• Burning, itching Greater levels of staining are often associated with
symptoms such as, ocular dryness, itching, and
• Decreased lens wearing time increased lens awareness (Businger et al., 1989).
In many cases the wearing time is reduced due to
• Dry eyes the onset of symptoms and increased apparent
ocular redness.
• Red eyes
97300-16S.PPT

7L397300-16
33 Three & Nine O’clock Staining: Aetiology
An inhibition of blinking leading to blinks that are
3 & 9 O'CLOCK STAINING
incomplete, and a reduced blink rate, is the primary
AETIOLOGY
cause of 3 & 9 o’clock staining. This leads to a
• Patient factors: disturbance of the tear layer that results in corneal
- dry eye and conjunctival desiccation. (Mackie, 1971, Korb
and Exford, 1970, cited in Mandell, 1988, Lemp et
- partial blinkers
al., 1970, 1970B, cited in Mandell, 1988, Lowther
- reduced blink rate and Paramore, 1982, Holden et al., 1987). As
blinking is inhibited (involving the upper eyelid
- inadequate mucin surfacing
primarily) the tears, especially the mucous layer,
of the cornea are not spread across the surface of the anterior
97300-17S.PPT
eye.
7L397300-17 Of perhaps greater significance was the
demonstration by McDonald and Brubaker (1971)
that tear film thinning occurred in a zone just
beyond the edge of tear menisci (slide 34). This
film thinning is compatible with the location of 3 & 9
o’clock staining in rigid lens wear. This film thinning
may be exacerbated in the dry, or marginally dry,
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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

34 eye because of the relatively inadequate tear

volume (with respect to the ‘needs’ of the post-lens
LENS EDGE MENISCUS tear volume, even in the normal eye) present on the
LOCAL TEAR FILM THINNING external eye. Tear fluid is drawn to and under an
Pre-lens tear film
in g RGP lens and this general insufficiency is a central
nn
thi
Lens edge
r fi
lm factor in the centration and fitting behaviour of all
tea
Lo
cal rigid lenses (Kikkawa, 1970, Hayashi and Fatt,
Pre-corneal 1980, Kikkawa and Salmon, 1990),
Cornea

Post-lens tear film tear film

Potentially, the corneo-scleral sulcus represents a
zone of no contact between the globe and the

Cornea
upper eyelid margin, i.e. it bridges the mid-
after McDonald & Brubaker, 1971
peripheral cornea and the perilimbal conjunctiva.
97300-182S.PPT
The presence of a lens may exaggerate the effect
by shifting the lid margin further from the cornea
7L397300-182
thereby increasing the size of the bridged zone
(slide 36). It is in this bridged zone that 3 & 9
35 o’clock staining occurs.
The fundamental cause of 3 & 9 o'clock staining is
3 & 9 O'CLOCK STAINING the irritation produced by the lens which inhibits the
AETIOLOGY normal blinking process leading to a
• Lens factors: disturbance/drying of the tear layer, and a failure of
- lid-lens ‘gap’ (bridging) wetting of the corneal epithelium adjacent to the
- centration (low) edge of the lens (slide 34).
- movement (limited)
The possible causes can be classified into the
- diameter (small)
following categories:
- edge thickness (excessive)
x Patient factors. Irregularities of the conjunctiva,
- edge clearance (excessive)
e.g. pinguecula, may assist in the bridging of
- edge defect(s)
97300-18S.PPT
conjunctival areas by the upper lid margin.
Tear film abnormalities include lipid
7L397300-18 contamination, mucin deficiency, and an
inadequate aqueous layer (Businger et al.,
1989).
36
x Lens factors. See slides 34 and 36. Holden et
3 & 9 O’CLOCK STAINING al. (1987) studied edge ‘liftoff’ (edge lift) and
UPPER LID MARGIN BRIDGING found that a lift of 0.08 mm was unlikely to
No Lens cause 3 & 9 staining while lifts of 0.10 to 0.12
Anterior Upper Lid Margin mm were almost certain to cause 3 & 9
Eye staining.
x Environmental influences. Examples include:
wind and air-conditioning.
Lens
Upper Lid Margin
Anterior
Eye In prospective studies, Schnider et al. (1996, 1997)
found that those wearers prone to 3 & 9 staining
97300-142S.PPT
exhibited the characteristics (of eyes and lenses)
7L397300-142 shown in slides 38 and 39.
37
Other theories appear in the literature, e.g.:
3 & 9 O'CLOCK STAINING x Bell (1997) presented a novel theory on the
AETIOLOGY aetiology of 3 & 9 o’clock staining based on
• Lens factors: tear fluid turbulence and viscous drag within
- low edge clearance the tear film slowly ‘abrading’ the corneal
- excessive edge clearance epithelium in the 3 & 9 o’clock regions.
- narrow edge width x Barr and Testa (1994) postulated that a
- wearing time contributing factor to the more serious
- poor wettability sequelae of 3 & 9 staining may be the result of
- daily or extended wear
a failure of the rate of mitosis in the affected
area to keep pace with the rate of cellular
97300-131S.PPT
damage. Such a discrepancy is greatest in EW
7L397300-131 in which the epithelium has no lens-free ‘repair’

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38 time. This failure to keep pace can lead to a

loss of epithelial tissue and a breakdown of the
3 & 9 O'CLOCK STAINING
AETIOLOGY epithelium may result.
after Schnider et al. (1996, 1997) Schnider et al. (1996) reported that a lens locating
• Increased conjunctival hyperaemia
inferiorly was an accurate predictor of an increased
• Longer inter-blink periods susceptibility of a wearer to developing peripheral
• Decreased tear film quality: desiccation staining (PCD) (3 & 9 o’clock staining).
- increased tear lipid Lindsay (2003, personal communication) has
confirmed this observation.
- increased tear debris
A summary of likely aetiologies appears as slide 40.
• Reduced lens surface wettability
• Faster front surface drying
97300-177S.PPT

7L397300-177

39
3 & 9 O'CLOCK STAINING
AETIOLOGY
after Schnider et al. (1996, 1997)
• Increased ratio: blink interval/lens drying time

• Inferior lens centration

• Narrow or shallow edges as seen with

fluorescein

• Smaller lens diameters

• More erratic blink-induced lens movement

97300-178S.PPT

7L397300-178

40
3 & 9 O’CLOCK STAINING
AETIOLOGY: SUMMARY
Incomplete
Discomfort
Blinking

Increased Tear
Dryness
Evaporation
Peripheral
Lens-Limbus Desiccation
Bridging by Thinned
Lid Margin Tear Film
3&9
Blinking Inhibition Corneal O’CLOCK
Mucus STAINING
97300-173S.PPT

7L397300-173
41 Three and Nine O’clock Staining: Management
Early detection of 3 & 9 o'clock staining is important
3 & 9 O'CLOCK STAINING
MANAGEMENT to the practitioner initiating an appropriate
• Dictated by cause management plan.
• Early phase: If the edge clearance is decreased excessively it is
- patient education possible to induce lens adherence which can
- use of tear supplements exacerbate 3 & 9 staining (Swarbrick and Holden,
- improve blinking 1987).
- redesign lens to improve fitting Schnider et al. (1997) showed that large diameter
- maximize lens wettability (TDs of 9.6 & 10.2 mm) lenses were better as long
as a moderately wide tear reservoir could be
- minimize surface deposits
97300-20S.PPT
maintained at the lens edge. To achieve the latter
they concluded that careful attention needed to be
7L397300-20
paid to the design of the lens periphery.

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42 If the staining is associated with a low-riding lens, it

may be helpful to refit with a lens that rides higher
3 & 9 O'CLOCK STAINING on the cornea.
MANAGEMENT
Blinking exercises provide some alleviation of 3 & 9
• Modify wearing time o’clock staining (Mackie, 1971, Kerr 1988, and
• Temporary discontinuation of lens wear
Cotie, 1990) and the use of in-eye comfort drops
(preserved or preservative-free) also help (Kerr,
• Vitamin A drops 1988, Jones et al., 1989).
• Punctal plugs
Despite the various techniques applied to the
• Fit SCLs elimination of 3 & 9 o’clock staining, none is
97300-21S.PPT
successful totally in treating the condition. The
most successful treatment is to improve the comfort
7L397300-21
of the lens through design, to allow a more natural
43 blink (Mandell, 1988).
3 & 9 O'CLOCK STAINING Generally, detection of 3 & 9 o’clock staining should
MANAGEMENT: LENS DESIGN be heeded as a warning sign of potentially more
To improve fit & optimize comfort: serious conditions that may follow should
• Thin edge remediation not be undertaken (Schnider et al.,
• Equatorial to posterior edge apex 1988).
• Thin lens
• Reduce edge clearance
• Centred or lid-attachment fit to facilitate
smooth lens movement
• Aspheric or blended back surface
• Larger TD (9.5 to 10 mm)
97300-179S.PPT

7L397300-179

II.D Corneal Dellen

44 Corneal Dellen: Introduction and Signs
DELLEN Dellen were first described by E Fuchs in 1911
SIGNS (Fuchs A, 1929) as dimples or saucer-like
• Localized thinning of the cornea excavations at the corneal margin that were usually
elliptical in shape and parallel to the limbus. In non-
• Saucer-like depressions contact lens cases, they usually last about 24 to 48
hours. The association between contact lenses and
• Fluorescein pooling/localized dellen (and 3 & 9 o’clock staining) was reported by
Mackie (1966, cited in Mackie, 1971).
tear film deepening Dellen are described as very localized areas of
peripheral corneal thinning with a sharp
• Often no overlying staining demarcation (slide 45). The depression has a
97300-22S.PPT

smooth, gradually sloping outer wall (limbus side)

7L397300-22 that rises to meet the normal thickness of the
surrounding corneal tissue. However, the slope of
the inner wall of the depression (corneal side) is
45 steep (Fuchs, 1911, cited in Fuchs, 1929).
Fluorescein and Rose Bengal pool in the dellen
(slides 45 and 46), but some claim there is no true
staining because the epithelium in the depression
remains intact. This has been disputed because a
precursor to dellen formation is desiccation, a
condition that involves staining.
Should significant corneal dehydration be present
adjacent to the lesion, localized staining of the
affected area(s) can be seen (the higher
magnification photograph [slide 46] shows a more
extensive area of staining than does slide 45 for
example). The eye is usually quiet and ‘white’ (this
section after Gutner, 1989).
7L31I27

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46 If the dellen are of long-standing, permanent

scarring and vascularization may result. If
treatment is delayed, the cornea may be
compromised and a permanent regional thinning
can result (Gutner, 1989).
Josephson (1986) expressed the concern that 3 & 9
o’clock staining left unchecked could lead to:
x A breakdown of elastic tissue locally.
x Conjunctival epithelial hypertrophy.
x Dellen-like changes in the cornea, with or
without vascularization.
Vascularized cases of dellen are more likely to
leave permanent scarring.

7L31I28
47 Corneal Dellen: Symptoms
Dellen usually occur in the absence of discomfort or
DELLEN
SYMPTOMS pain, or only a slight discomfort with a decrease in
corneal sensitivity in the depression itself (Insler et
• May be asymptomatic al., 1989).
Vague irritation or photophobia may be reported
• Associated conditions may cause irritation (Gutner, 1989). Visual acuity is not affected
because only the peripheral cornea is involved.
- 3 & 9 staining

- dry eye

97300-23S.PPT

7L397300-23
48 Corneal Dellen: Aetiology
DELLEN Most cases of dellen are not related to contact lens
AETIOLOGY wear, rather they are likely to be caused by the
• Elevations factors itemized in slides 48 and 49.
- pinguecula (& pterygium) Typically, dellen formation is secondary to a
- thick-edged RGP lenses localized breakdown of the tear film’s lipid layer
• Tear film evaporation followed by corneal surface evaporation and
- dry corneal surface
dehydration ensues (Baum et al., 1968, cited in
• Post-operative effects
- IOL implantation
Insler et al., 1989).
- subconjunctival injections The resulting desiccation produces localized
- rectus muscle surgery thinning of the underlying tissue. It is likely that a
- glaucoma procedures continued inability of the upper lid to resurface the
mucin layer of the cornea adequately, plays a
97300-24S.PPT

7L397300-24 crucial role in the process leading to dellen

formation. The elevation of the conjunctiva can
lead to bridging of the limbus by the lid margins.
49 Local elevations, e.g. pinguecula, pterygium, etc.
DELLEN can exacerbate such bridging. ‘Bridging’ of an
AETIOLOGY adherent lens may also contribute to the
• Old age development of dellen and corneal ulceration (Levy,
1985, Schnider et al., 1988).
• Episcleritis & scleritis
Dellen formation can be secondary to rigid lens-
• Cocaine administration (medical) induced 3 & 9 o’clock staining left unresolved. The
ways RGP lenses may contribute to dellen include:
• Paralytic lagophthalmos
x An excessively thick edge.
• Suture granuloma x Limited lens movement.
• Post-operative endophthalmitis x Lens adherence
97300-180S.PPT A pinguecula or a pterygium adjacent to the limbus
may cause dellen even without contact lenses
7L397300-180
being worn.
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50 Corneal Dellen: Management

DELLEN As dellen do not occur in isolation, it is important
MANAGEMENT that the underlying cause be determined. Any 3 & 9
o'clock staining should be minimized, and the RGP
• Determine cause lens fitting characteristics optimized as described
• Minimize 3 & 9 staining if present previously in this lecture.
Temporary discontinuation of lens wear allows the
• Ocular lubrication cornea to recover to normal thickness by re-
• Temporary discontinuation of lens wear epithelialization. Ocular lubricants and/or patching
have also been suggested as possible treatments
- monitor recovery (Insler et al., 1989 citing Duke-Elder, 1965, Baum et
al., 1968, and Gutner, 1989).
97300-25S.PPT

Baum et al. (1968, cited in Robin et al., 1986)

7L397300-25
suggest that rapid rehydration may lead to a
complete resolution and that delayed rehydration
may result in permanent local thinning.
The risk of serious corneal sequelae is low but can
include:
x Vascularization.
x Cicatrization.
x Stromal inflammation.
x Stromal degeneration leading to corneal
thinning (Insler, 1990).
x Chronic marginal keratopathy.
x Secondary infection.
If a case proves resistant to all treatments tried,
Josephson (1986) suggest that SCLs be considered
instead.
II.E Corneal Ulceration
51 Corneal Ulceration: Introduction
CORNEAL ULCERATION: Ulceration of the cornea is rare with RGP lens use.
INTRODUCTION Nanheim (1962) reported ulceration in a
serviceman following 3-4 weeks of unauthorized
• Ulceration in RGP lens wear is uncommon continuous wear of PMMA lenses.
Failure to heed the early warning signs would
• Failure to heed early warning signs
appear to increase the possibility of a serious
increases the risk of a serious adverse adverse event such as an ulcer occurring (Terry et
al., 1989).
event, e.g. a corneal ulcer

97300-139S.PPT

7L397300-139
52 Corneal Ulceration: Signs
Corneal ulceration may involve either the central
CORNEAL ULCERATION
SIGNS (less commonly) or peripheral cornea (slides 53 and
54).
• Associated with 3 & 9 staining
Ulceration may be associated with dense 3 & 9
• Focal infiltrate o'clock staining.
• Diffuse surrounding infiltrate The infiltrate typically appears as a dense focal
• Anterior stromal location zone surrounded by diffuse cellular accumulation.
The epithelial defect overlies this infiltrate.
• Redness
The eye is often very red and a watery or
• Tearing mucopurulent discharge can be seen.
97300-10S.PPT Other signs may include:
7L397300-10 x Significant tear layer debris.
x Obvious bulbar conjunctival redness.
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53 x Micropunctate epithelial staining. Terry et al.

(1989) recommended against EW when
persistent staining of grade 2 (on a 0 to 4 rating
scale) is observed.
x Significant stromal infiltration.
x Scarring normally follows a resolution of the
primary lesion.

7L3382-94

54

7L3518-99
55 Corneal Ulceration: Symptoms
Typically, a foreign body sensation is the first
CORNEAL ULCERATION
symptom experienced by the patient. As the
SYMPTOMS
condition develops, the severity of the symptoms
increases. Eventually, the condition becomes quite
• Mild to severe pain
painful and usually involves severe ocular
inflammation accompanied by photophobia.
• Foreign body sensation

• Photophobia

97300-11S.PPT

7L397300-11
56 Corneal Ulceration: Aetiology
CORNEAL ULCERATION Contributing factors to corneal ulceration especially
AETIOLOGY in extended wear (after Terry et al., 1989) include:
• Most likely to occur in extended wear x Selection of unsuitable patients.
• Epithelial breakdown x Lens design.
- chronic staining x Wearing schedule.
- 3 & 9 o'clock staining x 3 & 9 o’clock staining.
- lens adherence
x Patient non-compliance (failure to comply with
- ‘dry’ corneal surface
lens care and after-care requests and/or
• Bacterial toxins instructions).
• Most are culture negative
97300-12S.PPT
When the epithelium is damaged, the risk of an
opportunistic bacterial invasion increases.
7L397300-12
Potentially, this can contribute to the severe nature
of the inflammation, although the ulcers themselves
are usually culture-negative.

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While EW of RGP lenses is more likely to result in

conditions such as chronic 3 & 9 o'clock staining or
trapped foreign bodies, either of which can cause
epithelial damage, ulceration is a very rare
sequelae of RGP lens wear, even in EW.
57 Management of Corneal Ulceration
Any 3 & 9 o'clock staining must be eliminated to
CORNEAL ULCERATION
MANAGEMENT avoid the potential for corneal ulceration
subsequently, particularly in EW.
• Eliminate 3 & 9 o’clock staining if it is
An ulcer must be treated appropriately. In most
the precursor cases where a bacterial aetiology is suspected, the
• Cautious approach to extended wear use of topical antibiotics is sufficient to resolve the
condition. If an ulcer is established, the use of
• Topical antibiotics antibiotics is essential if corneal damage is to be
• Generally, will resolve with scarring
minimized.

97300-13S.PPT

7L397300-13

II.F Corneal Staining

58 Corneal Staining: Introduction
The health and vitality of the anterior segment
CORNEAL STAINING
depends, at least partially, on the integrity of the
• Assess with sodium fluorescein corneal epithelium. All types of contact lenses can
• Indicates cell damage, weakened affect the corneal epithelium and the extent of these
attachment, or cell loss effects can be observed clinically by the application
of a suitable vital stain, commonly sodium
• A common finding in contact lens wear fluorescein (slide 59).
• Other vital dyes include Rose Bengal and Other vital staining agents used in contact lens
Lissamine Green practice include Rose Bengal and Lissamine Green
both of which preferentially stain mucus and
- these stain dead cells and mucus
97200-19S.PPT
necrotic cells (slides 60 and 61). However,
Feenstra and Tseng (1992) have shown that,
7L397200-19
strictly speaking, Rose Bengal is not a vital stain as
it has demonstrated the ability to decrease the
59 vitality of cells stained by it.

Sequential sodium fluorescein instillation can cause

corneal staining (Korb and Herman, 1979).
Staining has also been referred to under various
names by different authors, e.g. superficial punctate
staining, Superficial Punctate Keratitis (SPK), or
Superficial Punctate Keratopathy (SPK).
Some degree of corneal staining even in non-
contact lens wearers should be considered ‘normal’
because it is common (see Schwallie et al., 1997,
Dundas et al., 2000).
It is likely that staining with RGP lenses is greater
7L31572-93 than with SCLs because of the incidence of 3 & 9
o’clock staining with RGP lenses (Fonn et al.,
1995). However, Hamano et al. (1994) reported the
opposite.

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60

7L30615-98

61

7L31175-96
62 Corneal Staining: Signs
Classifying and grading corneal staining is one of
CORNEAL STAINING the most common clinical activities a contact lens
• Classify by: practitioner undertakes. Traditionally, sodium
fluorescein stain is used. Because of the known
- type
difficulties of maintaining solution sterility, most
- depth practitioners choose to use dry, impregnated
fluorescein strips packaged individually.
- location
To be effective, sodium fluorescein stain needs to
- severity / extent be irradiated by light consisting mainly of the
shorter wavelengths of the visible spectrum and the
- possible aetiology
immediate near UV. This ‘blue’ light acts as a
97200-20S.PPT

fluorescein ‘exciter’.
7L397200-20
To disclose subtle epithelial disturbances the use of
a yellow barrier filter is essential. This barrier filter
63 prevents unfluoresced blue light from entering the
slit-lamp observation system (or any other
CLASSIFYING STAINING
BY TYPE observation system, e.g. a Burton lamp). Without a
barrier filter, this blue light acts as a veiling glare
• Micropunctate
source and renders any observation less sensitive
• Macropunctate by lowering the viewing contrast.
• Coalescent Fluorescence brightness requires some comment.
• Patch Should the quantity of sodium fluorescein be
• Linear inadequate, the brightness of any fluorescence will
• Arcuate be low. However, somewhat paradoxically, if the
Each can be graded (0-4) concentration of sodium fluorescein is too high, the
fluorescence may also be low because of self
absorption, i.e. the amount of fluorescein in the
97200-23S.PPT

7L397200-23 intervening fluorescein-stained tears actually

absorbs the incident ‘exciting’ light as well as
absorbing, and masking, any emitted fluoresced
light.
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64 The various aspects and methods of classifying and

grading corneal staining are presented in the slides
CLASSIFYING STAINING opposite.
BY DEPTH
One possible system
Another system Any epithelial area (corneal or conjunctival) altered
(from Guillon et al. 1990)
• 0 None
or damaged will imbibe fluorescein stain and
• Superficial epithelial
appear as an area of staining. When irradiated by
• Deep epithelial • 1 Superficial
blue light, e.g. the cobalt blue filter in the
• Stromal diffusion • 2 Full epithelial
illumination system of a slit-lamp or the ‘blue’ light
- immediate • 3 Stromal from the fluorescent tubes of a Burton lamp, the
- delayed fluorescein absorbs the blue light and re-emits it
Can be graded (0 - 4)
(the process of fluorescence) in the yellow region of
the visible spectrum. In this way the damaged area
97200-24S.PPT
is ‘disclosed’ by a yellow appearance.
7L397200-24 Staining from a mechanical cause can take many
forms. The most common form is lens-related, e.g.
65 lens defects including edge defects, insertion or
removal abrasions, or from foreign bodies trapped
CLASSIFYING STAINING Right Eye

BY LOCATION S
under a lens.
• By quadrant (S, I, N, T) T N

• By area (e.g. central, paracentral, etc.)

Central
Paracentral
Mid-peripheral Limbal
Peripheral Paralimbal conjunctiva
Paralimbal cornea

• By clock position (e.g. @ 3 o’clock)

97200-242S.PPT

7L397200-242

66
CLASSIFYING STAINING
BY SEVERITY
Simple From Lloyd, 1992
• 0 Absent • 0 No stain
• 1 Superficial • 1 Punctate/stippling
• 2 Mild • 2 Light confluent
• 3 Moderate • 3 Dense confluent
• 4 Severe • 4 Erosion/abrasion/ulcer

97200-26S.PPT

7L397200-26

67 Foreign body-induced epithelial damage as shown

in slides 67 (a FB tracking lens movement) and 68
(a trapped FB) is normally characterized by being
coarse and track-like in either a random or orbital
pattern and is usually unilateral. Profuse tearing
and bulbar hyperaemia result.
Corneal abrasions usually result in dense linear or
patch staining that can often be seen even in white
light.
RGP lens adherence produces both true epithelial
staining and tear pooling in the depression giving
the appearance of a circular ‘pseudostain’. The
7L30666-99 true staining may be in the form of a central patch
(inside the indentation ring, slide 70) and peripheral
arcuate staining (outside the indentation ring, slide
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68 71).
Corneal staining resulting from excessive lens
movement is usually limited to the peripheral area
traversed by the lens edge over time and is arcuate
(incomplete circle, slide 70) or doughnut-like (full
circle, slide 71) in appearance. The stained area is
normally outside the ‘average’ centred location of
the lens, i.e. the cornea normally located under the
centred lens is neither exposed nor traumatized by
the lens edge and hence sustains no damage.
Insertion or removal abrasions have a characteristic
linear appearance usually oriented along the
habitual direction of insertion or removal (slide 69).
More serious epithelial damage is usually termed
7L30668-99 an abrasion (slide 74) or an erosion (slide 72) and
69 the common signs are listed in slide 73.
In some cases of RGP lens binding, a combination
of fluorescein pooling and staining can be observed
after the lens has been removed (slide 75). The
pooling is usually in the epithelial indentation that
some binding causes. The staining may be the
result of excessive bearing, imprinting of trapped
post-lens tear film debris, or the result of attempts
to ‘loosen’ or dislodge the adherent lens.

7L30084-93
70

7L31835-92
71

7L3583-97
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72

7L30111-99

73
CORNEAL STAINING: EROSION
SIGNS
• Localized epithelial damage
- often visible in white light
- often full thickness
- sodium fluorescein
• Stromal penetration of fluorescein
if epithelial barrier breached - halo
• Bulbar redness
97300-34S.PPT

7L397300-34

74

7L31934-92

75

7L31883-92

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76 Corneal Staining: Symptoms

Unless the magnitude of epithelial damage is
CORNEAL STAINING: SYMPTOMS significant, corneal staining is often asymptomatic.
x Pain, esp. if FB or lens defect Vision will only be affected if the disturbance is
x Discomfort/foreign body sensation significant (Grade 3 or more) and central. Where
x Photophobia
significant damage has been sustained, symptoms
may include:
x Tearing
x Pain, especially if a FB or significant lens defect
x Lens intolerance, toxic/allergic is the cause. The pain can be intense, is of
x Decreased wear time, lens deposits and/or sudden onset, and lasts a relatively short time
poor surface condition
after the stimulus is removed. The FB is
97200-246S.PPT
usually flushed by reflex tears.
7L397200-246
x Discomfort. Potentially, this can be attributable
to almost all causes.
x Photophobia. Invariably, photophobia
accompanies discomfort/pain, tissue damage,
and tearing.
77 Corneal Staining: Aetiology
STAINING The main general categories of causes are
AETIOLOGY presented opposite. Many of these are covered in
• Mechanical: more detail under their own relevant headings, e.g.
- foreign body (FB) infection, and dry eye (see Lecture 7.4).
- lens removal
Corneal fluorescence following the instillation of
- lens edge / excessive lens movement
• Dehydration / incomplete blinking sodium fluorescein could be due to any of the
• Chemical toxicity / reaction to lens care causes presented in the slide opposite (after Efron,
• Infection / ulceration 1999).
• Adverse physiological conditions Wilson et al. (1995) showed that fluorescein
• Tear deficiency / tear film defect
• Idiopathic
staining was due to staining of individual cells and
97200-243S.PPT
not pooling in areas of cell drop-outs or filling of
intercellular spaces.
7L397200-243
If inferior staining due to superior lens decentration
is seen, exposure/dehydration should be suspected
78 (3 & 9 o’clock staining is dealt with separately in
AETIOLOGY OF STAINING
Section II.C 3 & 9 O’Clock Staining in this lecture).
Hamano et al. (1985) found that the main cause of
• Environmental influences damage in PMMA wearers was prolonged wear,
- wind whereas in RGP lens and SCL wearers the damage
inflicted was often the result of the condition of the
- UV light (esp. UV B) lens itself, especially scratches, material defects,
• Patient non-compliance with:
distortion and contamination.
Foreign body staining may be due to fine dust
- wear schedules particles, textile fibres, shed skin, or even dried eye
- solutions secretions that may masquerade as a transient FB
97200-22S.PPT
before they dissolve into the tears. Larger FBs, e.g.
grains of sand, can cause significant damage and
7L397200-22
give rise to severe symptoms. The incomplete
corneal coverage, the mobility of RGP lenses, the
edge tear reservoir and the edge clearance all aid
the ingression of FBs into the post-lens tear film.
Abrasions/erosions may be due to a myriad of
causes with the wearer’s fingernails among the
most common. Lens defects and lens deposits are
also known causes of corneal abrasions.

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79
CORNEAL STAINING: FOREIGN BODY
AETIOLOGY
• Material trapped behind lens:
- grit, sand, air pollution, etc.
- eyelash
- dried lid secretions/flakes of skin
• Lens mobility
• Greater edge clearance
- lens edge tear reservoir
97300-32S.PPT

7L397300-32
80
CORNEAL STAINING: ABRASION
AETIOLOGY
• Edge defect

• Back surface deposit - focal clump

• Trauma - fingernails, fingers, arm,

clothing, travelling FB, projectile, etc.

97300-36S.PPT

7L397300-36
81 Corneal Staining: Management
Generally, re-epithelialization is rapid provided the
CORNEAL STAINING: MANAGEMENT source of disturbance and/or contact lens is
• Remove cause promptly removed. The duration of discontinuation depends
on the severity and epithelial recovery rate. In
• Recovery:
some cases of mild SPK, the only management that
- rapid if superficial - hours is required is monitoring, i.e. there is no need to
discontinue lens wear.
- slower if more severe - few days
The healing process is almost certainly slowed or
• Change lens care system if toxic/allergy prevented in most instances if lens wear is
• If FB - prevention/eye protection
continued (see Hamano and Hori, 1983).
97200-245S.PPT
If foreign bodies are a recurring problem then some
form of eyewear, e.g. safety goggles, or sunglasses
7L397200-245
may be required.
As excessive edge lift is associated with greater
82 staining (by FBs) (Sorbara et al., 1996B),
CORNEAL STAINING: FOREIGN BODY decreasing the edge clearance may be required to
MANAGEMENT prevent such problems.
• Patient education If insertion or removal abrasions are observed,
some wearer re-education may be appropriate.
- expect foreign bodies occasionally
Ways of resolving problems produced by lens
• Lens removal
defects range from a simple repolish to lens
- rinse thoroughly and check replacement.
• Lens design If exposure due to lens decentration is detected
- minimize edge clearance then a larger lens and/or a lens fit alteration should
• n lens Dk/t be tried to both better cover the affected area and
97300-33S.PPT to encourage better lens centration.
7L397300-33 If staining is the result of epithelial fragility (easy to
suspect, difficult to confirm) it is possible that
refitting with a higher Dk/t lens (thinner lens and/or
higher Dk material) may assist the epithelium.
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83 Staining that is toxic/allergic/hypersensitive in origin

necessitates removal of the stimulus. If the source
CORNEAL STAINING: FOREIGN BODY
MANAGEMENT is a lens care product then a product with a different
• Flush debris from eye: formulation is required (see Module 5).
- sterile saline As it is difficult to prove exactly which of the solution
- artificial tears components (if any) is the offending one, a process
- in-eye comfort drops of trial and error is required to arrive at a suitable
- check under lids as well replacement.
• Discontinue lens wear temporarily Wearer compliance issues (dealt with later in
- minutes to a few hours Section VI.E Wearer Non-Compliance in this
- prophylactic antibiotics may be required lecture) are also worthy of investigation, e.g.:
97300-127S.PPT
x Is a cleaner being used?
7L397300-127
x Is the cleaner rinsed from the lens thoroughly
before proceeding to the next stage of the lens
care cycle?
x Is lens care being undertaken at all?
As some lens materials have different binding
and/or depositing properties it is possible that, in
rare cases, a change of lens material may reduce
or eliminate toxic or hypersensitivity reactions (after
Efron, 1999).
The major risk associated with corneal abrasions is
that of secondary infection particularly with
Pseudomonas aeruginosa (Ridder, 1992).
Clemons et al. (1987) recommended against
patching any patient with corneal abrasions and a
history of contact lens usage. Patching has been
found to have no significant effect on re-
epithelialization nor does it reduce the incidence or
severity of inflammation, nor relieve pain compared
with treatment without patching (Arbour et al.,
1997).
Prophylactic antibiotics can be used to guard
against abrasions/erosions becoming infected. If
pain is a problem, a soft lens as a bandage may be
appropriate, albeit at the risk of slowing healing.
Bandaging an abraded eye is generally inadvisable
as this step may enhance the risk of secondary
infection.
II.G Conjunctival Staining
84 Conjunctival Staining: Introduction
CONJUNCTIVAL STAINING: Conjunctival staining will often be seen in tandem
INTRODUCTION with corneal staining because the cause is usually
not limited to the cornea, and therefore may affect
• Often mirrors corneal staining
the whole of the anterior segment.
• Inferior conjunctival staining commonly Although they also reported occasional staining of
cells in the normal conjunctiva in the interpalpebral
seen in rigid lenses wearers area, Eliason and Maurice (1990) observed that
rigid lenses continually traumatized the inferior
• Staining allows monitoring of damage,
limbal conjunctiva in symptomless wearers. For
the healing process, and dry eye effects reasons of superior contrast (cf. sodium fluorescein)
these workers used sulphorhodamine B as their
97300-143S.PPT

preferred vital stain. They also found this stain to

7L397300-143 be a sensitive indicator of the effects of dry eye and
epithelial healing.

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85 Conjunctival Staining: Signs

Arcuate conjunctival staining is observed commonly
in RGP lens wearers. The majority of wearers
show a band of staining in the inferior limbal region
(5-7 o’clock) (slide 85). Additionally, the staining
may vary between an arcuate stain (slide 86)
defining only the extreme of all displaced lens
positions experienced by the wearer, and a
completely stained area encompassing a larger
area as shown in slide 87.

7L31770-92

86

7L30693-94

87

7L30680-94
88 Conjunctival Staining: Symptoms
Most cases of conjunctival staining cause few, if
CONJUNCTIVAL STAINING
any, symptoms. This is due partially to the
SYMPTOMS
conjunctival tissue being less sensitive.
Should moderate to severe staining be present, the
• Usually asymptomatic contact lens wearer may notice some non-specific
eye irritation. If conjunctival staining accompanies
corneal staining, symptoms are more likely to be
• Mild lens awareness induced by the corneal, rather than the conjunctival,
damage.

97300-27S.PPT

7L397300-27

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89 Conjunctival Staining: Aetiology

CONJUNCTIVAL STAINING Staining of the conjunctiva associated with RGP
AETIOLOGY contact lens wear is principally due to:
• Excessive limbal overlap x The mechanical effects of the lens edge.
- large overall diameter x A tendency for the lens to move beyond the
- tight edge
limbus (due to lid forces during a blink).
- lens movement
• Edge defect
A sharp edge is more likely to cause staining than
- micro-chip
one that is well rounded even when the apex is
- sharp edge biased towards the posterior surface (for more
• Poor blinking details on lens edge issues see Lecture 2.5,
• Underlying dry eye condition Section IV Back Surface Design and Edge
97300-28S.PPT Design).
7L397300-28 A poor lens fit – (too loose) will contribute to inferior
staining.
Other types of staining can be caused by:
x Incomplete blinking.
x Dry eye.
x Toxic/allergic reactions to environmental
factors, ocular pharmaceuticals, or lens care
products.
Conjunctival staining may also be due to
Vascularized Limbal Keratitis (VLK), an uncommon
condition affecting the nasal or temporal limbal and
paralimbal areas in some RGP lens wearers. VLK
is detailed separately in Section II.H Vascularized
Limbal Keratitis (VLK) in this lecture.
90 Conjunctival Staining: Management
CONJUNCTIVAL STAINING The conjunctiva, although filmy and flexible, is a
MANAGEMENT strong and resilient tissue that can usually
• Optimize lens fitting withstand the microtraumas of normal rigid contact
- centration
lens wear. Many contact lenses cause some
degree of staining. Excessive staining or staining
- diameter
associated with symptoms, e.g. discomfort, is
- movement
overcome generally by changing the design of the
• Lubrication during lens wear lens, especially the edge profile. A smaller lens
- artificial tears diameter and better centration will help minimize
• Punctal occlusion the level of conjunctival staining by limiting the
• Improved blinking excursions of the lens onto the areas beyond the
97300-29S.PPT
limbus. Steps that limit and/or minimize lens
7L397300-29 excursions include tightening the lens fit, and
decreasing the lens diameter.
II.H Vascularized Limbal Keratitis (VLK)
91 Vascularized Limbal Keratitis (VLK):
Introduction
VASCULARIZED LIMBAL KERATITIS
INTRODUCTION VLK is a rare condition involving the cornea, limbus
• Rare and conjunctiva and resulting primarily from DW,
and sometimes EW of RGP lenses (Grohe and
• Superficial vascularized lesion bridging Lebow, 1989). It is a superficial vascularized
conjunctiva, limbus & cornea corneal lesion adjacent to the limbus that is often a
• A sequel to chronic 3 & 9 o’clock staining sequel to chronic 3 & 9 o’clock staining. It is
• Usually in RGP EW - low edge lift
thought to be a result of poor tear wetting of the
cornea and of punctate corneal staining (after Bruce
• Due to inadequate tear wetting & punctate and Brennan, 2000). The condition was first
epithelial staining ? described by Lebow (1987) and was originally
97300-144S.PPT
termed limbal epithelial hypertrophy.
7L397300-144 VLK may develop after a long period of successful
RGP lens wear. Reports suggest that females are
more likely to be affected. RGP EW, especially in
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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

lenses with low edge lift, would appear to enhance

the risk of VLK.
92 Vascularized Limbal Keratitis (VLK): Signs
Some characteristics of VLK associated with RGP
VASCULARIZED LIMBAL KERATITIS
lens wear are presented in slide 92 (after Grohe
SIGNS
and Lebow, 1987). The elevated nodule is located
• Vascularized limbal mass some 0.25 – 0.5 mm from the limbus usually at 3 &
- opaque
9 o’clock or 4 & 8 o’clock (Anonymous, 1998).
The lesion’s properties include (after Grohe and
- elevated Lebow, 1989):
- ill-defined borders x Vascularized superficially (slide 94) and deeply
(slide 95).
- nasal and/or temporal
x Appears to form a bridge from the conjunctiva
97300-38S.PPT to the cornea but involves the tissue beneath as
7L397300-38
well.
x Exhibits extensive staining of the cornea and
93 less extensive concurrent staining of the
conjunctiva.
VASCULARIZED LIMBAL KERATITIS x Associated with limbal oedema.
SIGNS
x Has ill-defined, diffuse borders.
• Bulbar redness
x Appears semi-opaque.
- tuft of vessels x Has moderate to severe accompanying
• Conjunctival staining conjunctival injection.
• Limbal vessel engorgement
• Can develop after a period of
apparently successful wear
97300-39S.PPT

7L397300-39

94

7L30165-95

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95

7L3108-99
96 Vascularized Limbal Keratitis: Symptoms
Symptoms of VLK are listed in the slide opposite
VASCULARIZED LIMBAL KERATITIS
SYMPTOMS (after Grohe and Lebow, 1989):
• Minimal in early stages A raised corneal mass, and/or disturbed vision may
• Gradual increase in discomfort be noted, and reported by some wearers. The
– lens awareness
latter may be caused by:
— later, moderate discomfort, or pain x Optical effects of the lesion itself.
- decreased wearing time x Disorganization of the surrounding tissue.
• Redness x Tear film perturbations.
• Photophobia Lens awareness and ocular irritation increase as
• Lacrimation the condition develops. In the more advanced
97300-40S.PPT
stages, the patient may complain of a watery
7L397300-40 discharge, and slight photophobia. These
symptoms usually encourage the wearer to seek
professional help.
97 Vascularized Limbal Keratitis: Aetiology
The principal cause of VLK is mechanical insult to
VASCULARIZED LIMBAL KERATITIS
AETIOLOGY
the limbal region by the edge of RGP lenses.
Chronic lens irritation due to lens movement is most
• Large diameter lenses likely to occur during extended wear.
Repeated lens adherence in extended wear may
• Mechanical abrasion
also play a role in the development of VLK. Grohe
- chronic irritation and Lebow (1989) divided the development of VLK
into four stages. These are reviewed briefly below.
• Extended wear The original reference presents the details.
Stage 1.
• Lens adherence
97300-41S.PPT x Mild and Asymptomatic.
7L397300-41 x No conjunctival hyperaemia is apparent.

Stage 2.
x A response that is presumed to be inflammatory
with hyperaemia, peripheral staining, and
infiltrates.
x Mild ocular irritation reported along with
increased lens awareness.
x At this relatively early stage, VLK responds
rapidly to suitable treatment given.

Stage 3.
x Moderate conjunctival hyperaemia.
x More infiltrates.
x More severe staining.

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

x A vascular tuft emanating from the conjunctiva

and reaching across the limbus leads to, and
terminates in, an epithelial mass.
x Wearing time decreases.
Stage 4.
x An alarming increase in symptoms including
photophobia, significant discomfort, and
possibly pain whenever the lens encroaches
onto the raised lesion.
x Mass visible to the wearer and is likely to be
reported.
x Corneal hypoaesthesia may be detectable.
Grohe and Lebow believed that VLK was a lens
design issue rather than a lens material problem
while Anonymous (1998) reported that VLK may be
secondary to localized tear film disruption due to:
x Excessive drying and exposure.
x Excessive peripheral lens binding.
The same report also suggests that VLK produces
epithelial thinning above an intact Bowman’s layer
with significant subepithelial fibrotic tissue.
Miller (1995) reported an unusual case in which
VLK was apparently secondary to the
cracking/crazing of a siloxane acrylate RGP lens
(this is covered separately in Section V Vision
complications in this lecture).
98 Vascularized Limbal Keratitis: Management
VASCULARIZED LIMBAL KERATITIS
Sudden onset and rapid progression of the
MANAGEMENT condition necessitates prompt action by both
wearer and practitioner alike. Once again the ‘if in
• Regular after-care doubt take them out’ philosophy applies.
Grohe and Lebow presented a comprehensive
• Reversible condition differential diagnosis table for VLK (slide 100). The
table covers VLK, corneal vascularization, dellen,
• Reduce wearing time phlyctenulosis, and pseudopterygium, conditions
with some overlapping symptoms.
• Temporary discontinuation of lenses
It is believed that treatment at Stage 1 leads to a
97300-42S.PPT
rapid recovery. However, should VLK reaches
Stages 2 or 3 the recovery is somewhat slower. If
7L397300-42
Stage 4 is reached unchecked, the management
becomes complicated and protracted. One reason
99 is the substantial elevated and vascularized mass
that is established by then.
VASCULARIZED LIMBAL KERATITIS Grohe and Lebow suggested that changing to a
MANAGEMENT more conservative wearing schedule, and altering
• Lubricants, decongestants the lens design to result in only a moderate edge
lift, are cornerstones of VLK management
• Redesign lens: regardless of the stage VLK has reached. Their
- smaller diameter
suggested plan (presented only briefly here) is as
follows:
- optimize edge lift Stage 1:
• Reduce wearing time x Decrease wearing time.
x Peripheral lens design changed to produce
moderate edge lift.
97300-128S.PPT

7L397300-128 x Lubricating/comfort/in-eye re-wetting drops

applied on awakening, whenever required
during lens wear, and before sleep.

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100
Stage 2:
DIFFERENTIAL DIAGNOSIS: VLK x Discontinue lens wear for 5 days.
from: Grohe & Lebow, 1989
x Once wear is resumed, establish DW
Symptom VLK Vascularization Dellen Phlyctenulosis Pseudopterygium
successfully without reappearance of VLK.
Discomfort Mild None Mild Moderate Mild

Lacrimation Yes No No Yes No x Stage 3:

Lens
x Biopsy of elevated mass may be prudent to
Moderate None Mild Moderate Moderate
Awareness
differentiate between infectious and/or
Photophobia Yes No No Yes No inflammatory aetiologies.
x Consider topical corticosteroids.
97300-186S.PPT

7L397300-186 Stage 4:
x Discontinue lens wear for three weeks.
x Culture the anterior eye to eliminate the
possibility that the erosion is infectious in origin.
x Begin antibiotic/steroid combination therapy.

Grohe and Lebow noted a tendency for VLK to

recur, especially if only a temporary lens wear
discontinuation (3-5 days) occurred and the same
lenses were reused. They also suggest that this
approach might be considered a provocative test for
VLK, i.e. as confirmation that the case is one of
VLK.
Surgical removal of the nodule by superficial
keratectomy was also given as a possibility in
advanced cases.

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

III Oedema and Hypoxia-Related Complications

III.A Corneal Oedema
101 Corneal Oedema: Introduction
CORNEAL OEDEMA: INTRODUCTION Hypoxia-induced corneal oedema would seem to be
• Central to many adverse effects
central to many adverse effects in contact lens
• All lenses impede corneal access to
wear.
atmospheric O2 Tear exchange rates (per blink) for SCLs range
• Tear exchange <2% with SCLs & 10-20% with from 1-3% (Polse, 1979, Polse, 1981, and
RGPs
McNamara et al., 1999). RGP lenses on the other
• Tear exchange can n O2 by 1 -3% (Benjamin,
1994) hand exchange at a much greater rate, i.e. 10-29%
• In high Dk RGP lenses, tear exchange (Polse, 1979, Kok et al., 1992, and Yoshino et al.,
provides insignificant O2 1996). However, Fatt (1992) states that, based on
• Closed eye exacerbates any problems the data of Fatt and Liu (1984), when high Dk/t
97300-145S.PPT
lenses are utilized, transmission through a lens is
7L397300-145 more significant than the tear pump mechanism
because the latter can theoretically only increase
the oxygen delivered to the cornea by some 15-
102 20%.
TOPOGRAPHICAL CORNEAL Using practical data provided by manufacturers, the
SWELLING: PMMA & EYE CLOSURE (3h) following data on oxygen transmissibilities can be
12
Apex after Wang et al., 2003
generated:
Corneal Swelling (%)

10
After PMMA, at Removal
lotrafilcon A: Dk/t : 175 (Dk = 140, tc = 0.08)(SilHy)
8 balafilcon A: Dk/t : 110 (Dk = 99, tc = 0.09)(SilHy)
6 tisilfocon A: Dk/t : 109 (Dk = 163, tc = 0.15)(RGP)
4
2
After PMMA, 20 minutes
After Removal
A reduced contribution to oxygenation by tear
0
exchange will result if an RGP lens conforms to the
-5 -4 -3 -2 -1 0 1 2 3 4 5 shape of the cornea. This conformance reduces
Chord Distance (mm) the volume of the post-lens tear film and the lens-
97300-188S.PPT edge reservoir, thereby altering the tear pump
mechanism’s efficacy. If RGP lenses are too thin,
7L397300-188
(<0.1 mm) they are generally not practicable either
during manufacture or clinically.
An advantage of unknown significance to the
general wellbeing of the cornea is the incomplete
corneal coverage inherent in an RGP lens fitting.
However, RGP lens diameters in the range 10.5 to
12 mm are not unknown and are used successfully,
especially in high Dk materials. It is probable
however, that more attention needs to be given to
back surface design and its relationship to corneal
shape when large diameters are contemplated.
Corneal oedema should not occur in response to
RGP lens daily wear, as all lenses should satisfy
-9
the Holden-Mertz criterion of 24 X 10 . However,
‘at risk’ patients, e.g. diabetics, or wearers with an
endothelial dystrophy, should be observed more
carefully. If corneal swelling does occur, there will
be less paracentral , and no peripheral corneal
swelling as illustrated in slide 102 (Wang et al.,
2003).
In more recent times it would seem less
pachometry is being performed because it is now
possible to predict the approximate swelling
response of a cornea based on O2 transmissibility
and lens design. For more details on this and
related subjects see Module 6, Lectures 6.1, 6.2,
6.3.
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 Module 7: Contact Lens-Related Ocular Complications

Both lens wearers and non-lens wearers alike

experience closed-eye corneal swelling every night.
The challenge for the contact lens
designer/manufacturer is to aim for this level of
performance, i.e. no more swelling than the closed
eye without a lens.
103 Corneal Oedema: Signs
CORNEAL OEDEMA Daily wear, RGP lens-induced corneal oedema is
SIGNS most likely to be localized in, and restricted to, the
• Very subtle with RGP materials central to mid-peripheral corneal stroma. The low
- negligible in DW level of oedema likely with modern higher Dk/t
• EW lenses is very difficult to detect with a slit-lamp. An
extreme version of this central corneal oedema (so-
- greater overnight corneal swelling
called central corneal clouding, a visible central
- striae may be visible translucent corneal area) was seen in PMMA
- folds/black lines unlikely lenses (see Module 1: Lecture 1.4: slide 70).
- rapid recovery following eye opening Central corneal clouding should now be of historical
97300-43S.PPT
interest only.
7L397300-43 To observe subtle corneal oedema, an instrument
such as a pachometer (optical or, possibly,
ultrasonic) is required. Even pachometry is difficult
when the oedema level approaches that of
instrument error. Alternatives that have been used
to measure corneal thickness include:
x Contacting specular microscopes.
x Confocal microscopes that applanate the
cornea thereby allowing a measurement based
on apparent thickness.
x Interferometry and scanning partial coherence
interferometry (for more details see Module 9,
Lecture 9.1, Section V Pachometers).
Currently, the use of these newer techniques
appears to be confined to the research laboratory.
The oedema caused by contact lens wear can
affect both the structure and function of the cornea.
All layers can be involved and some signs are
visible with the slit-lamp. Such signs may include:
x Stromal striae (usually vertical, see slide 16,
Lecture 7.2 of this module).
x Descemet’s membrane folds (black lines, see
slides 22 and 23, Lecture 7.2 of this module).
x Hazy tissue.
All these signs, as induced by SCLs, are detailed in
detail in Lecture 7.2. The descriptions and
illustrations apply equally well to the RGP lens-
induced varieties.

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104 Corneal Oedema: Symptoms

CORNEAL OEDEMA The majority of cases are asymptomatic, especially
SYMPTOMS if only relatively minor signs such as a few striations
• Most likely to be asymptomatic are all that are present. Should symptoms be
associated with corneal oedema, they are usually
• Mild if present very mild and are more likely to be visual rather
than ‘comfort’ or physiological issues.
• More likely to be ‘visual’ than ‘comfort’ or Significant levels of oedema can result in reduced
vision and the patient may complain of blur with
physiology (e.g. haloes, blur, spectacle blur) their spectacles for some time after contact lens
removal. The latter is called spectacle blur, i.e. a
97300-44S.PPT
decrease in vision that has little or no refractive
7L397300-44 component (decreased visual acuity that does not
respond to a change in spectacle Rx).
If contact lens-induced corneal oedema is
significant the appearance of haloes, coloured
haloes around lights, or a general haziness
(reduction in contrast) of vision may be reported.
While most oedema-induced symptoms disappear
rapidly after lens removal, so-called spectacle blur
may take hours or even overnight to dissipate.
105 Corneal Oedema: Aetiology
CORNEAL OEDEMA The biggest single contributing factor to corneal
AETIOLOGY oedema is corneal hypoxia, i.e. a reduction in the
• Hypoxia (inadequate O2 transmissibility) cornea’s oxygen supply from the atmosphere
• In closed eye (EW) (Sweeney and Holden, 1991). This can occur as a
- little or no tear exchange result of eyelid closure, RGP contact lens wear
• Temperature increase under lens (Dk/t ) (Schnider et al., 1986), or a combination of
• Lowered tear osmolality during adaptation both, as occurs overnight when the lenses are worn
• Corneal pCO2 in open-eye wear (possibly) on an EW basis.
• Relative humidity (possibly) There are other causes of corneal oedema related
• Mechanical effect to contact lens wear, e.g. inflammation, allergy, and
97300-45S.PPT toxicity. Therefore, in a particular case it can be
7L397300-45
difficult for the contact lens practitioner to establish
with certainty the primary aetiology of corneal
106 oedema.
CLOSED-EYE CORNEAL OEDEMA: Other physiological issues such as a retarded efflux
CONTRIBUTION OF ELEMENTS of carbon dioxide from the cornea have been
(after Sweeney & Holden, 1991)
considered. Ang and Efron (1989) showed that
• Sleep: 3.1% RGP lenses had a CO2 permeability some 7X that
of O2 (SCLs have a 21X factor), figures that have
• Hypoxia: 1.6% been confirmed subsequently by Fatt and Fink
• Osmolality: 0.4% (1989), and Mitzutani (1990). However, research
• Temperature: 0.5% by Sweeney (1991) showed that CO2 was not a
• Relative Humidity: 0.4% significant factor in the oedema response of the
• Carbon dioxide: 0.2% (?) cornea. As eye closure probably results in
• Total: 3.1%
97300-146S.PPT
increases in corneal pCO2 each night with or
without contact lenses, any contribution must be
7L397300-146 minimal (e.g. 0.2% see (?) in slide opposite that
refers to closed eye, no lens) or negligible.
In addition to hypoxia and CO2 accumulation, other
potential contributing factors to lens-induced
corneal swelling include:
x A temperature increase due to the insulating
effects of the lens on the cornea and the
reduced evaporative cooling brought about by
the evaporation occurring at the front surface
of the lens rather than at the cornea.

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107 x Mechanical effects of the physical presence of

the lens.
CORNEAL OEDEMA x Hypotonicity due to stimulated tear production
CAUSES: Other at least in the early phases of RGP lens wear
(Harris and Mandell, 1969, Lowther et al.,
• Inflammation 1970, Hill, 1975, Terry and Hill, 1977).
Using rabbit corneas and a PMMA lens, Huff (1990)
• Allergy/hypersensitivity found lens-induced corneal swelling was:
x Metabolic in nature.
• Toxicity x Mainly involved the stroma.
x Required fluid absorption across the endothelial
97300-147S.PPT layer.
7L397300-147
x Not a direct result of epithelial or endothelial ion
transport inhibition.
108 Corneal Oedema: Management
CORNEAL OEDEMA The principal management strategy for dealing with
MANAGEMENT contact lens-induced corneal oedema is to
• Maximize Dk/t esp. for EW maximize the oxygen available to the eye. This can
- n material Dk be achieved by optimizing the level of oxygen
- thin lens judiciously (consider astigmatism) transmissibility provided by the lens (see slide
- alter lens fit (tend flatter) opposite), and then the fitting characteristics such
- n edge lift (consider comfort & risk of VLK) as movement.
- p lens diameter (TD) In cases where the lens fitting and oxygen supply
• p wearing time (if DW) are optimized for extended wear (even if not worn in
• Alter wearing mode (EW oDW) this mode) but corneal oedema remains, the only
97300-46S.PPT
option is to reduce the wearing time so that the
7L397300-46 adverse effects are minimized and contact lens
wear can continue. The latter should not be
pursued at all costs but with the designs and
transmissibilities possible now there should be little
difficulty meeting most of the cornea’s needs, at
least for DW. The minimum oxygen requirements
and related issues are covered in more detail in
Lectures 6.1, 6.2 and 6.3.
Chronic corneal oedema allowed to continue for
extended periods of time (many months to years)
can result in permanent alterations to the cornea.
These alterations include:
x Endothelial polymegethism.
x Stromal thinning.
x Vascularization.
x Swelling and thinning behaviour (possibly).
If intervention is early, the recovery is rapid and the
long-term effects negligible.

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III.B Corneal Vascularization

109 Corneal Vascularization: Introduction
CORNEAL VASCULARIZATION One of the more conspicuous signs of inadequate
INTRODUCTION corneal physiology is the growth of new blood
• A conspicuous sign of poor corneal vessels radially from the limbal area towards the
physiology centre of the cornea. The causes may not be
contact lens-related, e.g. corneal surgery, chemical
• Less likely in RGP lens wear
burns, etc. However, if an ocular history fails to
• Not always contact lens related elicit any other reason, it is reasonable to assume
• Must distinguish between filled ‘ghost’ that for contact lens wearers, the cause is probably
limbal vessels (limbal hyperaemia or physiological.
engorgement) & new blood vessels Vascularization of the cornea is generally less likely
(neovascularization) to occur as a result of RGP lens wear because the
97300-148S.PPT

corneal periphery/limbus remains uncovered by a

7L397300-148 centred, well-fitted lens when made in a common
diameter (TD ”9.8 mm).
Clinically, a distinction must be made between a
lens-induced filling of the limbal ‘ghost’ vessels
(hyperaemia or limbal engorgement) and the
ingression of new blood vessels
(neovascularization) between, and ultimately
beyond, these ghost vessels, progressing towards
the corneal centre.
110 Corneal Vascularization: Signs
CORNEAL VASCULARIZATION Vascularization of the cornea must be adequately
SIGNS described and documented. A baseline
assessment is essential for meaningful
• New vessels between and beyond limbal comparisons to be made of the effects of contact
‘ghost’ vessels lens wear. The key aspects of the documentation
are the extent to which the vessels encroach
• Vessels beyond limbal transition zone, i.e. beyond the limbal transition zone (slide 111) into
into the normally avascular cornea the clear cornea and their depth within the cornea,
i.e. epithelial, or sub-epithelial. Each of the corneal
• Pannus is more likely than single vessels quadrants should be assessed and described
independently.
97300-47S.PPT

It is important to distinguish between dilation and

7L397300-47
extension of blood vessels within the limbal zone,
i.e. limbal engorgement (slide 111 which is
111 suggestive of 3 & 9 o’clock staining as the cause)
and the growth of vessels beyond the corneo-limbal
transition into the clear corneal tissue, i.e.
neovascularization (slide 112).
With RGP lenses of low oxygen transmissibility, it is
more likely that a localized vascular pannus will
form rather than a ‘halo’ of circumlimbal discrete
vessels.
A detailed description of the anatomy of
vascularization is presented in Lecture 7.2, Section
II.I Corneal Vascularization.
Efron (1999) suggests that a vessel ingression of
about 0.4 mm from the limit of the visible iris is
7L31348-91 about normal for DW RGP lens wear. Vessel
trespass beyond this distance should be regarded
as abnormal and steps should be taken to improve
the physiological conditions to which the limbal and
paralimbal regions are exposed.

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112

7L31078-93
113 Corneal Vascularization: Symptoms
CORNEAL VASCULARIZATION Vascularization of the cornea occurs in the absence
SYMPTOMS of symptoms. Vascularization is best observed with
• Generally asymptomatic a slit-lamp using direct (slide 111) and retro-
illumination (slide 112).
• Vascularization may accompany non-

lens-related painful anterior segment

diseases. An ocular history will assist

differentiation
97300-48S.PPT

7L397300-48
114 Corneal Vascularization: Aetiology
CORNEAL VASCULARIZATION Lens-induced corneal vascularization is often
AETIOLOGY related to the hypoxia caused by inadequate lens
• Lens fitting
- decentred over limbus
oxygen transmissibility. For RGP lenses, other
- minimal movement factors such as poor lens centration and lens
- adherence adherence play a bigger role than does oxygen
• Oxygen supply transmissibility per se.
- inadequate Dk/t (large lenses only)
Typically, the growth of vessels into the cornea
• Persistent peripheral desiccation (3 & 9
staining of long standing [years]) occurs after some period of time. The length of the
• Peripheral ulcer this latent period is dictated by a number of factors
• Dellen including:
97300-49S.PPT

x Wearing schedule.
7L397300-49
x Lens oxygen transmissibility (unlikely).
x Individual variation.

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115 Corneal Vascularization: Management

CORNEAL VASCULARIZATION The key to successful management of ‘corneal
MANAGEMENT vascularization’ is early detection and appropriate
• Early detection essential intervention. The appearance of vessel spikes or
buds, and the extension of vessels within the limbal
• Increase lens Dk/t region, should be noted and action instigated
• Optimize lens fitting promptly. Such vessel changes should not be
permitted to progress and every endeavour made to
- no limbal overlap (better centration) prevent vascularization beyond the corneo-limbal
- good movement transition zone.
- decrease diameter (?) Suboptimal lens fitting should be addressed, and if
97300-50S.PPT
vascularization is a result of 3 & 9 o’clock staining,
7L397300-50 this should be rectified (see Section II.C 3 & 9
O’Clock Staining in this lecture).
Usually, lens oxygen transmissibility is not an issue
unless large, low Dk/t lenses are used. In this case,
a lens offering better oxygen transmission will
usually solve this problem.
If necessary, a smaller diameter may be required
but generally altering the fit to provide better
centration with adequate movement is all that is
required in addition to addressing the oxygen
transmissibility issue.
If vascularization is due to other, non-lens-related
causes, and lens wear is continued, all the
practitioner can do is monitor the condition of the
eyes on a regular basis.

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IV Mechanical and Pressure-Related Complications

IV.A Lens Adherence
116 Lens Adherence: Introduction
LENS ADHERENCE Adherence of rigid lenses to the cornea has been
INTRODUCTION observed almost from the commencement of
overnight rigid lens wear, the sanctioned use of
• Common consequence of overnight RGP
which commenced in the late 1970s. The first
lens wear published reports of lens adherence appeared in
1985 (Zantos and Zantos) followed by Levy (1985).
• Overall, 48% of RGP lens EW users Given the unsanctioned overnight wear of PMMA
lenses well before this time, it is surprising that lens
• 95% experience occasional adherence
adherence was not reported much earlier.
• Worse with flat-fitting lenses (84%) Although average figures as high as 49% have
been reported, overnight RGP lens wear results in
97300-149S.PPT

34% of wearers experiencing lens adherence

7L397300-149 (Swarbrick, 1991). However, when flat-fitting
lenses are applied, the incidence of lens adherence
rise to 84%.
For all fits and wearers, Swarbrick found a
frequency of 48% with 95% of wearers experiencing
at least occasional adherence.
Adherence can happen rapidly. Lin et al. (1989)
showed that adherence was apparent within two
hours in a significant number of experimental
subjects. Fortunately, the restoration of lens
movement can also be equally rapid, e.g. one hour
(Kenyon et al., 1988).
117 Lens Adherence: Signs
Adherence persists for an average of 15 minutes in
LENS ADHERENCE
SIGNS 50% of cases but has been observed to last for up
• Lens bound to the cornea to several hours. This means that a practitioner is
- often decentred unlikely to see the lens in the adherent phase of its
- usually nasal, overlapping the limbus behaviour (usually early morning).
• Indentation ring
While an RGP lens may adhere to the cornea at
- due to lens edge
- localized corneal distortion
any position, it most commonly occurs in the nasal
• Staining
quadrant (Swarbrick, 1991). A wide range of signs
- central may accompany a bound lens. Typical signs
- increased 3 & 9 o’clock include:
- outside lens edge (arcuate) x Corneal indentation by the adherent lens edge
97300-51S.PPT

(96% of cases) (slides 120 and 122).

7L397300-51
x Localized corneal distortion associated with
corneal indentation in 88% of cases.
118 x Central patch staining (76%). Kenyon et al.
(1988) listed ‘epithelial breakdown’ as one of
LENS ADHERENCE
SIGNS their findings in an experimental study group.
• Adherence lasts d15 min in 50% of cases x Peripheral arcuate staining (17%) (slide 121).
• Back surface debris: x Short BUT along the arcuate indentation
- adherent mucus & cellular debris (Kenyon et al., 1988).
- arcuate or ring-shaped
x Conjunctival indentation in the region opposite
- suggestive of adherence on waking
the corneal indentation (Kenyon et al., 1988).
• Conjunctival redness
• Rapid recovery: x Trapped debris, usually mucus and cellular
- once lens mobility re-established debris that is expelled rapidly from under the
- following lens removal lens once lens movement commences (slide
97300-129S.PPT 119).
7L397300-129 x Some central endothelial bedewing may also be
seen in rare instances.
x Ocular redness, especially of the conjunctiva.
234 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

119 Corneal recovery is rapid once lens movement is

regained. Only 30% of eyes still exhibited signs of
adherence two hours after lens movement had
been re-established (data from Swarbrick, 1991).
As both significant individual variation and variation
within individuals are also exhibited, the lens
behaviour seen on each occasion cannot be
predicted from that seen previously.
Generally, lenses that exhibited toric flexure (as
determined by front surface keratometry of the lens,
i.e. FSKs) were mirroring the toricity of the
underlying cornea.
Corneal patch staining that occurs in a majority of
7L340-99 cases of adherence resolves rapidly. However, it is
possible that some dots of staining may be
120
detectable up to four hours after removal of an
adherent lens. Dense peripheral arcuate staining
can still be seen some hours after lens movement is
achieved (Swarbrick, 1991).
Infrequently, staining associated with local, non-
wetting, peripheral corneal areas, and ‘bridging’ of
an adherent lens’ edge by the lid margins, may
contribute to the development of dellen and corneal
ulceration (Levy, 1985, Schnider et al., 1988).
When tear debris adhering to the posterior lens
surface is observed at an after-care visit (more
likely an early morning visit) of an RGP EW wearer,
it would be prudent to consider the possibility of
7L3E38-99 lens adherence.
Importantly, since corneal staining and corneal
distortion from episodes of adherence can resolve
121
rapidly, e.g. most staining disappeared within one
hour of the re-establishment of lens movement, it is
difficult to ascertain the facts of the case when
examining the eyes much later. Further, wearers
who do bind lenses do not necessarily do so every
day (Kenyon et al., 1988).

7L336-92

122

7L31883-92

IACLE Contact Lens Course Module 7: First Edition 235

 Module 7: Contact Lens-Related Ocular Complications

123 Lens Adherence: Symptoms

Few symptoms are usually associated with RGP
LENS ADHERENCE
SYMPTOMS lens adherence. Those that are reported are
• Often asymptomatic usually minimal. On many occasions, the level of
lens comfort increases when the lens adheres to
• Mild awareness
the cornea. This is due to the reduced movement
- blurred vision
and lens/lid interaction with each blink. The latter is
- dryness at least partially due to the ‘burying’ of the lens
- tiredness edge in the indented cornea.
• Ocular pain
The vision following lens removal may be distorted
• Foreign body sensation due to the irregular corneal topography remaining at
• Spectacle blur following lens removal the site of adherence, especially if the adherence
97300-52S.PPT

was eccentric, a common occurrence.

7L397300-52
Other symptoms reported include:
x Ocular pain.
x Eye Redness.
x Mild ocular irritation or discomfort.
x Tiredness.
x Foreign body sensation when debris trapped
beneath the lens is expelled as the lens starts
to move after an episode of adherence. Lens
removal usually relieves most symptoms except
any visual disturbance induced by alterations to
the corneal shape.
x Greater difficulty removing lenses (Molinari et
al., 1987).
124 Lens Adherence: Aetiology
LENS ADHERENCE Adherence rarely occurs during daily wear of RGP
AETIOLOGY lenses but, as has been detailed above, it is very
• Patient-dependent, EW phenomenon common in RGP extended wear.
- majority (95%) bind at least occasionally The principal cause of adherence is believed to be
- average: 48% but flatter > steeper a thinning of, and an increase in viscosity of, the
• Thinned and n viscosity of aqueous-depleted post-lens tear film precipitated by prolonged eyelid
Post-Lens Tear Film (PLTF) and:
- lid pressure pressure during sleep, i.e. thin-film adherence.
- dehydration and/or contamination of PLTF (Swarbrick, 1991).
- physical properties & topography of cornea This process may be exacerbated by the squeeze
• Monitor lenses exhibiting little movement in DW pressures applied by the lid-lens combination more
97300-53S.PPT
easily expelling the less viscous aqueous phase of
the tear fluid. This leaves behind a thin residual
7L397300-53
layer of a more viscous mixture of lipids and mucin,
the viscosity of which can be further enhanced by
125 dehydration, or contamination.
LENS ADHERENCE Lens adherence reflects the fact that the shearing
AETIOLOGY forces generated against the lens by the blinking
• Lens factors: eyelids that normally might move a lens laterally on
- flat central fitting the cornea, failed to overcome the viscous drag
- reduced edge lift between the lens and the thin, viscous, post-lens
- large total diameter (TD) tear film, i.e. the lens is ‘bogged’ or ‘glued’ in the
- limited movement
viscous, mucus-rich, residual tear film remaining
under the lens.
- lid pressure
- alterations unlikely to
Lens adherence is more frequent in flatter fittings
prevent adherence in (84%) than in steeper fits (49%). Lenses with
susceptible wearers looser edge fittings and flat central fittings promote
more persistent adherence while smaller diameters
97300-54S.PPT

7L397300-54 and steeper fits induced more severe clinical signs

of adherence (Swarbrick, 1991). Kenyon et al.
(1989) reported tendencies of flat and flattest
lenses reducing adherence while steep lenses
exacerbated the problem. These results are the
236 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

126 opposite to the findings of others, especially

Swarbrick and Holden (1987) and the modeling by
LENS ADHERENCE Taylor and Wilson (1995).
AETIOLOGY Lens fitting characteristics play a minor role in
• Patient Factors (factor that exacerbates) adherence and attempts to manipulate the lens fit
- physical properties of the cornea or lens parameters are unlikely to prevent most
– thickness (thin) cases of lens adherence.
– rigidity (low)
Lin et al. (1989) failed to elicit any differences in the
– indentation susceptibility (high)
adherence rates of two fluoro-siloxane acrylate
- eyelid tightness (tight)
lenses of differing rigidities. They also found that
- ocular rigidity (low)
- corneal toricity (low)
generally, both eyes of the same wearer were likely
- diurnal variation in IOP (a postulation) to be affected but the tendency for adherence was
97300-194S.PPT greater in the right eye than the left.
7L397300-194 Lens material specific gravity has been considered
(Jones and Jones, 1995) but conclusions are
difficult to make.
It is probable that there is also some contribution
from the physical properties of the cornea, i.e. is it
relatively rigid or flexible, resistant or susceptible to
indentation, etc. Corneal topography may also
have a role in lens adherence.
Patient factors elicited by Swarbrick and Holden
(1996) include:
x Tighter eyelids.
x Lower ocular rigidity.
x Thinner corneas (resulting in lower ocular
rigidity?).
x Low corneal toricity. This corneal shape
combined with a spherical back surface design
maximizes the uniformity of the thinned post-
lens tear film and the viscous drag that results
from thin films in shear.
Kwok (1992) postulates that a contributing factor to
lens adherence may be variations in the IntraOcular
Pressure (IOP) as both adherence and IOP peak at
about the same time of day in most people.
A modeling of the post-lens tear film by Taylor and
Wilson (1995) supports the finding of Swarbrick and
Holden (1987), i.e. flatter fits are more likely to
exacerbate the problem of lens adherence. They
also suggested that eyelid muscle tension and tear-
layer composition during sleep play a significant
role in lens binding.
A key characteristic associated with RGP
adherence in EW appears to be lack of lens
movement in DW.
It is postulated that the root cause of adherence is
thin-film adherence, an aetiology that is largely not
amenable to manipulation of lens or fitting factors.
Therefore, it is probable that patient factors such as
tear film quality and tear film properties are the
most important predisposing factors.

IACLE Contact Lens Course Module 7: First Edition 237

 Module 7: Contact Lens-Related Ocular Complications

127 Lens Adherence: Management

LENS ADHERENCE Relatively little can be done in extended wear to
MANAGEMENT reduce the likelihood of adherence. However,
• Adherence often not preventable education about the possibility may alert patients to
• Patient education: an event that they may experience unknowingly on
- assess lenses each morning a reasonably regular basis.
- use ocular lubricants Quinn (1990) found that in one case at least, the
- mobilize lens with lid pressure use of a minus carrier and a ‘lid attachment’ fitting
• Lens fitting: philosophy resolved a problem of RGP lens
- increase tear volume adherence. Molinari et al. (1987) suggested the
- fit with slight apical pooling use of smaller optic zone diameters as a means of
- reduce total diameter reducing lens adherence.
97300-55S.PPT

Jones and Jones (1995) found that most cases of

7L397300-55
adherence could be resolved by fitting smaller,
flatter lenses with increased edge clearance.
128 An aspheric back-surface design does not eliminate
the problem of lens adherence (Bennett et al.,
LENS ADHERENCE
MANAGEMENT 1987), nor does changing the lens material
• Revert to daily wear for: (Herskowitz, cited in Bennett, 1987).
The effects of adherence can be minimized by
- at-risk patients
taking the following steps:
- persistent lens binders x Patient education and follow-up.
- those showing persistent staining
x Fit the lenses with slight apical pooling, i.e.
steeper rather than flatter.
• Experiment with the in-eye solutions x Avoiding heavy apical touch.
used to re-establish lens mobility x Revert to daily wear if problems persist, i.e.
97300-56S.PPT
avoid the problem induced by EW altogether.
7L397300-56 Herskowitz (in Bennett, 1987) and Bennett and
Grohe (1987) suggest the use of RGP
reconditioning drops before going to sleep and
upon awakening. They also suggest wearer self-
assessment on awakening and, should it be
necessary after applying conditioning drops, lid
manipulation to assist in re-establishing lens
movement.
Realistically, self-assessment on awakening is the
only way to ascertain the occurrence and frequency
of lens adherence. The only other possibility is to
arrange a research-like overnight study so that lens
behaviour immediately before and after overnight
wear can be studied in detail. In normal contact
lens practice this would not be acceptable to either
the majority of wearers or practitioners.
IV.B Corneal Warpage
129 Corneal Warpage: Introduction
CORNEAL WARPAGE Alterations to the corneal shape may be:
INTRODUCTION x Intentional, e.g. orthokeratology, a reversible
• Alterations to corneal shape: procedure (both a disadvantage and an
- intentional – orthokeratology advantage) (orthokeratology is presented in
- unintentional: Module 8).
– regular
x Unintentional
– warpage or distortion
• More likely with rigid lenses, esp. PMMA – irregular, eccentric, transient and unwanted,
• Uncommon with RGP lenses: a result of RGP lens adherence (see
- less rigid previous section of this lecture)
- offer superior physiology – regular, readily explained but unwanted (see
97300-150S.PPT
next section of this lecture)
7L397300-150 – irregular, unpredictable, inexplicable and
unwanted (the subject to be dealt with here)
238 IACLE Contact Lens Course Module 7: First Edition
Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

that may be permanent or reversible (Wilson

et al., 1990B).
The latter is usually referred to as corneal warpage,
or corneal distortion, and is more common in rigid
lenses, especially those made of PMMA and,
occasionally, first-generation RGP lenses (Bennett
and Egan, 1986). Holden (1989) went to the extent
of asserting ‘PMMA should be banned by all
practitioners’. There is some suggestion from
Rengstorff (1966) that over 50% of PMMA lens
wearers had at least some temporary visual acuity
loss over the first 21 days after lens removal.
Reports of warpage or distortion began to appear in
the mid-1960s, e.g. Hartstein, 1965, Rengstorff,
1965. However, corneal changes due to PMMA
lens wear are mentioned in Grosvenor (1963) who
asserts that corneal oedema tends to steepen the
corneal curvature and that contact lenses can
increase corneal astigmatism although a decrease
was much more common. Long-term wearers of
thick hydrogel lenses have also exhibited these
effects (Sweeney, 1992).
It is probable that all lenses that maintain the
cornea in poor physiological circumstances are
capable of inducing these changes and, the longer
the exposure, the greater the effect. However,
Levenson (1983), using 50 cases of corneal
warpage, failed to establish a definite relationship
between the magnitude of the no-lens wear
astigmatism that developed, and the duration of
lens wear.
Therefore, it is to be expected that this condition is
now less common since modern rigid lenses are
generally less rigid and offer a much higher
physiological performance. Corneal warpage
should not be confused with an effect occasionally
seen with very thin SCLs in which an epithelial
wrinkling effect is observed (Ruben, 1975, Snyder,
1998, Pye, 2001 personal communication, see
Lecture 7.2, Section V.B Lens/Corneal Wrinkling).
One of the earliest reports of significant corneal
alteration caused by contact lenses was by
Dickinson (1960) who reported a case in which
PMMA, un-ventilated haptic lenses were worn
apparently successfully on a daily wear basis for
some 13 years. Vision with the lenses on was
normal but best corrected spectacle vision was only
6/60. Importantly, there was no direct mechanical
aspect to the aetiology in this case, since the lens
was fitted with limbal and corneal clearance.
As corneal warpage or distortion appears to be
physiological in origin, it is possible that in
susceptible individuals, EW of lenses with
inadequate transmissibilities may still result in some
cases being seen in practice. Widespread use of
the best materials the contact lens industry now
offers should make this condition increasingly rare.

IACLE Contact Lens Course Module 7: First Edition 239

 Module 7: Contact Lens-Related Ocular Complications

130 Corneal Warpage: Signs

CORNEAL WARPAGE PMMA lenses, first generation RGP lenses, or thick,
SIGNS low water hydrogel lenses, i.e. lenses providing the
• Irregular shape changes: cornea with less than ideal conditions, can cause
- distorted keratometer mires irregular changes in corneal shape. Such
- irregular retinoscopic reflex irregularity may be classified as mild, moderate, or
- indecisive subjective refraction endpoint severe.
- variable subjective Rx
- possible deep stromal hazing/opacities Keratometer mire distortion is one obvious clinical
- abnormal appearance of endothelium sign of corneal warpage. However, as always, it is
• Full topographical assessment desirable relevant to remember that the keratometer only
- irregular topography measures the central 3 mm (approximately) of the
- horizontal meridian tends to steepen cornea and offers no real information about corneal
97300-57S.PPT

curvature outside this zone (see Lecture 1.2). This

7L397300-57 issue is relevant because Wilson et al. (1990B)
reported that keratometer mires were usually
regular one month after cessation of wear yet
131 corneal topography took some five months to
CORNEAL WARPAGE ‘stabilize’. They also found a statistically significant
RE: Subject: VJT trend for PMMA wearers to show a steepening of
-5
mean corneal power. This had already been shown
-4
Horizontal by Rengstorff (1969, slide 134).
Irregular retinoscopic reflexes, and difficulties using
Dioptres

-3
either the direct or indirect ophthalmoscope, are
-2 Vertical also common findings. Using a binocular indirect
-1
ophthalmoscope may pose greater difficulties in
extreme cases of corneal warpage as stereopsis
0
0 12 48 96 144 240 360 1152 may be more difficult to achieve due to induced
ns ed Hours
Le ov
re
m
97300-152S.PPT
irregularities in image disparity.
The optical ramifications of such corneal changes
7L397300-152 can result in indecisive subjective refraction end
132 points and variable subjective refraction results.
This variability may be within sessions or between
CORNEAL WARPAGE
LE: Subject: VJT sessions in which the spectacle refraction is
-5 ascertained (see slides 131 to 133 for a typical case
Horizontal
that was monitored closely [Williams, 1988]).
-4
A detailed slit-lamp examination is likely to show
posterior stromal hazing or opacities (Korb, 1973,
Dioptres

-3
Vertical
-2
Sweeney, 1992), a finding also reported in long-
term PMMA and HEMA lens wearers by Remeijer
-1
et al. (1990). The latter group reported deep
0
0 12 48 96 144 240 360 1152
whitish central opacities adjacent to Descemet’s
n
Le ov
s d
e Hours membrane that reversed once lenses of higher
physiological performance were fitted. Endothelial
m
re 97300-153S.PPT

7L397300-153 changes including polymegethism were also

reported. Korb (1973) claims that these opacities
(‘edematous corneal formations’ as he called them)
133 were reversible by cessation of lens wear for one to
four weeks.
CORNEAL WARPAGE
Best Sphere: VJT: R & L Sweeney (1992) also reported pigmentary
-4 deposition on the endothelium at its posterior
Left
Right chamber interface. Persistent corneal staining may
-3
Right be seen in some cases (after Polse, 1974).
Dioptres

Left An assessment of the endothelial mosaic in

-2
specular reflection will probably reveal a bumpy,
-1
distorted, and polymegethous (moderate to severe)
mosaic (Sweeney, 1992). If the facilities were
0
available to assess the corneal swelling function, it
0 12 48 96 144
Hours
240 360 1152
would probably be found to be excessive during
97300-154S.PPT
open-eye wear of low or even moderate Dk/t
7L397300-154 lenses. This is suggestive of chronic endothelial
dysfunction induced by long-term contact lens wear.
240 IACLE Contact Lens Course Module 7: First Edition
Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

Such a dysfunction results in a compromised

endothelium that is no longer able to cope with the
stresses imposed by low transmissibility lenses
(after Sweeney, 1992). Any possible role played by
the restricted efflux of CO2 from the cornea is
difficult to determine. Bonanno and Polse (1987)
have shown acidic shifts in stromal pH under rigid
contact lenses. In their study, the poorer the
physiology offered, the greater is the corneal
acidosis.
In many cases, the use of a videokeratoscope or
other topographical measuring device, e.g.
photokeratoscope, is necessary if the extent of
corneal warpage beyond the corneal centre is to be
determined accurately.
In the so-called Fort Dix Report, Rengstorff (1965),
using fundal retro-illumination for disclosure,
showed that of 100 PMMA lens wearers whose
lenses were withdrawn for experimental purposes,
23% exhibited ‘marked’ distortion (bilaterally in all
but 2 cases), 38% ‘slight’ distortion, 37% ‘very
slight’, and only 2% ‘none’.
In the case of ‘marked’ distortion, the 23% initial
incidence had decreased to just 7% of cases on the
first day and only 2.5% of cases by day 7.
Correctable visual acuity was reduced in most
instances.
‘Slight’ distortion cases (bilateral in all but six cases)
reduced from the initial 38% to 23% by the first day,
and 5% by day 7. Since Rengstorff frequently
found retinoscopy difficult in cases of corneal
distortion, it is probable that such a procedure will
disclose even subtle cases of distortion, whereas a
keratometer, measuring only the central 3 mm of
the cornea, may show relatively regular mire
images. Rengstorff did report frequent mire
distortion, but tellingly, the greatest distortion was
not necessarily immediately after lens removal.
Frequently, he found ‘scissor’ motion and
meridional inequalities. Subjective cylinder findings
often showed 90° axis swings and power changes
of 2.00 D or more were common during the first
seven days of no-lens wear. Changes of 1.00 D in
the spherical equivalent were common, >20% of
cases showed >2.00 D of change, and two cases
showed >5.00D of change.
Significantly, Rengstorff (1965) also reported that
frequently, corneal curvature changes were
considerably less than the respective subjective
refraction changes and, in some cases, bore no
apparent similarity at all. He also found aspherical
changes to be common within the first seven days
of lens removal.
The development of irregular astigmatism was also
a common finding (Levenson, 1983) that usually
resolves over time if an RGP lens is used to refit the
patient (Levenson and Berry, 1983). These authors
also found that there is a regular astigmatic
component to corneal warpage that was either slow
to resolve (under an RGP lens), or became
permanent.
IACLE Contact Lens Course Module 7: First Edition 241
 Module 7: Contact Lens-Related Ocular Complications

134 Rengstorff (1967, 1969) reported progressive

flattening (negative change, decreasing minus Rx)
CORNEAL WARPAGE of both the vertical and horizontal corneal meridians
RENGSTORFF, 1969
Steepening
+0.25 over the first three days following cessation of lens
Vertical wear (slide 134).
Mean corneal change

0.00

-0.25
This phenomenon was then followed by a
(Dioptres)

progressive steepening (positive change, increasing

-0.50
Horizontal plus Rx) of both meridians over the following
-0.75 weeks.
-1.00 An associated decrease in myopia was found over
-1.25
the first three days followed by an increase over the
Flattening 0
ns ed
24 72 168 336 504 1152 following weeks until a steady state was reached.
Le ov Hours
re
m 97300-156S.PPT
The data from subject VJT (slides 131 to 133) also
7L397300-156 shows such a change. Others have found the
same basic corneal behaviour pattern following
cessation of wear of low physiological performance
rigid lenses.
Rengstorff (1973) showed that even after diurnal
variation was taken into account, PMMA lens
wearers exhibited a steepening of corneal curvature
(also reported by Wilson et al., 1990B) the
magnitude of which was directly related to the
number of years of contact lens wear. Levenson
(1983) failed to show such an effect in relation to
the amount of astigmatism that developed following
cessation of lens wear.
Using a videokeratoscope to monitor the corneal
shape, Wilson et al. (1990B) found that warpage
cases were characterized by:
x Central irregular astigmatism.
x Loss of radial symmetry.
x Frequent reversal of the normal shape of
progressive flattening towards the periphery,
i.e. warped corneas steepened towards the
periphery.
They also found that lenses locating superiorly
induced corneal topography changes similar to that
of early keratoconus. Stable corneal topography
was not realized until five months after cessation of
lens wear.
135 Corneal Warpage: Symptoms
CORNEAL WARPAGE Usually, very few symptoms are associated with
SYMPTOMS corneal warpage and most cases are asymptomatic
(Wilson et al., 1990B). When the lens is on the eye,
• Usually, asymptomatic
the corneal surface irregularities are masked by the
- otherwise minimal if lens is comfortable contact lens/tear lens/cornea combination to the
• Significant ‘spectacle blur’ extent of some 90% (see Module 2, Lecture 2.3,
- may be long-lasting Section VII The Tear lens for a detailed treatment
• If lens wear ceases of this and related areas). Alternatively, the corneal
- astigmatic spectacle Rx shape may be dictated by the back-surface design
of the lens. As a direct result, vision remains at an
- Rx/vision stabilization takes time
acceptably high level in most instances and the
97300-58S.PPT
wearer often remains unaware of anything
7L397300-58 untoward.
Some wearers may report sudden intolerance to
lenses that proved to be satisfactory (though not
necessarily desirable) over many years of use.
Corneal exhaustion syndrome (CES) may be a
more appropriate classification for some of these

242 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

136 cases and this topic is detailed separately in

Lecture 7.2, Section II.H Corneal Exhaustion
CORNEAL WARPAGE Syndrome (CES) in this module.
SYMPTOMS However, upon lens removal, the vision with
• Sudden intolerance to lenses may
spectacles is often reduced significantly. The
develop
cornea may take days or even weeks to recover its
• Corneal surface irregularities are
normal shape and during this time the vision
‘masked’ by lenses
remains somewhat compromised even when the
• Corneal shape may be influenced by
best spectacle correction determinable is worn.
lens back surface design
Although some wearers may report lens discomfort,
• Vision often reduced significantly upon
lens removal if the lens’ physiological performance is so low as to
result in corneal hypoaesthesia, such reporting is
• Effects likely to span weeks or months
97300-195S.PPT unlikely. Reduced corneal sensitivity was reported
7L397300-195
by Korb (1973).
If corneal distortion is severe, corneal curvature
changes may occur for many weeks (Rengstorff,
1979B). Rengstorff’s Fort Dix Report (1965) found
that 10% of a sample of 100 subjects that usually
wore PMMA lenses exhibited corneal distortion that
increased in the first seven days of no-lens wear
(lenses withdrawn for experimental purposes).
These distortions decreased over time. The visual
consequences of this variable corneal topography
can be both serious and disturbing to a previously
successful contact lens wearer. Rengstorff (1985)
studied the contributions of the corneal components
to changes in corneal refraction. Although anterior
corneal curvature made the greatest contribution,
other factors also played roles. In descending order
of importance these were:
x Refractive index.
x Depth of anterior chamber.
x Posterior corneal curvature.
x Least significantly, corneal thickness.
Generally, the changes in corneal curvature
measured only explain about half the refractive
change determinable (Rengstorff, 1967, 1969,
Lowther, 1994).
Furthermore, the need to track the resulting
refraction changes can be frustrating and expensive
for both the patient and practitioner. Prudent
management suggests immediate refitting (see
Corneal Warpage: Management later in this
section).
137 Corneal Warpage: Aetiology
CORNEAL WARPAGE While the apparent cause of corneal warpage with
AETIOLOGY rigid lenses is mechanical, the underlying cause is
• Apparently, mechanical but..... poor physiology. The resulting chronic corneal
• Underlying cause is prolonged oedema (mainly stromal) oedema would appear to be the
- inadequate lens Dk/t root cause (after Bennett and Gilbreath, 1983).
- CO2 (possibly) However, oedema cannot be the sole cause of
• Ill-fitting lens these changes because oedema resolves very
- eccentric location quickly whereas the refractive and/or topographical
- localized heavy bearing changes resolve much more slowly (Wilson et al.,
- excessive movement 1990B, Lowther, 1994).
- lid pressure translated to cornea A contributing factor to chronic corneal oedema
97300-59S.PPT

may be contact lens-induced endothelial

7L397300-59 dysfunction (Remeijer et al., 1990, Sweeney, 1992).
This condition, which is part of the so-called

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 Module 7: Contact Lens-Related Ocular Complications

138 Corneal Exhaustion Syndrome (CES), is a possible

result of many years of seemingly successful lens
CORNEAL WARPAGE wear using lenses of low physiological
AETIOLOGY after Rengstorff, 1985 performance. However, the onset of CES is usually
• Curvature changes only ‘explain’ about sudden.
half the refractive change measurable A possible contributing factor is a stromal pH
• Other factors (in decreasing order of decrease resulting from corneal hypoxia. This is
contribution):
probably exacerbated by a reduced CO2 efflux from
- refractive index
the cornea when wearing a rigid lens (see Holden
- depth of anterior chamber et al., 1987 and Ang and Efron, 1989). As reported
- posterior corneal curvature by Bonanno and Polse (1987), the stromal pH
- corneal thickness (the least significant) decrease under rigid lenses was inversely
97300-196S.PPT proportional to the oxygen transmissibility of the
lens.
7L397300-196
Localized areas of heavy corneal bearing due to a
poor fit, combined with a decentred fitting, can
rapidly change the shape of the ocular surface in an
irregular manner. Lens decentration produces
relative flattening of the cornea beneath the
decentred lens and a relative steepening in the
diametrically opposed corneal area (Smolek and
Klyce, 1995). Lens resting position has been
shown to influence alterations in corneal
topography both regularly and irregularly and, in
extreme cases, can give rise to keratoconic-like
topographical alterations (Wilson et al., 1990, Ruiz-
Montenegro et al., 1993). Furthermore, Rengstorff
(1967) showed that the changes in the vertical and
horizontal meridians followed different patterns.
It is difficult to attribute warpage to a lens being too
steep or too flat because it has been shown already
that a steep lens can result in a corneal steepening
(the most likely outcome), a flattening, or no
change. Hill and Rengstorff (1974) studied 40 eyes
when fitted with steep lenses. Of these, 24
steepened, 12 flattened and 4 remained the same.
A later study by Rengstorff (1977) used steep,
aligned, and flat lenses and a similarly
unpredictable outcome was found.
The relative insignificance of lens back surface
shape (assuming a reasonable initial lens fit) is
further supported by the finding of significant
astigmatism in previously spherical corneas,
sometime after cessation of lens wear even though
the cornea may have been spherical immediately
after lens removal. Generally, the horizontal
meridian was found to steepen slightly, while the
vertical tended to flatten slightly. The corneal
curvature changes shown by Rengstorff (1967,
1968, 1969) and others, can be explained largely by
Polse’s (1972) results from a study of corneal
hydration. He found that only those wearers who
demonstrated an increase in corneal thickness
(increased corneal hydration) following lens
withdrawal showed significant corneal thickness
changes. The changes reported by Polse lasted
several weeks. He proposed that the thickness
changes were not uniform because the refractive
changes that resulted were also not uniform.
The changes described here are more likely to
occur when a very low oxygen transmissibility lens
244 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

material is used, as this results in corneal oedema

that renders the corneal tissue ‘softer’ and more
susceptible to molding. Examples of such lenses
are PMMA, thick, first generation RGP lenses, or
thick low water hydrogels (especially torics or high
spherical Rxs)
139 Corneal Warpage: Management
Because of individual differences and the relative
CORNEAL WARPAGE rarity of the condition now, corneal warpage needs
MANAGEMENT
Basic approaches: to be managed on a case by case basis.
• Change to lenses with nn transmissibility An accurate assessment of the corneal shape and
• Cease lens wear its irregularity requires the use of a
• Programmed withdrawal of original lenses
photokeratoscope, or videokeratoscope. While a
Other management issues:
• Need to convince wearer of the need to change keratometer is useful, it provides incomplete, or
• Several pairs of lenses may be required even misleading data on corneal topography and its
• Corneal sensitivity returns recovery. The different stabilization time courses
- initial comfort of new lenses may be lower found by each of these instrument categories
• Wearer requests to return to ‘old’ lenses must (Wilson et al., 1990B, Lowther, 1994, Smolek and
be resisted
97300-197S.PPT
Klyce, 1995) need to be reconciled by the
7L397300-197
practitioner. This is because, if lens wear is to be
discontinued for a length of time, any management
plan will depend on a decision as to when the
140 corneal topography has ‘stabilized’.
CORNEAL WARPAGE Improve Physiology
MANAGEMENT The most obvious issue to be tackled is that of the
• Pre-lens ocular data invaluable (available?) physiological performance of the lenses. Corneal
• Assessment by videokeratoscope warpage or distortion is indicative of poor corneal
desirable circumstances under the lenses worn. This
suggests strongly that the lenses must be changed
• Refit immediately if at all possible
for something better, promptly. The maintenance of
- lens parameters similar to originals corneal optical and shape integrity is also important
- make diameter larger if good vision is to be maintained. However, Pence
- make slightly flatter (1988) and Sweeney (1992) both reported that
97300-60S.PPT
PMMA wearers exhibiting CES and refitted initially
with relatively low Dk/t RGP lenses (the only type
7L397300-60
available at the time), only received short-lived relief
that required a further refitting with even higher
141 transmissibility lenses (once they became available)
some time later.
CORNEAL WARPAGE Cessation
MANAGEMENT
• Discontinuation: Some authors believe that temporary
- avoid if possible discontinuation of lens wear may be required in
– poor vision some cases to permit the cornea to return to its
– no or inadequate spectacles
– corneal astigmatism may develop
original shape. In view of the changes in spectacle
– stabilized shape may be permanent & Rx that are expected, it is prudent to warn the
significantly astigmatic patient of what is likely to happen to their spectacle
- need to await stabilization
- reinforces negative impressions of CLs
vision once they cease contact lens wear (Polse,
• Refitting 1974, Harris, 1975).
- improve corneal alignment However, if the distortion is a result of long-term
- deliver more oxygen
97300-151S.PPT PMMA lens usage, it is imprudent to discontinue
lens wear (Rengstorff, 1977, 1979, Bennett, 1983,
7L397300-151
Bennett and Tomlinson, 1983, Williams, 1988).
This is because the cornea can develop permanent
astigmatic changes of significant magnitude
(approximately 3.00D but as high as 6.00D within
one month of lens removal in corneas that were
spherical previously) (Hartstein, 1965, Rengstorff,
1965B, 1977B, 1978, and Williams, 1988). Slides
131 to 133 refer to subject VJT who ultimately
developed a stable -2.75D cyl in one eye and a –
2.50D cyl in the other. Rengstorff (1977B) presents
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 Module 7: Contact Lens-Related Ocular Complications

four cases in which significant with-the-rule

astigmatism resulted from sudden cessation of rigid
lens wear.
There is some evidence that the length of exposure
to inadequate lenses influences the magnitude of
the induced changes (Rengstorff, 1965B, 1969, and
Ing, cited in Rengstorff, 1977, 1977B). If in doubt,
the cornea should not be allowed to ‘run free’ as the
restoration task becomes more difficult, takes
longer to achieve, and may have some permanent
residual effect. Some authors even describe the
cessation of contact lens wear as ‘dangerous’, e.g.
Rengstorff (1979B). Ing measured the ocular
rigidity indirectly in 131 eyes and found that, after
lens removal, the greatest with-the-rule astigmatism
developed in those eyes that exhibited the lowest
ocular rigidity. Furthermore, the lowest ocular
rigidity was noted in the eyes that had worn PMMA
lens for the longest time.
The withdrawal of lenses that provided good or
better vision often leaves the wearer visually
handicapped because they have no, or inadequate,
spectacles. From a safety point of view, e.g.
driving, riding, and navigating through congested
environments, this can pose a danger to the
individual (Rengstorff, 1981).
Additional complications may also overlay the
fundamental problems of corneal topography.
These include dry eye and epithelial erosions
(Bennett and Gilbreath, 1983).
Despite much data supporting alternative
approaches, Wilson et al. (1990B) still suggested
waiting for as long as 5-6 months without lenses
before refitting, to establish that corneal topography
had stabilized.
Although most experienced RGP lens practitioners
would avoid this alternative if possible, hydrogel or,
preferably, siloxane hydrogel lenses are a viable
alternative in some cases. However, if significant
astigmatism is induced (during or after lens wear),
not only is the wearer unlikely to see well
(uncorrected astigmatism when only spherical
lenses are used or available), it seems unlikely that
such lenses will reverse the induced astigmatism
over time.
Programmed Withdrawal
Arner (1977) studied abrupt cessation of lens wear
and found severe corneal deformations and loss of
visual acuity. As a result, he advised a gradual
reduction of lens wear over several weeks as a way
of reducing the effects of eventual cessation. If
refitting immediately, Rengstorff (1979) also
suggested that the original lenses (assuming they
are not PMMA) be modified and used until a lens of
higher transmissibility can be delivered.
Modifications suggested include: reducing the
diameter, decreasing the BOZD and flattening the
peripheral curves. The new lens to be ordered
should mirror the experience with this modified lens
and incorporate a flatter BOZR (0.50D), especially if
the problem lens tended to fit steeply. Bennett
246 IACLE Contact Lens Course Module 7: First Edition
Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

(1983) suggested an alignment, or possibly flatter,

fit with a larger (TD: 8.8 – 9.00 mm) RGP lens
intended to provide a ‘lid-attachment’ fit. Until the
lenses were delivered, PMMA lens usage should be
limited.
Lens delivery should be made at about the same
time of day as the RGP prescribing visit. This
advice is based on the assumption that this would
be after about the same amount of PMMA lens
wearing time on both occasions, i.e. corneal shape
at the time of RGP lens delivery should mirror that
at the earlier RGP trial lens session.
Immediate Refitting
An alternative, and probably preferred method is to
refit the patient promptly with a lens of substantially
higher oxygen transmissibility and essentially
similar parameters (depending on the practitioner’s
assessment of the fit of the problem lenses, or
observation with a new trial lens).
Snyder and Gordon (1985) studied the effect of
refitting PMMA wearers with an early RGP lens and
found a dramatic decrease in corneal thickness, a
slight flattening of corneal curvature, and no change
in refraction. A simple reorder of the original lens
parameters in an RGP material was their study’s
recommendation. More recent RGP materials
probably allow larger lenses to be fitted to
advantage.
Bennett and Tomlinson (1983) compared the
complete cessation philosophy with the immediate
refitting approach. They found that refitting may
have slowed corneal recovery slightly (stability of
parameters took longer to achieve, also a finding of
Harris et al. (1972). However, there were no
apparent disadvantages to this approach and many
advantages, especially the achievement of better
and more stable vision. Further, less myopic
astigmatism developed in the group refitted
immediately. Immediate refitting has also been
supported by Levenson (1983), Hom (1986),
Williams (1988), and Bennett and Henry (1994). If
RGP lenses are fitted without delay, the return to
corneal regularity may take from six months to two
years (Stein et al., 1995).
Proactive Approach
The other approach presented in the literature is
more relevant to those cases in which there is a
practitioner-detected need for more desirable rigid
lenses, rather than an adverse event that makes
the same point more dramatically. In these
situations, it has been suggested that lens wear
with the original lenses be reduced progressively
before eventually replacing them with RGP lenses
with higher physiological performance (after
Rengstorff, 1975, 1989, Arner, 1977).
In such circumstances, a knowledge of pre-lens
wear corneal data is invaluable. Kastl (1987) used
the expression ‘absolutely mandatory’ but
regrettably such data is often not available
regardless of its desirability. When pre-fitting data
is not available, the fit should be optimized to
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 Module 7: Contact Lens-Related Ocular Complications

reduce any localized pressure points or zones on

the cornea. Clear corneas, the absence of
spectacle blur, and wearer comfort are the criteria
that apply to deciding whether the replacement
lenses are satisfactory (Polse, 1974).

Patient Management Issues

An important aspect of the clinical management of
corneal warpage cases is the frequent need to
convince a satisfied and experienced PMMA (or
low-Dk RGP) lens wearer that, for the sake of their
corneas, the lenses about which they have no
complaints need to be replaced (Bennett and
Henry, 1994). The possibility that several changes
of lenses may be required before a final Rx can be
issued adds to the challenge of any such
explanation.
Another pressing clinical matter that receives little
coverage in the literature, but which almost always
arises when refitting PMMA wearers, is the issue of
returning corneal sensitivity. With low
transmissibility lenses, the cornea is at best
hypoaesthesic, and at worst anaesthetized. Once a
lens with higher transmissibility is worn, the
functions of the corneal sensory nervous system
start returning to normal. In so doing, the wearer is
much more aware of their new, ‘superior’ lenses on
their eyes and they often request a return to their
‘more comfortable’ (but quite undesirable) original
lenses. To forestall such a request requires ‘selling’
them on the benefits of refitting and forewarning
them before any refitting is undertaken. Taking a
reactive approach to problems as they arise
diminishes the credibility of the practitioner and
makes the ‘selling’ of the idea to the patient much
more difficult.
IV.C Corneal Shape Changes
142 Corneal Shape Changes: Introduction
CORNEAL SHAPE CHANGE While previous sections of this lecture dealt in detail
INTRODUCTION with lens adherence and contact lens-induced
• Unintentional corneal irregularity/warpage, this section deals with
• Regular & correctable regular corneal curvature changes that result from
• Often reflects lens-cornea fitting relationship
contact lens wear. Frequently, these changes
reflect the lens-cornea fitting relationship, tend to be
• Largely a ‘mechanical’ effect
relatively small, and apparently completely
• However, intuitive result (steeper reversible once either the lens design is altered, or
lensosteepening) not always the case lens wear ceases, at least temporarily. Such
• Reversible (usually rapidly) changes can be either intentional (see
• Little or no physiological component orthokeratology presented in Module 8) or
97300-158S.PPT
unintentional. It is the latter that are covered here.
7L397300-158 The previous section on corneal warpage has
significant overlap with the present topic and should
probably be considered an adjunct to it.
Although intuitively it is expected that lenses fitted
steeper should result in a steepening of the corneal
curvature, it has been shown that the reverse is
also quiet likely to occur. No change is a less likely
outcome (after Hill and Rengstorff, 1977).
Providing lenses cater adequately for the cornea’s
physiological needs, any effect they have on
248 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

corneal topography will probably be largely

mechanical in origin rather than physiological.
If the cornea responds optimally to contact lens
wear, corneal changes will be minimal (Harris,
1975). A study of 89 PMMA lens-wearing myopes
by Brungardt and Potter (1971) found that 76.3% of
the group had spectacle blur refractions (Rxs taken
immediately after lens removal) that were within
±0.37D of their pre-fitting Rx. Interestingly, unlike
corneal warpage cases, the changes in contact lens
in situ Rx, and the spectacle blur Rx, were almost
identical (Fig. 7 of Brungardt and Potter’s paper).
These authors believed their fitting philosophy to be
‘correct’ when the spectacle Rx, spectacle blur Rx,
and the original pre-lens fitting spectacle Rx were
judged to be the same and each offered the same
visual acuity, i.e. the introduction of contact lens
wear has had no refractive/acuity effect.
Figures from Rengstorff’s ‘Fort Dix Report’
(Rengstorff, 1965) suggest that up to 30% of rigid
lens wearers show corneal shape changes.
143 Corneal Shape Changes: Signs
CORNEAL SHAPE CHANGES Assessment of the extent of RGP lens-induced
SIGNS corneal shape changes depends to some extent on
the method(s) used to determine them. Arguably,
• Regular shape change the least informative method is keratometry
because of its 3 mm central-area limitation. Such K
- keratometry readings should be regarded as the ‘tip of the
iceberg’ and have less significance than the
- videokeratoscopy peripheral cornea (Iacono, 1989A). The corneal
periphery can only be assessed with either a
• Sphericalization of the cornea photokeratoscope, or a videokeratoscope (see
Module 9, Lecture 9.1, Section III.B
97300-61S.PPT
Videokeratoscopes).
7L397300-61 More recently, Hettiger (2000) stated that spectacle
blur was an easy ‘test’ of what a contact lens had
done to alter the corneal surface. He suggested
144 that a comparison be made between the spectacle
CORNEAL SHAPE CHANGES refraction before contact lens wear, and the
SIGNS spectacle Rx ‘caused’ by the current contact lenses
• Spectacle blur (cf. before & after CL wear) (at least four hours of wear was recommended).
• Sphericalization may p manifest astigmatism Supporting evidence that showed decreasing
topographical distortion was accompanied by
- unaided VA may improve
improvements in visual acuity has been supplied by
• Both flattening & steepening of the cornea Iacono (1989B). He also showed that with reduced
have been reported
corneal distortion in myopes, there was a reduced
- flattening is more common need for minus power, and a decrease in with-the-
- Rx changes correlate poorly with curvature rule astigmatism. In hyperopes, a reduction in
changes distortion was accompanied by a reduction in
refractive astigmatism but with little or no alteration
97300-198S.PPT

7L397300-198 to the spherical component.

Commonly, the shape is changed towards a more
spherical surface, i.e. a process of sphericalization.
Provided any manifest spectacle astigmatism is
mainly corneal in origin, such shape changes
should lead to a reduction in ocular astigmatism
along with the potential for improved unaided vision
(see above).
Polse et al. (1987) found that in RGP EW, the mean
flat K flattened by 0.37 D and the mean steep K

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 Module 7: Contact Lens-Related Ocular Complications

flattened by 0.87 D. However, Polse et al. (1988)

found than in RGP EW (35 subjects, 6 months
wear) corneal curvature:
x Flattened 0.24 r0.59 D in the steep meridian.
x Steepened 0.13 r0.42 D in the flat meridian.
x Overall effect: Total corneal astigmatism
reduced by an average of 0.50 D.
A comparison of pre-lens K readings with post-lens
wear K readings should mirror these changes.
Alterations to the spherical component or the
spherical equivalent may also be detected if an
overall steepening or flattening of the corneal
curvature has also been effected. The keratometer
mire reflexes (or the screen images or plots from a
videokeratoscope) are expected to be regular,
suggesting a system that is symmetrical about a
‘centre’ and essentially normal.
However, keratometry is unlikely to disclose subtle
lens-induced corneal shape changes. Most
instruments measure a 3 mm (approximately)
diameter circle. Changes within this central area
affect vision but may not be detected by the
keratometer.
Further, any corneal shape change should be
reflected in logical and relevant changes in the
sodium fluorescein-fitting pattern. If they are not,
corneal distortion or warpage should be suspected
(detailed in the previous section).
Although unlikely with most RGP lenses,
conjunctival curvature changes may also occur with
lenses that are excessively mobile and that traverse
the limbal ‘boundary’. Staining may disclose this
mobility but assessing the changes quantitatively is
difficult and beyond the capabilities of most
topographical instruments with the possible
exceptions of the PAR, Humphrey, and Euclid
instruments (see Lecture 9.1).
Badowski and Carney (1990) studied the effects of
high Dk RGP lenses on corneal topography. They
varied the fit by making it aligned, flatter than
aligned or steeper than aligned and found that there
was an overall flattening of the cornea.
Paradoxically, the flatter fitting lenses produced the
greatest deviations from this tendency towards
corneal flattening. In a three-month study of RGP
and low water SCLs, Gauthier et al. (1991) found
the RGP lenses showed a significant reduction in
refractive sphere, refractive cylinder, and corneal
cylinder compared with SCLs. Polse et al. (1987)
found refractive changes were smaller than
changes in K readings, and were not correlated with
the latter.
Following a 12-month EW study, Kamiya (1986)
reported changes in corneal thickness (thinning).
However, these changes were relatively
inconsequential with respect to refractive changes.
He also found that corneal curvature flattened in
both meridians by about 0.36 D within the first week
of EW, a result similar to those reported by others.

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

145 Corneal Shape Changes: Symptoms

CORNEAL SHAPE CHANGES
Few symptoms are associated with a regular
SYMPTOMS change in corneal shape. If the change is
substantial, the lens fitting characteristics may be
• Minimal with contact lens wear affected adversely, making the presence of the lens
more noticeable to the wearer.
• Change in lens comfort After lens removal, the patient may be aware of a
change in their vision both unaided, and with
• Spectacle blur spectacles. These changes may be for the better,
i.e. orthokeratology-like changes, or for the worse,
- fluctuating vision i.e. a deterioration of vision.
97300-62S.PPT
Where vision is not correctable to an ‘acceptable’
standard (Dixon, 1964), a judgment usually based
7L397300-62
on pre-lens wear performance, the term ‘spectacle
blur’ applies. Spectacle blur implies that a non-
refractive component is at least partially responsible
for any reduction in vision detected, i.e. some
factor, probably physiological, that does not
respond to correction by lenses. Spectacle blur is
related more to the previous section
(warpage/distortion) than this section, and will not
be dealt with further here.
While refractive changes parallel those of corneal
curvature, generally they are smaller (Polse et al.,
1988). Further, reports appear in the literature of
‘wide excursions’ of Rx with no accompanying
changes in keratometer readings or pachometry
results (e.g. Dixon, 1964, at a time when only
PMMA lenses were available). A change in corneal
refractive index (change in water content) was
proposed as a possible explanation.
146 Corneal Shape Changes: Aetiology
CORNEAL SHAPE CHANGES The dominant factors in alterations to corneal shape
AETIOLOGY during contact lens wear are the relative rigidity,
and thicker profile, of an RGP lens combined with
• Mechanical the pressure exerted by the upper eyelid, when at
rest and during blinking (especially). The duration
• Lens fitting of lens wear (hours per day) and the prolonged use
of the lenses (months/years) both influence the
- corneal bearing
magnitude of the changes induced (Rengstorff,
- pressure from the upper lid 1989). A partial explanation of the underlying
mechanism comes from Dixon (1964) who
attributed the changes to alterations to the
97300-63S.PPT
epithelium.
7L397300-63 However, since lenses fitted flatter do not
necessarily flatten the cornea, the situation must be
more complex than first appearances and intuition
may suggest, e.g. Carney (1975), Rengstorff
(1977), Rengstorff (1989). The resting position of
the lens has also been shown to be a factor. In
extreme cases of decentration, keratoconic-like
topographies can result (Wilson et al., 1990, Ruiz-
Montenegro et al., 1993).

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 Module 7: Contact Lens-Related Ocular Complications

147 Corneal Shape Changes: Management

CORNEAL SHAPE CHANGES Small and regular changes in corneal shape are
MANAGEMENT usually of minimal concern and require little or no
intervention by the practitioner.
• Dictated by degree Harris (1975) suggested that when visual acuity
either with contact lenses or with best post-lens
• Minimal change requires no intervention wear spectacle Rx was worse than 6/7.5 (20/25),
further testing for stabilization of corneal curvature
• Lens fitting was indicated. He also cautioned against pursuing
significant cylindrical components in post-wear
- minimize bearing
spectacles. If such changes are demonstrated, and
they are believed to be contact lens-induced, it is
97300-64S.PPT

probable that a case of warpage or distortion is to

7L397300-64 hand and not a simple shape change.
The following refitting criteria are modified from
Polse (1974):
x Prolonged spectacle blur (> 45 minutes
duration) of 6/9 (20/30) or worse.
x Irregular corneal curvature (see previous topic).
x Changes in corneal curvature of 1D or more.
x Persistent oedema or oedematous lines (striae,
folds, black lines). These are less likely with
RGP lenses, Polse was referring to PMMA
lenses.
x Persistent corneal staining.
x Patient discomfort. Not particularly likely with
modern lens materials and designs.
Lens fitting characteristics should be optimized to
ensure good centration and minimal bearing on the
cornea. Once refitted, it may be prudent to reduce
initial lens wearing times with the replacement
lenses (Polse, 1974). The corneal behaviour under
the new lenses should then be monitored carefully
to ascertain that minimal corneal curvature changes
are occurring, and that some improvements have
been effected.
Should corneal oedema be suspected because the
minus spherical component of the current spectacle
Rx has increased, Hettinger (2000) suggested the
BOZR of any new lens be ordered 0.50D flatter
than the current pair. The reverse alteration, i.e. a
steeper fit, was required for increases in the plus
component of the spectacle Rx.
Modern lens designs, high-performance materials
and a good working knowledge of RGP fitting
principles should be sufficient to solve all the
problems likely to arise in current routine contact
lens practice. Usually, the lens type does not need
to be changed, i.e. RGP to SCL, in the event of
finding changes in corneal curvature.

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

IV.D Ptosis
148 Ptosis: Introduction
PTOSIS Sometimes, rigid lens wearers adopt abnormal
INTRODUCTION head gaits, eye/lid positions, and blinking behaviour
while wearing their lenses. Many of these
• Sign of an RGP lens wearer ‘adaptations’ can be explained by eye positions and
• Upper lid rests in a lower than normal
lid behaviours that minimize the wearer’s
discomfort, e.g. looking down while wearing rigid
position lenses, and infrequent blinking, to reduce the lid-
• Upper lid is more swollen and often redder lens interaction. The eyelids of rigid lens wearers
tend to appear more swollen than those of non-
• Reversible (dependent on cause) wearers or SCL wearers. A comparison of lid
photographs of non-wearers, SCL wearers, and
97300-159S.PPT
rigid lens wearers usually results in reliable
7L397300-159 identification of the rigid lens users because of their
abnormal appearance and/or lid margin resting
position. What is less obvious is a mild to moderate
ptosis that can also develop while wearing rigid
lenses.
Rigid lens-induced ptosis in extended wear was first
reported by Fonn and Holden (1986). Others have
since presented similar findings, e.g. Fonn and
Holden (1988), Levy and Stamper (1992), van den
Bosch and Limij (1992), Jupiter and Karesh (1997),
Thean and McNab (2004).
While earlier reports of similar effects exist, they
referred to embedded lenses (e.g. Yassin et al.,
1971 and Sebag and Albert, 1982, both cited in
Fonn and Holden, 1986), CLPC (Sheldon et al.,
1979, cited in Fonn and Holden, 1986, and a
permanent ptosis (Epstein and Putterman, 1981
and Thean and McNab 2004) postulated by the
authors to be due to dehiscence (disinsertion) of the
aponeurosis of the levator from the tarsus caused
by excessive eyelid manipulation and rubbing
induced by rigid lens wear over many years.
The Fonn and Holden cases were different in that
they were all resolved by the cessation of rigid lens
wear. This finding has also been presented by
Fonn and Holden (1988), Levy and Stamper (1992),
and Jupiter and Karesh (1997).
The dehiscence was associated with long-term
wear of rigid lenses. The paper by van den Bosch
and Limij (1992) suggests that lens-induced ptosis
is more common that most practitioners realize.
149 Ptosis: Signs
Ptosis refers to an upper eyelid position that is
PTOSIS lower than normal, i.e. the resting position of the
SIGNS upper lid margin is lower than would be the case if
• Narrowed palpebral aperture no rigid lenses were worn. This lowered lid position
results in a narrowing of the Palpebral Aperture
• Unilateral or bilateral Size (PAS). The upper eyelid appears thickened or
‘puffier’ and is often redder (slide 150). Slides 151
• Often with accompanying and 152 show differences between the two
apertures and shows clearly the smaller PAS of the
thickening of the upper lid RGP lens-wearing eyes. The changes in PAS
induced by wearing (and subsequent removal) an
• Cosmetic problem
97300-65S.PPT RGP lens in one eye and an SCL in the other were
presented graphically by Fonn and Holden (1988,
7L397300-65 slide 153). Similar differences were shown by Fonn
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 Module 7: Contact Lens-Related Ocular Complications

150 et al. (1991) in a daily wear clinical trial using the

same protocol of subjects wearing a soft lens in one
eye and an RGP lens in the other. One would
expect that EW exacerbates the ptosis, and
perhaps hastens its onset.
The difference in PAS between rigid lens wearers
and non-wearers was 0.5 mm on average (van den
Bosch and Lemij, 1992). Fonn et al. (1995)
reported an identical result.
In a comprehensive study of wearers of rigid, soft,
and non-wearers, Fonn et al. (1996) found that rigid
lens wearers had significantly smaller PASs
compared with SCL wearers and non-wearers.
7L3046-99
The PASs were:
x RGP wearers: 9.76 r0.99 mm.
x SCL wearers: 10.24 r0.94 mm*.
151 x Non-wearers: 10.10 r1.11 mm*.
* No significant difference existed between SCL
wearers and non-wearers.

Thean and McNab (2004) reported on 15 wearers

of rigid lenses who exhibited non-senile
blepharoptosis. Four of the 15 were RGP lens
wearers, the remainder wore PMMA lenses.
Thirteen of the 15 cases had worn rigid lenses for
7L3UPAS-1
more than 17 years but all 15 were reported to have
normal levator palpebrae superioris function.
152 Interestingly, only four of the cases had bilateral
involvement. Eleven of the 15 cases underwent
ptosis repair successfully. Aponeurosis
thinning/dehiscence was noted during surgery.
Compared with all causes of blepharoptosis,
contact lens-related ptosis was uncommon across
all age groups.

7L3UPAS-2

153
PTOSIS
Larger Palpebral Aperture Size (PAS)
9

6
SCL
3 RGP
(% change)

-3
PAS

Lenses OFF

-6

-9

-12

-15
Smaller 0 5 10 13 15 20
Weeks
(from Fonn & Holden, 1988) 97300-160S.PPT

7L397300-160

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154 Ptosis: Symptoms

In many cases, the onset of ptosis occurs
PTOSIS asymptomatically (see van den Bosch and Lemij,
SYMPTOMS
1992). Generally, a lens-induced ptosis is more
• None likely to be found in long-term wearers of RGP
lenses. A slow onset may mean that a ptosis
• Lens awareness passes unnoticed for long periods of time unless it
develops unilaterally. Because the lids are likely to
• Reduced superior visual field be affected similarly, and the onset is usually
subtle, most wearers are unlikely to notice the early
- only if severe (lowered lid position) stages of any lid changes.
In other cases, the wearer may complain of
97300-66S.PPT

increased lens awareness, or general lid awareness

7L397300-66 due to the altered lens-lid interaction. Alternatively,
the wearer may complain of swollen and/or reddish
upper eyelids.
Unilateral ptosis of moderate degree is usually of
cosmetic concern to the patient.
155 Ptosis: Aetiology
PTOSIS RGP lens-induced ptosis is principally caused by
AETIOLOGY mechanical effects associated with blinking. In
• Mechanical interaction long-term wearers the upper lid appears thickened
- lid riding over the lens edge and oedematous.
• Oedema of the lid tissue Fonn and Holden (1986), and Levy and Stamper
- gravity (1992), postulated that the ptosis was caused by lid
• Inflammation oedema from mechanical irritation of the lids by the
• Lid traction during lens removal lens edge.
• Lid hypertrophy Van den Bosch and Limij (1992) and Thean and
• Nerve dysfunction McNab (2004) attributed some of their cases of
• Dehiscence (unlikely) ptosis to the rigid lens removal technique in which
97300-67S.PPT

the eyelids are pulled laterally. However, Van den

7L397300-67
Bosch and Limij were unable to explain disinsertion
of the aponeurosis of the levator palpebrae
156 superioris (slide 156) from such a lid manipulation.
Instead they postulated that the removal method
RGP PTOSIS: UPPER LID may lead to a thinning of the levator or its
Superior orbital septum
disinsertion because of the powerful blink that
Orbicularis Oculi muscle Orbital fat
accompanies this removal technique. The
Orbital portion Levator Palpebrae Superioris
(LPS)
antagonistic action of the orbicularis and the levator
Superior palpebral muscle may increase traction on the levator eventually
Superior fornix
leading to its disinsertion. A suction cup was
Fibres of the
aponeurosis of the LPS
Tarsal plate
suggested as the preferred removal method.
However, two of their subjects did use suction
holders yet still developed ptosis (this observation
Meibomian gland has also been confirmed by Lindsay, 2003, in a
Orbicularis Oculi muscle
Palpebral portion
97300-185S.PPT
private communication). This suggests that other
mechanisms may also be involved. Another
7L397300-185 contributing factor they presented was the weight of
the oedematous lid(s). In the short term, any
changes may be reversible, e.g. the short-term
Fonn and Holden studies (Fonn and Holden, 1988,
Fonn et al., 1991) whereas in the long term, the
ptosis and changes may not be reversible.
Lid hypertrophy may also be an outcome of chronic
irritation and oedema.
A ptosis may also be caused by nerve fibre
dysfunction that is unrelated to contact lens wear.
This is an important differential diagnosis that
needs to be made by the practitioner.

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157 Ptosis: Management

PTOSIS The extreme approach to managing lens-induced
MANAGEMENT ptosis is to cease lens wear altogether, or refit with
• Temporary discontinuation of lens wear SCLs. However, even with this extreme approach,
• Refit with SCLs
the condition may take months to resolve (Fonn &
Holden, 1986, Fonn and Holden, 1988, Jupiter and
• Preventative Karesh, 1997).
- optimize lens edge shape In the case reported by Levy and Stamper (1992),
- reduce lens thickness the PAS had increased from 8 mm to 9 - 10 mm
four weeks after lens wear ceased. By 12 weeks
- regular after-care the difference in PAS between eyes was almost nil.
• Rule out other causes The lid oedema noted in their case took some eight
97300-68S.PPT

weeks to resolve.
7L397300-68
An optimal RGP lens edge shape, and minimum
lens thickness reduce the degree of lid-lens
interaction resulting in greater wearer comfort. In
the long-term, should lens wear be pursued, it is
essential that steps be taken to lessen the
mechanical impact of the lens on the lids.
Other potential causes of ptosis must be ruled out if
the condition is to be managed successfully.
A point made in the literature is the need to cease
lens wear to ascertain whether or not the condition
will resolve without other interventions. This is
necessary to exclude the possibility of an
unnecessary investigation of the condition or even
cosmetic surgery to correct it.
Van den Bosch and Limij’s (1992) suggestion of a
suction holder reduces any form of lid manipulation
to a minimum. However, many would argue that
suction holder use should not be encouraged
because of the potential for accidentally ‘attaching’
a suction holder to the cornea should a lens be
missing, e.g. when a lens has been lost from the
eye and the wearer in unaware of their loss.
Furthermore, wearers should be encouraged to be
independent of such aids to lens removal because
at some point in time they may need to remove a
lens urgently and find that a suction holder is not
available.
IV.E Discomfort
158 Discomfort: Introduction
DISCOMFORT Comfort is one of the issues central to the
INTRODUCTION acceptance of a lens type (rigid versus soft) or lens
• Probably the most common contact design (thick/thin, aspheric/blended spherical curve,
lens-induced condition small/large edge lift, etc.).
• Influencing factors are almost too Hydrogel lenses are initially more comfortable than
numerous to cover comprehensively RGPs, even when RGP surface wettability is
• May be accompanied by redness & insignificantly different (Hatfield et al., 1993). This
corneal staining
is due largely to the interaction between the lens
• May not always be contact lens-related and the eyelids. Common wisdom has it that the
• Wearer descriptions vary widely initial discomfort of rigid lenses is their greatest
• Descriptions can mislead barrier to wider acceptance. However, the possible
causes of discomfort with RGP lenses generally are
97300-161S.PPT

7L397300-161 almost too numerous to cover comprehensively.

Cornish and Sulaiman (1996) state that 30% of
prospective RGP wearers fail to adapt to RGP
lenses because of issues with their initial comfort.
Holden (1990) presented data suggesting that 18%

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

of RGP lens EW dropouts were due to discomfort

(cf. only 5% in SCL EW). However, Fonn and
Holden (1988) reported only two out of 40 subjects
dropped out of an eight to 13 week SCL and RGP
EW study (one lens type in each eye concurrently)
because of discomfort.
In a comparison study by Pole and Lowther (1987),
patient preference for a particular lens material, or
lens series (lenses made as alike as possible but
more than one laboratory supplied lenses for the
study), was usually based on comfort.
Citing a practitioner survey, Shulman and Zagar
(1981) stated that a successfully designed contact
lens was one that was comfortable to the wearer.
In a large (n=3,517) 1999 survey of Japanese
contact lens wearers (most of whom were rigid gas
permeable lens wearers) by the Japan
Ophthalmologist Association, 36.8% of wearers
reported discomfort (cf. 51% who reported
bloodshot eyes, 49.3% pain, 15.1% lens-induced
tears) (Schreiber, 2001).
159 Discomfort: Signs
DISCOMFORT Irritation associated with RGP lenses generally
SIGNS produces an increase in ocular redness. This
• Increased bulbar and/or redness may involve both the bulbar and palpebral
palpebral conjunctival redness conjunctival vasculature.
• Narrowed palpebral aperture Lens discomfort often results in the wearer reducing
- minimizes lid-lens interaction both the quantity and quality of blinking. This
• Incomplete blinking minimizes the interaction between the upper lid and
the lens edge that is often the cause of RGP lens-
• Epithelial damage/staining
induced discomfort.
- corneal
Lens-induced ocular surface damage produces not
- conjunctival only discomfort but also redness and epithelial
97300-69S.PPT

staining. The latter can be detected by the

7L397300-69
application of sodium fluorescein and has already
been covered earlier in Section I.F Corneal
160 Staining.
The lenses themselves should also be examined
DISCOMFORT carefully both in situ and in vitro, paying attention to
LENS SIGNS the condition of their surfaces as well as their
• Poor surface wettability overall integrity. If discomfort is experienced with a
lens that was once comfortable, it is probable that
• Surface deposits some aspect of the lens has changed, e.g.
deposits, altered wettability, or the lens has
• n lens mobility sustained damage probably during handling or lens
care.
• Manufacturing defect

• Damage
97300-162S.PPT

7L397300-162

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161 Discomfort: Symptoms

DISCOMFORT When assessing the level of comfort with an RGP
SYMPTOMS lens it is important to distinguish between any
sensation experienced immediately upon lens
• Upon lens insertion or delayed insertion and that which might be experienced
• Edge awareness some time into a wearing period.
- upper lid (almost constant?) Awareness of the lens during blinking is the most
common symptom and this is usually associated
- on blinking
with the edge shape, and/or thickness of the lens.
• Foreign body sensation A foreign body sensation can occur at any time
• Dryness during wear and is a relatively common symptom.
97300-70S.PPT Lens surface dryness or poor wettability is often
related to ocular discomfort and may be the cause
7L397300-70
of upper lid irritation or epithelial staining. Lack of a
continuous tear film constitutes a loss of lubricity
that can result in uncomfortable traverses of the
lens by the lids. This can be expected to result in
palpebral conjunctival irritation, conjunctival
hypertrophy, and possible conjunctival epithelial
staining.
Menstrual cycle phases can also influence contact
lens comfort. Symptoms reported include dry eyes,
blurred vision, and other forms of discomfort
(Serrander and Peek, 1993). Menopausal women
may experience dryness, tearing, decreased visual
acuity, red and swollen lids, foreign body
sensations, and visual coordination problems
(Metka et al., 1991, cited in Serrander and Peek,
1993).
Dry eye is treated in detail as a separate subject in
Lecture 7.4 in this module.
162 Discomfort: Aetiology
DISCOMFORT Many different factors cause the discomfort that
AETIOLOGY may be associated with RGP lens wear.
• Edge profile
Some causal categories include:
x Lens:
- blunt
– condition (edge defects, warpage)
- sharp – thickness
- poorly rounded front surface – edge design
• Inadequate blending – fit (excessive edge clearance, lens too flat,
too steep)
• Lens surface defect
97300-71S.PPT
– surface condition (poor polish, deposits)
– errors of insertion or removal.
7L397300-71
x Airborne contaminants (includes ‘sick’ building
163
syndrome, Nilsson and Andersson, 1986,
DISCOMFORT Backman and Haghighat, 1999)
AETIOLOGY
– gaseous
• Excessive movement
– particulate (foreign body), or aerosol
• Trapped foreign body
– liquid
• Tight lens fitting
– microbiological.
• Ocular dryness
x Hand-borne contaminants
- associated staining
– particulate (foreign body)
• Lens surface deposits
– liquid
- especially back surface
– microbiological.
x Lens care products
97300-72S.PPT

7L397300-72 – inappropriate

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164 – contaminated
– sensitizing
DISCOMFORT
AETIOLOGY – incompletely rinsed/removed.
• Care and maintenance products x Endogenous
- sensitivity – pregnancy
- incorrect use
– menstrual cycle
- incomplete removal (rinsing)
• Environmental – hormonal imbalance
- wind, dust, etc – illness
• Binocular vision anomaly – systemic disease
- asthenopia – acquired disease
• Photophobia
97300-73S.PPT
– failure of psychological adaptation.
7L397300-73 x Dry eye issues (see Lecture 7.4)
– true dry eye
– marginally dry eye
– low relative humidity (RH)
– dry eye secondary to a transient condition.
Of the possibilities presented above the most
common factors are probably:
x Lens manufacturing defects.
x Fitting characteristics.
x Trapped foreign bodies.
x Lens deposits, and/or poor wettability
x Epithelial staining (multiple causes).
Environmental air pollution including the so-called
‘sick building syndrome’ can be a source of chronic
discomfort and eye irritation (Klopfer, 1989). A
useful patient-history question to come out of her
paper was whether air conditioning lessens the
symptoms. This is because air conditioners filter
the air they treat, and reduce the relative humidity.
The former may ‘improve’ the quality of the air in
the environment while the latter may exacerbate the
sensations of dryness and evaporative tear film
issues.
165
In a 12-subject (all adapted wearers) study of the
DISCOMFORT effects of alterations to the BOZR and TD of rigid
AETIOLOGY: LENS FACTORS lenses, Williams-Lyn et al. (1993) found that larger
Factors tending to give greater comfort include: diameter lenses were more comfortable (i.e. 10.0
• Larger TDs (d 10 mm) versus 9.5 or 9.0 mm) and the steeper fitting (0.2
• Optimal or slightly flatter fits
mm steeper than optimal) was less comfortable
than the optimally or flatter (optimal + 0.2 mm)
• Aspheric back surface designs
fitting lenses. This finding had been reported
• Narrow peripheral curves & smaller axial edge lifts
previously (Fonn and Gauthier, 1990). Custom
• Well-rounded anterior edges designing of larger RGP lenses has been detailed
• Interpalpebral fits (as opposed to lid-attachment) by Hazlett (1997).
97300-199S.PPT These findings of larger lenses being more
comfortable are the opposite of those reported by
7L397300-199 Sarver (1966). However, Sarver’s use of PMMA
lenses probably meant that discomfort was at least
partially attributable to poor physiology rather than
‘physical’ factors (after Williams-Lyn et al., 1993).
Although Williams-Lyn et al. felt that the flatter lens
tended to exhibit upper lid-attachment behaviour,
and that this might explain their greater comfort, not
all are agreed that upper lid attachment results in
greater comfort. For example, Sorbara et al.
(1996A) designed a series of lenses specifically for
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upper lid attachment to be used in a comparison

study with centred, interpalpebral lenses (Sorbara
et al., 1996B). They found that upper lid-
attachment lenses produced more incidents of
discomfort, as well as more incidents of corneal
topography changes and ‘mechanical’ staining.
Pritchard et al. (1999) surveyed a large number of
contact lens wearers to ascertain the number of
dropouts (temporary or permanent) and the reasons
for such occurrences. Of the discontinuation cases,
almost half had been refitted at least once, primarily
for reasons of discomfort. Discomfort also headed
the reasons for abandonment of lens wear followed
by ‘dryness’ and ‘red’ eyes.
To ascertain the effect of lens design on comfort,
Andrasko (1989) used lenses with either a
biaspheric design, or four different spherical
designs, all manufactured in the same material.
Generally, there was a significant preference for the
aspheric design especially initially, i.e. initial comfort
was better with the aspheric design. However, the
data was not overly convincing because one of the
three spherical designs, the one with low edge lift,
was preferred to the aspheric design. In a report of
a round-table conference of practitioners
(Anonymous, 1990), a particular aspheric design
was generally reported to be more comfortable than
alternative RGP designs and almost as comfortable
as some toric SCLs (i.e. a more liberal ‘standard’ of
SCL comfort).
In a sequel to the Andrasko (1989) paper, Picciano
and Andrasko (1989) investigated other factors
influencing comfort. They concluded:
x Tricurve lenses with narrow peripheral curves
are more comfortable than either bicurve or
tricurve lenses with wide peripheral curves.
x Lenses with large axial edge lifts are less
comfortable than those with normal or small
edge lifts. This is the opposite of what had
already been shown by Bennett (1986).
x Blended curve lenses were slightly more
comfortable than those that were unblended.
The authors also concluded that while low edge lift
designs may be more comfortable, at least in the
short term, there was some evidence that they also
were likely to adhere more and produce more
peripheral corneal staining.
Poorly manufactured RGP lenses can also cause
significant discomfort during wear. The most
common cause of irritation on blinking is inadequate
rounding of the anterior aspect of the lens edge.
Edge design issues are detailed in Lecture 2.5, and
in La Hood (1988).
The role of lens material, if any, remains unclear.
Collins et al. (1984) compared the comfort of PMMA
and various rigid gas permeable materials. PMMA
was found to be the most comfortable (or the least
uncomfortable) and the authors attributed this to the
material’s ability to deliver a superior surface finish.
In retrospect, it is probable that the reason was
260 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

actually the depressed corneal sensitivity resulting

from the poor physiological performance of PMMA
lenses. Andrasko (1988) compared the comfort of
siloxane acrylate (SA) and fluoro-siloxane acrylate
(FSA) RGP lenses and found that the majority of
wearers preferred the FSA lenses. This outcome
was attributed to less than optimal surface
wettability and surface deposits of SA lenses.
In female wearers, the influence of the menstrual
cycle and pregnancy is a consideration. During the
normal menstrual cycle, corneal sensitivity may
decrease (premenstrual and ovulatory phases) but
ultimately sensitivity returns. The comparison
allowed by this shift means that lenses that were
comfortable can become a source of discomfort
subsequently. During pregnancy, any change in
lens tolerance may be due to alterations in the tear
film or its properties (most of this section after
Guttridge, 1994). In a study of the effects of oral
contraceptives and the menstrual cycle on tear film
physiology, Tomlinson et al. (2001) found no
significant effects.
Upon entering an RGP lens-wearing eye, airborne
pollutants can behave as a foreign body and, once
under the lens, can lead to epithelial damage.
Turner et al. (1993) studied patient compliance
issues and reported that non-compliance posed a
significant risk to both safety and comfort. Factors
that posed risks to comfort were less likely to
induce non-compliance than were safety-related
issues (34% versus 91% of patients).
166 Discomfort: Management
DISCOMFORT Managing comfort issues requires the cause be
MANAGEMENT ascertained first. This can only be done by a careful
evaluation of the symptoms and signs by the
• Determine cause
practitioner to determine the underlying problem.
- dictates management Once the cause is found, suitable steps can be
• Optimize fitting characteristics taken to eliminate, or at least reduce significantly,
the resulting discomfort.
• Change environment
Should the apparent cause be more general, e.g.
• Use different lens care products the lens type (an RGP lens?), little can be done to
eliminate the mild initial discomfort inherent in the
• Replace lens
use of such lenses except for the use of a local
97300-74S.PPT

anaesthetic at trial fitting as suggested by Kenitz

7L397300-74 (1992), Bennett and Schnider (1993), and Bennett
et al. (1998). While steps can be taken to optimize
167 the comfort of RGP lenses, the elimination of such
discomfort is probably impossible. A realistic
DISCOMFORT
MANAGEMENT: LENS FACTORS
approach is recommended (Bennett and Schnider,
• Modify lens edge profile 1993).
- round & polish anterior edge It is common for two or more factors to play a role in
- centre apex lens-related discomfort. Some of the factors
- polish posterior edge uncovered may be inter-related or mutually
• Minimize axial edge lift exclusive, i.e. the solving of one problem may mean
• Use a larger TD (within reason, e.g. d 10 mm) that another problem cannot be resolved completely
• Minimize front surface junction angles or at all. For example, a simple lens design such as
• Thin the lens (however, too thin may p comfort) a tricurve, executed as a potentially more
• Polish lens surface comfortable larger lens (larger TD), means
97300-200S.PPT
relatively large peripheral curve widths that may
7L397300-200 actually reduce comfort (see slide 165). In such

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 Module 7: Contact Lens-Related Ocular Complications

cases, a balance between the two factors may need

to be sought.
Rakow (1989) and Ames and Erickson (1987)
suggested that a lid-attachment, slightly flatter than
‘K’ (+0.1mm), fitting philosophy provided the best
comfort in both blended spherical and aspheric
RGP lenses. However, Sorbara et al. (1996B)
found lid attachment decreased wearing comfort.
Hazlett (1997) suggested the use of large-diameter
(9.5 mm and larger [Ames and Erickson used
lenses with a TD of 9.6 mm]), custom-designed
lenses for cases of RGP lens-induced discomfort.
The design of the lens edge has often been raised
as a key issue in RGP lens comfort (Shulman and
Zagar, 1981, La Hood, 1988, Andrasko, 1991,
Bennett and Schnider, 1993). Suggestions relevant
to the edge include:
x Rounding the anterior lens edge.
x Centring the apex of the edge.
x Minimizing the axial edge lift.
x Posterior edge shape has little effect.
x Edge thickness (within reason) has little effect.
It has also been suggested that minimizing front
surface junction angles may also improve lens
comfort (Shiobara and Holden, 1989).
Other fitting characteristics are also important,
especially lens centration and movement. A
decentred lens is not usually a comfortable lens.
This is especially true if the lens decentres
inferiorly, because of the abnormal edge clearance
this induces superiorly. While edge clearance
should not be excessive or non-uniform, minimal
edge clearance is also undesirable as it can lead to
inadequate tear exchange, redness, and dryness
(Bennett and Schnider, 1993).
Making a lens thinner does not increase lens
comfort and making a lens very thin may actually
decrease comfort (Cornish and Sulaiman, 1996).
However, Holden (1990) claimed that less rigid (or
more flexible) RGP materials improved wearer
comfort significantly (the optical effects of this lens
flexure is covered later in this lecture).
It is possible to consider a solution-based approach
to comfort improvement using lens care products
that form a stable coating on the lens (Raheja and
Ellis, 1995). However, the ‘stay time’ of such
coatings is usually finite. The main benefit relates
to improved comfort upon insertion, arguably almost
as important as lens comfort towards the end of the
wearing period. Seidner and Sharp (1984) advised
the use of effective cleaners on RGP lenses if long-
term success is to be achieved. This was because
they found problems attributed to ‘poor wetting’
were often actually cases of ‘dirty lenses’. Nolan
and Nolan (1985) recommended the use of a
contact lens polish for 30 sec or more, with or
without a facial tissue applicator (which was found
to enhance the ‘abrasiveness’), on siloxane acrylate
lenses.

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Should non-compliance be detected, patient re-

education on matters of lens wear and lens care is
required.
If menopause is implicated in RGP lens discomfort,
oestrogen replacement therapy may mitigate the
symptoms (Metka et al., 1991, cited in Serrander
and Peek, 1993).
If wearer comfort decreases in the longer term
(months), regular replacement of the lenses may be
an option. Although Woods and Efron (1996)
recommended 6-monthly RGP lens replacement for
lens worn on a daily wear basis, they found no
significant difference between replaced and
unreplaced lenses (3-monthly replacement) with
respect to comfort. However, they did find
differences in surface drying, mucous coating, lens
deposits, surface scratching, and corneal staining,
all of which may ultimately affect comfort.
A difficulty arises when the air quality in the
patient’s workplace is suspected of being the cause
of, or at least a contributing factor to, wearer
discomfort. In such cases the difficulty of
addressing the issue of air quality may be ‘bigger’
than the wearer’s problem.
More recently, a study of the efficacy of cyclosporin
A solutions (0.05% and 0.1%) on patients with
moderate to severe dry eye (Sall et al., 2000) found
it to be efficacious in the treatment of dry eye.
If addressing the probable, or even the possible,
causes of contact lens-related discomfort fails to
disclose the source of the problem, attention needs
to be redirected towards non-lens causes. It is
probably prudent to keep this possibility in mind
from the outset, even while lens-related causes are
being explored.

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V Vision Complications
168 Vision Complications: Introduction
VISION COMPLICATIONS Because vision correction is the most common role
INTRODUCTION for contact lenses, any deviations from the normal
• Answers sought when vision is: or expected vision with contact lenses usually
- below normal results in the wearer seeking answers from their
- less than expected practitioner as to why.
• Intermittent disturbances can be common Because vision problems discourage contact lens
• Causes may be related to: wear, attention to visual performance with contact
- lens lenses is important (after Lowther, 1986).
- cornea Reductions, or perturbations, of vision are usually
- tear film the result of shortcomings of lens design, material
97300-163S.PPT
selection, tear film and/or lens wettability issues, or
disturbances of the cornea. These are the issues
7L397300-163
addressed here. Issues such as poor fit and
incorrect Rx are not ‘complications’ per se and are
presented elsewhere in this course, e.g. Lectures
2.3, 3.4.1, 3.4.2
Although some comparison studies of visual acuity
(VA) with spectacles, RGP contact lenses, and soft
contact lenses have shown slight reductions in VA
with CLs, the reduction is usually least with RGP
lenses (e.g. Wechsler, 1978, Iwasaki et al., 1986,
Sheedy et al., 1992). However, results of
Modulation Transfer Function (MTF) testing of all
types of spectacle and contact lenses by Grey and
Sheridan (1988) suggest that the optical
performance of the lenses per se is an unlikely
source of reduced vision in contact lens wearers.
169 Vision Complications: Signs
VISION COMPLICATIONS
Vision-Related Problems
SIGNS: GENERAL x Can be associated with a number of signs,
• Reduced acuity most of which depend on the cause.
- high contrast (?) x Are not necessarily revealed by a high-contrast
- low contrast (more telling) Snellen acuity chart (Wechsler, 1978, Lowther
1986, Guillon and Sayer, 1988). However,
• Narrowed PAS (squinting)
such an assertion is more applicable to SCLs
- stenopaeic-slit effect than RGP lenses.
• Frowning and other obvious x Revealed by low-contrast charts (letter, sine-
signs of vision-induced stress
wave, or other) are usually indicative of ‘real’
97300-75S.PPT visual performance, and often support patient
7L397300-75
complaints of ‘unsatisfactory vision’ despite
good high-contrast chart acuity being recorded.
If a low-contrast chart reveals a vision deficit,
170 other clinical signs should be sought.
VISION COMPLICATIONS x May induce the wearer to narrow their
Flare: SIGNS: LENS-RELATED palpebral aperture size (PAS) to produce a
• Poor lens centration stenopaeic-slit effect (thereby increasing the
• Small: TD, BOZD, FOZD eye’s depth of focus) to improve their vision.
Poor wettability (lens front surface)
Such a sign may be apparent immediately
upon the wearer’s arrival at a practice.
• Rapid drying/thinning of the tear film
- BUT < 5 sec
Poor Lens Wettability
- @ any position on the surface or .... x A slit-lamp examination of the front surface of
- repeatable locations the lens should disclose the wetting properties
of its front surface. Direct and specular
• Aqueous fringes (thin-film interference)
97300-80S.PPT reflection illumination may prove useful.
7L397300-80
Ideally, the lens should support a stable and
regular tear film that promotes both visual

264 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

171 performance and wearer comfort (see Rankin

and Trager, 1970 for an explanation of surface
wetting).
x Typically, poorly wetting lenses have a rapid
tear drying time following each blink (slides 171
and 172). Either a non-wetting, rapidly-
appearing haze enveloping the lens surface, or
tiny hydrophobic spots that can not sustain a
complete tear film even during a normal blink,
may be seen.
– Walker (1990) described a case of CLPC
that developed as a direct result of the
failure of the surface to wet because of
7L3894-92 overpolishing during lens manufacture
172 – if a dry eye, marginally dry eye, or other
tear film condition exists for whatever
reason, poor lens wettability may also be
observed. This topic is presented in detail
in Lecture 7.4 of this module.
Lens Surface Crazing
Lens surface crazing (also known as lens surface
cracking) affected a few RGP materials in the late
1980s and early 1990s. Most were siloxane
acrylates (SA), few were FSA. It occurs very rarely
in modern materials.
x The appearance is very distinctive (slides 174
and 175 [a more extreme example]) and
7L31783-93 include multiple cracks or a mesh-like lattice of
fissures (Walker, 1990) with ‘frosting’ of the
‘islands’ between fissures (secondary
173 deposits?).
VISION COMPLICATIONS x Lens fracture, or disintegration into component
SIGNS: LENS-RELATED pieces, has been reported (Sandy, 1987, Polk,
Surface Crazing: 1987).
• Uncommon with modern materials x Walker (1990) described rapidly-forming, small
menisci around the fissures after each blink.
• Surface deterioration over time
x Fissure widths range from 1 to 8 µm (Grohe et
- multiple cracks al. 1987B, Lembach et al., 1988) with those in
FSAs being narrower (1 µm according to
- frosting of the islands between cracks
Caroline, 1988, cited in Walker, 1990).
- surface subject to secondary deposits x Depths range from 10 to 15 µm (Grohe et al.
97300-105S.PPT
1987B).
7L397300-105 x The anterior central zone of the lens is affected
174 at first but ultimately, the whole lens surface is
involved (Grohe et al., 1987).
x The onset of crazing can range from 3 to 24
months (Grohe et al., 1987, Seidner, 1987,
Seidner, 1987B, Bingham in McGeehon, 1987,
Sandy, 1987, Sanford, 1987, Silk, 1987, Polk,
1987, Lembach et al., 1988, McGeehon,1987,
Phillips and Gascoigne, 1988, Walker, 1990).
x Sanford (1987) suggested the worst affected
material (pasifocon B) had a 15% problem rate
although only a little later, the manufacturer’s
data suggested a figure of less than 1%
(Ratkowski, 1987, Walker, 1990).
7L30500-99
x Theoretically, even modern materials cannot
be guaranteed immunity since many of the
possible causes are ever-present and/or
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 Module 7: Contact Lens-Related Ocular Complications

175 inherent in all aspects of the RGP lens supply

and use chain.
x In an unusual case, Miller (1995) reported the
occurrence of vascularized limbal keratitis
secondary to RGP (SA) lens crazing.

Cornea-Related: Spectacle Blur

x Reduced spectacle vision immediately
following removal of RGP lenses.
– ‘normal’ vision cannot be restored by altering
the spectacle Rx.
x This vision reduction is most notable
7L3051-99
immediately after lens removal. Over time
(hours), or following a period of sleep, the
vision may improve to a near ‘normal’ level.
176 x In PMMA lens wearers, Rengstorff (1966)
VISION COMPLICATIONS found that when lens wear was terminated
SIGNS: SPECTACLE BLUR suddenly, fewer than 50% obtained 6/6 vision
• Reduced vision with spectacles immediately after, or on the first day of, wear
cessation.
- follows RGP lens removal
– almost 10% of the wearers had worse
- may improve over time (hours) correctable vision at the end of the first week
- or after a period of sleep
than was attainable on the first day of
cessation.
• Change of spectacle Rx ineffective x Polse et al. (1987) found that RGP lens
- not refractive wearers had spectacle acuity decreased about
97300-84S.PPT ‘half a Snellen line’ compared with SCL
7L397300-84
wearers.
x If the vision loss is unilateral, binocular vision
may be affected adversely.
177 Corneal warpage and related issues are explored in
VISION COMPLICATIONS more detail in Section III of this lecture.
SIGNS: DIMPLE VEILING
• Gas bubbles trapped in post-lens tear film Post-Lens Tear Film-Related: Dimple Veiling
- bubbles act more like solids than gases x Has a very distinctive and characteristic
• Small, hemispherical pits in the epithelium
appearance (slides 178 and 179).
x Disclosure is effective with either direct or
• Pool with fluorescein after lens removal retro-illumination techniques (both can be seen
• Irregular topography decreases vision in slide 178 [white light]) following the
instillation of sodium fluorescein.
• Takes time to disappear
97300-88S.PPT
x Numerous gas bubbles are obvious in all but
the most subtle cases (slide 178 shows a case
7L397300-88
photographed using sodium fluorescein under
178 cobalt blue light while slide 180 shows a more
subtle case resulting from the nitrogen
propellant of an aerosol saline coming out of
solution, once under the lens [photograph
taken with the lens off]).
x Small, hemispherical pits form in the
epithelium, resulting in an irregular corneal
surface. With the lens removed, the pooling of
sodium fluorescein in these pits presents a
startling, but characteristic, appearance.
x The dimpling reduces the cornea’s optical
efficacy and reduced vision results. Extreme
cases can result in a serious reduction of
7L3530-98 vision.
x Usually, only seen in cases of excessive
266 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

179 corneal clearance. An optic section of the lens

and cornea in the region of bubbles will usually
disclose this fact. It is more likely to be seen
under the edge of an RGP lens if the cornea is
significantly toric and the BOZR is spherical.
Central bubbling is unlikely in a well fitted lens.
x Bubbles trapped under lenses at lens insertion
are usually few in number, and tend to be
large. Usually, these diminish or disappear
over time because they are not sustained by
conditions under a well-fitting lens.

7L3HARE96

180

7L3LAU99

181 Vision Complications: Symptoms

General
VISION COMPLICATIONS
SYMPTOMS: GENERAL
Typical symptoms relating to vision problems
include:
• Blurred vision x Blur.
- distance, near, all distances x Hazy, cloudy, misty, foggy vision.
• Ocular discomfort x Haloes.
- asthenopia x Flare from light sources.
• Flare and/or glare x Glare.
• What did onset correlate with?
The patient may experience some ocular or visual
discomfort related to reduced vision. This may be
associated with long periods of concentrated vision
97300-76S.PPT

7L397300-76 such as when reading or using a computer.

Methods of assessing visual acuity (VA) include:
x Snellen-type letter charts
– high contrast
– low contrast.
x Sine-wave gratings
– high contrast
– low contrast.
x Screen-based letter or sine wave charts.
x Contrast sensitivity tests (slide 183).
x Measurement of border contrast enhancement.
(Guillon and Sayer, 1988)
x Any of the above with a glare test added (glare

IACLE Contact Lens Course Module 7: First Edition 267

 Module 7: Contact Lens-Related Ocular Complications

182 source introduced into the field of view

concurrently). Carney and Jacobs (1984)

D F
suggested the incorporation of a glare source,
whereas Ruben (1979) nominated the Miller
Glare Test.
Luminance per se is also a factor to be considered

EF DE when assessing vision with contact lenses. Millodot

(1969) showed that, compared with spectacles, the
deterioration of vision with decreasing luminance
PRU ZUR with contact lenses is greater. The effect he found
was more marked at low luminances and was due
ZHUV PVNF largely to spherical aberration. The British
Standard (1968) for externally illuminated Snellen-
ENDFUZE DNEZFU
type acuity charts suggests illuminances of 480 –
PRUDENVHZF VZFHENUDRP 600 lux, with only small differences between chart
and room light levels.
7L3HILOVACHART
Lens-Related: Flare
x Lens-induced flare cannot be observed by a
183 practitioner because it is a subjective
phenomenon.
CONTRAST SENSITIVITY: TESTING
Square Wave
x Cause is difficult to assess because
Sine Wave conventional examination techniques involve
the use of local illumination that usually masks
Sine Wave
the most common causes (see later). If lens
Low
decentration is seen, this should be noted as it
ohzawa-lab/izumi/CSF/A_JG_RobsonCSFchart.html
http://www.bpe.es.osaka-u.ac.jp/

too may be partially, or wholly, responsible for

Dr Izumi Ohzawa. URL:
Used with permission of:
CONTRAST

the flare reported.

Symptoms reported may include:
High x Disturbing reflections.
Low High
SPATIAL FREQUENCY [cycles per degree]
97300-190S.PPT x Glare.
x Double (or even multiple) images.
7L397300-190
x Unstable vision.
x Radiating ‘shafts’ of refracted light emanating
184 from bright light sources.
VISION COMPLICATIONS x Haloes or coloured haloes
SYMPTOMS: LENS-RELATED – single
Flare: – herringbone and figure-8
• Distracting reflections, glare – possibly compounded with other flare types.
• Perceived by the wearer (very subjective)
• Variable vision Lens-Related: Poor Lens Wettability
Poor wettability:
An unstable tear layer on a lens front surface can
• Reduced vision disrupt the optical performance and result in
- variable & unstable compromised vision. The wearer may complain
- progressive deterioration over time that their vision is clear immediately after a blink
97300-81S.PPT
and deteriorates very quickly subsequently. This
corresponds to the rapid thinning and, ultimately,
7L397300-81
the absence of the pre-lens tear layer.
A lens that wets very poorly, may show immediate
tear break-up. In such cases, the vision is severely
reduced, as is wearer comfort.

Lens-Related: Lens Surface Crazing

Mild crazing of the lens is usually asymptomatic
(Kastl, 1990, Walker, 1990). In cases where the
crazing is extensive and central, it is probable that
the wearer will notice a reduction in vision quality.
Due to surface roughness, and possibly reduced
wettability (reduced lubricity), wearer comfort may
268 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

185 also decrease (after Walker, 1990), or a vague

awareness of the lenses may develop (Grohe et al.,
VISION COMPLICATIONS 1987). The wearer will also complain of an inability
SYMPTOMS: LENS-RELATED to clean their lenses satisfactorily in the mistaken
belief that what they see is a lens coating and not
Surface Crazing:
the lens surface defect (cracking) that it really is.
• Generally asymptomatic
Cornea-Related: Spectacle Blur
• Affects vision if severe Typically, the wearer reports that their vision with
the contact lenses was relatively good before lens
removal, and that blurred vision is experienced with
• May also affect comfort if severe
spectacles worn after contact lens removal.
97300-106S.PPT
However, variable vision throughout the spectacle
wearing period is also often experienced.
7L397300-106
Rengstorff (1966) found poor subjective responses,
an inability to detect relatively large dioptric
186 changes (of sphere and cylinder), and difficulty with
subjective refraction end points.
VISION COMPLICATIONS
SYMPTOMS: SPECTACLE BLUR
Post-Lens Tear Film-Related: Dimple Veiling
Following lens removal On most occasions there are no symptoms
associated with the dimple veiling that occurs
• Blurred vision with spectacles but... during RGP lens wear. If the dimples are located
centrally (within the entrance pupil zone), and are
- vision was good with CLs significant in number, vision may be affected.

- nothing improves spectacle vision

97300-85S.PPT

7L397300-85

187
VISION COMPLICATIONS
SYMPTOMS: DIMPLE VEILING
• Generally asymptomatic

• Decreased vision if bubbles are:

- central

- numerous

- large
97300-89S.PPT

7L397300-89

188 Vision Complications: Aetiology

VISION COMPLICATIONS General
AETIOLOGY: GENERAL Contact lens-induced poor visual performance can
• Numerous possibilities be the result of:
- requires a careful history x Refractive blur. When the VA with a lens is
below expectation it is important that a sphero-
- determine onset, duration cylindrical over-refraction be done. Often the
- detailed description reason for reduced VA is uncorrected ocular
- any other associated factors
astigmatism. This is sometimes a result of the
practitioner’s assumption that a spherical rigid
- miscellaneous observations lens virtually eliminates ocular astigmatism,
97300-77S.PPT
whereas in fact it only eliminates corneal
astigmatism (only 90% actually) (see Module
7L397300-77
2, Lecture 2.3, Section VII The Tear Lens).
IACLE Contact Lens Course Module 7: First Edition 269
 Module 7: Contact Lens-Related Ocular Complications

189 Astigmatism elsewhere in the eye may

become manifest after fitting with a spherical
VISION COMPLICATIONS
rigid lens. This refractive error component
AETIOLOGY: LENS-RELATED
may be the cause of the refractive blur, and
Lens fitting
may be apparent in the over-refraction.
• Inadequate pupil coverage x Diffusive blur.
• Inappropriate BS or FS design x Both refractive and diffusive blurs.
• Excessive movement These effects can not be differentiated by
• Excessive bearing or vaulting conventional, routine, VA measuring techniques
(Guillon and Sayer, 1988).
• Variable tear lens (due to movement
Both types of blur may be due to the contact lens,
& decentration)
97300-78S.PPT and/or the cornea affected by contact lens wear.
7L397300-78 High contrast (approx. 90%) VA charts are only
sensitive to refractive blur.
190 Diffusive blur-mediated losses can be estimated by
the use of low-contrast charts (10 and 20%) (Ho
VISION COMPLICATIONS and Bilton, 1986). Guillon and Sayer (1988)
AETIOLOGY: LENS-RELATED
Lens parameters: suggested the use of two illuminance levels; high
2 2
• Small BOZD/FOZD (>200 cd/m ), low (1-5 cd/m for distance, 50-75
2
• Small TD cd/m for near). They also suggest two contrast
Lens wettability: levels; 90% and 10%.
• Poor surface hydrophilicity
- a material property? Lens-Related: Flare
- a result of a manufacturing procedure? Although less common in the era of relatively large
• Deposit build-up (poor care and maintenance?) diameter lenses, flare associated with RGP contact
• Environmental influences
- low humidity lens wear is related typically to:
- high temperatures x A small back optic zone diameter (BOZD).
97300-82S.PPT

x Significant lens decentration.

7L397300-82
x Both a small BOZD and lens decentration.
x Larger pupil sizes (e.g. individual anatomical
variation, and/or lenses worn under low light
levels) increase the possibility that the
entrance pupil of the eye may exceed the
BOZD, or the FOZD, which ever is the smaller.
x Peripheral transition curves entering the optics
of the eye (by virtue of pupil size, and/or lens
decentration), degrade visual performance.
x The degree, and/or asymmetry of:
– the pupil size exceeding the lens optic
zone, and/or…..
– lens-decentration. In extreme
decentration, the significant flare reported
is due to the lens edge and its attendant
meniscus entering the eye’s ‘optics’.
x The possible confounding, or compounding,
effects of any residual refractive error.
x The time of day. Flare is usually only reported
at night and is most common when one or few
relatively bright, relatively small light sources
are in the wearer’s field of view.
x Of unknown significance is the finding (Fonn
and Holden, 1988) that nine of 29 subjects
wearing RGP lenses exhibited increased pupil
sizes transiently and inconsistently.
Other causes of flare include:
x A deficient pre-lens tear film.
x Poor lens wettability.
x Both tear film deficiency and poor lens
270 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

wettability. See under separate headings in

this section

Lens-Related: Poor Lens Wettability

x Relative to SCLs, RGP materials are less
hydrophilic.
x Tear break-up times (BUTs) are shorter.
– a BUT of 5 to 6 seconds is common with
most RGP materials.
x Excessive heat generated during lens
manufacture may reduce substantially the
wettability of the material (Walker, 1989).
x Formation of front surface deposits on the lens
may affect wettability adversely and reduce
visual performance. Both deposition and
surface wettability may be affected by the
methacrylic acid content (7-9%) of the higher
Dk materials, especially the siloxane acrylates
(Seidner, 1987).
x Environmental factors can reduce RGP lens
surface wettability. Heat, wind, and low
humidity enhance evaporation of the tear film
(especially the aqueous phase) from the lens.
191
VISION COMPLICATIONS Lens-Related: Lens Surface Crazing
AETIOLOGY: LENS-RELATED The exact cause of crazing of higher Dk RGP lens
Surface Crazing: materials remains unknown. Possibilities include:
x Flaws inherent in the manufacturing process.
• Material flaw
x Stresses introduced during the lens fabrication
(McLaughlin and Schoessler, 1987, Ratkowski,
• Lens manufacturing flaw
1987, Walker, 1990), e.g.:
• Interaction with lens care products – excessive localized heating during surfacing
– susceptibility of particular polymers to
• Individual anterior eye environments normal surface heating
– inadequate annealing of rod or button lens
97300-107S.PPT

7L397300-107 blanks.
x Stress relieving circumstances. Seidner noted
that RGP materials can contain more than 2%
water when hydrated fully, and hydration-
dehydration cycles may play a role. Supporting
this possibility is the observation that almost all
cracking/crazing is a front surface phenomenon,
i.e. the surface that experiences the full effect of
a hydration-dehydration cycle (Ratkowski,
1987). However, Grohe et al., (1987) reported
a case (mild) of back surface crazing. Other
factors may include:
– UV light
– lens flexure
– temperature variations (after Polk, 1987,
Seidner, 1987, Silk, 1987, Walker, 1990).
x Peculiarities of the anterior eye environment
unique to the wearer.
x The misuse of particular lens care products.
Lowther (1987) and Phillips and Gascoigne
(1988) showed that an isopropyl alcohol-based
cleaner was able to alter SA and FSA lens

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 Module 7: Contact Lens-Related Ocular Complications

materials, and parameters significantly if it

remained in contact with a lens for an extended
period of time.
192 Cornea-Related: Spectacle Blur
VISION COMPLICATIONS Blurred vision with spectacles after wearing RGP
AETIOLOGY: SPECTACLE BLUR
lenses may be due to:
• Corneal shape change
- alters refractive error x A change in corneal shape, and/or ….
- not all VA loss attributable to altered x Corneal oedema.
refraction, i.e. some blur not correctable
x Factors unknown.
• Lens pressure on the cornea
- central or peripheral
Rengstorff (1966) found no correlation between
- bearing
lens design and fitting factors. However, he
- complicated by lid forces
showed a dosage relationship, i.e. the effects were
• Corneal oedema
worse when lenses were worn for many years, or
97300-86S.PPT
were worn for many hours a day, especially when
occasional overnight wear or napping was involved.
7L397300-86
Polse et al. (1987) found that refractive errors were
smaller than K reading changes, and were not
correlated with them.
Subtle corneal shape changes induced by RGP
lens wear may also reduce VA. A partial
explanation may have been provided by Greenberg
and Hill (1973). They showed that PMMA lenses:
x Left an ‘imprint’ (corneal indentation?).
x Compressed all epithelial layers, although the
changes were more obvious in the basal cell
layer.
x Resulted in one fewer wing cell layer.
x Increased the frequency of cell mitosis.
It is conceivable that less obvious epithelial effects
may have essentially similar anatomical (physical)
sequelae.
In studying visual loss in corneal oedema, Carney
and Jacobs (1984) used the contrast sensitivity
function to assess the resulting visual disability.
They found that despite normal acuity (as assessed
by a high contrast letter chart), the magnitude and
type of visual loss depended on the origin of the
oedema (osmotic, hypoxic/anoxic) and the site of
the corneal response (epithelial, stromal, total
corneal).

193 Post-Lens Tear Film-Related: Dimple Veiling

VISION COMPLICATIONS Trapped air bubbles under an RGP lens may result
AETIOLOGY: DIMPLE VEILING from excess blink-induced lens movement and tear
• Poor lens-cornea relationship
exchange. Bubbles are more likely to form if a lens
- excessive corneal clearance is fitted with excessive central or peripheral
- too flat (most common), too steep clearance, or bearing (which also raises the
possibility of excessive clearance elsewhere). The
• Trapped air bubbles
minimum clearance required for bubble formation is
- break up when pressure applied unknown but is probably > 120 µm and may be as
- numerous small bubbles result high as 250 µm (Pullum, personal communication,
2002). Probably, no single figure is applicable,
• Aerosol saline (bubbles of propellant) rather it is likely to be a combination of
97300-90S.PPT

circumstances including on-eye lens behaviour,

7L397300-90
cornea-lens clearances, blink characteristics, and
tear film properties.
A large post-lens bubble may break-up into smaller
bubbles that remain trapped by the lens.

272 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

Regardless, all indent the corneal epithelium in a

characteristic fashion.
A spectacular, but preventable, case of dimple
veiling can be due to the use of aerosol saline. If
the saline is ‘sprayed’ into the concavity of a lens,
and the fluid-filled lens applied to the eye
immediately, a large number of bubbles of
propellant (usually nitrogen) may appear in the
PLTF. More bubbles may appear after lens
insertion as the warmer eye drives more propellant
out of solution in to the PLTF/saline mix.
194 Vision Complications: Management
General
VISION COMPLICATIONS
MANAGEMENT: GENERAL
As the aetiology of vision-related problems in RGP
contact lens wear may involve multiple factors, the
• Dictated by cause practitioner must obtain a detailed and careful
history from the wearer. Key questions should
• If cause not ascertained, consider investigate a number of areas including the
following:
sequential elimination of the possibilities x Time of onset of the symptoms.
x Duration.
• Alter lens BVP to optimize VA
x Exacerbating conditions.
97300-79S.PPT x Previous problems.
x General health.
7L397300-79
x Medications.
Correction of any obvious problems in lens fitting,
care and maintenance, wear schedules, etc.
permits the practitioner to assess subsequently the
possible roles of more subtle problems.

195 Lens-Related: Flare

VISION COMPLICATIONS When flare is reported, attention should be paid to:
MANAGEMENT: LENS-RELATED x Lens design including:
Flare: – lens diameter (TD)
– back optic zone diameter (BOZD)
• Optimize fitting characteristics
– front optic zone diameter (FOZD).
- improve centration x Fitting characteristics to improve lens
centration.
- decrease lens movement
x Pupil size (actually the entrance pupil size) in
• Increase BOZD/FOZD and/or TD various disparate light levels.
97300-83S.PPT
x Optic zone and total diameter increases to
reduces flare (after Lowther, 1986) by
7L397300-83 improving centration and minimizing the optical
influence of the lens back surface’s peripheral
curves. An increased optic zone diameter also
decreases the likelihood of the OZD (as
determined by the FOZD or the BOZD
whichever is the smaller) being exceeded by
the size of the entrance pupil in most light
conditions.
x The use of a continuous aspheric back surface
design that has no distinct BOZD. The lack of
a distinct transition should reduce the
magnitude of any flare resulting. However,
vision will still degrade with large pupils.

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 Module 7: Contact Lens-Related Ocular Complications

196 Lens-Related: Poor Lens Wettability

If a lens surface is damaged by excessive heat,
VISION COMPLICATIONS excessive pressure, or over-polishing during
MANAGEMENT: LENS-RELATED
manufacture, a lens remake is necessary.
Poor wettability:
Reduced lens wettability is best managed by
• Remake lenses
optimizing the lens surface properties. This can be
• Polish existing lenses achieved in the following ways:
• Change lens material x Improved lens care to minimize deposits.
• Optimize care products x Polishing the surface to remove tenacious
- re-educate wearer on their usage deposits.
• Change environment x Refitting with a different material.
97300-104S.PPT x Changing the patient’s environment to minimize
the effects of surface dehydration. This is not
7L397300-104 an easy option in most cases, and impossible in
some instances.
197
Lens-Related: Lens Surface Crazing
VISION COMPLICATIONS x Management requires the ordering of new
MANAGEMENT: LENS-RELATED
lenses (Grohe et al., 1987, Phillips and
Surface Crazing: Gascoigne, 1988).
• Replace problem lens x Once a crazing pattern (surface cracking) is
present, the deterioration is unlikely to stop, and
• Change lens material
it certainly cannot be reversed.
- maintain lens physiology x An alternative lens material should be ordered
• Change lens care products provided its physiological performance equals,
or exceeds that of the original material.
• Check lens care procedures x If the lens material cannot be changed for some
97300-108S.PPT

reason, lens care procedures and products

7L397300-108 should be reviewed and optimized.
x Polishing often makes the situation worse and
is not the solution to the problem (Grohe et al.,
1987B).
x Once crazing is confirmed, the lenses should
not be used because concerns have been
voiced about the microbiological implications of
possible colonization of the fissures by ocular
pathogens (Grohe et al., 1987B, Walker, 1990),
and the cracks acting as ‘footholds’ or
foundations for deposits subsequently.
198
VISION COMPLICATIONS Cornea-Related: Spectacle Blur
MANAGEMENT: SPECTACLE BLUR Lens fitting characteristics must be optimized if
• Improve lens fitting characteristics spectacle blur is apparent after lens wear. Key
factors for evaluation include:
- minimize bearing
x Localized bearing on the cornea.
- maintain lens mobility
x Decentration.
• Increase lens Dk/t significantly x Limited movement.
• Educate wearer (re-educate) x Lens thickness.
x Lid forces.
• Wearer compliance
97300-87S.PPT
x Physiological performance of the lenses.
In many RGP lens wearers, a small amount of
7L397300-87 spectacle blur may be experienced after lens
removal even when high-Dk materials are used.
Wearer education is required to minimize their
concerns, and to enlist their support for monitoring
their own visual performance. If a particular cornea
proves to be susceptible to spectacle blur with
274 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

several different rigid lenses, a soft lens may prove

to be a more appropriate form of correction.
199
VISION COMPLICATIONS Post-Lens Tear Film-Related: Dimple Veiling
MANAGEMENT: DIMPLE VEILING Repeated episodes of dimple veiling indicate a lens
• Alter lens fitting/design fit that is sub-optimal and must be improved. Any
central clearance should be minimized to achieve a
• Decrease clearance near-alignment fitting. If the fluorescein fitting
pattern indicates excessive edge width and/or
- central
clearance, the peripheral curves should be
- edge
‘tightened’ to prevent bubble formation.
Cautious use of aerosol saline with any type of lens
• Use non-aerosol saline should avoid the induction of an artificial dimple
97300-91S.PPT veiling. Alternatively, a non-aerosol saline could be
used.
7L397300-91

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 Module 7: Contact Lens-Related Ocular Complications

VI Lens and Fitting-Related Complications

VI.A Blink-Related Problems
200 Blink-Related Problems: Introduction
Usually, the presence of a rigid lens alters the blink
BLINK-RELATED PROBLEMS response of neophyte wearers. The effects of
INTRODUCTION
these alterations may require the intervention of the
• RGP lenses modify blinking esp. in
practitioner.
neophyte wearers
If the blink response remains abnormal after a
• Has adaptation to lenses occurred?
‘reasonable’ adaptation period, an investigation is
• Is a lid-attachment fit being pursued? necessary. Problems remaining, prima facie, are
• Many visually demanding tasks depress not an adaptation issue, and need investigation
the blink rate significantly, e.g. VDU usage (after Mandell, 1988).
• Corneal nerves can detect tear film If a ‘lid-attachment’ fitting philosophy is employed
changes 97300-167S.PPT
(introduced by Korb and Korb, 1970) some blink-
related problems may be inherent in such a fit. Lid-
7L97300-167
attachment can eliminate the visual disturbances
that occur when a lens drops (lens lag), after the
upper lid retreats to its ‘open’ position (movements
of 1.5 to 1.8 mm are common [Fonn et al., 1984]).
While lid-attachment has been claimed to improve
comfort by reducing lens-lid interaction, Sorbara et
al. (1996B) did not find this to be the case.
When wearers use computers or read intently, a
decreased blink rate can be expected (York et al.,
1971, Patel et al., 1991, Cho et al., 1997). Patel et
al. also found a correlation between blink rate and
tear thinning time (time from a blink to a
keratometer mire appearance change) while a
computer was being used.
201 Blink-Related Problems: Signs
BLINK-RELATED PROBLEMS Commonly, lens-induced modifications to the blink
SIGNS response take two forms:
• Excessive or slowed blinking
x An increased blink rate or, perhaps more
• Excessive lens movement
significantly, excessive and erratic blinking due
• Incomplete blinking (band deposits,
band of FS dryness) to the interaction between lens edge and lid
• BUT and blink frequency may be margins (Brown et al., 1973, Hill and Carney,
inversely related 1984). Brown et al. also showed rigid lenses
• Staining increased the blink amplitude, and some
- corneal wearers kept their eyes open wider (increased
- conjunctival Palpebral Aperture Size [PAS]) between blinks
• Ocular redness
97300-92S.PPT
to avoid lid-lens contact.
x Alternatively, lens-caused discomfort can
7L397300-92
induce a reduction in both blink rate and blink
completeness. This can result in epithelial
desiccation staining (Hill and Carney, 1984).

Some blink characteristics that can be observed

include (after Mandell, 1988):
x Blink rate.
x Completeness of the blink.
x Forcefulness of the blink.
x Regularity of the blink.
Any changes from the pre-lens wear blink
characteristics are noteworthy. Possible causes
need to be investigated.
Should it be necessary to differentiate between
voluntary and involuntary blinking, see the summary
276 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

in Mandell (1988).
Involuntary blinking, especially in rigid lens wearers,
tends to be incomplete (Mandell, 1988), a factor
that is difficult to detect under normal
circumstances. Indirect evidence of blink
incompleteness can take the form of tear film debris
‘bulldozed’ into a band (sometimes referred to as a
‘prowline’, e.g. McMonnies, 1989) corresponding to
the gap between the lids at the maximum blink
position. Other evidence is a poorly wetting lens
exhibiting a dry band corresponding to the lid gap.
With non-rotating lenses (e.g. a toric), a band-like
front surface deposit formed by ‘bulldozed’ material
may appear eventually.
Accumulation of tear debris, atmospheric pollutants,
and other airborne matter may be detectable in the
stagnant post-lens tear film of the static lens of an
infrequent blinker (Efron, 1998).
The head posture and eye positions should also be
noted, looking particularly for a backward head tilt
and/or a downward gaze. These characteristics,
202 and incomplete blinking, are signs of incomplete or
abnormal adaptation.
Other signs of blink-related complications can
include (after Gasson and Morris, 1992):
x Oedema (insufficient tear pumping if blink rate
decreases significantly – only a problem with
low Dk materials).
x 3 & 9 o’clock staining.
x Other corneal and conjunctival desiccation
(slide 202, outside the lens area)…
and (from Lowther and Snyder, 1992):
x A decentred lens. If the lens fit is too ‘loose’,
7L30249-94
extreme excursions of the lens will be observed
with each blink.
203 Blink-Related Problems: Symptoms
BLINK-RELATED PROBLEMS Typical symptoms associated with blink-related
SYMPTOMS problems, especially if the blink rate decreases,
• Discomfort include:
x Lens awareness.
- burning
x Irritation.
- lens/edge awareness x Disturbances of vision.
• Dry eyes x Dryness of the eyes.
• Tired eyes – if severe, the wearer may experience a
burning sensation or other symptoms
• Transient disturbances of vision appropriate to dry eyes (see Lecture 7.4 of
this module).
97300-93S.PPT

7L397300-93
x Eyes feeling ‘tired’, and possibly ‘dry’,
especially towards the end of a normal wearing
period. This may be associated with excessive
blinking.
x If lid-attachment is intended but not achieved,
or the lens is more mobile than intended, the
variable lens position may lead to disturbances
of vision.

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 Module 7: Contact Lens-Related Ocular Complications

204 Blink-Related Problems: Aetiology

BLINK-RELATED PROBLEMS The most common cause of blink-related problems
AETIOLOGY in RGP lens wear is lens edge awareness. In most
• Edge awareness cases, the upper eyelid margin touches the lens
- discomfort edge during the course of a blink (interpalpebral fit
- reduced blink frequency
assumed). Support for this assertion comes from
Collins et al. (1989) who found that topical
– increased blink frequency
anaesthesia lowered the blink frequency. If the
- incomplete blinks
edge shape is suboptimal, the movement of the lids
• Inadequate lens fit over the lens front surface can be hindered, and/or
• Large interpalpebral aperture made more apparent, resulting in partial or
• Not relative humidity incomplete blinking. Alternatively, failure to adapt
97300-94S.PPT
to new lenses may indicate an edge defect, or a
7L397300-94 loose fit (excessive lens mobility, excessive edge
clearance, or both).
Alterations in blink rate are also produced by:
x Anxiety, potentially relevant in cases in which
contact lens wearing success has yet to be
achieved.
x Stifling atmospheres, an environmental factor
that may have some significance in CL wear.
Interestingly, low relative humidity does not alter the
blink rate (Ruskell, 1989).
The amount of lens movement depends on a
number of factors including:
x Lens fitting factors.
x Anatomical issues such as the position of the
upper lid, e.g. a high upper lid enables more
vertical movement during a blink (after Fink et
al., 1990).
A large interpalpebral aperture implicit in a high
upper lid position also influences (improves) the
tear pump efficiency by allowing greater lens
movement (Fink et al., 1990). While moderate to
small PASs may limit lens movement, and reduce
tear pump efficiency, they, along with moderate or
greater blink rates, do prevent or reduce corneal
desiccation. Tear evaporation increases with the
area of exposed ocular surface, and the blink rate.
Therefore, people with large PASs may be more
prone to ‘dry eye’, or sensations of dry eye (some of
this section after Tsubota and Nakamori, 1995).
Stagnation of the post-lens tear film is usually the
result of little, or infrequent, blinking possibly of the
twitch, partial, or incomplete type. Apart from
corneal oxygenation issues that, in high Dk
materials at least, are less important, the lack of
lens movement/tear exchange leads to retention of
acquired and accumulated material.

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

205 Blink-Related Problems: Management

BLINK-RELATED PROBLEMS Optimization of the RGP lens edge shape is central
MANAGEMENT to the achievement of maximum comfort during
• Optimize lens edge profile or fit wear. Each lens should be evaluated before
- improve comfort dispensing, and if indicated, modifications made.
• Improve lens centration
If lid-attachment is intended but not achieved, a
lens alteration, or a re-order, may be required.
• Patient education
Patient education on issues related to lens
- understand problems adaptation and comfort is important as it imparts to
• Difficult to overcome by training the wearer some understanding of the effects of
lens wear. Blink exercises are recommended as
• As a last resort - SCLs part of the patient education process. However, the
97300-96S.PPT

likely success of such ‘training’ is debatable.

7L397300-96
McMonnies (1989) suggested 20 blinks, 20 times
per day for one week to improve voluntary blinking
with the following characteristics:
x Complete.
x Relaxed.
x Rapid.
x Facial muscle involvement in blinking of any
description should be avoided and facial muscle
relaxation highlighted if necessary.
The effect of RGP lenses on the PAS has been
covered earlier in this lecture (Section IV.D Ptosis)
and should not be regarded as inconsequential.
Other issues include:
x The effects of lid geometry, lid position, and lid-
lens interactions, be considered before fitting
rigid lenses (Carney et al., 1997).
x If discomfort is a significant problem, RGP
lenses should be fitted optimally, or slightly flat,
in a large diameter (TD=10 mm rather than the
more common 9.0 or 9.5 mm) Williams-Lyn et
al. (1993).
x Centration difficulties are more difficult to
resolve.
x Generally, it is more difficult to improve the
centration of a high-riding lens than of a low-
riding one (Carney et al., 1996).
x For high-riding lenses, the lens thickness, and
if prudent, the lens diameter, should be
increased as changing the material (to a lower
specific gravity to decrease lens mass) is
relatively ineffective (Carney et al., 1996).
x For low-riding lenses, a change of material (to
one of lower specific gravity to lower lens
mass), and an increase in diameter are
effective. Changing the lens thickness is not
(Carney et al., 1996).
Lens fitting characteristics may need changing,
because of the magnitude of lens movement
(excessive or inadequate), or post-lens tear film
stagnation due to infrequent blinking. In such a
case, either the lens parameters or lens design
need alteration, blink exercises should be tried, or a
combination of both strategies may be required.
If all attempts to rectify blink-related problems fail,
SCLs may be required.
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 Module 7: Contact Lens-Related Ocular Complications

VI.B Fitting Problems

206 Fitting Problems: Introduction
Put simply, if a contact lens is to perform well, and
FITTING PROBLEMS obvious lens-induced problems be avoided, the lens
INTRODUCTION
must fit the eye well. Without a good fit, the range
• A good lens fit is the cornerstone of
of difficulties that might arise for the wearer, and
good contact lens practice
therefore the practitioner, expand enormously.
• Ill-fitting lenses are a potential source of:
In addition to physical and pathophysiological
- discomfort problems, ill-fitting lenses are, potentially, sources
- a residual Rx or a variable over-Rx of discomfort, residual refractive error, and visual
- visual disturbance disturbance.
- pathophysiological problems
97300-168S.PPT

7L397300-16

207 Fitting Problems: Signs

In the interests of sustaining/maintaining the health
FITTING PROBLEMS
SIGNS
of the anterior eye, the fitting characteristics of rigid
lenses must be assessed carefully.
• Decentration
- slight The primary fitting factors to be assessed are:
- excessive x Lens centration.
- over the limbus
• Movement x The bearing relationship between the lens and
the corneal surface.
- limited
- excessive x The amount and type of lens movement.
- variable Poor centration results in:
97300-133S.PPT

x Inadequate coverage of the pupil. This can

7L397300-133 disturb/reduce vision significantly by allowing
non-optical lens zones to intrude into the
optical path of the eye.
208
x Decreased comfort.
FITTING PROBLEMS
SIGNS Lens bearing on the cornea can be assessed with
• Unstable fitting sodium fluorescein instilled into the post-lens tear
film. Excessive bearing appears as a dark (or
- variable location
absent) zone in a fitting pattern because of the lack
- variable movement of fluorescein-stained tears locally. Excessive
• Fluorescein pattern bearing pressure can cause localized epithelial
- bearing (pressure) damage that will stain eventually with fluorescein.
- pooling (bubbles if too deep) Some caution is required when interpreting
- centre, mid-periphery, peripheral (edge) fluorescein patterns:
97300-134S.PPT
x Some RGP materials are UV-absorbing.
These fail to show any fluorescence of the
7L397300-134
post-lens tear film leading to the false
impression of a ‘perfect’ alignment fit.
x Wetting agents used in most lens care
products aid the retention of a fluorescein-
stained pre-lens tear film, especially if they are
formulated with a higher viscosity. The film
behaves as a source of veiling fluorescent
glare on the lens’ front surface, making the true
fitting pattern indiscernible (saline rinse
eliminates the wetting function of adherent lens
care products [Caroline and Norman, 1991]).
Once sodium fluorescein is instilled,
x
voluminous, or abnormally thick (deep) tear
films exhibit ‘self absorption’, i.e. incident and
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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

209 fluoresced light are absorbed by the dyed

tears. The fluorescence brightness (the
FITTING PROBLEMS analogue of film thickness) may appear
SIGNS constant (Young, 1988) or, paradoxically,
• Staining sometimes even darker (greater absorption of
incident and fluoresced light). Gas bubbles
- corneal (where is it located?)
(dimple veiling) are a second clue to excessive
- conjunctival film thickness (>125 – 250 µm [Pullum, 2002
personal communication]).
• Effects on blinking
- rate increased or decreased x Thin, post-lens tear film thicknesses (below a
critical level), do not fluoresce and can lead to
- incomplete false estimations of the fitting relationship
97300-135S.PPT
(Young, 1988).
7L397300-135 Adequate lens movement is a key factor in
successful RGP lens performance.
Restricted movement hinders the removal of post-
210 lens tear film debris.
Excessive movement may cause:
x Tearing.
x Limbal irritation.
x Corneal and conjunctival staining. These are
adverse signs, indicative of excessive lens
movement, and/or a lens that traverses the
limbus, see slide 211).
x Increased ocular redness.
Decentring, or ill-fitting lenses (slide 210 illustrates
most fitting relationships) affect the tear lens power,
resulting in reduced or variable vision. The effects
7L31310-91
may be either cumulative, or may cancel one
another and mask shortcomings in fit,
measurements, and clinical technique (Haynes,
211 cited in Mandell, 1988).

7L31617-91

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 Module 7: Contact Lens-Related Ocular Complications

212 Slide 212 shows a lens that probably decentres

statically and which is too flat (lens has moved to
the flatter corneal periphery to seek corneal
alignment). Slide 213 shows a very flat fitting lens
that bridges the corneal centre and the limbus at 9
o’clock. Slide 214 shows the result of a lens with
too much vertical movement (note the staining
beyond the limbus between 4 and 8 o’clock).
Evidence of a developing 4 and 8 o’clock (3 & 9
o’clock) stain is also apparent.
Slide 215 is a spherical lens fitted to a significantly
toric cornea (with-the-rule).

7L3192-91

213

7L31751-93

214

7L31768-93

215

7L3894-94

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

216 Fitting Problems: Symptoms

A wide range of symptoms can be associated with
FITTING PROBLEMS
SYMPTOMS poor RGP fitting characteristics. Most commonly,
• Discomfort the patient complains of:
- lens awareness x Decreased comfort.
- staining x Unstable vision.
• Variable vision x Reduced wearing time.
• Reduced wearing time x Altered blinking pattern, e.g. blink rate may
- cessation of lens wear increase or decrease, blinking may become
• Altered blink pattern incomplete, or the proportion of incomplete
97300-110S.PPT blinks may increase.
7L397300-110 x Sustained problems are likely to lead to a
cessation of lens wear.
Symptoms may follow the commencement of lens
wear, or begin some time later. This distinction is
important to the practitioner’s determination of the
likely cause of the problem(s), i.e. are they inherent
in the lens, lens fit, or lens condition, or are they the
result of changes that occurred subsequently?
217 Fitting Problems: Aetiology
FITTING PROBLEMS Despite the number of RGP lens designs available,
AETIOLOGY the practitioner’s initial choice may not always prove
• Numerous to be optimal for a particular wearer, and an
• Fitting relationship alternative will be required.
• Lens parameters:
- radius (BOZR, BPCR, etc. Issues include:
- diameter (TD, BOZD, etc.)
- edge design x Alterations to the lens parameters while the
– width lenses have been in use. If key parameters
– clearance change after dispensing, the original
– shape satisfactory fit will no longer be exhibited.
• Old lenses, swapped lenses
97300-111S.PPT x Key parameters such as lens diameter (TD),
7L397300-111
lens thicknesses, and BOZR are frequently the
focus of deliberations on ‘lens design’.
Problems related to these factors are usually
among the more overt, e.g. decentration,
excessive looseness or tightness, induced
corneal curvature changes, discomfort, lens
awareness, shortened wearing times, etc.
x Subtle factors that may decide ultimate
success include issues such as BOZD,
peripheral curves (radii and widths), junction
angles and thicknesses, edge shape, and
edge lift. The latter two factors influence not
only lens centration and movement but also
the tear exchange rate (Ueda and Nishida,
1997).
x A poor lens-cornea fitting relationship at any
location under a lens can result in corneal
and/or conjunctival staining due to local
pressure excesses. This is more likely to
occur at junctions on the back surface,
especially between the optic zone and the first
peripheral curve, or between the penultimate
peripheral curve and the edge curve.
x Generally, rigid lenses tend to decentre
towards the steeper region of a cornea.
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 Module 7: Contact Lens-Related Ocular Complications

However, if they are a ‘flat’ fit, they tend to

decentre upwards (sometimes temporally, or
supero-temporally) where, generally, they can
find a flatter (better aligned) fitting relationship.
However, in corneas with asymmetric
astigmatism, e.g. inferior steeper than
superior, or nasal steeper than temporal, the
lens migrates towards the steeper region. This
can be observed in against-the-rule
astigmatism where, for example, a lens will
decentre nasally should the nasal cornea be
steeper than the temporal sector, especially if
the lens is spherical (Lindsay, 2003 personal
communication).
x If vision is unsatisfactory, excess tearing, lens
centration, lens movement, and lens BVP
warrant investigation. Decentration is an
obvious cause of decreased vision, the others
possible causes are often less obvious.
x Simple answers to lens fit questions should
not be overlooked, e.g. old lenses pressed
back into service unintentionally, swapped
lenses if significantly different lens parameters
are used in each eye, etc.
218 Fitting Problems: Management
FITTING PROBLEMS In the era of easy-to-fit, disposable soft lenses, the
MANAGEMENT ability to design and fit RGP lenses competently,
• Fit to achieve near-alignment centrally has become something of a hallmark of a ‘real’
contact lens practitioner.
• Revisit lens parameters chosen initially
The appropriateness of the lens design and fit, and
• Re-measure lens parameters at after-care the amount and quality of lens movement, remain
the keys to successful RGP lens wear and RGP
• Optimize edge design
contact lens practice.
• Ensure adequate movement The availability of several diagnostic trial lens sets
- a key success factor is recommended and dry storage, while a
97300-112S.PPT
controversial recommendation, is probably more
7L397300-112 practical in a practice setting (Bennett, 1990).
Usually, the signs and symptoms of a poor fit assist
the practitioner’s determination of the most likely
cause(s). Regular after-care and lens evaluation by
the practitioner is necessary to ensure that the
initial fitting characteristics, lens performance, and
eye health are maintained. Rigid lenses should be
re-measured if there is any hint of a problem that
may be caused by alterations in lens parameters
(after McMonnies, 1988), especially BOZR, or
regularity of the lens (see later section on lens
warpage).
Corneal topography is useful to the monitoring of
corneal changes, and as an adjunct to the lens
fitting process (after Lowther, 1996, and Szczotka,
1995, 1997, Bufidis et al., 1998, Jeandervin, 1998,
Evardson and Douthwaite, 1999).
If decentration is a problem, the lens fit, BOZD, or
TD may need to be changed to ensure the pupil is
covered by the optic zone only. Other changes
related to lens fit are covered in Lecture 3.4.2.
When lens parameters are being altered,
284 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

compensation for their interdependencies need to

be made, e.g. changing the BOZR needs BVP
compensation, BOZD alterations need BOZR
compensation, and TD alterations need BOZR
compensation (unless the lens is aspheric and the
alterations relatively minor).
If lens thickness is excessive, the lens can be
modified (thinned) within practical limits. Large
changes require a lens re-make.
If a more flexible material is to be used on a toric
cornea, thought needs to be given to increasing the
new lens thickness to increase rigidity. This may be
required if residual astigmatism is to be controlled
or avoided (after Veys and Davies, 1995).

VI.C Lens Flexure

219 Lens Flexure: Introduction
LENS FLEXURE Lens flexure is an unwanted, unaccounted for, lens
INTRODUCTION shape change that occurs in situ. It is usually
Lens flexure may lead to: transient, does not exceed the lens’ elastic limits,
• The induction of residual astigmatism and has ramifications for lens fit, corneal health,
• A reduction of residual astigmatism and vision quality. Most flexure is transient, i.e.
• Variable vision (blink-modulated?) only occurs while the lens is on the eye, and lens
• The need for a: shape returns either upon lens removal, or soon
- thicker lens after. Permanent lens alterations are possible (see
- more rigid material warpage later).
- a material that is both rigid & more O2 Flexure of (spherical) RGP lenses, especially when
permeable
fabricated from the less rigid RGP materials, is
significant because of the residual astigmatism that
97300-169S.PPT

7L397300-169 remains in cases of corneal astigmatism (after

Lowther, 1986).
In general, RGP lenses on spherical corneas flex
little and any alteration in shape is likely to retain
the lens’ basic spherical shape.
Toric flexure (or an approximation thereto, see
later) is more likely to be restricted to spherical
lenses fitted to toric corneas, or back-surface
toric/bitoric lenses flexing to align more closely with
toric corneas.
Lens flexure may be beneficial, e.g. if lens flexure
reduces residual astigmatism, visual acuity will be
improved (see Patel et al., 1988, and Salmon,
1992). Alternatively, lens flexure may exacerbate
the refractive error (Silbert, 1990).
In cases of corneal astigmatism, should flexure be
variable or blink-modulated, the variable vision may
necessitate a more ‘rational’ approach to solving
the problem such as a toric periphery, a toric back
surface, or a bitoric RGP lens.

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 Module 7: Contact Lens-Related Ocular Complications

220 Lens Flexure: Signs

LENS FLEXURE A spherical RGP lens may bend, flex, or conform to
SIGNS the cornea during wear such that it is no longer
• Front surface keratometry (FSK) spherical (slide 221). Such a form is bitoric, i.e.
both front and back surfaces are toric. However,
- front is toric in situ (spherical in vitro) Fatt (1987) pointed out that flexed lenses with
• Decreased and/or variable visual acuity power incorporated are not truly toric or bitoric but
were better described as being ‘tacoicitic’ or
• Cylindrical over-refraction demonstrating the property of ‘tacoicity’. These
terms have not entered common usage.
• Less than expected residual astigmatism
Assessing lens flexure:
(ocular astig. < 90% of corneal astig.)
97300-113S.PPT
x The flexure of a lens, whose front surface is
nominally spherical, can be measured by a
7L397300-113
keratometer (after Wechsler, 1979, Goldberg,
1990). This is the ‘front surface K’ or sometimes
221 the ‘FSK reading’.
x Videokeratoscopy (see Module 9, Lecture 9.1,
LENS FLEXURE: SPHERICAL Section III.B Videokeratoscopes).
(WTR CORNEAL ASTIGMATISM)
Tear
lens
Lens remains Lens is now Lens is now Transformations similar to those of spherical lenses
SPHERICAL BITORIC more BITORIC
on toric corneas can also occur with bitoric lenses
ep a
t)
te rne

on toric corneas. Traditionally, a bitoric lens is not

es
Co

fitted with both its principal meridians aligned with

(s
surface
Lens
back

C
Tear lenses
(fl orne
at t a
es
the cornea, rather its steepest meridian is fitted
t)
Horizontal: ALIGNED slightly flatter in the interests of post-lens tear
exchange. If the lens flexes (slide 222), it is
Vertical: NO flexure Vertical: SOME flexure Vertical: ALIGNED
(UNLIKELY)
possible that the lens aligns both meridians by
SPHERICAL
becoming more bitoric and tear exchange is
97300-170S.PPT affected adversely.
7L397300-170 Once lens flexure is confirmed (e.g. by FSK
assessments), the optical ramifications can be
calculated using paraxial theory (see Lecture 2.3 in
222 Module 2). However, a difficulty arises when
estimating the changes at the back surface
LENS FLEXURE: BITORIC because a choice needs to be made of which ‘lens
(WTR CORNEAL ASTIGMATISM)
flexure model’ is to be used. This is a complex area
and will not be covered here (see Holden et al.,
Lens is now 1976 for theories on lens flexure that have been
more BITORIC

Tear lenses
advanced). As a clinical approximation, it is
reasonable to assume that an identical
Horizontal ALIGNED Horizontal ALIGNED
transformation occurs on the reverse surface.

Vertical Almost Vertical ALIGNED

ALIGNED (flatter
by 0.05 - 0.1 mm)
BITORIC (normal fit) BITORIC FLEXED
97300-171S.PPT

7L397300-171
223 Lens Flexure: Symptoms
LENS FLEXURE Small amounts of lens flexure are expected with
SYMPTOMS RGP lenses. However, excessive flexure may
• Vision result in a reduction in the quality of vision.
- variable Typically, the wearer reports that their vision is
variable (unstable), blurred (Egan and Bennett,
- reduced quality 1985), and fluctuates with each blink.
Possibly: Although unlikely, it is possible that lens comfort
• Decreased comfort and/or wearing times may decrease. This is more
likely when bitoric lenses of low transmissibility flex,
- reduced lens tolerance
thwarting the intentions of the fitter to avoid aligning
• Decreased wearing time both meridians (in the interests of adequate tear
97300-114S.PPT

exchange).
7L397300-114
The general subtlety of the symptoms, or their
absence, with the possible exception of the
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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

occasional vision problem, means lens flexure

borders on being a problem to the practitioner
rather than to the wearer, i.e. the condition is often
subclinical.
224 Lens Flexure: Aetiology
LENS FLEXURE Lens flexure is related to the lens material (but
AETIOLOGY probably not its Dk, see below), lens design
• Centre of lens too thin (especially thickness), and the lens fitting
- material characteristic characteristics (especially if fitted steeply).
- large BOZD If a lens is unable to withstand the forces applied by
- high minus BVP the upper lid, it is forced into closer alignment with
the cornea. However, it is known that the cornea
• Corneal toricity
does not resist these forces completely either, i.e.
• Lid force on blinking there is some reciprocal conformance (see corneal
- possibly a low lid position changes, corneal warpage and spectacle blur in this
• Steep central fitting lecture, and Module 8, Lecture 8.9:
97300-115S.PPT

Orthokeratology).
7L397300-115
Lens flexure increases with the following (after
Salmon, 1992 unless indicated otherwise):
x Decreasing lens thickness
x More flexible materials (see also Harris et al.,
1982, 1982B).
x Larger BOZDs.
x In WTR astigmats:
– low upper lid positions
– flatter BOZRs.
x In ATR astigmats:
– high upper lid positions
– steeper BOZRs.
x The steepness of fit, i.e. the steeper the fit, the
greater the flexure (Pole, 1983, Pole and
Kochanny, 1984, Caroline and Norman, 1988).

Are lens flexure and Dk correlated?

The following are relevant:
x Fatt (1986) (and later Fatt, 1987, and Miller and
Andrasko, 1989), showed a correlation between
Dk and rigidity with early generation RGP
materials (mostly SAs).
x Stevenson (1988, 1991), Cornish et al. (1991),
and Sorbara et al. (1992) studied the lens
flexure of rigid lenses including PMMA, SAs,
FSAs, and fluorocarbons on corneas of varying
toricities. Except for the fluorocarbon lenses
that did flex, they found no significant
differences between the materials tested (Dks
to 115), and no correlation between Dk and
either, susceptibility to flexure, or visual acuity
achieved.
x Pole and Kochanny (1984) using a siloxane
resin and two SA RGP lenses, found no
consistent or significant difference in flexure
between these lenses.
x Given the conflicting results, it may be that the
outcome of each study depends on the actual
materials used and/or their basic chemistry
rather than simply just the Dk of the materials.

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 Module 7: Contact Lens-Related Ocular Complications

Other relevant issues include:

x Herman (1983, 1984) and Egan and Bennett
(1985) found that a spherical lens fitted flatter
than the cornea tended to minimize the induced
residual astigmatism, or reversed it (i.e. flexure
became against-the-rule on a with-the-rule
cornea). The changes were small (usually 0.25
to 0.50D). This may be due to the flat spherical
lens being more likely to attempt to align with
the flattest corneal meridian (i.e. the lens
steepens over this meridian) rather than with
the less accessible steepest meridian. In
steepening, the lens meridian over the steepest
corneal meridian is likely to become flatter, i.e.
the lens warps, and residual astigmatism
increases because of changes to the tear lens.
x Edwards (1990) found a poor correlation
between corneal astigmatism and lens flexure.
Ballentine et al. (1980, cited in Harris et al.,
1982) found that PMMA lenses, and an early
SA lens, flexed little on corneas with ” 1.00 D
WTR corneal toricity.
x Goldberg (1990) suggests that flexure is more
likely in decentred, immobile lenses regardless
of their resting position. Lenses fitted flatter
than the cornea tend to locate higher on the
cornea (Herman, 1984). This lens position
maximizes the influence of the upper lid on the
lens, and may maximize lens flexure effects, or
increase ATR flexure (Herman, 1983).
x To resist lens flexure on toric corneas, the
following thicknesses have been recommended:
– PMMA: 0.12 – 0.13 mm (Harris, 1970, Harris
and Chu, 1972)
– SAs: 0.15 – 0.20 mm (Harris et al., 1987)
– RGPs: 0.15 mm as a minimum (Holden,
1984).
x Varying the total diameter (TD) did not alter
flexure or residual astigmatism in PMMA (Harris
and Appelquist, 1974), or SA lenses (Herman,
1983, 1984).
x Increasing minus BVP reduced flexure and
residual astigmatism compared with low minus
power (probably because of enhanced mid-
peripheral thickness).
x Corzine and Klein (1997) concluded that
surface tension forces acting on a lens
maintained, rather than caused, lens flexure.
x Fatt (1989) found that flexure was more
sensitive to thickness and diameter than to
material properties. Not all agree on the
influence of diameter however.

Blehl et al. (1991) postulated that the increased

flexure seen with hybrid lenses (e.g. SoftPerm™)
on toric corneas may be the result of the toric
conformance of the peripheral hydrogel skirt
influencing the more rigid central zone.

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225 Lens Flexure: Management

LENS FLEXURE x PMMA trial lenses do not reflect the flexure and
MANAGEMENT residual astigmatism of RGP lenses (Harris et
• Use trial lenses made of the same
al., 1982) and trial lenses should be made of
material as the lenses to be dispensed
the same material as the lenses to be
• Increase lens thickness dispensed (Henry et al. (1990).
• Seek alignment or a slightly flat fitting x If a lens is too thin, and vision quality is reduced
• Choose a newer material by lens flexure, a remake is necessary.
- e.g. higher Dk with greater rigidity
Subsequent lenses must be either thicker, or
made of a more rigid material. However, thicker
• Decrease the BOZD lenses reduce oxygen transmissibility and a
• Fit a back surface toric or a bitoric lens
97300-116S.PPT
compromise, dependent on material properties,
is required. Previously, compromises required
7L397300-116 clinical judgment, and some experience.
Newer materials offer greater rigidity, long-term
stability, and high oxygen permeability (see
Harty, 2001).
x For minimum flexure, the lens-cornea fitting
relationship should be either aligned or slightly
flat (up to 0.50D flatter) (Herman, 1983,
Caroline and Norman, 1988).
x If beneficial (‘with-the-rule’) flexure is required
to reduce residual astigmatism (Harris, 1970,
Harris and Chu, 1972, Salmon, 1992), a slightly
steeper fit may be successful (Herman, 1984).
x Brown et al. (1984) reported that lenses with
smaller BOZDs flexed less. Therefore, the
simple expedient of decreasing the BOZD may
reduce flexing enough to resolve some of the
lesser cases of lens flexure. Pupil size remains
a consideration.
x Residual refractive error correction may require
a lens with a spherical back surface, a toric
front surface, and prism ballast (Silbert, 1990).
If the cornea is somewhat toric, predicting or
measuring lens flexure in situ, even after a
settling period, is difficult. Some lens BVP
compensation may be required to offset the
induced tear lens effects.
x Dealing with lens flexure in against-the-rule
(ATR) astigmats can be difficult (Herman,
1984). Herman found that altering the BOZR,
to modulate lens flexing, was ineffective in ATR
astigmats, and recommended soft torics in
myopic ATR astigmats.
x If lens flexure is to be minimized, significant
amounts of corneal toricity require a toric lens
back surface. If the disparity between corneal
curvature and lens back surface shape is too
great, simple physical factors may thwart
contact lens success with spherical lenses,
despite the achievement of adequate vision.

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VI.D Lens Warpage

226 Lens Warpage: Introduction
Perhaps for reasons of intuition rather than good
LENS WARPAGE
INTRODUCTION science, RGP lenses, especially the fluoro-siloxane
• Intuitively, thought to be a problem of
acrylates (FSAs), have been perceived as being
more ‘exotic’ RGP materials more susceptible to transient (flexure, see previous
section), or permanent warpage. However, Quinn
- intuition NOT supported by the literature (1989) studied the stability of FSA lenses over a 9-
- therefore other causes month period and found that, under daily wear
• Can cause: circumstances, the lenses demonstrated excellent
- corneal warpage stability. More recently, Harty (2001) showed that
at least for one material, siflufocon B, dimensional
- reduced vision stability was maintained despite its high oxygen
97300-172S.PPT
permeability.
7L397300-172 Thus, it would seem that despite earlier perceptions
that stability and rigidity were related to DK
inversely, modern RGP materials offer what the
contact lens practitioner needs – high Dk with
rigidity and stability.
227 Lens Warpage: Signs
A number of signs are present when the shape of
LENS WARPAGE an RGP lens is warped. These include:
SIGNS
• Irregular mires x Irregular or distorted mires on the focimeter and
- radiuscope radiuscope (in vitro).
- focimeter/lensometer x Irregular or distorted keratometer mires (in
- keratometer/ophthalmometer
vivo).
• Over-refraction x Reduced visual acuity (in situ).
- no precise end-point x Difficulty obtaining a precise end-point to an
over-Rx while the lens is worn.
- irregular or inexplicable result
• Altered lens fit/fluorescein pattern
x Altered lens fit.
97300-117S.PPT
x Irregular fluorescein pattern (slide 228).
7L397300-117 x Induced residual astigmatism (Bailey, 1961,
cited in Silbert, 1990).

228

7L31764-93

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229 Lens Warpage: Symptoms

Typically, the irregular optics of a warped RGP lens
LENS WARPAGE results in complaints of reduced vision.
SYMPTOMS
A warped lens may also decrease wearer comfort.
• Reduced vision Along with reduced vision, this can result in a
reduction in wearing time, or even the cessation of
• Decreased: lens wear.
Distortions of vision are unlikely to be reported.
- comfort

- wearing time
97300-118S.PPT

7L397300-118

230 Lens Warpage: Aetiology

LENS WARPAGE The most common cause of RGP lens warpage is
AETIOLOGY inappropriate lens handling (Henry et al., 1988)
• Heavy handling during which significant pressure is applied to the
- previous PMMA wearer lens. Slide 231 shows careful, but imprudent RGP
- poorly instructed patient
- cleans between thumb & forefinger lens handling, while slide 232 shows the effect of
• Lens case issues: lens mishandling. Note the difference in the shapes
- flat base of the reflections of the flash diffusers in each
- smooth walls (eccentric storage) image (in slide 232 the lens is extremely bitoric).
- lens ‘pressed’ into bottom of well Such abuse can lead to transient, or permanent
- dry storage
- allowed to dry-out lens warpage.
• Thin lens design Typically, lens warpage occurs in wearers who
clean lenses between their thumb and forefinger
97300-119S.PPT

7L397300-119 (Henry et al., 1987, 1990). Henry et al.

recommended cleaning lenses in the palm of the
hand (slide 233).
231
Distorted lenses take either some time to return to
their original shape (elastic deformation, perhaps
with some viscoelastic properties), or do not return
fully to their original shape (plastic deformation or
distortion).
Often, wearers of PMMA lenses developed bad
lens care habits because the material was (is) very
durable, and does not flex easily. When refitted
with RGP lenses, their ‘normal’ (PMMA) methods
can prove to be overly vigorous, and RGP lens
warpage can result.
Other causes of lens warpage include:
7L3RGPB-01
x Inadequate thickness of the finished lens.
x Negative pressure (‘suction’) between the
232 storage case and a lens. This often occurs in
cases that are not designed for rigid lenses,
e.g. those with a flat bottom. Negative pressure
can hold a lens in a flatter than normal shape
that may also prove to be somewhat irregular.
x Insertion into, and storage in, a spring-clip lens
holder (slide 234) that loads the lens laterally
due to inadequate holder size, or the lens being
too large.
Other causes (after Henry et al., 1990) include:
x Use of hot water to rinse lenses.
x Dry storage, or allowing the lens case to dry-out
inadvertently.
7L3RGPA-01 x Leaving lenses in tilted, and/or non-conforming
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 Module 7: Contact Lens-Related Ocular Complications

233 positions for long periods, especially if the lens

case dries out.
x Placing a lens concave down in a smooth-
walled case well. In addition to negative
pressure generation, the lens may be stressed
beyond its limits, if pushed down, and/or
‘locked-on’ to the case during attempted
removal.

7L31206-94

234

7L30LW1-98
235 Lens Warpage: Management
LENS WARPAGE Once an RGP lens warps, it is usually not possible
MANAGEMENT to ‘restore’ the lens to its original shape. A new
• Replace lens lens of appropriate design, probably in a different,
more rigid, more stable material, is required.
• Patient re-education
If the warpage is suspected of being laboratory
• Optimize lens design induced, suitable feedback to the quality manager,
- thickness or professional services staff is appropriate so that
- change materials the issue(s) can be investigated and appropriate
steps taken to eliminate the problem(s).
- hands-off cleaning
Frequently, manufacturers are a reliable source of
• Do not revert to lower transmissibility information about materials that are easy to deal
97300-120S.PPT

with during production, that are more rigid, etc. The

7L397300-120 practitioner must base their final choice on their
own experience, the laboratory’s advice, and the
physiological performance offered by the materials
suggested.
Re-education of the patient is required when
warpage is due to poor lens handling techniques.
Henry et al. (1990) suggested that if all else fails,
the use of a ‘hands-off’ cleaning technique be used
(they suggested a lens ‘swisher’ but these are no
longer available in most markets). Alternatively,
regular replacement programmes are available from
some RGP lens suppliers.
Patients should not be returned to wearing more
‘durable’ lenses with lower transmissibilities.
The importance of after-care visits needs emphasis,
and at subsequent visits, the regularity of lens
shape and fluorescein fitting pattern must be re-
assessed.

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VI.E Wearer Non-Compliance

236 Wearer Non-Compliance: Introduction
WEARER NON-COMPLIANCE: Compliance is defined as acting in accordance with
INTRODUCTION a request, command, instruction, etc. (after The
Non-compliance is a failure to act in New Shorter Oxford English Dictionary, 1993).
accordance with valid requests, Practitioners regard non-compliance as the most
commands, instructions, etc. from: significant, and/or the most common problem
confronting them, and their patients. It is probably
• The practitioner the biggest single barrier to long-term successful
• The lens manufacturer contact lens wear.
Sources of ‘alternative’ behaviour include:
• The lens care product manufacturer
97300-164S.PPT
x Misunderstanding instructions given verbally.
7L397300-164 x The wearer finding a more ‘convenient’, or
‘easier’ way.
237 x Misinterpretation of written (and in most cases
WEARER NON-COMPLIANCE: illustrated) instructions issued at dispensing, or
INTRODUCTION at subsequent after-care visits.
Sources of non-compliant behaviour: x Laziness.
• Misunderstanding - verbal, printed
• Seeking of greater ‘convenience’ x Erroneous information from well-intentioned,
• Laziness ‘helpful’ friends.
• Erroneous/irrelevant information from:
x Correctly following instruction given to others
- friends
using different, and irrelevant, lenses or lens
- family
• Independent personality care products.
• Poor wearer-practitioner communication x A personality that leads to independent ideas
regardless of their efficacy, safety, or relevance.
97300-165S.PPT

7L397300-165
x The awe-struck wearer who is afraid to question
or confirm the information they believe was
238 supplied by their practitioner.
COMPLIANCE ISSUES x Inappropriate practitioner attitudes that create
after Claydon & Efron, 1994
unnecessary communications barriers. Such
• The use of: attitudes can prejudice the chances of wearer
success, and may affect the long-term viability
- cleaner of the practice as well (see Module 10, Lecture
- rinsing solution 10.4: Standards of Practice).
- disinfectant Factors that affect compliance (after Shannon,
1987):
- protein remover
x Complexity of procedures recommended.
Length of time required to perform prescribed
97300-166S.PPT
x
7L397300-166 tasks correctly.
239 x Cost of regimen.
COMPLIANCE ISSUES x Poor understanding of verbal, and/or written
after Claydon & Efron, 1994
instructions.
x Poor, or no, patient-practitioner relationship.
• Hygiene:
Factors not affecting compliance include (after
- hand washing Shannon, 1987):
- lens case care x Age.

- lens case replacement x Sex.

x Occupation.
97300-201S.PPT

Perception of threat, or consequences of

x
7L397300-201 disease.
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240 x Race.

COMPLIANCE ISSUES x Education.

after Claydon & Efron, 1994
x Socio-economic group.
• Recommendations/advice on:
Various levels of compliance have been reported.
- wearing times These include:
- lens replacement scheme x Collins and Carney (1986, 1986B) showed that
- a ‘red eye’ only 26% of wearers were compliant fully.
- swimming in lenses x Chun and Weissman (1987), using a simplified
- storing lenses for the longer term definition, found 60% were compliant.
97300-202S.PPT x Schwartz (1989) reported that only 75% of
wearers used the lens care products
7L397300-202
recommended by their contact lens
practitioner. This figure may be high given
compliance levels reported in relation to other
aspects of lens wear and care (see above).
x Chun and Weissman also found compliance
decreased among the younger (10 – 30), the
older (>50), and the more experienced (>2
years of wear). However, this finding is
controversial.
x Sokol et al. (1990) found that being <30 years
of age, and using contact lenses for reasons of
cosmesis or convenience, were associated
with non-compliant behaviour.
Some have suggested that patient education is
central to compliance (Schwartz, 1987, McGeehon,
1988, Turner et al., 1993, Ky et al., 1998).
However, Radford et al. (1993) found an
improvement in compliance (to 85%) only after ‘re-
instruction’, suggesting that the information
conveyed initially did not meet wearer needs
completely. However, Claydon et al. (1996, 1997)
found that additional education had no significant
effect.
Anonymous (1986) also suggested that the
variations in recommended procedures that existed
between practices, was a difficulty for wearers
changing practitioners.
Philosophically, it is sometimes difficult for the
practitioner to accept that non-compliance is not
always a patient/wearer problem only (Gleason,
1999). Patient education should be viewed as a
‘partnership’ between the wearer, and the
practitioner and practice staff.

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241 Wearer Non-Compliance: Signs

WEARER NON-COMPLIANCE A recurring difficulty for wearer and practitioner
SIGNS alike is the perplexing issue of the varying levels of
• Numerous
• Depend on the cause wearer compliance with the instructions of:
- lens-related x The practitioner.
– surface contamination
– surface scratches x The lens manufacturer.
– corneal staining
- lens care-related x The lens care product manufacturer.
– surface deposition
– corneal infections Signs associated with non-compliance are
– chemical irritation/staining numerous and typically relate to the effects of the
– chronic conjunctivitis inappropriate actions of the wearer.
97300-121S.PPT

Methods of assessment, according to Claydon and

7L397300-121
Efron (1994), include:
Direct:
242
x Self-reporting by:
WEARER NON-COMPLIANCE – questionnaire
SIGNS
• Ocular – interview.
- staining x Demonstration and observation.
- redness
x Direct solution bottle and tablet counts (or
volume measurements) to ascertain the
• Care solutions quantities used.
- improper use x Therapeutic outcome:
- infrequent use – ocular health
- not used – contact lens condition (e.g. scratched
97300-132S.PPT
surfaces, slides 243 and 244)
7L397300-132 – wearing success.
Indirect:
243 Collins and Carney (1986, 1986B) found a strong
relationship between non-compliance and signs and
symptoms indicative of potential lens wearing
problems. These signs included:
x Corneal staining.
x Lens surface deposits (including fungal
contamination).
x Lack of wearer awareness of their non-
compliance.
x Non-compliance ranging from total to
occasional.
Wearer characteristics (traits) were poor indicators
of compliance levels.
7L31786-93
To the list above could be added (after Asbell,
1988):
244 x Chronic conjunctivitis.
x Corneal abrasions.
x Corneal infections.
x Chemical irritations/staining.
and:
x Ocular redness (lids and globe)
x Appointments attended or missed.

The use of products that are not non-contact lens-

related such as make-up and skin preparations can
also create problems (Backman, 1987). Signs
include discolored lenses, easily removed lens
7L30528-94
deposits, greasy films, and filamentous material (as
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 Module 7: Contact Lens-Related Ocular Complications

used in eyeliners/mascara).
Fingerprint-pattern bleaching of tinted contact
lenses can be the result of using skin preparations
containing the oxidizing agent benzoyl peroxide. If
a finger contaminated with the preparation is used
to handle tinted lenses, the lens areas in contact
with the peaks of the finger print pattern can be
bleached leaving a distinctive pattern. Furthermore,
such chemical entities should never be permitted to
come in contact with the eye via any vehicle (e.g.
finger, lens, etc).
245 Patient Non-Compliance: Symptoms
WEARER NON-COMPLIANCE Wearer non-compliance often results in a reduction
SYMPTOMS
• Increased lens awareness
in lens performance. This may result in:
• Decreased wearing time x Poor vision should the level of lens front-
• Cessation of lens wear (drop-out)
- is it temporary or permanent? surface deposits increase.
- more likely if onset is rapid x Decreased wearer comfort.
• Reduced vision
- deposits x Decreased lens tolerance.
- excessive lens movement
• Lens care issues x Decreased wearing time.
- stinging x Reduced motivation to wear lenses.
- pain
- burning x Cessation of lens wear.
x Stinging or pain, and ocular hyperaemia may
97300-122S.PPT

7L397300-122 be a consequence of a failure to neutralize

hydrogen peroxide disinfectant, or to rinse lens
cleaner from the lenses thoroughly.
x In extreme cases, the wearer may attempt to
attribute blame, and question the practitioner’s
competence.
246 Patient Non-Compliance: Aetiology
WEARER NON-COMPLIANCE The most common cause of non-compliance is a
AETIOLOGY failure of patient education. This results in the
• Patient’s personality patient either not being informed adequately, or
• Poor patient education misunderstanding the importance of their own role
- misunderstandings in successful contact lens wear. A failure of the
- lack of reinforcement (e.g. after-care education process cannot be attributed to just one
appointments rushed or not kept) party and the practitioner must accept some of the
• Practitioner shortcomings
blame for a less than ideal outcome.
Solution costs are not a significant contributor to
• Use of inappropriate LCPs
non-compliance (Sheard et al., 1995).
• Failure to replace lenses
97300-123S.PPT Reduced vision may be due to lens deposits. The
7L397300-123
vision reduction may be because of the scattering
of light by the deposition, or corneal distortion
caused by the deposits if nodular and large (see
Hansen, 1990). The failure of a lens to
maintain/sustain a complete tear film also has
negative ramifications for vision quality.
Discomfort may be due to the use of inappropriate,
or unapproved, lens care products. Too many
wearers also assume that protein removal does not
need to be accompanied by disinfection (Lowther,
1988).
If a wearer fails to replace lenses on schedule, any
resulting CLPC may induce discomfort, lens
intolerance, and lid redness.
Collins and Carney (1986) found that a lack of
understanding of the functions of the lens care and
maintenance recommended did not affect
compliance adversely.
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247 Patient Non-Compliance: Management

WEARER NON-COMPLIANCE
MANAGEMENT It is rare that a patient deliberately sets out to
• Patient education/instruction disregard, or be non-compliant with, their
practitioner’s instructions.
- at lens dispensing
- at each after-care Compliance according to Claydon and Efron (1994)
- ongoing reinforcement
includes the following facets of contact lens wear:
- enthusiastic delivery is best x The use of:
- avoid arousing ‘fear’ – cleaner
- signed consent forms
– rinsing solution
- printed instructions & hints
97300-124S.PPT
– disinfectant
7L397300-124
– protein remover (enzyme) tablets.
x Hygiene recommendations:
– washing hands
– washing lens cases.
x Recommended:
– wearing times
– lens replacement period
– lens case replacement period.
x Attendance at after-care appointments.
Other issues that are relevant include:
x Behaviour in case of a ‘red’ eye, or other
complication (see Smith, 1996).
x Swimming while wearing contact lenses.
x Lens storage for longer periods of time, e.g.
when lenses are only worn intermittently.
In a round-table conference (Bailey, 1986):
x McEachern advised practitioners to assess the
cleanliness and neatness of a prospective
contact lens wearer at their first appointment.
Those presenting well were potentially good
contact lens candidates.
x Poster suggested wearers be trialled in DW
before progressing to EW, to demonstrate
responsibility and compliance.
x Polse recommended that:
– the lids, lid margins, and conjunctivae be
examined
– the lids be everted, and the tarsal plate
zones studied for CLPC-like changes.
– the tears be assessed for debris, excess
mucus, corneal dry spots, and thin or poor
film coverage/spreading
– conjunctival and corneal epithelial cell loss
be assessed using sodium fluorescein
and/or Rose Bengal (or Lissamine Green).
Some other relevant issues are:
x Smith (1996) and Sigband (1988) suggested
tracking wearer lens ordering patterns as a way
of monitoring non-compliance with lens
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 Module 7: Contact Lens-Related Ocular Complications

replacement recommendations.
x Simplified lens care (theoretically, easier to
comply with) is often suggested as a way of
reducing lens drop-outs and wearer problems,
e.g. Anonymous, 1986, McGeehon, 1987B,
Cedrone et al., 1992, Radford et al., 1993.
However, others have presented data to refute
this assertion, e.g. Sager et al., 1992, Phillips
and Prevade, 1993 (who showed only a 32.4%
compliance rate with a one-bottle system),
Turner et al., 1993, and Gower et al., 1994.
x The incidence of Microbial Keratitis (MK) and
lens spoilage has not decreased with the
introduction of simplified lens care systems
(Sokol et al., 1990, Trick, 1993), an observation
they attributed to lens care non-compliance.
x Proper instruction should commence as soon
as the contact lens fitting cycle commences.
Instructions should be reinforced at every
opportunity, e.g. after-care, and phone calls
(after Turner et al., 1993), if the wearer is to
remain aware of the need for compliance.
Failure to do so may allow the wearer to lapse
into bad habits and poor hygiene practices.
x Bennett et al. (1998B) showed that instructions
issued enthusiastically with a neutral (non-fear-
arousing) tone, were the most effective in
raising wearer compliance.
x A wearer who continues to disregard
instructions should be discontinued for their
own safety.
x If compliance issues arise, the prudent
practitioner should note the details in their
records, and inform the wearer of their action.
Legally, the practitioner should practice
defensively (see Module 10). Steps may
include (especially in EW):
– a signed consent form
– written instruments explaining wearer and
practitioner rights, as well as obligations
– written and illustrated instructions covering
procedures, potential problems, and steps to
be taken in cases of emergency (see Smith,
1996). In most legal jurisdictions, signed
waivers of patient rights carry little, or no
legal weight. Proof that instructions were
given, and the recipient’s understanding of
them was assessed, is probably more useful
legally (see Farkas et al., 1987 for a
checklist of what one practice supplies).
x When a lens material is changed to one that is
more deposit prone, or more fragile, etc., extra
attention should be paid to re-educating the
wearer at delivery (Terry et al., 1989B).
Understandably, many wearers assume that
their ‘old and proven ways’ are adequate.
x If lens deposits problems persist, proteolytic
enzyme treatments may be helpful. If
necessary, more frequent lens replacement, or

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even a planned replacement programme, can

be instigated.
x Regardless of the level of compliance, the ‘Look
good, Feel good, See well’ trilogy (Yamane and
Kuwabara, 1987) should be imparted to all
wearers so that they become their own first line
of detection and defence. The ‘if in doubt, take
them out’ philosophy should also be
communicated.
x Theoretically and practically, disposable lenses
address some non-compliance issues
(compliance levels of up to 90% have been
claimed [Lane, 1990]). Surprisingly, both DW
and EW disposable lenses have been
associated with a higher risk of microbial
keratitis (Matthews et al., 1992). Poor hygiene,
disinfectant system failure, and lens type, were
implicated.
x While a pro rata extension of lens life may
seem reasonable (to many practitioners as well
as patients), a more conservative approach is
warranted when lenses are worn for fewer than
seven days per week (DW). Once a lens is
worn, it is an expiring commodity. This means
that time absolute (time since opening for the
first time) is a lens-life factor, in addition to the
time the lens is actually worn on the eye (actual
usage). For example, if worn five days a week,
12 uses, rather than the nominal 14 uses, might
be suggested. Similarly, if worn for only three
or four days a week, the recommendation might
fall to just 10 uses. If lens usage is less
frequent than this, it is probably more
appropriate for daily disposable lenses to be
used. These lenses do not present the
problems of longer-term lens storage in LCPs
that may not be suitable, e.g. one-bottle
systems which are unsuitable for safe, long-
term storage.
x Even wearers without difficulties, be they
compliant or non-compliant, can harbour
potentially pathogenic micro-organisms in lens
storage cases (Donzis et al., 1992).
x Generally, the use of water-based (water-
soluble) make-up products is advisable.
x Given the nascent market for ‘no rub’
disinfectant products, lens condition will have to
be monitored more closely in the future. For
deposit-prone wearers, adjustments to lens life
(a shortening) may be prudent if wearer comfort
and safety are to be maintained. It may also be
prudent to examine RGP lenses on, and off the
eye before cleaning, to assess more accurately
the condition of the lens surfaces (Terry et al.,
1989). If lens care is poor, the lens condition
usually mirrors this failing.

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 Lecture 7.3: Rigid Gas Permeable Contact Lens Complications and their Management

Ling T (1987). Osmotically induced central and peripheral corneal swelling in the cat. Am J Optom
Physl Opt. 64(9): 674 – 677.
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Lowther GE (1988). Patient compliance. ICLC. 15(5): 142.
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Lowther GE (1996). Can corneal topographers and computer programs fit RGP contact lenses. ICLC.
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Madigan MC, Holden BA (1992). Reduced epithelial adhesion after extended contact lens wear
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th
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McGeehon M (1988). Guidelines to handling problem patients. CL Forum. 13(4): 23 - 28.
McLaughlin WR, Schoessler JP (1987). Manufacturing defect in a rigid gas-permeable lens. ICLC.
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McMonnies CW (1983). Contact lens-induced corneal vascularisation. Int Contact lens Clin. 10: 12 –
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McMonnies CW (1984). Risk factors in the etiology of contact lens-induced corneal vascularisation. Int
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Stone J, Contact Lenses. 3rd ed. Butterworths, London.
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lens wear. Brit J Ophthalmol. 63: 478 – 481.

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McNamara NA et al. (1999). Tear mixing under a soft contact lens: Effects of lens diameter. Am J
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Polse KA et al. (1988). Ocular effects of hard gas-permeable-lens extended wear. Am J Optom Physl
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Rengstorff RH (1979B). Changes in corneal curvature associated with contact lens wear. J Am Optom
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Rengstorff RH (1981). Postwear Refractive Changes. In: International Ophthalmology Clinics:
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Rengstorff RH (1985). Corneal refraction: Relative effects of each corneal component.. J Am Optom
Assoc. 56: 218 – 219.
Rengstorff RH (1989). Chapter 20: Refractive changes after wearing contact lenses. In: Phillips AJ,
Stone J, Contact Lenses. 3rd ed. Butterworths, London.

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Ridder TR (1992). Pseudomonas corneal ulcer following patching of a corneal abrasion. Clin Eye Vis
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Robin JB et al. (1986). Peripheral corneal disorders. Surv Ophthalmol. 31: 1 – 36.
Ruben M (1975). Contact Lens Practice: Visual, Therapeutic and Prosthetic. Baillière Tindall, London.
Ruben M (1979). Visual disturbances from contact lenses. Ophth Opt. 19(Mar 17): 186 – 194.
Ruiz-Montenegro J et al. (1993). Corneal topographic alterations in normal contact lens wearers.
Ophthalmology 100: 128 – 134.
Ruskell GL (1989). Chapter 2: Anatomy and physiology of the cornea and related structures. In:
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Sager DP et al., (1992). ReNu system: A compliance study. CL Spectrum. 7(12): 39 – 44.
Sall K et al. (2000). Efficacy and safety of Cyclosporin ophthalmic emulsion in dry eye disease.
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Salmon TO (1992). Beneficial flexure – Using thin RGPs to correct residual astigmatism. CL
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Sandy LM, 1987). “Cracked glaze” phenomenon not so unusual. CL Spectrum. 2(4): 17.
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Sarver MD (1966). Comparison of small and large corneal contact lenses. Am J Optom Arch Amer
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Schnider C et al. (1986). Critical factors in avoiding adverse responses with hard gas permeable (HGP)
extended wear. Invest Ophth Vis Sci. 27(3)(Suppl.): 139.
Schnider CM et al. (1988). Unusual complications associated with RGP extended wear. ICLC. 15: 124
– 129.
Schnider CM et al. (1996). Effect of patient and lens performance on peripheral corneal desiccation. J
Am Optom Assoc. 67(3): 144 – 150.
Schnider CM et al. (1997). Effect of lens design on peripheral corneal desiccation. J Am Optom Assoc.
68(3): 163 – 170.
Schoessler JP, Woloschak M (1981). Corneal endothelium in veteran PMMA contact lens wearers. Int
Contact Lens Clin. 8: 19 – 25.
Schreiber M (2001). Tabloid squints over contact lens squabble. Japantoday (Japan Today Japan
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Schwallie JD et al. (1997). Corneal staining patterns in normal non-contact lens wearers. Optom Vis
Sci. 74(2): 92 – 98.
Schwartz C (1987). Solutions update ‘87: Beyond compliance. CL Forum. 12(10): 22 - 47.
Schwartz C (1989). Solutions survey: How does your practice compare? CL Forum. 14(9): 55 – 59.
Seidner L (1987). Wettability vs. surface deposits: Searching for a solution. CL Forum. 12(10): 50 –
52.
Seidner L (1987B). Balance: The key to RGP materials. CL Spectrum. 2(10): 32 – 34.
Seidner L, Sharp MS (1984). Surface deposits with gas permeable lenses. CL Forum. 9(Oct): 55 – 65.
Serrander A-M, Peek KE (1993). Changes in contact lens comfort related to the menstrual cycle and
menopause. A review of articles. J Am Optom Assoc. 64: 162 – 166.
Shannon BJ (1987). Don’t quit with the fit. CL Forum. 12(5): 46 – 48.
Sheard GM et al. (1995). Does solution costs affect compliance among contact lens wearers. J Brit CL
Assoc. 18(2): 59 – 64.
Sheedy JE et al. (1992). Task and visual performance with contact lenses and spectacles. Optom Vis
Sci. 69(5): 337 – 341.
Shiobara M, Holden BA (1989). The effect of front surface design on RGP lens comfort. Optom Vis
Sci. 66(12)(Suppl.): 162.

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Shulman PF, Zagar LA (1981). A study of the lens edge. CL Forum. 6(11): 45 – 55.
Sigband DJ (1988). Disposable contact lenses: The answer to noncompliance. ICLC. 15(12): 367 –
370.
Silbert JA (1990). Conquering residual astigmatism and RGP flexure. CL Forum. 15(11): 15 – 27.
Silk AA (1987). Puzzle of the polymers. Trans Br CL Assoc. 4: 57 – 61.
Simmons PA et al. (1996). Comparison between evening and morning surfactant cleaning of hydrogel
lenses. ICLC. 23(Sept/Oct): 172 – 175.
Smith RE, Flowers CW (1995). Chronic blepharitis: a review. CLAO J. 21: 200 – 207.
Smolek MK, Klyce SD (1995). Chapter 2. Physiology of the Cornea. In: Kastl PR (Ed.). Contact
Lenses: The CLAO Guide to Basic Sciences and Clinical Practice. Vol. I: Basic Science. Kendall/Hunt
Publishing Company, Dubuque.
Smith SK (1996). Patient noncompliance with wearing and replacement schedules of disposable
contact lenses. J Am Optom Assoc. 67(3): 160 – 164.
Snyder C (1998). A unique hydrogel phenomenon. CL Spectrum. 13(3): 16.
Snyder AC, Gordon A (1985). Refitting long-term asymptomatic PMMA lens wearers into gas
permeable lenses. J Am Optom Assoc. 56(3): 192 – 196.
Sokol JL et al. (1990). A study of patient compliance in a contact lens-wearing population. CLAO J.
16(3): 209 – 213.
Sorbara L et al. (1992). Effect of rigid gas permeable lens flexure on vision. Optom Vis Sci. 69(12):
953 – 958.
Sorbara L et al. (1996A). Centrally fitted versus upper lid-attached rigid gas permeable lenses: Part I.
Design parameters affecting vertical decentration. ICLC 23(May/June): 99 – 103.
Sorbara L et al. (1996B). Centrally fitted versus upper lid-attached rigid gas permeable lenses: Part II.
A comparison of the clinical performance. ICLC 23(July/August): 121 – 126.
Solomon J (1986). Causes and treatments of peripheral corneal desiccation. CL Forum. June: 30 –
36.
Stein HA et al. (1995). Chapter 8. Postfitting of Rigid Lenses. In: Kastl PR (Ed.). Contact Lenses: The
CLAO Guide to Basic Sciences and Clinical Practice. Vol. II: Soft and Rigid Contact Lenses.
Kendall/Hunt Publishing Company, Dubuque.
Stein RM et al. (1988). Infected vs sterile corneal infiltrates in contact lens wearers. Am J Ophthalmol.
105: 632 – 636.
Stevenson RWW (1988). Flexibility of hard gas permeable contact lenses. Optom Vis Sci. 65(11): 874
– 879.
Stevenson RWW (1991). Young’s Modulus measurements of gas permeable contact lens materials.
Optom Vis Sci. 68(2): 142 – 145.
Swarbrick HA (1988). A possible etiology for RGP lens binding (adherence). Int Contact Lens Clin. 15:
13 – 19.
Swarbrick HA (1991). Rigid Gas-Permeable Contact Lens Adherence: Frequency, Features and
Etiology. PhD Thesis. School of Optometry, The University of New South Wales, Sydney.
Swarbrick HA, Holden BA (1987). Rigid gas permeable lens binding: significance and contributing
factors. Am J Optom Physiol Opt. 64: 815 – 823.
Swarbrick HA, Holden BA (1996). Ocular characteristics associated with rigid gas-permeable lens
adherence. Optom Vis Sci. 73(7): 473 – 481.
Sweeney DF (1991). Factors Contributing to the Human Corneal Oedema Response. PhD Thesis.
School of Optometry, The University of New South Wales, Sydney.
Sweeney DF (1992). Corneal exhaustion syndrome with long-term wear of contact lenses. Optom Vis
Sci. 69: 601 – 608.
Sweeney DF, Holden BA (1987). Silicone elastomer lens wear induces less overnight corneal edema
than sleep without lens wear. Curr Eye Res. 6: 1391 – 1394.
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Sweeney DF, Holden BA (1991). The relative contributions of hypoxia, osmolality, temperature and
humidity to corneal edema with eye closure. Invest Ophth Vis Sci. 34(4)(Suppl.): 739.
Szczotka LB (1995). Interactive rigid contact lens fitting with the TMS-1 computerized
videokeratoscope contact lens program. ICLC. 22(Nov/Dec): 244 – 248.
Szczotka LB (1997). Clinical evaluation of a topographically based contact lens fitting software. Optom
Vis Sci. 74(1): 14 – 19.
Taylor AJ, Wilson SDR (1995). Post-lens tear film thinning in rigid gas permeable lenses. Optom Vis
Sci. 72(12): 849 – 856.
Terry JE, Hill RM (1977). The osmotic variable. J Amer Optom Assoc. 48(3): 311 – 313.
Terry R et al. (1989). Peripheral corneal ulceration in rigid gas permeable extended wear: A case
report. ICLC. 16(11&12): 323 – 326.
Terry R et al. (1989B). Rigid gas permeable lenses and patient management. CLAO J. 15(4): 305 –
309.
Thean JHJ, McNab AA (2004). Blepharoptosis in RGP and PMMA hard contact lens wearers. Clin Exp
Optom. 87(1): 11 – 14.
Tomlinson A et al. (2001). Effect of oral contraceptives on tear physiology. Ophthal Physl Opt. 21(1): 9
– 16.
Trick LR (1993). Patient compliance – don’t count on it! J Am Optom Assoc. 64(4): 264 – 270.
Tsubota K, Nakamori K (1995). Effects of ocular surface area and blink rate on tear dynamics. Arch
Ophthalmol. 113: 155 – 158.
Tsubota K et al. (1996). Quantitative videographic analysis of blinking in normal subjects and patients
with dry eye. Arch Ophthalmol. 114(6): 715 – 720.
Turner FD et al. (1993). Compliance and contact lens care: A new assessment method. Optom Vis
Sci. 70 (12): 998 – 1004.
Turner FD et al. (1993B). A new method to assess contact lens care compliance. CLAO J. 19(2): 108
– 113.
Ueda K, Nishida T (1997). The influence of the edge design on hard contact lens fitting performance. J
Jpn Cl Soc. 39: 284 – 289.
van den Bosch WA, Limij HG (1992). Blepharoptosis induced by prolonged hard contact lens wear.
Ophthalmology 99: 1759 – 1765.
Veys J, Davies I (1997). Basic contact lens practice: Part 6: Rigid contact lens fitting. Optician
210(5513): 16 – 23.
Walker J (1988). Overpolishing fluorosilicone-acrylates – the consequence and the cure. Trans Br CL
Assoc. 6: 29 – 32.
Walker J (1990). Cracking and crazing: A practitioner’s viewpoint. Optician 199(Apr 6): 19 – 21.
Wang J et al. (2003). Topographical thickness of the epithelium and total cornea after hydrogel and
PMMA contact lens wear with eye closure. Invest Ophth Vis Sci. 44(3): 1070 – 1074.
Wechsler, S (1978). Visual acuity in hard and soft lens wearers: a comparison. J Am Optom Assoc.
49(3): 251 – 256.
Wechsler, S (1979). Effects of rigid lens flexure on vision. J Am Optom Assoc. 50(3): 327 – 328.
Williams LJ (1988). The effects of contact lenses on the cornea with special reference to corneal shape
and the endothelium. A paper presented at the 30th Anniversary Conference of the New Zealand
Contact Lens Society, Wellington, New Zealand.
Williams-Lyn D et al. (1993). The effect of rigid lens back optic zone radius and diameter changes on
comfort. ICLC. 20(Nov/Dec): 223 – 229.
Wilson SE et al. (1990). Rigid contact lens decentration: A risk factor for corneal warpage. CLAO J. 16:
177 –182.
Wilson SE et al. (1990B). Topographic changes in contact lens-induced corneal warpage.
Ophthalmology 97: 734 – 744.
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Wilson G et al. (1995). Corneal epithelial fluorescein staining. J Amer Optom Assoc. 66(7): 435 – 441.
Woods CA, Efron N (1996). Regular replacement of daily-wear rigid gas-permeable contact lenses. J
Br Cont Lens Assoc. 19(3): 83 – 89.
Yamane SJ, Kuwabara DM (1987). Ensuring compliance in patients wearing contact lenses on an
extended-wear basis. ICLC. 14(3): 108 – 111.
Yap M (1991). Tear break-up time is related to blink frequency. Acta Ophthalmol. 69: 92 – 94.
York M et al. (1971). Variation in blink rate associated with contact lens wear and task difficulty. Am J
Optom Arch Am Acad Optom. 48: 461 – 466.
Yoshino M et al. (1996). Measurement of tear replenishment rate under a hard contact lens. Invest
Ophth Vis Sci. 37(3)(Suppl.): S75.
Young G (1988). Fluorescein in rigid lens fit evaluations. ICLC. 15(3): 95 – 100.
Zantos SG (1983). Cystic formations in the corneal epithelium during extended wear of contact lenses.
Int Contact Lens Clin. 10: 128 – 146.
Zantos SG (1984). Management of corneal infiltrates in extended-wear contact lens patients. Int
Contact Lens Clin. 11: 604 – 612.
Zantos SG, Holden BA (1977). Transient endothelial changes soon after wearing soft contact lenses.
Am J Optom Physiol Opt. 54: 856 – 858.
Zantos SG, Zantos PO (1985). Extended wear feasibility of gas-permeable hard contact lenses for
myopes. Int Eyecare. 1: 66 – 75

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314 IACLE Contact Lens Course Module 7: First Edition

Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

Unit 7.4
(2 Hours)

Lecture 7.4: Diagnosis and Management

of Dry Eye in Contact Lens
Wear

IACLE Contact Lens Course Module 7: First Edition

 Module 7: Contact Lens-Related Ocular Complications

Course Overview

Lecture 7.4: Diagnosis and Management of Dry Eye in contact

Lens Wear
I The Normal Tear Film and Lacrimal System
II Patient History
III Symptoms and Signs of Dry Eye
IV Mechanisms of Dry Eye
V Clinical Tests for Dry Eye
VI Laboratory Tests for Dry Eye
VII Management of Dry Eye
VIII Contact Lenses and Dry Eye

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Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

Lecture 7.4
(2 Hours)

Diagnosis and Management of

Dry Eye in Contact Lens Wear

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 Module 7: Contact Lens-Related Ocular Complications

Table of Contents

I Dry Eye and Contact Lenses: Introduction......................................................319

II The Tear Film ....................................................................................................321
III The Normal Lacrimal System..........................................................................326
IV Dry Eye .............................................................................................................341
IV.A Mechanisms of Dry Eye .............................................................................. 359
IV.A.1 Sjögren's Syndrome ................................................................................. 368
IV.B Clinical Tests for Dry Eye ............................................................................ 380
IV.B.I Clinical Test for Dry Eye: Non-Invasive..................................................... 381
IV.B.II Tear Film Interferometry........................................................................... 384
IV.B.III Clinical Test for Dry Eye: Invasive........................................................... 393
V Management of Dry Eye ...................................................................................410
VI Contact Lenses and Dry Eye ..........................................................................425
References ............................................................................................................445

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

I Dry Eye and Contact Lenses: Introduction

1 Of all the conditions presenting, or symptoms
reported, dry eye and/or dryness are among the
most common clinically, and all too frequently, the
most perplexing. The latter is partly due to the
nebulous nature of the condition, the vagueness of
DIAGNOSIS & MANAGEMENT the symptoms, and the frequent lack of supporting
signs/evidence.
OF DRY EYE IN
CONTACT LENS WEAR However, given the significance of the condition(s)
and its almost pervasive presence, especially in
SCL wearers, it warrants an in-depth coverage.
Fortunately, it is usually not a serious condition in
that it seldom threatens the health and vitality of the
97400-1S.PPT
anterior eye. However, along with discomfort and
7L497400-1 inconvenience, it is a major cause of lens wear
discontinuation. Jones (2001) attributed drop-out
rates of between 25% and 40% of wearers over
2 three years to the trilogy of dryness, discomfort, and
inconvenience.
DRY EYE & THE TEAR FILM A complete tear film is central to the health of the
Dry eye is due to a disorder, or anterior eye, and the optical performance of the
cornea (confirmed by Thibos et al., 1999).
disturbance, of the tear film
As any factor affecting the tear film has the potential
A complete tear film is essential to:
to affect the success of contact lens wear, the
• Ocular health existence of a dry eye is significant. It will be shown
that SCLs have a greater need for tear film integrity
• Optical performance of the eye than RGP lenses. This is probably because of their
• Successful contact lens wear complete coverage of the cornea and their
97400-275S.PPT
significant water content. Further, it will also be
shown that contact lenses affect the tear film. The
7L497400-275 most notable effect being a dramatic reduction in
tear break-up time, an indication of a reduction in
tear film stability.
3

DRY EYE & CONTACT LENSES

Dry eye is a common condition that affects:
• 20 to 75% of CL wearers
Nichols, 2000, Brennan & Efron, 1989

• 11 to 35% of non-CL wearers

Evans, 2001

• 25 to 50% of CL discontinuations
Fonn, 1999, Jones, 2001

97400-276S.PPT

7L497400-276

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4 Some of the difficulties that arise when trying to

diagnose dry eye are presented in the slide
DRY EYE: A DIFFICULT DIAGNOSIS
opposite.

• Ill defined
This lecture examines the tear film, dry eye, and dry
• The term given to a number of signs & eye and contact lens wear.
symptoms Note: In this lecture, the words mucus and mucous
are used extensively. Mucus is used to refer to the
• Wide range of vague symptoms tear component whereas mucous is used as the
related adjective, e.g. a layer of mucus, or the
• Not always accompanied by signs
mucous layer.
97400-277S.PPT

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

II The Tear Film

5 The Classic Tear Film:

CLASSIC TEAR FILM The classic tear film is presented as a three-layered

Air STRUCTURE structure dominated by its central aqueous
0.1Pm Lipid component. It is founded on a microvilli-anchored
Phase thicknesses

(after Holly & Lemp 1977 & Efron 1998)

layer of mucus overlying the corneal epithelium and

phases
Layer thicknesses not to scale
is topped by an evaporation-reducing (Iwata et al.,
1969) layer of lipids. Traditionally its thickness is
7Pm Aqueous given as being about 7 µm (Ehlers, 1965, cited in
Danjo et al., 1994, Holly and Lemp, 1977) to 10.3-
Tear

12 µm (Danjo et al., 1994).

.02-.05Pm Microvilli Mucus

In the traditional model, the mucous layer is
Epithelium 97400-87S.PPT
assigned to the corneal and conjunctival epithelia
with some justification because it is held in place by
7L497400-87 microplica of the epithelia’s superficial cells.
6 Alternative Structures from the Literature

ALTERNATIVE STRUCTURES Generally, there is broad agreement in the literature

Lipid
FROM THE LITERATURE
that the tear film is a three-layered structure whose
Aqueous
after Efron’s interpretation, 1998 thickness is of the order of 7 µm.
However, alternative structures have been
proposed, e.g. Lambert’s (1994) view is that the tear
41-46Pm

film is a 7 µm thick, two-layered structure.

Mucus
A more radical alternative, that of Prydal et al.
Lipid Mucinous
(1992), is that the majority of the tear film consisted
4-12Pm

glycoprotein Fibronectin

of mucus rather than aqueous, and presented tear

Aqueous matrix
Glycocalyx Lipid
Microvilli Microvilli Microvilli Microvilli
Mucus
Epithelium Epithelium Epithelium Epithelium film thicknesses of between 34 and 46 µm in human
Wolff
subjects. The differences between their results and
Prydal et al. Baier & Thomas Hodson & Earlam
1946 1992 97400-85S.PPT 1996 1994

7L497400-85
the commonly accepted thicknesses, were
explained by the optical (non-disturbing, non-
contact) interferometric method (described in Prydal
7 and Campbell, 1992) used to measure the film
thickness. To date there has been little support in
PROBABLE TEAR FILM STRUCTURE: the literature for these figures.
CURRENT THINKING ??
Non-polar lipids, Baier and Thomas (1996) proposed an ‘inverted’
Lipid Bilayer e.g. cholesterol
Aqueous Polar lipids, tear film, i.e. mucin on the outside, and the deeper
l
ge
e.g. phospholipids
layers composed of lipids. The authors assert that
ic
st lipids cannot form superficial layers as thick as the
la
continuum

oe
sc 0.1 µm film thicknesses observed clinically. Little or
vi
a
m
is no support for their views has been forthcoming to
fil
te
ar date.
e
Th
Mucin Current Thinking
Epithelium
97400-157S.PPT
Using in vivo cryofixation and scanning electron
7L497400-157 microscopy, Chen et al. (1997) found the rat to have
a tear film composed primarily of mucus with a lipid
layer covering its surface but without a free aqueous
layer as shown in the classic model of the tear film.
Anderton and Tragoulias (2000) also supported the
theory that relatively thick tear films were supported
by an elaborate mucous gel. Pflugfelder et al.
(2000) described the tear film similarly, i.e. a
hydrated mucus gel (slide 7).
Evans (2001) concluded that, since the literature
suggests that at least two thirds of the tear film
thickness is contributed by, or attributable to, mucin
which is extremely hydrophilic, it is unlikely there is
separation of the mucous and aqueous layers as in
the classic model of the tear film. Rather, she
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 Module 7: Contact Lens-Related Ocular Complications

believes it is more likely to be a gradient of aqueous

through to mucin in the form of a viscoelastic gel
with an overlying discrete lipid bilayer.
Wong et al. (1996) developed a ‘coating’ model of
the tear film that predicted tear film thinning and
break-up times close to experimental data. The
Break-Up Time (BUT) was related to:
x Tear viscosity.
x Surface Tension (ST).
x Tear Meniscus Radius (TMR).
x Initial and final tear film thickness.
8 The Tear Film: Published Data

THE TEAR FILM: SUMMARY (1 mm=1,000µm=1,000,000nm=10,000,000Å [Å is

an obsolete unit and is not used here])
• Total thickness: 3 - 12 Pm
• Lipid layer: 40 - 150 nm Thicknesses:
• Aqueous layer: 7 Pm x Lipid (oily) layer:
• Tear volume: 6.5 - 8.5 PL
– 40 to 150 nm (Holly & Lemp, 1977, Holly,
• Tear turnover rate: 15-16%/min
1978B, Norn, 1979, Olsen, 1985).
• Tear meniscus volume: 0.51 – 3.15 PL
• Osmolarity: 295 - 318 mOsm/L x Aqueous layer:
• Production rates: 0.5 - 1.78 PL/min – 7 µm (Holly & Lemp, 1977).
• Evaporation: 1.58 - 14.7 X10–7g/cm2/sec
97400-179S.PPT
x Aqueous layer: Thickness at tear break-up:
7L497400-179 – 1.5 to 4 µm (Holly & Lemp, 1977, Licznerski
et al., 1999).
Tear Volume
x 6.5 to 8.47 µL (Mishima et al., 1966, cited in,
Lamberts, 1994, Furukawa & Polse, 1978,
Lawrenson, 1993).
Tear Meniscus Volume – Lower
x 0.51 to 3.15 µL (Mishima et al., 1966, cited in
Mainstone et al., 1996, Holly, 1986, cited in
Mainstone et al., 1996, Mainstone et al., 1996).
Tear Turnover Rate:
x 15 to 16%/min (Mishima et al., 1966, cited in
Puffer et al., 1980,Puffer et al., 1980).
Refractive Indices:
x 0.9% saline: 1.33419 (Craig et al., 1995).
x ‘Tears’:
– 1.3357 to 1.337 (von Rötth, 1922, cited in
Duke-Elder, 1968, Fischer, 1928, cited in
Duke-Elder, 1968, Golding & Brennan, 1991,
Seal et al., cited in Craig et al., 1995, Patel et
al., 1994, Craig et al., 1995, King-Smith et al.,
1999).
x Tears in dry eye:
– 1.3351 ±0.0004 (Golding & Brennan, 1991).
x Tear lipids:
– 1.482 (1.46 – 1.53) (Tiffany, 1986).

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

9 x Epithelium:
– 1.376 to 1.401 (Aubert, 1876, cited in Duke-
THE TEAR FILM: SUMMARY Elder, 1968, Gullstrand, 1911, cited in Duke-
• pH: 6.50 - 7.83 Elder, 1970, Duke-Elder, 1932, cited in Clark
• Temperature (corneal): 34.2 - 34.8 °C & Carney, 1971, Patel et al., 1995).
• Temperature (conjunctival): 34.9 - 35.4°C Lactoferrin Levels:
• Surface tension: 35 - 43.6 mN/m x Normals:
• Lactoferrin levels: 1.5 - 1.68 mg/mL – 1.5 to 1.68 mg/mL (Janssen, 1986, cited in
• Refractive index (epithelium): 1.376 - 1.401 Craig et al., 1995, Craig et al., 1995, Foulks
• Refractive index (tears): 1.3357 - 1.3370 et al., 1999).
97400-180S.PPT
x KeratoConjunctivitis Sicca (KCS) (dry eye)
7L497400-180 cases:
– 0.35 ±0.2 mg/mL (Foulks et al., 1999).
Osmolality:
x 0.9% saline: § 292 mOsm/kg (Craig et al.,
1995).
x Tears:
– 294.9 to 318 mOsm/L (Gilbard & Farris,
1978, Benjamin & Hill, 1983, Craig et al.,
1995, Aragona et al., 1999, Foulks et al.,
1999).
– 0.96% sodium chloride equivalence (Terry &
Hill, 1977).
x KCS cases:
– 333.6 mOsm/L (Foulks et al., 1999).
x Diabetes:
– 332.2 mOsm/L (Aragona et al., 1999).
x With PMMA lenses:
– 0 to –0.1% change (i.e. 0.96 to 0.95%) (Terry
& Hill, 1977).
Tear Production Rates:

x –
x = 0.5 to 1.78 µL/min (Mishima et al., 1966,
cited in Puffer et al., 1980, Furukawa & Polse,
1978, Smolin, 1987, Maurice, 1990).
Tear Evaporation Rates:
x Normal:

– – –5 –7 2
x = 1.58 x 10 to 14.7 x 10 g/cm /sec
(Mishima & Maurice, 1961, cited in Hamano
and Kaufmann, 1987, Iwata et al., 1969,
Hamano et al., 1980, cited in Hamano and
Kaufmann, 1987, Rolando and Refojo, 1983,
Tsubota & Yamada, 1992, Tomlinson and
Cedarstaff, 1992, Mathers et al., 1993).
x Abnormal tear films (dry eyes):

– – –7 2
x = 8.17 to 47.6 x 10 g/cm /sec (Rolando
and Refojo, 1983, Tsubota & Yamada, 1992,
Mathers et al., 1993).

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10 Surface Tension:
x Normals:
TEAR FILM: NORMAL vs DRY EYE
– 35 to 43.6 mN/m (Holly, 1973, Holly & Lemp,
Parameter Normal Dry Eye
1977, Tiffany et al., 1989, Nagyová and
• Refractive index: • 1.3357-1.337 ƒ 1.3351 Tiffany, 1999).
• Lactoferrin • 1.5 - 1.68 ƒ 0.35
• Osmolality • 295 - 318 ƒ 334
x Dry Eye:
• Surface tension • 35 - 44 ƒ 50 – 49.6 ±2.2 mN/m (Tiffany et al., 1989).
• Evaporation • 4.07 - 14.7 ƒ 7.3 - 47.6
x Epithelium:
• NIBUT • 53% > 30 ƒ All <20
• Corneal temperature • 34.8 - 36.2 ƒ 34 – 67.5 to 69.3 mN/m (Tiffany, 1990, Tiffany,
97400-280S.PPT
1990B).

7L497400-280
pH of the Tear Film:
x Normal tear film:
– 6.5 to 7.83 (Chen and Maurice, 1990, Norn,
1990, Lawrenson, 1993, Lamberts, 1994).
x Under contact lenses:
– 7.3 behind PMMA & RGP lenses (Chen and
Maurice, 1990).
Corneal Temperature (Tsubota et al., 1997):
x @ RH 20%, 20°C
– 34.8 to 36.2°C.
x @ RH 80%, 20°C
– 35.9 ±1.1°C.
x @ RH 20%, 50°C
– 36.2 ±0.6°C.
x Open eye:
– 34.2 to 34.5°C (Martin & Fatt, 1986, Efron et
al., 1989, Fujishima et al., 1996)
x Closed Eye:
– 36.2 (±0.1)°C (Martin & Fatt, 1986)
x Other:
– dry eye 34.0 (±0.5)°C (Fujishima et al., 1996)
– under 0.07 mm SCL 34.6°C (Martin & Fatt,
1986)
– under 0.30 mm SCL 34.9°C (Martin & Fatt,
1986).
x Conjunctiva (Isenberg & Green, 1985)
– 34.9°C (±0.6)°C
– 35.4°C in 20-30 year olds
– 34.2°C > 60 years of age.

NIBUT (Tiffany et al., 1989)

x Tear NIBUT ‘normals’:
– 53% of normals > 30 sec.
x Tear NIBUT Dry Eye:
– All below 20 sec. (8.9 ±5.1 sec).

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

11 The Tears
Information about the apparent tenacity of the
TEAR FILM
human tear film has appeared in the literature.
• Tenacious Ehlers (1965, cited in Clark and Carney, 1971) and
Clark and Carney (1971) commented on the
- difficult to disrupt, even with significant force difficulty experienced in trying to forcibly disrupt the
tear film even when probes were applied ‘edge-on’.
- lids are incapable of exerting the necessary force
Clark and Carney believed that the eyelids normally
• Resilient only applied about 10% of the pressure required to
disrupt the normal tear film.
- once diluted, can restore osmolality in seconds
Furthermore, the tears have also been shown to be
97400-282S.PPT
resilient when diluted by hypotonic artificial tears
and other non-isotonic solutions. Holly and
7L497400-282 Lamberts (1981) found it took only seconds for the
tears to restore their osmolarity following the
instillation of non-isotonic solutions, provided the
dilution was not sustained. They believed that the
mild irritation and the volume increase caused by
such instillations contributed to the rapidity of the
recovery.
12 The Tear Proteins
Tear proteins account for about 1% of the tears
TEAR PROTEINS
Kijlstra & Kuizenga, 1994 (Holly, 1987). The main proteins are listed in the
slides opposite.
Principal proteins:
Berta et al. (1990) reported elevated levels of
• Secretory Immunoglobulin A (sIgA) plasminogen activators (PAs) in cases of corneal
and conjunctival diseases, especially contact lens-
• Lactoferrin
associated erosions, ulcers, keratitis, acute
• Tear-Specific PreAlbumin (TSPA) keratoconus, recurrent erosions, and bullous
keratopathy.
• Lysozyme
The tear protein TGF-D (Transforming Growth
97400-181S.PPT
Factor alpha) probably originates in the lacrimal
7L497400-181 gland. It also interacts with Epidermal Growth
Factor (EGF) receptors suggesting a role in corneal
physiology and wound healing (van Setten et al.,
13 1993). Other TGFs include:
x TGF ȕ-1 and ȕ-2 (Gupta et al., 1996).
TEAR PROTEINS
Other proteins: Holly and Hong (1982) found that, at physiological
• Amylase pHs, most tear proteins were negatively charged
• Plasminogen Activators (PAs) while the remainder were positively charged
– urokinoase (u-PA), tissue (t-PA) (lysozyme among them). Few were neutral.
• Plasmin
• Fibronectin (a high molecular wt. glycoprotein)
• Tryptase (from mast cells during inflamm. episode)
• Protease inhibitors
• Epidermal Growth Factor (EGF)
• Transforming Growth Factors (TGFs DEE)
97400-182S.PPT

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III The Normal Lacrimal System

14 Role of the Lacrimal System
A functional lacrimal system is vital to the health of
THE LACRIMAL SYSTEM
FUNCTIONAL ASPECTS the anterior eye. It has three main functions:
x Secretion of lacrimal (tear) fluid onto the surface
• Secretion of the anterior eye. This maintains a ‘moist eye’
and is responsible, at least partially, for the
• Distribution optical regularity of the anterior corneal surface.
x Distribution of tear fluid across the ocular
• Drainage surface.
x Drainage of tear fluid, and the subsequent
97400-2S.PPT
discharge of any contaminants the tear fluid has
‘collected’.
7L497400-2
Any malfunction or disturbance of any aspect of the
system’s processes has the potential to cause
anterior eye disease, not just a tear problem.
15 The Lacrimal System

THE LACRIMAL SYSTEM

Lacrimal Gland
The lacrimal gland consists of lobes of secretory
Aponeurosis of LPS
LPS (ts.)
Superior (orbital)
acini separated by connective tissue. The lobes
Superior canaliculus
La

Ou
crim
alg
portion
have tubular columnar secretory cells that form the
lan
Common canaliculus
tle
td
uc
ts
d
Inferior (palpebral)
acini (aicinar = berry or grape-like) (see slide 15 for
an artists interpretation). These empty into
.
portion
Puncta
.
secretory ducts leading to the lobes’ main ducts that
Lacrimal sac
Tears

Preseptal muscle
(deeper part)
(sectioned) Inferior canaliculus empty into the outlet ducts of the lacrimal gland
Naso-lacrimal duct
(after Walcott et al., 1994).
A so-called valve
(non-functional) Main lid actions In addition to the dominant secretory cells, other cell
Tear fluid
exits to nose 97400-155S.PPT
types associated with acini include:
7L497400-155 x Myoepithelial cells. These cells are located
about the duct, and in the basal portion of the
acini. The secretory products accumulate in
16 membrane-bound granules that increase in size
as they move towards the apex of the cell.
TEAR LAYER ORIGINS
PRIMARY GLANDS They are extruded from the granules into the
lumen of the excretory duct. The tears, as they
• Lacrimal glands
now are, are propelled along the ducts under
the contractile influence of the myoepithelial
• Accessory lacrimal glands cells that constrict the walls in peristaltic wave-
like contractions (after Lamberts, 1994).
- Wolfring (superior margins of tarsal
x Scattered throughout the interstitial spaces
conjunctiva: 4 in upper lid, 2 in lower lid)
between the secretory tubules are small groups
of:
- Krause (lateral, upper fornices, | 40)
97400-183S.PPT – lymphoid cells.
7L497400-183 – mast cells.
– fibroblasts.
The dominant immunoglobulin actively transported
across the secretory epithelium and secreted into
the tears is IgA (as a dimer coupled by a secretory
component) (Walcott et al., 1994).
Lacrimal gland secretion is viewed as a two-stage
process. The primary fluid resembles an ultrafiltrate
of blood plasma and is located in the region of the
acinus, and the proximal duct regions. Secondary
stages add potassium chloride-rich fluid in the more
distal parts of the ducts (Mircheff, 1989).
326 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

17 Accessory Lacrimal Glands

Normally, lacrimal fluid is supplied by both the
TEAR LAYER ORIGINS
lacrimal gland, and the accessory lacrimal glands
SECONDARY GLANDS
(of Wolfring and Krause). The latter number about
Mucus Secreting
60 in each eye (see slides 18 and 19).
• Goblet cells (conjunctiva)
• Subsurface vesicles (corneal) While these accessory glands have similar
structures and functions, the glands of Wolfring are
slightly larger (this section after Lamberts, 1994).
Lipid Secreting
• Meibomian glands (lids) It has been shown by Maitchouk et al. (1999), that
tear production by the accessory lacrimal glands is
• Glands of Zeis (lid margins)
sufficient to maintain a stable tear film. They
• Glands of Moll (lash roots) suggest it would be necessary to remove the
97400-184S.PPT

lacrimal gland, and partly remove the accessory

7L497400-184 lacrimal glands, to create a dry eye model in a
primate.
18

ORIGINS: TEAR FILM COMPONENTS

Lacrimal gland from Tiffany & Bron, 1978
(orbital portion)
Fornix

Meibomian
gland
orifices
Punctum
Caruncle
Punctum
Lacrimal gland
(palpebral portion)
Meibomian
gland
Glands of Krause orifices
Conjunctival
goblet cells

FRONTAL VIEW 97400-230S.PPT

7L497400-230

19
ORIGINS: TEAR FILM COMPONENTS
Upper fornix Glands of Krause

Palpebral conjunctiva (Conjunctival)

Goblet cells
Bulbar conjunctiva (MUC5AC, MUC2)
Glands of Wolfring
Tarsal plate

Meibomian gland
(Corneal)
Subsurface vesicles
(MUC1, MUC4)
Glands of Zeis emptying
into a lash follicle
Glands of Moll
Gland of Moll emptying emptying onto lid margin
into a gland of Zeis 97400-291S.PPT

7L497400-291

20 The Layers of the Tear Film: The Lipid Layer

The lipid layer is a holocrine secretory product
LIPID LAYER: ROLES
after Golding, 1994 mainly of the Meibomian glands located in the upper
• Retard evaporation (if stable & intact) and lower lids (for details see Lecture 7.2, III.E
• Stabilize tear film (lowers surface tension [ST]) Meibomian Gland Dysfunction (MGD) in this
module). Contributions are made by the glands of
• Prevent overflow onto lids (hydrophobic barrier)
Moll and Zeis, and less directly, by blood from the
• Lubricate passage of lids over eye Meibomian gland vasculature.
• Smooth surface for optical quality Nicolaides et al. (1981) proposed the name meibum
• Prevent film disruption by skin lipids for the excretory product of the Meibomian glands to
• Seal lids during eye closure. differentiate it from sebum, the sebaceous excreta
97400-185S.PPT
of glands in the skin, a different (Moore and Tiffany,
1981) and somewhat incompatible entity. However,
7L597400-185
as the Glands of Zeis and Moll are also involved in

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 Module 7: Contact Lens-Related Ocular Complications

21 the supply of lipids to the tear film, this suggests

that the tear lipid layer is not just meibum, rather it is
LIPID LAYER a complex of secretory products.
• Holocrine secretory product of: Meibomian The 0.1µm thick lipid layer consists mainly of (after
glands, glands of Zeis & Moll, blood serum Tiffany, 1979):
(vessels of Meibomian gland)
x Wax esters.
• Mainly wax and esters (59%)
x Cholesterol esters).
• Contains both polar & non-polar components
(outer layer) x Mono, Di, and Triglycerides.
• Phospholipids 15% (inner layer) (cholesterol, x Fatty alcohols.
triglycerides, free fatty acids)
x Free fatty acids.
97400-186S.PPT

x Phospholipids (these make up 15% of the

7L497400-186
Meibomian lipids [Nicholaides, 1986, cited in
22 Evans, 2001], see separate slide 22 on roles).
LIPID LAYER Obviously, to form a useful layer on and over the
PHOSPHOLIPIDS: ROLES aqueous phase of the tears in the normal eye, the
• 15% of Meibomian lipids
lipid layer must be in liquid form. However, with a
• Surfactant (probably anionic [–ve] phospholipids) :
hydrophobic lipid layer/underlying aqueous phase melting point of about 35°C, the lipid layer is always
- polar groups towards watery tear components close to its transition temperature when the eye is
(Korb et al., 1996) open. During eye closure, the temperature of the
- non-polar groups associate with non-polar tear
components (Shine and McCulley, 1999) anterior eye rises, due mainly to reduced
• May interact with mucus and other evaporation of the aqueous phase of the tear film,
macromolecules to: and the proximity of the palpebral vasculature to the
- p surface tension normally exposed cornea and lateral conjunctivae.
- n film structural integrity (stability)
97400-284S.PPT Lamberts (1994) makes the point that it is important
to understand that the lipid layer behaves essentially
7L497400-284
as a film, independent of the underlying aqueous
layer. The lipid film is anchored above and below at
23 the orifices of the Meibomian Glands on the lid
margins. Importantly, the lipid layer does not take
LIPID LAYER part in the flow of tears as they pass from the lateral
ABSENCE or NON-CONFLUENCE canthus to the nasal lacrimal puncta (see slide 15).
• 4X n in evaporation & an unstable tear Debris, including cellular debris, travels under the
lipid layer as it makes its way to the exit (the
film (Craig & Tomlinson, 1997)
lacrimal puncta). However, atmospheric tear film
• 7X n in evaporation (p corneal thickness) contaminants can be seen ‘floating’ upon the lipid
(Mishima & Maurice, 1962) layer. This material is more likely to find its way
onto the lid margins and roots of the lashes rather
• Thickness less critical than completeness than pass down the puncta and into the nose via the
and stability, for retarding evaporation canaliculi and lacrimal sac.
97400-285S.PPT

7L497400-285

24
LIPID LAYER
FACTORS AFFECTING

• n relative humidity
- increases lipid layer thickness
- increases comfort
• Expression of Meibomian glands
- p evaporation rate
- alters lipid interference patterns
• Lid scrubbing
97400-286S.PPT

7L497400-286

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

25 The Layers of the Tear Film: The Aqueous Layer

AQUEOUS LAYER The aqueous phase of the tears is mainly water
ORIGIN (98.2%) but also contains other entities. Some of
Derived mainly from: these are:

• Lacrimal gland &

x Soluble proteins:
– primarily lysozyme
- Glands of Wolfring (palpebral
conjunctiva) – lactoferrin
– tear-specific prealbumin.
- Glands of Krause (fornices)
x Electrolytes:
• Water: 98.2%
97400-187S.PPT – primarily sodium
7L497400-187 – potassium
26 – chloride
AQUEOUS LAYER Caffery, 1991 – calcium.
ORIGIN COMPOSITION
• Acinar cells • Proteins & enzymes; x Peptides.
(lacrimal gland) amylase, lysozyme,
lactoferrin, tear-specific
albumin, x Metabolites.
glycoproteins
• Plasma cells • Immunoglobulins (IgA, IgG) Details of the origin and composition are explored
(lacrimal gland)
• Blood serum further in slide 26.
• H2O, NaCl, urea,
(lacrimal gland) pyruvate, glucose, K+,
Ca++, Mg++,
some proteins
• Epithelial cells • Sloughed cells
(conjunctiva & cornea)
• Blood vessels • Serum components
(conjunctiva) 97400-166S.PPT

7L497400-166

27
The roles of the aqueous layer are presented in
AQUEOUS LAYER: ROLES slide 27 while those of the lipocalin component of
after Golding, 1994)
the aqueous appear as slide 28.
• A vehicle for O2 transfer to cornea
• Removal of metabolic wastes
• Flushing of noxious substances
• Antibacterial activity
• Lubrication (lid-globe)
• Corneal swelling (osmotic gradient, tear/cornea)
• Route for leucocytes & IgA
97400-188S.PPT

7L497400-188

28
AQUEOUS LAYER
LIPOCALIN
• The tear film’s lipid-binding protein
• Scavenges lipids
- delivers them to the aqueous
- n solubility of lipids in the tear film
- n surface tension (ST) of the tear film
- lipocalin & a polar lipid fraction o ST
• Maintains tear film integrity
after Glasgow et al., 1999, Pandit et al., 1999, Nagyyová & Tiffany, 1999
97400-287S.PPT

7L497400-287

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29 The Layers of the Tear Film: The Mucous Layer

MUCOUS LAYER The mucous layer is in intimate contact with the 3
ORIGIN nm lipid layer that covers the anterior surface of the
A layer of high-molecular weight muco-
glycoproteins
epithelial cells of the cornea and conjunctiva, and
probably originates from them (Blümcke et al.,
Derived from:
1967, cited in Hogan et al., 1971).
• Conjunctival goblet cells
• Subsurface vesicles The mucous layer is a layer of high molecular
• Crypts of Henle (tarsus)
weight muco-glycoproteins, described by Holly and
Lemp (1977) as a hydrated layer of mucoproteins
• Glands of Manz (limbus)
rich in sialomucin, derived primarily, but not only,
• Epithelial cells (cornea & conjunctiva)
from:
• Glands of Moll (lid margins)
97400-190S.PPT
x The goblet cells of the conjunctival epithelium.
7L497400-190 x Subsurface vesicles of the conjunctival and
30 corneal epithelium (Dilly, 1985). Sometimes
this source is described as being ‘non-goblet’
MUCOUS LAYER epithelial cells.
COMPONENTS
• MUC5AC main gel-forming mucin The other sources of mucins are listed in slide 29.
Ocular mucins are different from mucins elsewhere
• Some MUC1, MUC2, and MUC4 in the body including the skin of the adjacent lids.
• Goblet cell: MUC5AC & MUC2 Disulphide bonds in mucins help them form
viscoelastic gels. The main gel-forming tear film
• Subsurface vesicles: MUC1 & MUC4 mucin is known as MUC5AC.

• Sialomucins, sulphomucins Some MUC1, MUC2, and MUC4 (a messenger

97400-191S.PPT
RNA protein) are also present. Both MUC5AC and
MUC2 (the gel-formers) are derived from the goblet
7L497400-191 cells of the bulbar and palpebral conjunctiva. They
may contribute to the lubrication of the ocular
surface as well as the surface tension of the tear
31 film. They are also responsible for the envelopment
SUBSURFACE VESICLES (wrapping) and removal of debris from the anterior
CONJUNCTIVAL EPITHELIUM Mucoprotein
eye surface.
chains
ell
tc MUC1 (mainly) and MUC4 (to a lesser extent) are
Mucus layer

[long-chain
ble us ,
Go muc 5AC ] glycoproteins,
UC C
2 MUC1 & membrane-bound mucins produced by subsurface
Microvillus

[M MU MUC4]
& vesicles. They cover the superficial cells of the
corneal and conjunctival epithelia (slide 31).
Cell membrane According to Dilly (1985), membrane-bound mucin
is integrated into the epithelial surface by fusion of
Surface cell

conjunctival
of

epithelium

Subsurface vesicle fused with cell membrane

after Dilly, 1985
Subsurface vesicle: the epithelial cell membrane with mucin vesicles
Mucoproteins
MUC1
migrates towards cell’s
anterior surface
below the epithelial surface. These vesicles contain
&
MUC4
97400-152S.PPT
long-chain mucous glycoproteins joined to the
7L497400-152
vesicle’s membrane. The vesicle membrane
becomes incorporated in the cell membrane and
supplies the membranes of the microvilli that cover
32 the epithelium’s exposed surface.

MUCOUS LAYER It is believed that the role of subsurface vesicle-

ROLES derived mucus (MUC1 and MUC4) is to anchor the
goblet cell-derived mucus (MUC5AC and MUC2) to
• Removing debris
the surface membranes of the epithelial cells
• Preventing adhesion of debris & bacteria covering the eye (see Nichols et al. (1985).
• Spreading mucus Released glycoprotein extends some 2-5 µm into
• Anchoring mucins the tears forming the so-called glycocalyx (of MUC1
and MUC4). The roles of the mucous layer are
• Stabilizing the tear film summarized in slide 32. The mucous layer,
• Protecting the ocular surface particularly its glycocalyx component, may play a
97400-288S.PPT
role in maintaining the stability of the pre-corneal
tear film in the open eye, as well as providing
7L497400-288 surface protection (Nichols et al., 1983).

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

33 Significant lipid contamination (the presence of

lipids in the mucous layer in humans) was shown by
MUCOUS LAYER Caffery, 1991 Moore and Tiffany (1981). They found that the lipid
ORIGIN COMPOSITION in the mucus they assayed was virtually identical to
• Goblet cells • Sulphomucins, that from the Meibomian glands. Interestingly, Holly
(conjunctiva) sialomucins
stated that, should the mucus become saturated
• Crypts of Henle • Sulphomucins
(tarsus) with lipids, it begins to roll up under the shear forces
• Glands of Manz • Sialomucins generated by the moving lids, forming a fine fibrillar
(limbus) network initially. This network then collapses into
• Epithelial cells • Sulphomucins, coarser mucus threads (Adams, 1979).
(conjunctiva & cornea) sialomucins
• Glands of Moll • Little contribution Adams suggests that the formation and collapse of
(lid margins) the mucus network represents a system for the
97400-165S.PPT
removal of exfoliated surface cells and debris,
7L497400-165 invading organisms, foreign matter, and lipid-
contaminated mucus from the surface of the normal
eye. Tellingly, mucus of this network stains
positively for lipids (see Holly 1980).
It is conceivable that the so-called ‘mucin balls’
seen under some siloxane hydrogel lenses are the
result of these same shear forces breaking mucus
into small pieces (approximately spherical, probably
their free-form shape).
Contaminated mucus, containing the trapped
material it has gathered while on the anterior eye, is
ejected finally onto the skin of the lid at the nasal
angle as a ‘crust’ (Maurice, 1990). This is a
common finding on awakening and is sometimes
called ‘sleep’. Crusts can also be detected
occasionally during the day especially in dusty, dry,
or windy conditions. Maurice also considers mucus
entrapment to be a possible defence against
invading bacteria.
Using guinea pig data, Nichols et al. (1985)
suggested that the thickness of the mucous layer
over the cornea is thinner than that over the more
irregular conjunctiva. Using rats, Kessler et al.
(1995) concluded that conjunctival goblet cell
mucous secretion is mediated neurally, and that
such secretion could serve as an immediate
response to a need for ocular surface protection.
34 Tear Film: Protective Substances

TEAR FILM The tear film contains several protective substances

PROTECTIVE SUBSTANCES (slide 34).
from Dilly, 1994
• Lactoferrin Lactoferrin, present in the tears at a concentration
• Lysozyme of about 2mg/mL (Smolin, 1987), works by chelating
• Non-lysozyme antibacterial factor iron. Once iron is chelated, micro-organisms are
• Complement either killed, or attenuated, by iron deprivation.
• Anti-complement factor Lactoferrin may also:
• Interferon x Modulate complement activity in vivo.
• Immunoglobulins (esp. A, E & G)
• Lymphocytes x Be synergistic for a specific antibody.
97400-150S.PPT
x Enhance the action of lysozyme.
7L497400-150 Lysozyme is lytic to glycosaminoglycans and, in the
presence of complement, facilitates IgA
bacteriolysis.
Immunoglobulins:
x IgA neutralizes viruses and inhibits bacterial

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 Module 7: Contact Lens-Related Ocular Complications

adherence to the epithelial surface.

x IgG promotes phagocytosis and complement-
mediated bacteriolysis.
x IgE presence is increased in allergic
responses.
The concentration of immunoglobulins increases
during prolonged eye closure (sleep), and falls
again after eye opening.
35 The Normal Eye and Its Tear Film: Diagrammatic
The tear film on a normal eye is the result largely of
THE NORMAL EYE
inspired by Tsubota, 1998 a dynamic equilibrium between tear production, and
Tear tear drainage and evaporation. This state is
production
Tear
Lipids maintained at least partially by the antievaporative
Meibomian gland
Lacrimal gland
Glands of Wolfring
evaporation Glands of Moll properties of its surface lipid layer and the stabilizing
Glands of Zeis
Glands of Krause
influence of the mucin layer interface between itself
and the corneal epithelium.
Tear fluid
Puncta &
Mucin Lacrimal drainage system
Goblet cells MUC5AC, MUC2
Subsurface vesicles MUC1, MUC4
97400-218S.PPT

7L497400-218

36 Tear Film Secretion: Lacrimal Gland Innervation

LACRIMAL GLAND The lacrimal gland is innervated by the autonomic
INNERVATION nervous system and has both parasympathetic
• Autonomic nervous system: (acetylcholine, primarily [Lamberts, 1994]) and
- parasympathetic (secretion?) sympathetic (norepinephrine) nerve fibres, as well
- sympathetic (modulation of output?) as fibres that contain neuropeptides such as those
- fibres containing neuropeptides: listed in slide 36 (after Walcott et al., 1994).
– Vasoactive Intestinal Polypeptide (VIP)
– Substance P (SP) Mircheff (1989) and Lamberts (1994) state that the
– Leu-Enkephaline (L-Enk) rate of lacrimal gland fluid secretion is controlled
– Neuropeptide Y (NPY) primarily by the parasympathetic system, with
– Calcitonin Gene-Related Peptide (CGRP) modulation by the sympathetic system.
97400-192S.PPT

7L497400-192

37
LACRIMAL GLAND:
INNERVATION

• Lacrimal gland - a parasympathetic

organ

• Relationship between parasympathetic

& sympathetic systems is unclear

97400-274S.PPT

7L497400-274

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38
LACRIMAL GLAND
INNERVATION
• Parasympathetic:
– originate in the superior salivatory nucleus (in
brain stem)
– fibres synapse in pterygopalatine ganglion
– post-ganglionic secretory fibres pass to the
zygomatic n. (branch of trigeminal n. [N5])
– from the zygomatic n. they form connecting
branches that enter the lacrimal n.
– lacrimal n. innervates the lacrimal gland
97400-273S.PPT

7L497400-273

39
LACRIMAL GLAND
INNERVATION
• Sympathetic agonists may be able to
alter tear fluid quality/quantity
• Sympathetic:
- originate in the hypothalamus
- pass to the superior cervical ganglion
- then the carotid plexus
- and on to the lacrimal gland
97400-376S.PPT

7L497400-376

40 Innervation and Control of the Other

Components of the Lacrimal System
CONTROL OF OTHER LACRIMAL
SYSTEM COMPONENTS The control of the other components of the lacrimal
• Mucous secretion (Kessler & Dartt, 1993, Kessler et al., 1995): system are either neural, or by intracellular
– reflex neural stimulation of conjunctival messenger substances, e.g. the release of goblet
mucous cells
cell mucins by cGMP, or the release of fluids and
• Release of mucins from conjunctival goblet cells
by intracellular messengers (Jumblatt et al. 1993): electrolytes from the accessory lacrimal glands by
– Ca++ cAMP (see slides opposite).
– cyclic Guanosine MonoPhosphate (cGMP) The roles external factors may have in the control of
• Fluid & electrolyte secretion from accessory the lacrimal system, and the mechanisms involved,
lacrimal glands (Gilbard & Rossi, 1993): are not well understood.
– cyclic Adenosine MonoPhosphate (cAMP)
97400-193S.PPT
Some details of the types of innervation used to
7L497400-193 control the accessory lacrimal glands are presented
in slide 41.

41
CONTROL OF UPPER LID GLANDS
(in sheep) (Aisa et al., 2001)

• Acetylcholinesterase-positive innervation:
- glands of Zeis
- glands of Moll (some effect only)
- Meibomian glands
- lacrimal gland
• Paraformaldehyde-induced-fluorescence-
positive (FIF+) innervation
- glands of Moll
- glands of Zeis (less effective than AChase)
- Meibomian glands
- lacrimal gland
- conjunctiva (scarcely)
97400-292S.PPT

7L497400-292

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42 The Blink

THE BLINK: UPPER LID Eyelid motion, eyeball movement, tear distribution,
Doane, 1980 and tear drainage are all intermittently related in
• Descent begins with rapid acceleration serving the crucial function of maintaining a clean,
• Peak velocity reached | @ visual axis: stable tear film layer over the corneal surface
- 17 - 20 cm/sec (max. recorded 40 cm/s) (Doane, 1980).
• Remains closed 3 - 5 msec The flow of tears from the lacrimal gland, under the
• Accelerates upwards rapidly upper and lower eyelids, around the menisci, and
along the lid margins towards the puncta, and also
• Slows as starting position is approached
their drainage, depends upon the viscous properties
• Remaining movement (‘parking’) is performed of the tear fluid (after Pandit et al., 1999).
relatively slowly
97400-203S.PPT
Gravitational forces are relatively ineffective
7L497400-203 because of the thinness of the tear film. Surface
and interfacial forces between its various layers may
be relatively large and predominant in determining
43 the overall behaviour of the film (Pandit et al., 1999).
THE BLINK: LOWER LID Doane (1980) also provided some distinctions
Doane, 1980 between the two main types of blinks. These are:
• Movement is almost entirely HORIZONTAL x Normal (involuntary): (see slide 43).
• Movement is directed nasally: Incomplete blinks are faster (shorter distance to
- some 2 - 5 mm is normal travel?), and the stationary phase at the lowest
• In some individuals the lower lid may move point of travel is usually shorter. This may be
downwards 1 - 2 mm related to gaze fixation/concentration, and the
• Lower lid movement has ramifications for: need to have the vision obstructed minimally
- tear fluid and tear debris movement (see comments on concentration and dry eye
- tear drainage induction in Factors Affecting Blinking,
- toric lens rotation opposite slide 53). It is the downward motion of
97400-204S.PPT

the upper eyelid that wipes the cornea clean of

7L497400-204
accumulated debris. The mainly horizontal
44 movement of the lower lid moves the debris-
carrying tears towards the nasal puncta.
TYPES OF BLINK Once tear film debris arrives at the nasal
(Doane, 1980)
canthus it may:
• Normal (involuntary):
– pass through the puncta to the lacrimal sac
- no movement of the globe and then into the nose
- usually incomplete (up to 75%) – gather in the corner of the eye encased in
- not controlled consciously mucus. It can be removed from there with a
finger
- complete blinks must occur (to rewet
& resurface cornea completely) – be discharged onto the skin adjacent to the
lid margin, and possibly be associated with,
97400-205S.PPT
or attached to, the root of an eyelash.
7L497400-205 Miller (1967, cited in Doane, 1980) found that
the eyeball moved backwards some 10.3 mm
45 on average, with each blink. Doane, who found
only 1-6 mm displacement, postulated that this
TYPES OF BLINK movement is central to the removal of lipid-
(Doane, 1980) contaminated mucus from the epithelium, and
the resurfacing of the epithelium with mucus.
• Forced (voluntary or when lid movement
x Forced (voluntary) blink, e.g. when upward lid
restrained): motion is restrained forcibly.
- complete Owens and Phillips (2001) found that, after a blink,
tears spread upwards over the cornea rapidly, and
- Bell’s phenomenon seen
stabilized (zero velocity) in 1.05±0.3 seconds.
Meibomian gland expression reduced the initial
velocity markedly. However, the stabilization time
remained normal. The inhalation of an irritant
97400-206S.PPT

7L497400-377 decreased stabilization time but left the initial

velocity unchanged.
334 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

46 The in situ Tear Film During Blinking

The tear film undergoes a cyclic, almost concertina-
A BLINK: THE TEAR FILM
OPEN CLOSING CLOSED OPENING
like, compression/thickening and stretching/thinning
cycle, under the influence of the closing and
opening eyelids respectively. This is especially
Local
lipid thickening &
applicable to the superficial lipid layer.
crumpling
Duplex
lipid Lipid The tear drainage system is also affected by the
film
100-150 nm
thick
monolayer
blink (see next).
Local
lipid thinning &
Thick
spreading
crumpled
100 Pm thick
lipid layer

97400-228S.PPT
after Holly, 1980

7L497400-228

47 Blinking and Tear Film Drainage

The blink also plays a major role in the drainage of
THE BLINK: ROLES tears from the anterior eye. The main aspects of
• Sweeps tear-borne debris towards the tear drainage are listed in the slide opposite.
puncta It has already been shown that both eyes blink in a
• Assists the envelopment of tear debris harmonious and conjugate way (Stava et al., 1994).
by mucus Stava et al. showed that even though differences
• Renews/re-lays the superficial lipid layer may be induced in the amplitude of the blinks and
their peak velocities, the duration of the blinks
• Resurfaces the mucous layer
remain ‘time-locked’, i.e. synchronous.
• Powers tear removal by modulating the
calibre of the canaliculi Wilson and Merrill (1976) showed that voluntary
97400-206S.PPT
blinks, tight lid squeezing, eye movements, and
7L497400-206
pressure changes in the nose all resulted in
pressure changes in the canaliculi.

48
TEAR DRAINAGE

• Lacrimal sac not essential to process (Toti,

1904 cited by Sahlin & Chen, 1997)

• Affected by blink rate and gravity (Shalin

and Chen, 1997)

• | 2 PL per blink
97400-207S.PPT

7L497400-207

49
TEAR DRAINAGE
• Canaliculi are the ‘pumps’ (Frieberg, 1917
cited in Sahlin & Chen, 1997)

- blink-powered ‘compression-dilation’
cycle (Frieberg cited in Sahlin & Chen, 1997)
- inner orifice of canaliculus acts as a
one-way valve (directing flow towards
the lacrimal sac)
- mutual occlusion of the puncta
97400-208S.PPT

7L497400-378

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50
TEAR DRAINAGE (PUMP)
after Doane (1980)
• Canaliculus filled with | 1.5 PL of tear fluid
• Orbicularis oculi (OO) contracts, eye starts to close
- upper lid moves down, lower moves nasally
• Lid margins near puncta protrude towards each
other
• Both puncta meet forcefully when eye is only half
closed
• Their forced meeting occludes both puncta
• Further eye closure compresses the canaliculus &
the lacrimal sac
• Fluid in canaliculus is expelled into the nose
97400-296S.PPT

7L497400-296

51
TEAR DRAINAGE (PUMP)
• Canaliculus/sac volumes are minimal at the moment
of maximum eye closure (maximum lid
compression)
• As eye reopens, compressive forces p
• Elasticity of canaliculus & sac walls induce volume n
• ‘Valve’ action of the distal (sac) end of the
canaliculus and valve of Hasner (at distal end of
nasolacrimal duct) prevent tear fluid & air being
drawn back into the tear drainage system, i.e. flow is
unidirectional (outwards)
97400-297S.PPT

7L497400-297

52

TEAR DRAINAGE (PUMP)

• The puncta are still occluded (by each other)
• Expanding canaliculus & sac volumes induce an
increasing negative pressure within their system
• The eye continues to open
• As the puncta finally part, the negative pressure
generated draws tear fluid from the local lid-globe
meniscus (lacrimal lake) for 1-3 sec
• This re-primes the canaliculus and the cycle is
ready to be repeated
97400-298S.PPT

7L497400-298

53 Factors Affecting Blinking

Blinking is central to the propulsion of tears from the
FACTORS CONTROLLING BLINKING
• Reciprocal innervation of the LPS (opening)
temporal anterior eye towards the nasal puncta.
& the OO (closing) Any blink abnormality has the potential to disturb
• Smoothness of lid movements depends on tear spreading (distribution) and/or cause anterior
coordination of two brain-stem cranial motor eye surface problems (Doane, 1980).
nuclei:
- LPS motorneurones (in caudal central The normal blink rate is quite variable although it is
subnucleus of N3 [oculomotor n.]) usually between 15 to 20 blinks per minute under
- OO motorneurones (a subdivision of the relaxed conditions according to Tsubota (1998).
facial nucleus of N7 [facial n.]) Other rates have been reported, e.g. 12 per minute
- neither location nor pathway of (Carney and Hill, 1992) and 24.8 per minute (17.2
coordination is known Stava et al., 1994 with anaesthetic) (Collins et al., 1989).
97400-294S.PPT

7L497400-294
The literature on the blink and relevant factors
affecting it are summarized in the slides opposite.
336 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

54 Ponder and Kennedy (1928, cited in Tsubota, 1998)

noted that blinking does not change in a dry sauna
FACTORS AFFECTING BLINKING (high temperature, >50°C, low relative humidity
Ocular Surface: [RH]). Mori et al. (1997) and Tsubota et al. (1997)
• Tear evaporation (Tsubota & Nakamori, 1995) hypothesized that this lack of change was due to the
• Ocular surface condition (Tsubota et al., 1996, Nakamori et
primary determinant of the blink rate being
al., 1997) decreased corneal temperature, which does not
• Ocular surface area exposed (Nakamori et al., 1995) occur in a sauna. Tsubota et al. (1997) actually
reported a decline in blink rate (from 17.5 to 6.2
• Lipid contamination of the mucous layer (Holly, 1973,
Doane, 1980) blinks per minute) in saunas.
• Tear stability (Collins et al., 1989, Al-Abdulmunem, 1999) Various studies by workers associated with Tsubota
• Tear thickness (Prause & Norn, 1987, Collins et al., 1989) showed that at any given humidity under more
97400-194S.PPT
normal circumstances, the blink rate was inversely
7L497400-194 proportional to the ambient temperature. However,
in a dry sauna, it seems likely that any cooling effect
due to tear evaporation is swamped by the high
55 ambient temperature. Consequently, dry eye
sufferers are advised to close their eyes as much as
FACTORS AFFECTING BLINKING possible while in a dry sauna.
External Factors:
• Air temperature (p rate with n temperature)
Discomfort has been reported when concentrating
• Topical anaesthesia (p Collins et al., 1989, Nakamori et al., 1995) on games, and computers screens (e.g. York et al.,
• Wind (n rate) 1971, Campbell and Durden, 1983, Patel et al.
• Humidity 1991, and Suber et al., 2001). This was postulated
Tasks Demanding Concentration (York et al., 1971): to be caused by a thinning of the lipid layer resulting
• VDUs, computers, computer games
• Conversing (Records, 1979 cited in Collins et al., 1989)
from the reduced blinking inherent under these
No Effect (Tsubota, 1998) circumstances (reduced Meibomian gland output,
• Age lack of spreading/resurfacing of the tear layer,
• Sex prolonged opportunity for evaporation?). High
97400-293S.PPT
relative humidities reduced problems of infrequent
7L497400-293 blinking significantly (from an Optistock [2001B]
56 summary of an article appearing in the 2001 May
Review of Optometry).
Sharma and Ruckenstein (1985) suggested that the
FACTORS AFFECTING BLINKING
blink was induced by the aqueous phase of the tear
• Dry eye (compensates by rate n) (Tsubota & film coming in contact with the hydrophobic corneal
Nakamori, 1995)

• In dry eye cases, artificial tears almost

epithelium.
normalize blink rates and MBIs (Nakamori et al., Alternatively, Mengher et al. (1985) suggested that
1995)
the breakdown of the anterior eye tear film over the
• Low blink rates are associated with long
bulbar conjunctiva, i.e. a breakdown of the tear film
BUTs and vice versa (Prause & Norn, 1987)
outside the confines of the cornea, stimulates a
- in Sjögren’s syndrome (short BUTs), blink before a break over the cornea occurs.
n blink rate prevents tear break-up
97400-295S.PPT
Holly (1973, cited in Collins et al., 1989), and Doane
(1980), suggested that tear film break-up was
7L497400-295
based on gradual lipid contamination of the mucous
57 layer.
A parameter, the Maximum Blink Interval (or MBI),
MAXIMUM BLINK INTERVAL was introduced by Nakamori et al. (1997), to
after Nakamori et al., 1997
describe clinically one aspect of blinking (slide 57).
Nakamori et al. suggested MBI is a more useful
measurement of tear film stability than tear BUT
measurements.
Maximum Blink Interval
(MBI)

MBI: The longest time subjects

can keep their eyes open comfortably
97400-156S.PPT

7L497400-156

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58 Epithelial Wettability
Based on the early work of Holly and Lemp (1971),
EPITHELIAL WETTABILITY
the epithelial surface per se was believed to be
• Early opinion was that the epithelial surface hydrophobic.
was hydrophobic
• More recent thinking suggest it is hydrophilic: However, Cope et al. (1986) stated that the
– ST higher than previous estimates assumption of epithelial hydrophobicity conflicted
– ST of bare epithelium similar to mucus- with most current theories of cell membranes.
covered epithelium (Tiffany, 1990) Additionally, Levenson (1973, cited in Cope et al.,
— therefore mucus NOT essential to 1986) found that, in the rabbit eye, any direct air
epithelial wettability drying of the cornea resulted in severe and
– different cell ages = different wettability of irreversible damage. Cope et al’s results showed
individual cells? (Tiffany, 1990)
97400-208S.PPT
that wiping the epithelial surface to remove mucus
was also damaging (confirmed by Tiffany, 1990,
7L497400-208 and Tiffany, 1990B using two different techniques).
Since these issues were applicable to the original
Holly and Lemp studies, doubts arose about the
veracity of the conclusion of epithelial
hydrophobicity.
If the epithelium is not hydrophobic, the concept of a
layer of mucus being essential to epithelial
wettability is questionable.
Current thinking favours a hydrophilic epithelium.
59 Tear Film Break-Up
TEAR FILM BREAK-UP The exact mechanism of tear film break-up is not
THEORIES known but many theories exist. In no particular
• Mucous layer thinning: order these include:
- aqueous phase comes into contact with the
epithelium (assumed to be hydrophobic?) Mucous Layer Thinning:
• Lipid contamination of the mucous layer: Most theories depend on the supposition that, at
- excess lipid contamination of the mucous some stage in the process that leads to tear film
layer thins it break-up, the aqueous phase of the film comes in
- mucous layer becomes unstable contact with the supposedly hydrophobic epithelium.
- lid shear forces roll mucus fibrils that
contain contaminants Sharma and Ruckenstein (1985) postulated that,
- mucus is resurfaced & cycle repeated because thin films eventually become destabilized
97400-209S.PPT
and rupture due to the van der Waal’s dispersion
7L497400-209 forces acting on them (sometimes also referred to
as London forces, or simply dispersion forces, see
Moore et al., 1978), contact between the aqueous
60 phase and the underlying epithelium is inevitable.
Simple contact between the aqueous and
TEAR FILM BREAK-UP
epithelium is claimed to result in tear film break-up.
THEORIES
• Simple evaporation is not a plausible Lipid Contamination of the Mucous Layer:
explanation (Sharma & Ruckenstein, 1985)
Holly (1973), Holly and Lemp (1977), and Holly
• Usually, tear break-up occurs over the cornea
and not the conjunctiva (1981) maintain that the crater-like breaks that form
- the mucous layer may be thinner over the
in the tear film, and increase in area the longer a
cornea (no goblet cells) blink is delayed, are not the result of breaks in the
- thinner layers are easier to rupture (Sharma & lipid layer as was originally thought. Rather, they
Ruckenstein, 1985)
believe that film rupture is the result of excess lipid
• Tear film rupture tends to occur over
irregularities in the aqueous-mucous layer
contamination of the underlying mucous layer, and
interface that once this contamination occurs, tear film break-
97400-299S.PPT
up is immediate.
7L497400-299
Holly and Lemp (1977) assert that the normally
hydrophilic mucus is rendered hydrophobic by the
lipid contamination that occurs from the constant
bombardment of the mucous layer by lipids
presumably in the aqueous. Eventually, the mucous
layer becomes unstable in its thin-layer form. At this
point the heavily contaminated mucus, with the
assistance of the shear forces generated by the
338 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

blinking lids, rolls up to form mucin fibrils that in turn

aggregate to form threads of mucus. Thus the
mucous layer has two roles, that of an agent to
lower the surface tension of the tear film (increase
wettability), and that of a renewable vehicle for the
removal of tear film contaminants.
Tear Film Evaporation:
Early theories relied on the simple supposition that
excessive tear film evaporation (of the aqueous
layer mainly) was sufficient to cause the tear film to
rupture. However, citing data from Mishima and
Maurice (1961), Sharma and Ruckenstein argue
that, in the presence of a normal lipid layer, a break
in the tear film due to simple evaporation is
impossible in the short term (<10 min). The tear
film thins at an approximately linear rate during the
interval between normal blinks, and has a terminal
thickness of between 1.5 and 4 µm before the tear
film ruptures. Therefore, simple evaporation is not
a plausible explanation for tear film failure because
under normal circumstances only about 7% of the
aqueous layer evaporates in one minute. On this
basis, a full-thickness loss to evaporation would
take more than 10 minutes. On the other hand, dry
spots can appear in less than one minute after
blinking.
Tomlinson et al. (1991) investigated the relationship
between tear production and tear evaporation in the
normal eye, and found no significant correlation
between these two factors. It had been suggested
that tear production was triggered by the elevated
tear osmolality that results from evaporation. They
concluded that tear production regulation through
the mechanism of tonicity change may not be the
only, or principal, mechanism in the normal eye and
that other mechanisms may apply.
Surface Irregularities:
Liu et al. (2002) studied the reoccurrence of tear
break-up using an invasive (fluorescein) technique
and failed to show that epithelial, or bound mucin
layer, irregularities were implicated in the location of
any tear film break-up. Instead, they attributed the
location to lid-tear film interactions, or blink-induced
shear stresses within the tear film.

61
TEAR FILM BREAK-UP
SUMMARY
• Not simply evaporation
• At some stage, the aqueous phase comes in
contact with the epithelium
• The mucus layer:
- lowers tear film surface tension
- is renewable
- is contaminated by tear lipids
• Epithelial or other surface irregularities do not
determine the location of tear film breaks
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62 Basal and Reflex Tears

TYPES OF TEARS Two main types of tears are generally recognized,

BASAL & REFLEX although not all authorities agree on this division:
Basal:
x Basal tears. While acknowledging that true
• The tear film covering the eye constantly basic tearing may not exist, Fujishima et al.
Reflex: (1996) define this term as basic tearing caused
• Tears stimulated physically or emotionally by such subtle and constant stimuli as blinking,
and the temperature changes due to tear
BOTH types are produced by the main & evaporation. In this way, a tear film covers the
accessory lacrimal glands anterior eye constantly. Most patients with low
Usually, good reflex production exists even basal tear volumes (low Schirmer Test results)
when basal tear volume is low
97400-283S.PPT
still have good reflex tear production. Tsubota
presented one possibility as being a
7L497400-283 neurosensory abnormality involving either the
production or reception of a neurotransmitter.
x Reflex tears. This type of tearing is produced
by strong physical or emotional stimulation of
the lacrimal gland. These tears contain
essential components such as vitamin A and
EGF for the proliferation and differentiation of
corneal and conjunctival epithelia.
63 The Tear Film During Eye Closure
THE TEAR FILM DURING EYE Gilbard et al. (1992) studied the normal tear film at
CLOSURE Sack et al., 1992 the instant of eye opening following a period of
• Increases (open o closed): sleep. They found the tears had decreased
- total protein (2 X) osmolarity, and the inferior marginal tear strip (lower
- secretory IgA (10 X) tear meniscus) was absent. These findings were
- serum albumin (18 X) postulated to be of significance to SCL binding
• Complement C3 activation during sleep and the development of recurrent
• Unchanged: corneal erosions on awakening.
- lysozyme
Sack et al. (1992) concluded:
- lactoferrin
- tear-specific albumin x Reflex tears and closed-eye tears represented
97400-210S.PPT
opposite extremes in both composition and
7L497400-210 likely origins.
x Reflex tears are derived from lacrimal or
accessory gland secretions that are inducible
64 neurologically.
THE TEAR FILM: CLOSED EYE – reflex tears are composed mainly of
Sack et al., 1992 lysozyme, lactoferrin, tear-specific albumin,
• Reflex secretion either ceases or diminishes
greatly and a minor mixed alpha to beta globulin
• Ongoing slow flow maintained by secretions fraction.
that are mainly sIgA The conclusions of Sack et al. (1992) regarding the
• Eye is in a state of sub-clinical inflammation changes to the tears resulting from eye closure are
- marked rise in albumin presented in slide 64.
- n sIga (n protection?)
- but….closed eye may have n susceptibility
to inflammation & immune-mediated
processes during EW
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IV Dry Eye
65 Dryness Sensation
The ‘dryness’ sensation is not well understood and
DRYNESS SENSATION ‘dryness’ receptors have yet to be identified in the
• No ‘dryness’ receptors in the eye human eye. Further, some stimuli can be
• Coding of afferent neural input misinterpreted as the sensation of ‘dryness’, or
simply the absence of the normal level of ‘wetness’
• Misinterpretation of neural stimuli
or simply not ‘wet’.
- mechanical
- lens dehydration/surface effects
- vasodilation
- temperature
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66 Dry Eye: Prevalence

DRY EYE General:
PREVALENCE The terms dry eye and KeratoConjunctivitis Sicca
Difficult to determine: (KCS) imply a highly reduced or absent tear film that
• Ill-defined condition often is not clinically demonstrable, despite the
Depends on the: presence of other signs or symptoms (Rolando et
• Definition used al., 1983). KCS, a term frequently used in a
• Diagnostic test used to assess collective, or cover-all sense, most often refers to
that form of dry eye occurring in middle-aged and
• Practitioner
elderly adults, especially post-menopausal women,
• Patient tolerance that is of gradual onset.
• Time of day
97400-90S.PPT
The condition is ill defined, and the term ‘dry eye’,
like KCS, is used commonly as a cover-all
7L497400-90 description in a variety of circumstances.
67 Although contact lens wearers often describe
DRY EYE feelings of dryness, the majority of dry eye sufferers
PREVALENCE are not, and have never been, contact lens wearers.

Related to: In a questionnaire-based study of the Japanese

general population, Shimmura et al. (1999) found a
73% awareness of a condition called ‘dry eye’. Most
• Age
information about ‘dry eye’ was obtained from the
general media, and relatively little came from health
• Gender care professionals. As many as 33% of
respondents had self-diagnosed ‘dry eyes’, 25% of
• Environment whom were already using over-the-counter dry eye
97400-95S.PPT
preparations on a daily basis. Interestingly, most
respondents using some form of eyedrops were
7L497400-95 dissatisfied with their therapeutic efficacy.
Erickson et al. (2001) cautioned that the
68 patient/sufferer’s interaction and communication
styles, and their sense of well-being, influence self-
DRY EYE: PREVALENCE reporting of dryness symptoms and that these
SUMMARY: GENERAL POPULATION
factors need to be taken into account when
• 6.6% (female) • Schaumberg et al., 2000 interpreting questionnaire responses.
• 2.8% (male) • Schaumberg et al., 2000 Brewitt and Sistani (2001) claimed that one in four
• 10.8% (average) • Albietz, 2000 (25%) ophthalmological consultations in Germany
were for dry eye complaints, and called for
• 15.3% • Toda et al., 1993
standardization of both the terminology and tests for
• 15.5% (25.5%?)(<45) • Bowden & Harknett, 2001 dry eye.
• 33% • Shimmamura et al., 1999 Toda et al. (1993) reported 15.3% of subjects in a
97400-306S.PPT
large study (n=524) were diagnosed as having dry
eye with symptoms, and 21.2% had symptoms of
7L497400-306 ocular fatigue. Importantly, more than half (51.4%)
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69 of the fatigue sufferers had dry eye, an association

that was statistically significant.
DRY EYE: PREVALENCE
SUMMARY: EFFECT OF AGE
The incidence of dry eye in general ophthalmic
practice has been estimated to be 2% or higher
• 7.3% (<40) • Albietz, 2000 (Golding and Brennan, 1992).
• 18.1% (>40) • Albietz, 2000 Age:
• 11.3% (>60) • Schein et al., 1996 Strickland et al. (1987, cited in Evans, 2001) found
• 14.9% (aged pop.) • Jacobsson et al., 1989 a prevalence of 35% in an aged population (63 to 92
• 15.5% (25.5%?)(<45) • Bowden & Harknett, 2001 years) while Schein et al. (1996) presented a figure
of 11.3% for a similar population. In a younger
• 20% (>45) • Brewitt & Sistani, 2001)
population (55 to 72 years), Jacobsson et al. (1989,
• 35% (>60) • Strickland et al., 1987 cited in Evans, 2001) the prevalence of dry eye was
given as 14.9%.
97400-307S.PPT

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Albietz (2000) gave an overall dry eye prevalence of
10.8% (n=1584), but her figure rose to 18.1% in
70 those over 40 years of age, and declined to 7.3% in
those under 40.
DRY EYE: EFFECT OF GENDER Albietz found the following subtypes:
• 3 : 2 F : M (Caffery, 1998) x Lipid anomaly dry eye: 4%. Lipid anomalies
were also more prevalent in those over 40 years
• 46 : 1 F : M severe dry eye
of age.
• 11 – 35% females (Evans, 2001)
x Primary mucin anomalies, allergy, toxic dry eye:
• 6.6% : 2.8% F : M (Schaumberg et al., 2000) 3.1%.
• HRT may increase incidence (Schaumberg et al., 2000)
x Lid surfacing/blinking anomalies: 1.8%.
• Oral contraceptives: no difference (Tomlinson et al., 2001)
x Aqueous tear deficiency: 1.7%. This type of dry
97400-303S.PPT eye was also the only subtype that was more
prevalent in women. Aqueous deficiency was
7L497400-303
also more prevalent in those over 40 years of
age.
71 Albietz’s finding that lipid anomalies are more
common that aqueous deficiencies is at odds with
DRY EYE: EFFECT OF ENVIRONMENT
Lamberts (1994B) who reported the reverse.
• 72% in aircraft (McCarty & McCarty, 2000) Brewitt and Sistani (2001) accepted published data
that suggested up to 20% of adults over 45 years of
• 51% contact lens wearers (Bowden et al., 2001) age experience dry eye symptoms.
• 15% contact lens wearers (Schaumberg et al., 2000) Bowden and Harknett (2001), using a McMonnies
Dry Eye Questionnaire, surveyed students (98% of
• 40% VDU users (Harknett & Bowden, 2001) respondents were <45 years of age) for dry eye.
They found 15.5% had scores suggestive of
• 60% air-conditioning (Harknett & Bowden, 2001)
marginally dry eye and a further 10% gave
97400-304S.PPT borderline dry eye scores.
7L497400-304 Sex:
72 Females have a greater incidence of lacrimal gland
adenitis and autoimmune disease than males, and
THE DRY EYE are more susceptible to fibrotic and atrophic
inspired by Tsubota, 1998 changes (after summary of Evans, 2001).
Although there is widespread reporting of a higher
Tear incidence of dry eye in females, e.g. Bowden and
Tear
production
evaporation Harknett (2001), the ratios reported vary greatly,
especially when severity is factored in. Caffery et al.
(1998, cited in Evans, 2001) found only a 3:2 ratio
Drainage overall. However, when the focus of the data was
shifted to severe dry eye symptoms only, the ratio
rose dramatically to 46:1. Evans (2001)
97400-219S.PPT summarizes the range reported as 11% to 35%.
This may be due, at least partially, to gender
7L497400-219
differences in the morphology and function of the

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73 lacrimal gland mentioned above.

DRY EYE PREVALENCE Schaumberg et al. (2000, cited in Nichols, 2001)

SUMMARY reported the female dry eye rate was 6.6% while the
• 7.3% to 33% of the population affected male rate was 2.8%. They also suggested there is
evidence that the use of hormone replacement
• More common in females
therapy in post-menopausal women is associated
• Increases with age with an increase in the incidence of dry eye.
• Higher in: Mamalis (1997) reported that women with severe
- low relative humidity cases of dry eye were more likely to have low
testosterone levels.
- contact lens wearers
- users of Video Display Units (VDUs) Tomlinson et al. (2001) studied the effects of oral
97400-380S.PPT contraceptives on tear physiology and found no
differences between study subjects and controls,
7L497400-380
despite the test battery that covered almost every
aspect of tears.
Environment:
Harknett and Bowden (2001) found that 31% of
contact lens wearers reported ‘slightly dry eye’ and
9% ‘very dry’ when using a computer monitor. In
air-conditioning, 49% reported ‘slightly dry’ and 11%
‘very dry’ eyes. In aircraft, the driest atmosphere
most people are exposed to, the same group
reported 29% ‘slightly dry’ and 10% ‘very dry’.
These latter findings were not supported by McCarty
and McCarty (2000) who surveyed Australian pilots
on this issue. Dryness was reported by 72.3% of
respondents but only 5.4% reported dry eye under
other circumstances. The authors also found an
association between dry eye and flying time, and
class of aircraft (i.e. large jets, propellor-driven
planes, etc.).
A report by several authors (see Bowden et al.,
2001) found up to 51% of contact lens wearers
reported mildly dry eyes at some time.
Schaumberg et al. (2000, cited in Nichols, 2001)
showed that 15% of contact lens wearers were
diagnosed as having dry eye.
74 Effects of Aging on Tears and Related
Structures
EFFECT OF AGING ON TEARS
PRODUCTION Production:
With age, the following decrease: Lacrimal Gland
• Lacrimal gland secretion Over a lifetime there is a progressive decrease in
tear secretion from the lacrimal gland.
• Meibomian gland function
This may be due to the obstruction of the secretory
• Bulbar conjunctival average cell area
ducts most commonly because of chronic
• Schirmer Test lymphocytic infiltration, periductular fibrosis, and
• Phenol Red Thread Test (PRTT) ductal abnormalities (Damato et al., 1984, Roen et
al,. 1985, and Stasior and Roen, 1994). Damato et
• Tear volume
97400-301S.PPT
al. postulated that obstruction of the secretory
ducts, and a depletion of the functional reserves of
7L497400-301
both the main and accessory lacrimal glands, could
contribute to dry eye later in life.
No statistically significant differences have been
reported between males and females (Patel and
Farrell, 1989).
Tomlinson and Cedarstaff (1992) reported that tear
production (and evaporation) was lowest on
awakening and rises to its final level within two
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 Module 7: Contact Lens-Related Ocular Complications

75 hours after eye opening. This finding was attributed

to the thick lipid layer on awakening. Because of
EFFECT OF AGING ON TEARS this diurnal variation, they also suggested that the
ELIMINATION time of day when production rates are assessed
should be standardized.
• p in drainage
• Evaporation ? (conflicting data) Tomlinson and Giesbrecht (1993) postulated that in
normal eyes, the decreased elimination (drainage)
• n in tear osmolality that has been found with age may be a
• n in lipid viscosity compensatory factor offsetting the declining tear
• p in BUT fluid production, thereby combating the potential for
dry eyes in the older population.
Does the p in drainage compensate
for the p in tear production ? Tear Volume and Tear Flow
Mathers et al. (1996) showed that the tear volume
97400-302S.PPT

7L497400-302 decreased with age, but the lipid volume did not.
The tear flow also decreased with age (Furukawa
and Polse, 1978, Mathers et al., 1996). However,
Xu and Tsubota (1995) found no correlation
between age, tear volume, tear flow, tear clearance
rate (an estimate of tear drainage), or basal tear
turnover (the % decrease per minute of sodium
fluorescein concentration in tears after fluorescein
instillation).
Schirmer Tear Test
Mathers et al. (1996) found that the wet length of a
Schirmer Test (detailed in Section IV.B.III Clinical
Tests for Dry Eye: Invasive) declined with age.
Phenol Red Thread Test (PRTT)
Hamano et al. (1990) found that the wet length of
the PRTT decreased with age. This mirrors the
findings of Manthers et al. (1996) with the Schirmer
test.
Meibomian Gland Drop-Out
Using an infrared video imaging system (see
Mathers et al., 1994), the Meibomian gland
participation rate was found to decline with
advancing age (Mathers et al., 1996). Furthermore,
the incidence of MGD increases with age (Driver
and Lemp, 1996). In the normal eye, about 10
Meibomian glands are ‘expressible’ but this number
decreases with age (Norn, 1987).
Bulbar Conjunctival Cell Area
Blades et al. (1998) showed a tendency for the
bulbar conjunctiva of older eyes to have increased
numbers of smaller cells resulting in a decrease in
the average cell area.
Elimination:
Evaporation
It has been estimated that evaporation of the tear
film accounts for about 10 to 40% of tear fluid
elimination. Studies by Rolando and Refojo (1983)
and Tomlinson and Giesbrecht (1993, 1994) failed
to show any correlation between evaporation rate
and aging, although males over 40 years of age did
exhibit a reduced rate of evaporation. Mathers et
al., (1996) presented an opposite finding, i.e.
evaporation rates increased with age.
However, it would seem that Mathers et al’s results,
i.e. that osmolarity increased with age, cannot be
explained completely by evaporation (the most

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

logical and simplest explanation) because their

subjects were predominantly female whose
evaporation rates vary little with age (Tomlinson and
Giesbrecht, 1993, 1994). The partial or total
dependence of osmolarity on evaporation, along
with data showing a diurnal variation in tear film
evaporation rates (Tomlinson and Cedarstaff,
1992), clouds these findings.
Mathers et al. (1993) concluded that evaporation of
water from the tears is accelerated by tear
production decreases and that this acceleration was
sufficient to exacerbate any existing dry eye
condition. The evaporation rate in dry eye cases
was approximately three times that of a normal eye.
Lipid Viscosity
Mathers et al. (1996) found that the viscosity of tear
lipids increased with advancing age.
Drainage
While Sahlin and Chen (1996) found that tear
drainage capacity declined with age, they also found
that the level of variation within each age group was
considerable. This tended to make broad
76 generalizations difficult. Xu and Tsubota (1995)
failed to show a correlation between age and tear
EFFECT OF AGING ON TEARS clearance rate.
SUMMARY
• Lacrimal gland output declines BUT:
BUTs decrease with age, especially in those over
• Anterior eye tear volume decreases 30 years of age (Tonge et al., 1991). This result
was alluded to by Patel and Farrell (1989) but
- tests of ‘tear volume’ mirror this decrease statistical significance was not reached in their
study. Patel and Farrell found that the stability of
• Tear viscosity and osmolality increase the tear film decreases with age (decreasing BUTs
with advancing age) and suggested that this was
• BUT decreases the main factor in the higher incidence of tear-
97400-381S.PPT
related problems associated with aging.
7L497400-381
77 Definition of Dry Eye
DRY EYE A wide range of terms is used to describe ‘dry eye’.
• Also known as: The terms applicable are often used
- keratoconjunctivitis sicca (KCS) interchangeably in the literature. The most common
- keratitis sicca alternative term is KeratoConjunctivitis Sicca (KCS).
Other names appear in slide 77.
- xerophthalmia
- xerosis
- sicca syndrome
More recently:
• Ocular surface disease
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78 A widely accepted definition resulted from a series

of meetings of qualified and interested parties
DRY EYE (presented in slide 78) (Lemp, 1995).
Definition
Dry eye is a disorder of the tear
film due to tear deficiency or
excessive tear evaporation which
causes damage to the
interpalpebral ocular surfaces
and is associated with symptoms
of ocular discomfort.
Report of the National Eye Institute / Industry Workshop
(1993-1995)
97400-83S.PPT

7L497400-83

79
An alternative definition is shown in slide 79.
DRY EYE

A dry eye (kerato-conjunctivitis sicca)

is a result of the inability of the pre-
ocular tear film to maintain the integrity
of the epithelial surface of the cornea
and/or conjunctiva.

97400-3S.PPT

7L497400-3

80
A detailed classification of dry eye is presented in
DRY EYE: A CLASSIFICATION slides 80 to 83 (see Lemp, 1995).
NEI / INDUSTRY WORKSHOP - 1995

Dry Eye - KCS

The Nature of Dry Eye

Tear-deficient Evaporative
As the tear film is a complex of components, it may
be affected adversely by disturbances to:

Sjögren’s Non-Sjögren’s x Any of its components.

syndrome syndrome
x Related structures, e.g. the lacrimal gland.
97400-237S.PPT
x Anterior eye features, e.g. the lids.
An unstable tear film can result from a break down
7L497400-237 in any one or more of the layers of the tear film.
81 Alterations can compromise the ability of the tears
to wet the anterior eye adequately.
DRY EYE: A CLASSIFICATION In dry eye, the most common pathological condition
NEI / INDUSTRY WORKSHOP - 1995 that results is a breakdown in the integrity of the
Sjögren’s Non-Sjögren’s epithelial cell layer, thereby compromising its
syndrome syndrome function.
Primary Secondary
Sjögren’s Sjögren’s
• Rheumatoid arthritis
• Systemic lupus erythematosus
• Wegener’s granulomatosis
• Systemic sclerosis
• Primary biliary cirrhosis
• Other autoimmune diseases
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82

DRY EYE: A CLASSIFICATION

NEI / INDUSTRY WORKSHOP - 1995
Sjögren’s Non-Sjögren’s
syndrome syndrome

Lacrimal Lacrimal Reflex

disease obstruction hyposecretion

• Trachoma • Neuroparalytic
• Cicatricial keratitis
• Cong. alacrima • Sarcoidosis
pemphigoid • CLs
• Acquired prim. • HIV
lacrimal gland • Erythema • N VII palsy
disease • Graft vs host multiforme
Primary •Xerophthalmia • Burns
•Ablation
Secondary 97400-239S.PPT

7L497400-239

83

DRY EYE: A CLASSIFICATION

NEI / INDUSTRY WORKSHOP - 1995
Evaporative

Oil Lid-related Surface Contact

deficient change lenses
Xerophthalmia
Primary Secondary
• Blink
• Absent glands abnormalities
• Posterior
• Distichiasis blepharitis • Aperture
• Obstructive abnormalities
MGD • Lid surface
incongruities
• Anterior
blepharitis
• Other ? 97400-240S.PPT

7L497400-240

84

THE NATURE OF DRY EYE

Due to disturbances of one or more:
• Anterior eye structures
• Related structures
• Tear film layers
Disturbances can result in:
• Breakdown of the epithelium
• Compromises in epithelial functions
97400-308S.PPT

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85 Abnormalities of the Tear Film

TEAR FILM ABNORMALITIES Categories of Dry Eye
AETIOLOGY
(after Holly, 1980) Holly and Lemp (1977) and Holly (1980, 1987)
• Deficiency of the aqueous phase categorized dry eye five ways (slide 85). These are
based on the clinical realities of dry eye, and are
• Deficiency of mucin somewhat arbitrary (Lamberts, 1994B):
• Changes in the lipid layer The first four of these categories are all
characterized by an unstable, discontinuous, or
• Inadequate blinking/lid surfacing abnormalities absent tear film (Holly, 1987). The findings in the
• Epithelial pathology final category depend on the underlying condition(s)
and its/their severity.
97400-125S.PPT

Tsubota (1998) stated that an abnormality of any of

7L497400-125 the following can cause dry eye:
x Production.
x Distribution.

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86 x Evaporation.
x Drainage.
DRY EYE: ALL AETIOLOGIES
COMMON FEATURES
• Symptoms
• Interpalpebral surface damage
(commonly but not always)

• Tear stability

• Tear hyperosmolality
97400-142S.PPT

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87 Related Issues: Impaired Tear Fluid Excretion:

While a dry eye can be a serious problem, the
IMPAIRED TEAR FLUID EXCRETION opposite extreme, involving an excess of tear fluid,
• The epiphora resulting from an excess of can have unpleasant consequences as well.
tear fluid causes problems
• Common at subclinical level Excessive tearing can result from impaired drainage
• Causes include: due to damage to the puncta, the congenital
- impaired drainage absence of which is rare. The puncta can be
- congenital absence of puncta damaged by, or lost to, trauma, or the chronic use
- damaged puncta of certain medications such as idoxuridine.
– trauma
– iatrogenic Obstruction of the canaliculi can occur either
- obstruction of the canaliculi congenitally, or as a result of injury or medication.
97400-250S.PPT
The lacrimal sac or the nasolacrimal duct can be
7L497400-250 obstructed by infection, dacryocystitis, or trauma,
especially to any of the adjacent facial bones (e.g.
the nasolacrimal duct passes through the maxilla).
Subclinical delayed tear clearance is common and
potentially pathogenic, and can cause ocular
irritation, medicamentosa (undesired effect of a
medication, especially as a result of
overuse/overexposure), pseudopemphigoid, and
ocular hypertension (Prabhasawat and Tseng,
1998).
Delayed clearance can be associated with moderate
to severe dry eye but can also be found in other
external eye diseases. Tseng (2000) suggests the
treatment of delayed tear clearance with topical,
preservative-free steroids.
88 Patient History Taking in Dry Eye

DRY EYE: SYMPTOMS Evaluation of the patient’s history is a vital

component in the assessment and diagnosis of dry
• Often the key to a diagnosis, but…. eye. The practitioner can use the history provided
- association with signs may be weak by the patient to assist in determining the most
appropriate tests to undertake.
- other associations? (air-conditioning,
occupation, computer monitor usage, etc.) Use of a dry eye questionnaire (e.g. McMonnies,
• Frequency
1986, Begley et al., 1999, Begley 2003) can provide
valuable information that is useful to the
• Duration determination of the presence of a dry eye prior to
• Intensity
performing any invasive tests. However, while most
97400-109S.PPT
studies have found the McMonnies Dry Eye
Questionnaire valuable, Mainstone et al. (1996)
7L497400-109 reported that it showed poor correlation with the tear
meniscus parameters they evaluated, with the
exception of the Tear Meniscus Height (TMH).
McMonnies and Ho (1987) reported that, at least in
348 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

89 women over 45, the performance of a McMonnies

questionnaire was such that supplementary ocular
PATIENT HISTORY sicca examination procedures were not required for
the majority of cases, i.e. the questionnaire alone
• Age and gender
was sufficient to identify dry eye cases correctly,
• Occupation (any difficulties most of the time. A sensitivity (the test’s ability to
in previous jobs?)
identify TRUE cases correctly) of 98% and a
• Contact lens history (if any) specificity (the test’s ability to identify TRUE
– current CLs cf. previous? negatives [non-cases] correctly) of 97% were
• Time of day problems arise claimed.
– when is it worse/worst? Many different factors may play a direct or indirect
• Exacerbating factors role in the development of ocular dryness. A wide
97400-105S.PPT range of questions and careful assessment of the
patient’s answers permits the practitioner to build a
7L497400-105
potential dry eye profile.
Dry Eye History
90
Targeted questioning is important to the diagnosis
PATIENT HISTORY: GENERAL of dry eye. Lamberts (1994B) suggested that the
• General health following questions be asked routinely because the
occurrence of dry eye is so high.
– diabetes
– thyroid eye disease “What sorts of things bother your eyes?”
– rheumatoid arthritis Dry eye sufferers are extremely sensitive to drafts,
– nasal congestion, sinusitis wind, air-conditioning, and smoke. Reading may be
another activity that results in symptoms of
– facial nerve palsy
discomfort. Reading, like VDU usage, tends to
– autoimmune disease lower the blink rate, and therefore increases the
• Family history Maximum Blink Interval (MBI). As an increased MBI
approaches or exceeds the BUT, discomfort will be
97400-19S.PPT

7L497400-19 experienced.
“At what time of the day is your problem worst?”
91 Either at night, or on awakening, are most likely to
be the reported ‘worst time’ for symptoms of dry
PATIENT HISTORY eye. This may be due to altered tear production
• Allergies during sleep. This is exacerbated by a concurrent
• Skin diseases blepharitis, or lagophthalmos. Smoke, cigarette or
other, is almost universally intolerable to most
• Medications
people but tear-deficient individuals tolerate smoke
– decongestants even less well.
– antihistamines
“Do you have any problems with your skin, skin
– diuretics
conditions, areas of skin that itch, or skin that
– oral contraceptives requires a lot of moisturizer?”
• Is reflex tearing noticed?
97400-20S.PPT These sorts of questions are useful, especially in
Sjögren’s syndrome cases (detailed in Section
7L497400-20
IV.A.I Sjögren’s Syndrome). Various skin
92 disorders have dry eye and itching as attendant
features. Some of these disorders are:
PATIENT HISTORY: DRY EYE
• Previous episodes x Seborrhoeic dermatitis (see opposite slide 165).
• Family history (of DE) x Psoriasis.
• Dry eye questionnaire
• Environmental influences:
x Ichthyosis.
– humidity x Keratosis follicularis (Darier’s disease).
– temperature “What medication are you on/what medications do
– air flow you take?”
– smoke
– air-conditioning While few well-controlled clinical studies have been
97400-106S.PPT done on the association between systemic
medications and tear flow, some results are now
7L497400-106
available.

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93 x The oral contraceptive does not appear to have

any manifest adverse effect on the tears despite
DRY EYE: PATIENT HISTORY some anecdotal suggestions to the contrary
(Tomlinson et al., 2000).
• Allergies
The following have been shown to decrease tear
• Skin diseases production:
• Medications: x Chlorpheniramine maleate (an antihistamine)
- decongestants (Koffler and Lemp, 1980, cited in Lamberts,
- antihistamines
- diuretics 1994B).
- HRT
x Isoretinoin.
• No reflex tearing ?
97400-107S.PPT
x Hydrochlorothiazide.
7L497400-107 x Propranolol hydrochloride.
94
DRY EYE: PATIENT HISTORY Caffery (2000) observes that most clinicians find a
weak association between symptoms of dry eye and
Exacerbating conditions: the signs of dry eye. Some patients with severe
• Blepharo-conjunctivitis corneal and conjunctival staining report little ocular
• Thyroid disease discomfort while others, who report extreme
discomfort and other symptoms, show few ocular
• Vitamin A deficiency
signs.
• Lagophthalmos
Begley et al. (1999) found that patient self-reporting
• Recurrent corneal erosions
of dry eye was more successful in isolating
• Contact lens wear symptomatic cases than the use of a specially
97400-108S.PPT
developed dry eye questionnaire. Further,
Chalmers et al. (2001B, Begley was a co-author),
7L497400-108 found self-assessment of dry eye was more efficient
than professional diagnosis, and generally more
accurate when the results were compared with the
graded symptoms.
95 Symptoms of Dry Eye
As with most ocular conditions, any classification of
DRY EYE: SYMPTOMS
dry eye is usually based on:
• More noticeable in dry, warm environments x A relevant history.
x The symptoms reported.
• Tend to get worse:
x An examination of the eyes.
- as the day progresses
x Diagnostic tests performed by or for the
- with concentration (e.g. reading, games, practitioner.
computer use) Symptoms described by the patient are a key factor
97400-111S.PPT
in diagnosing ocular dryness. In most cases of dry
eye, significant symptoms are present. However,
7L497400-111 the practitioner must determine the degree of
96 association between the symptoms and any signs
observed during subsequent testing.
DRY EYE: SYMPTOMS Tears in the normal eye form a hydrodynamic
• Sandy, gritty, scratchy, FB • Redness lubricant. A possible explanation for the symptoms
• Stinging • Vague discomfort of ocular discomfort may be the ten-fold increase in
ocular surface roughness that can accompany dry
• Irritation • Excessive mucus
eye. Additionally, if the tear film is thinner, its
• Tiredness/fatigue
• Dryness lubricating ability is reduced. This results in an
• Burning • Excessive tearing increased frictional coefficient that can result in
• Soreness • Epiphora ocular surface damage (increased rate of cell death
• Blurred vision (that clears and cell loss, and potentially, an overwhelmed
• Photophobia
with blinking) tissue repair process), and ocular discomfort (this
97400-309S.PPT
section after Holly and Holly, 1994).
7L497400-309 Lamberts (1994B) asserted that symptoms
350 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

described by a patient are not particularly helpful in

making a diagnosis of dry eye. He based this
assertion on the fact that the cornea has no
‘dryness’ receptors. A complaint of dryness does
not necessarily indicate the underlying problem
specifically. Rather it may be just another way of
describing ‘discomfort’. The dry eye sufferer may
complain of a wide-range of irritating symptoms that
may fluctuate, and that may be more pronounced
on awakening.
Some possible symptoms are listed in slide 96 (after
Korb et al., 1996, and others).
Toda et al. (1993) found ocular fatigue to be a major
symptom of dry eye. Conversely, they also found
that dry eye was a common underlying cause of
ocular fatigue.
Patel et al. (1991) concluded that the corneal nerves
can detect tear changes and this faculty allows the
perception of various sensations leading to
symptoms such as gritty or itchy eyes.
97 Signs of Dry Eye

PHYSICAL EXAMINATION A slit-lamp evaluation of the anterior segment is the

Look for: minimum necessary to detect the presence, or
absence, of objective signs of ocular dryness.
• Ocular hyperaemia The eye’s appearance may be altered in a number
• Mucus strands & filaments
of significant ways, even if only a mild dry eye state
is suspected, or claimed. Examination of the
• Floaters (debris) in tear menisci adnexa, tear film, epithelial integrity, and lids in a
systematic manner forms the basis of a physical
• Papillary conjunctivitis evaluation of a patient with suspected dry eye.
Some signs include:
• Parallel folds in the conjunctiva
97400-25S.PPT
x A statistically significant increase in tear
7L497400-25 evaporation rate in dry eyes compared with
normals (Rolando et al., 1983).
98 The authors felt this was the probable
explanation for the hyperosmolality of tears
PHYSICAL EXAMINATION observed in KCS cases. Interestingly, Wilson
• Meibomian glands (1996) showed that tear hyperosmolality in dry
- plugs and blockages eye did not increase the shedding rate of the
epithelial cells of the ocular surface.
- orifice appearance
• Eyelids x Decreased Maximum Blink Interval (MBI)
(Nakamori et al., 1997).
- structure
Strictly speaking, the MBI, and the inverse of the
- position blink rate, are not the same because the
- function maximum time a person can keep their eyes
97400-26S.PPT
open while remaining comfortable might be
unrelated to how often they blink routinely.
7L497400-26
However, Nakamori et al. found that the two
factors were strongly related (i.e. MBI parallels
blink rate inversely) and concluded that factors
affecting the cornea and conjunctiva directly
were the primary determinants of both the MBI
and blink rate. They postulated that MBI might
be a more useful measurement of tear film
stability.
x The mean corneal epithelial cell area is
significantly larger (Fujishima et al., 1991).
x Rose Bengal, or sodium fluorescein staining of

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 Module 7: Contact Lens-Related Ocular Complications

99 any damaged epithelia.

Other signs include (after Lamberts, 1994B):
PHYSICAL EXAMINATION
x A reduced or absent tear meniscus (Whitcher,
1987).
• Punctal patency
x Reduced Tear Meniscus Height (TMH).
• Papillary conjunctivitis In about 85% of normals, this is about 0.2 to 0.3
mm (Lamberts et al., 1979). Confusingly, there
• Blink frequency and completeness was no correlation found between a Schirmer
test and TMH, suggesting that factors other
• Dry skin
than tear flow are involved in determining TMH.
Such factors may include the length of the lid,
97400-27S.PPT the location of the puncta, lid-globe apposition,
the distance of the Meibomian glands from the
7L497400-27
inner lid edge, and relevant physical properties
of the tear fluid itself.
100 x Reduced Tear Meniscus Radius (TMR) (see
later under IV.B.I Clinical Tests for Dry Eye:
DRY EYE: SIGNS Non-Invasive).
• p MBI
x Meniscus floaters.
These are small pieces of particulate matter
• p TMH
that are carried along in the lacrimal lake.
Some are dead epithelial cells sloughed from
• p TMR
the anterior eye and some are small fibrils of
lipid-contaminated mucin. They are also seen
• n Corneal epithelial cell areas
in blepharitis and conjunctival infections. Also
apparent in slide 102 are coloured fringes
• n Tear evaporation rate
97400-310S.PPT
resulting from thin-film interference of a thinned
tear film (see Section IV.B.II Tear Film
7L497400-310 Interferometry). Interference in cases of
101 normal tear function is colourless (Elçioglu et
al., 1990).
TEAR FILM DEBRIS
x Mucous strands (and clumps).
These are strings (slide 103) of lipid-
contaminated mucus (sometimes along with
increased levels of lipid) that have been rolled
• Excess floating debris
up and propelled towards the fornices by the
shearing action of the lids. They are common in
• Degraded mucus both aqueous-deficient and mucin-deficient
states. They are believed to be the result of the
intermingling of mucin with excess lipid.
Characteristically, dry eye of gradual onset
97400-34S.PPT
occurring in middle-aged and elderly adults,
7L497400-34 especially post-menopausal women, has mucus
102 strands that are not indicative of mucus
overproduction. Paradoxically, mucin secretion
may even be deficient in such cases because of
the decreased goblet cell population.
x Filaments.
Commonly, these are associated with dryness,
but dryness is not their only cause. The
filaments are less than 2 mm long, appear as
‘tails’ emanating (hanging) from the corneal
surface. When sectioned, they will be found to
have a core of mucin surrounded by epithelial
cells (shed from the corneal surface).
x Papillary conjunctivitis.
7L40005-99 Papillary changes are a non-specific
conjunctival reaction to irritation. They are seen
in many conditions other than dry eye, e.g.

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

103 allergy, infection, acne rosacea, and

staphylococcal blepharitis.
x Allergic conjunctivitis is sometimes associated
with dry eye cases involving only a decreased
BUT (Toda et al., 1995).
Toda et al. proposed that the decreased BUT
was due to the decreased goblet cell density
caused by allergic conjunctivitis. Such cases
have also been found to be serum antigen-
specific IgE negative, and total IgE negative
(Fujishima et al., 1996). It was proposed that
such cases form a type of dry eye.
x In aqueous-deficient KCS cases, the
7L41163-96
conjunctiva can appear dry and lustreless, and
104 may show redundant parallel folds
(www.merck.com, 2003) due to a reduced
resident tear volume.
This cannot be taken as a definitive sign
because Miller et al. (2001) found only a slight,
but statistically insignificant, increase in the
number of conjunctival folds in moderately dry
eyed subjects.
x An increased blink frequency (Prause and Norn,
1987).
Slide 103 highlights a build-up of mucus in the tear
film that has formed into a ‘clump’ on the lower lid
margin.
Slide 104 shows the presence of small filaments
attached to the surface of the corneal epithelium.

7L42919-93

105
Slide 105 shows the lower puncta of the right eye. A
high magnification, slit-lamp assessment of the
punctal orifice with a slit-lamp can reveal its
patency.

7L40791-94

106
Slides 106 show the effect of partial blinking on the
health of the inferior epithelium. Repeated non-
wetting of the inferior cornea results in punctate
staining as disclosed by the instillation of
fluorescein.

7L42125-95

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107

TEAR FROTHING

• Foam on the lid margin

• Bubbles

- abnormal tear composition

- blinking expels air from under the lids

97400-33S.PPT

7L497400-33

108
x Frothing in the tears is a distinctive feature in
some cases of dry eye.
Usually, froth forms on the lower lid margin near
the canthii (slide 108). Froth may also form
along the upper lid margin (slide 109). Frothing
is due an abnormal tear film composition. The
blinking lids generate sufficient force to aerate
the tears (air is expelled from under the lids).

97400-326S.PPT

7L497400-326

109

7L40004-99

110 Diagnosis of Dry Eye Requires More Than One

Diagnostic Test
DIAGNOSING DRY EYE
A ‘STANDARD’ TEST ? Individual clinical tests may provide only a small
• As yet, NO ‘standard’ test & NO single test amount of information relevant to the diagnosis of
• A battery of common tests include: dry eye. However, when a number of tests are
- careful history & McMonnies-type questionnaire positive, and the history is indicative of a dryness
- biomicroscopy/staining (fluorescein, Rose Bengal)
problem, the practitioner is well placed to confirm a
- tests for tear film secretion, stability
– Schirmer test diagnosis of dry eye.
– BUT
- tear sampling
A major clinical consideration is the potentially
– tear osmolality invasive nature of some of the tests. The
– lactoferrin concentration practitioner must ensure that the order in which the
– composition
97400-249S.PPT
testing is undertaken maximizes the value of the
data. For example, the lids must not be
7L497400-249 manipulated prior to an assessment of the tear film
lipid layer, as the expression of Meibomian fluid will

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

111 disrupt or distort the lipid pattern.

Nichols et al. (2000) concluded that the
DIAGNOSING DRY EYE performance of at least one test for dry eye in
A single test is unlikely to be adequate because dry eye has: addition to an assessment of symptoms was
• Symptoms probably sufficient, although most practitioners
surveyed for their report performed two tests as well
• Ocular surface damage as assessed symptoms. However, many studies
• Decreased tear stability have concluded that it is not feasible to make or
confirm the diagnosis of dry eye on the basis of just
• Tear hyperosmolality one single test, e.g. Lamberts (1994B), Roth and
• An inflammatory component MacKeen (1994), Korb, (2000), Narayanan et al.
No single test can explore all of these satisfactorily
(2001).
97400-382S.PPT

As a dry eye condition is characterized by

7L497400-382 symptoms, ocular surface damage, reduced tear
stability, and tear hyperosmolality, as well as an
inflammatory component, there may be no direct
112 correlation between the number or severity of
DIAGNOSING DRY EYE symptoms, and the degree of ocular surface
OTHER ISSUES damage or tear deficiency. Once a diagnosis of dry
• Dry eye is not a single condition. It can be eye has been made, the need to classify the
further classified as:
condition, e.g. into tear deficiency or evaporative dry
– tear deficient
eye, may arise. Furthermore, these two forms of
– evaporative
the condition are not mutually exclusive and often
— not mutually exclusive, can co-exist co-exist. Therefore, an optimal diagnosis depends
• Dry eye testing on the suspicion of dry eye on the results of several tests (Bron, 2001).
amounts to ‘preselection’
• Sequence of dry eye tests is significant Following a survey of eyecare practitioners, Korb
• Time between tests, especially if invasive, also (2000) found the preferred tests to be:
important
97400-383S.PPT
x A questionnaire.
7L497400-383 x BUT (invasive).
x Ocular surface staining.
x Schirmer test.
Golding and Brennan (1993) evaluated the
diagnostic accuracy of 20 clinical tests for dry eye
and found that diagnostic accuracy was greatest for
Rose Bengal staining followed (in descending order)
by McMonnies questionnaire, Anderson
questionnaire, sodium fluorescein staining, NIBUT,
and BUT (using sodium fluorescein dye). Their final
recommendation for the clinical diagnosis of dry eye
was:
x Rose Bengal staining.
x McMonnies questionnaire.
x BUT (with sodium fluorescein dye).
Lamberts (1994B) suggested an overlapping suite
of tests, namely:
x Rose Bengal staining.
x BUT (with sodium fluorescein dye).
x Schirmer test.
The ‘assessment standard’ of Abelson and Knight
(1994) is simply:
x Rose Bengal staining.
Bron (1994) believes that there is no ‘standard’
possible, especially when the tests are often applied
because of the suspicion that dry eye is present, i.e.

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some preselection has already occurred. When

diagnosis is to be based on a battery of tests, the
sequence of their execution, and the time allowed
between tests may be important, especially if
invasive tests are involved (Bron, 1994). Bron
suggests the following as a suitable sequence:
x Tear sampling.
x NIBUT
x BUT (invasive).
x Sodium fluorescein staining.
x Schirmer test (type I or II?).
x Rose Bengal staining.
Farris (1994) believes that tear osmolarity, as
determined by the freezing-point depression
technique applied to nanolitre samples of tears, has
the potential to become the ‘standard’ of KCS
diagnosis. However, this suggestion has not been
adopted widely.
Farris et al. (1983) found the most sensitive tests for
the diagnosis of dry eye to be the increase in
lactoferrin concentration from basal to reflex tears
(% increase in lactoferrin), and tear osmolarity in
that order. A similar conclusion was reached by
Foulks et al. (1999).
Goren and Goren (1988) found that in cases of
minimally irritated dry eye, the Schirmer test in
combination with a lactoferrin immunological assay
(not the Lactoplate™ Test) was more effective.
However, in moderate to severe cases of dry eye
without systemic signs such as xerostomia or
arthritis, the lactoferrin assay alone was adequate.
Similarly, cases with both ocular and systemic
complaints were diagnosed by lactoferrin assay
alone, but BUT and Rose Bengal staining were not
useful. The Schirmer test had limited value in
measuring the rate of tear secretion in symptomatic
cases.
Despite reporting favourably on the Lactoplate™test
for dry eye diagnosis, Lucca et al. (1990) concluded
that their ‘standard’ for dry eye diagnosis was a
good clinical history combined with an analysis of
tear osmolarity.
[Note: osmolality is the number of moles of solute in
1 kg of solvent, which is an easier concept to deal
with than osmolarity which is the number of moles
of solute in 1 L of solution].
Yolton et al. (1991) concluded that lactoferrin
concentration alone was insufficiently sensitive or
specific to diagnose mild to moderate dry eye.
It would appear that, despite some common ground
in the opinions of some authorities in the field of dry
eye, there as nearly as many ‘standards’ as there
are opinion providers (see slide 110).
It can be concluded that the use of a suitable
questionnaire features frequently in many authors’
recommendations of how dry eye should be
diagnosed. Such an approach is not only useful but
356 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

is also simple, economic, and ancillary staff can

explain and supervise their completion.
Following a survey of eyecare practitioners, Holly
(1989) concluded that there was clearly an
overwhelming need for improved diagnostic
methods for dry eye.
More recently, Korb’s Dry Eye Test (D.E.T., Akorn
Inc.) was found to be a valid and reliable test for dry
eye (Narayanan et al., 2001). The DET involves the
instillation of consistent microvolumes of sodium
fluorescein into the eye using a small strip, to
improve the reliability of a BUT determination.
113 Differentiating Normal from Dry Eyes: Less
Conventional Methods
DRY EYE
Common Features Global Tests
Roth and MacKeen (1994) used a series of
conventional dry eye tests (e.g. Schirmer I & II,
• Symptoms • Validated questionnaire Rose Bengal staining, TMH, BUT with fluorescein),
of symptoms
and less conventional tests (e.g. tear fluid electrical
• Interpalpebral • Demonstration of ocular conductivity, and pachometry) to assess their
surface damage surface damage relative abilities to differentiate between the various
• Demonstration of tear types of dry eye. They concluded that the status
• Tear instability instability and severity of dry eye can be based on
• Tear • Demonstration of tear ascertaining whether or not the cornea is normal,
hyperosmolality hyperosmolality thinned or swollen.
97400-103S.PPT

Corneal thickness was correlated:

7L497400-103
x Positively with Schirmer I and Schirmer II
results, i.e. short Schirmer wet-lengths were
114 found in eyes with thinner corneas (as
measured centrally).
DIFFERENTIATING DRY EYES FROM
NORMAL EYES x Negatively with short (”1 sec) BUTs, i.e. short
LESS CONVENTIONAL BUTs were associated with thickened corneas
Pachometry after Roth and MacKeen, 1994 probably due to corneal surface damage.
• Increased corneal thickness correlated with: x Positively with decreasing BUTs (within the
– decreased tear fluid conductivity range from 10 ĺ 3 seconds), i.e. BUTs in this
(decreased osmolality) range were associated with thinner corneas
– greater Schirmer wet-lengths [centrally] generally, but as the BUT shortened,
– short BUTs (up to 1 sec)
the cornea thickened, see previous point).
– greater Rose Bengal staining x Positively with Rose Bengal staining, i.e. the
97400-271S.PPT
greater the corneal swelling, the greater the
7L497400-271 staining.
x Negatively with tear fluid conductivity (due to
115 decreased osmolality), i.e. with decreased tear
osmolality (which decreases tear electrical
AESTHESIOMETRY conductivity), the corneal thickness was found
after Xu et al., 1996 to be greater.
• Measures corneal sensitivity

• Both Sjögren’s & NSDE have |p sensitivity

Findings related to aesthesiometry, so-called
• Corneal sensitivity correlates with: meibometry, the bromothymol blue test (of tear pH),
and tear viscosity are presented in slides 115 to
- Schirmer test 118.
- TFI

- Rose Bengal & fluorescein staining

97400-311S.PPT

7L497400-311

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116
MEIBOMETRY
after Yokoi et al., 1999
• Meibometer – a device for blotting lipids from
the centre of the lower lid
– uses special plastic tape
– tape is analysed optoelectronically
— optical density of blot centre is assessed
– optical density is an analogue of lipid content
• p lipid volume in MGD
• n lipid volume in aqueous deficient women
- along with n lipid layer thickness
97400-312S.PPT

7L497400-312

117

TEAR VISCOSITY
• Essentially, the resistance to tear flow or
movement
• n by n in protein & lipid content
• Grading Scale 1 to 5 (Fink, 2001):
- 1 = watery, rapid flow, no detectable drag
of surface particles
- 5 = viscous, no flow, oily, much debris
97400-313S.PPT

7L497400-313

118

BROMOTHYMOL BLUE TEST

• Dye is a pH indicator

- colours yellow to blue (Lupelli, 1986)

• 10 µL, 0.2% solution o lower fornix

- note colour after 5 sec

- ascertain pH from table of colours

97400-314S.PPT

7L497400-314

119 Differentiating Between Types of Dry Eye:

DIFFERENTIATING BETWEEN
Lee and Tseng (1997) used Rose Bengal staining of
the unexposed zones of the anterior eye, along with
TYPES OF DRY EYE
Aqueous vs Lipid Deficiencies the lytic cytological changes in the conjunctiva
(provided there was no squamous metaplasia)
• Rose Bengal staining of the unexposed areas
revealed by impression cytology, to differentiate lipid
of the eye after:
Lee & Tseng, 1997
deficient states from aqueous deficient states.
• Impression cytology Patel et al., 1998
Typically, the aqueous deficient show squamous
• PRTT or PRTT clones
metaplasia with mucous aggregation and Rose
• Surface tension determination Bengal staining in the exposed areas of the anterior
• Tear protein profiles eye (slide 119).
• NIBUTs 97400-272S.PPT Patel et al. (1998) found they could differentiate
7L497400-272
between aqueous deficient and non-aqueous
deficient dry eye, using their own version of the

358 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

120 Phenol Red Thread Test (PRTT) (see Blades and

Patel, 1996 for details) (slide 119).
DIFFERENTIAL DIAGNOSIS:
Other factors that may assist in differentiating
MUCIN vs AQUEOUS DEFICIENCY
MUCIN AQUEOUS aqueous from lipid deficiencies are also listed in
• Shorter BUT (but perhaps • Low Schirmer result slide 119.
adequate Schirmer 1 early) • Variable (or low) BUT
• Associated with Stevens- • Reduced marginal tear strip The differences between mucin and aqueous
Johnson syndrome, or… • Rose Bengal staining deficiencies are tabulated in slide 120 (after
• Associated with vitamin A • Associated with: McMonnies, 1980).
deficiency - rheumatoid arthritis (SS), or…
- menopause, or…
- endocrine imbalance, or…
- drug side-effect
from McMonnies, 1980
• Age >50 (10%), >80 (50%)
97400-236S.PPT

7L497400-236

IV.A Mechanisms of Dry Eye

121 Aetiology of Dry Eye

DRY EYE In many cases the cause of dry eye is unknown and
POSSIBLE AETIOLOGIES remains so.
• Aqueous deficiency Hormonal
• Mucin deficiency In females at least, some possible clues come from
a study of premature ovarian failure. More than half
• Lipid abnormalities of the 67 subjects studied reported two or more
signs of dry eye. It was suggested that the
• Lid surfacing abnormalities disruption to sex hormones, and immune
dysfunction, may have roles in their causation (from
• Epithelial pathology a summary of an article appearing in the 2001 May
97400-96S.PPT
Review of Optometry published by Optistock,
7L497400-96 2001B).
122 Caffery (2000B) summarized a paper by Stern thus:
Considering dry eye as a local inflammatory
DRY EYE process, the age-related (especially menopause-
AETIOLOGY related) reduction in androgen levels that occur in
• Hormonal (in females at least): women afford a lower level of ocular surface
– p androgen protection from inflammation. Stern proposed that
– sex hormone disruption ocular cells make cytokines that attract T cells,
– immune dysfunction thereby producing dry eye symptoms.
– local inflammatory processes Cermak et al. (1999) also proposed that androgen
• Systemic: deficiency is a contributor to the pathogenesis of dry
– diabetes mellitus eye.
– Myalgic Encephalomyelitis (ME)
97400-315S.PPT
Health

7L497400-315
Nepp et al. (2000) showed a relationship between
the severities of diabetic retinopathy and KCS.
They concluded that KCS can be yet another
manifestation of diabetes mellitus.
In rare instances, dry eye may be due to myalgic
encephalomyelitis (ME) especially in adult cases
(Macintyre, 1994).
Recently, Mathers (2000) proposed a ‘cornea and
lacrimal gland feedback’ model to explain why the
eye becomes dry. Essentially, Mathers supports a
model in which the ocular surface and lacrimal
gland are viewed as a tightly integrated functioning
unit. Dry eye-induced ocular surface damage leads
to lacrimal gland damage. It seems that this model
is also supported by Pflugfelder et al. (2000).
Sindt (1999) reported on two cases in which

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 Module 7: Contact Lens-Related Ocular Complications

123 unusual causes of dry eye were involved, namely

incomplete blinking in a contact lens wearer, and
DRY EYE nocturnal lagophthalmos.
AETIOLOGY
• Associated with: Ocular Health
– allergic conjunctivitis op goblet cell density Toda et al. (1995) showed that the decreased
– lagophthalmos goblet cell density resulting from allergic
– incomplete blinking conjunctivitis can cause reduced BUTs and dry eye.
• Refractive surgery
– LASIK The relationship between ocular fatigue and dry eye
– LNE (LASIK-induced Neurotrophic is ambiguous. Toda et al. (1993) found a
Epitheliopathy) statistically significant relationship between the two
– post-surgical p tear production (51.4% of the ocular fatigue sufferers had dry eye).
• Ocular fatigue (?)
97400-385S.PPT They concluded that not only was ocular fatigue a
major symptom of dry eye, but dry eye was a
7L497400-385
common underlying cause of ocular fatigue.
Ocular Surgery
As the role of refractive surgery in eyecare expands,
there is a growing number of reports of dry eye
symptoms occurring post-surgically.
Wilson (2001) raised the subject of LASIK-induced
Neurotrophic Epitheliopathy (LNE) as being the
most likely cause of post-LASIK dry eye, rather than
diminished tear production. Both signs and
symptoms (including vision compromises) of LNE
tend to disappear by about 6 months, providing no
‘enhancement’ surgery is performed in the interim.
Wilson suggested that surgical procedures on the
contralateral eye, and/or enhancements to the
operated eye, be separated by more than 6 months
so that the patient’s visual function can be
maintained. Choi and Wilson (2001) report that
existing dry eye sufferers may have their symptoms
exacerbated by LASIK.
Decreased tear secretion post-surgically was
reported by Benitz-del-Castillo et al. (2001). They
also found that myopic LASIK depressed tear
secretion for 6 months after surgery, i.e. the same
critical time period reported by Wilson.
124 The following summaries are after Holly (1987) and
Lamberts (1994B).
AQUEOUS TEAR DEFICIENCY
AETIOLOGIES Aqueous Deficiency:
Most common of the dry eye syndromes This is by far the most common dry eye syndrome
• Defect of: (Lamberts, 1994B). The aqueous forms the bulk of
- lacrimal gland (LG), or nerve supply the tear film. Its main contributor is the lacrimal
- accessory glands, Krause and Wolfring gland itself, with some support from the accessory
• Idiopathic lacrimal glands of Wolfring and Krause.
• Acquired This deficiency may be the result of any condition
- numerous causes (see separate slides) that causes decreased secretion, e.g. diseases of
• Congenital (see separate slide) the lacrimal gland, or the nerve supply to it. Some
97400-6S.PPT
conditions that can cause an aqueous deficiency
7L497400-6 are detailed in the slides opposite. Further
explanations follow:
x Riley-Day syndrome (crying without tears,
corneal hypoaesthesia or anaesthesia, sleeping
with open eyelids, and symptoms of
dehydration. An autosomal recessive condition
of young children).
x Obstruction or obliteration of the lacrimal ducts
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125 following any destructive condition of the

conjunctiva, e.g. radiation, chemical, or thermal
AQUEOUS DEFICIENCY AETIOLOGIES: burns.
ACQUIRED
x Destruction of the lacrimal gland following
• Neuroparalytic hyposecretion
surgery or trauma of the eyelids, or orbit.
• Brainstem lesions
x Drugs. The most common drugs that decrease
• Bone lesions, esp. of the orbit aqueous secretion include:
• Lesions of the sphenopalatine ganglion – antihistamines
• Primary & Secondary Sjögren’s syndrome – anticholinergics, e.g. atropine

• Adie’s syndrome – diuretics

97400-211S.PPT
– beta-blockers
7L497400-211 – antimuscarinics
126 – general anaesthetics
AQUEOUS DEFICIENCY – nasal decongestants
AETIOLOGIES: ACQUIRED
– isoretinoin (Accutane™).
• Multiple endocrine neoplasia
The actual cause of decreased lacrimation may not
• Lymphoma, or leukaemia always be obvious, or identifiable. This may be
especially so in cases involving a varying ability to
• Sarcoidosis (conjunctival)
lacrimate. The minimum tear production rate is
• Obstruction/obliteration of the LG ducts unknown, but it is suspected that about 0.1 µL/min
could maintain a normal tear film under favourable
• Pharmaceutical drugs conditions.
97400-212S.PPT The mucous strands that are seen in aqueous-
7L497400-212
deficient dry eye occurring in the middle-aged or the
elderly are not indicative of mucus overproduction.
They also contain considerable quantities of lipids
127 that are believed to cause the aggregation of mucus
into hydrophobic fibrils and particles. Therefore,
ACQUIRED AQUEOUS DEFICIENCY excessive mucin precipitation could result from
LACRIMAL GLAND AFFECTED increased lipid contamination, or a decreased tear
• Trauma/destruction removal facility.
• Infection Normally, the lipid-carrying hydrophobic mucus is
- trachoma ‘blinked’ into the inferior fornix, propelled towards
the nasal canthus (by the lower lid’s largely
- mumps
horizontal action), and accumulated at the canthus,
• Inflammation or discharged onto the adjacent lid areas.
• Infiltration
Decreases in the lacrimal gland function/output
• Sarcoidosis (LG) have an attendant drop in tear protein content.
97400-8S.PPT

Declines in the antibacterial factors, e.g. lysozyme,

7L497400-8 lactoferrin, and sIgA, may leave the anterior eye
more susceptible to opportunistic infection.
Practitioners may instigate prophylactic antibiotic
128 therapy in some cases. Conservative practitioners
do not use such therapy in mild to moderate cases
ACQUIRED AQUEOUS DEFICIENCY
LACRIMAL GLAND AFFECTED of KCS, in the belief that susceptibility only
increases when the epithelium’s barrier function is
• Drug induced
compromised.
- antihistamines
The occurrence of KCS in post-menopausal women
- anticholinergics suggests that oestrogen deficiency is a possible
cause of this problem. In a study of contact lens
• Neuroparalytic
wear in presbyopes presented by du Toit et al.
- facial nerve (N7) (2001), more than twice as many women as men
• Lacrimal gland excision reported symptoms of dryness. Interestingly, no
97400-9S.PPT
age differences were found.

7L497400-9
KCS, as part of a systemic disease, is commonly
associated with Sjögren’s syndrome (dealt with in
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 Module 7: Contact Lens-Related Ocular Complications

129 Section IV.A.I Sjögren’s Syndrome). Most

commonly, such KCS is associated with rheumatoid
arthritis, a collagen-vascular disease.
Congenital Syndromes and Aqueous Deficiency
Although rare, a congenital absence of the lacrimal
gland can occur.
Riley-Day syndrome is a familial dysautonomia that
affects peripheral autonomic, sensory and motor
neurons. Autonomic abnormalities include defective
lacrimation.
The amyloid diseases constitute a group of
conditions characterized by the accumulation of
7L40001-98 fibrillar material in various component tissues in
quantities sufficient to compromise organ function.
Such deposition in the lacrimal gland reduces
130 aqueous production.
Acquired Aqueous Deficiency
The ability of the lacrimal gland to produce aqueous
fluid can be compromised by a number of
conditions. Most commonly, chronic inflammation
results in destruction of the tissue due to the build-
up of infiltrative material (slides 129 and 130).
Trauma, drug side-effects, and neuropathology
should be considered in the differential diagnosis of
aqueous deficiency.

7L40014-98

131

CONGENITAL AQUEOUS DEFICIENCY

• Many congenital syndromes can result in a dry

eye condition including:

– Alacrima (lacrimal gland does not secrete)

– Riley-Day Syndrome (neural abnormalities)

– Amyloidosis (fibrillar deposits in LG)

97400-7S.PPT

7L497400-7

132 Mucin Deficiency: Aetiology

Mucin deficiency caused by goblet cell destruction
MUCIN DEFICIENCY: CAUSES can result in an unstable tear film. Although not
• Hypovitaminosis A essential to epithelial wettability, mucin may play a
• Ocular pemphigoid role in maintaining it in the presence of the lipid-rich
• Stevens-Johnson syndrome environment of the anterior eye.
• Chemical burns
Possible causes of goblet cell loss include:
• Radiation damage
• Trachoma x Hypovitaminosis A.
• Pharmaceutical drugs: x Ocular pemphigoid, e.g. cicatrical pemphigoid.
- practolol
- echothiophate iodide x Stevens-Johnson syndrome, an acute purulent
97400-213S.PPT
form of erythema multiforme exudativum in
7L497400-213 which vesicles appear on the mucous
membranes of the conjunctiva, mouth, nose,
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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

urinogenital orifices, anal canal and, eventually,

similar eruptions appear on the skin.
x Chemical burns, especially by alkalis.
x Radiation damage.
x Trachoma.
x Drugs:
– practolol
– echothiophate iodide.
Essentially, mucous deficiency is caused by
conjunctival disease, i.e. anything altering or
reducing the conjunctival contribution to the tears.
133 Abnormality of the Mucin Layer
The mucin layer forms a foundation for the tear film.
MUCIN ABNORMALITY Dysfunction or disease may compromise production
• Epithelial glycocalyx disruption of mucus by the conjunctival goblet cells. Slide 134
- cell related shows the effect of an alkali burn on the upper
palpebral conjunctiva. Such an injury will affect the
• Goblet cell dysfunction
normal functioning of the goblet cells.
- chronic conjunctivitis
The epithelial cells also produce a component of the
• Goblet cell destruction
mucin layer, the so-called glycocalyx. Disruption of
- cicatricial conjunctival disease this layer may occur due to epithelial cell
- chemical burns abnormality.
97400-10S.PPT
Drug side effects and inadequate supply of vitamin
7L497400-10
A may also decrease the quality of the mucin layer.

134

7L40593-92

135

MUCIN ABNORMALITY
• Drug induced

• Vitamin A deficiency

• Associated with an over-supply of aqueous

– irritation

– trigeminal nerve stimulation

97400-11S.PPT

7L497400-11

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136 Lipid Abnormalities:

Only in severe anhidrotic ectodermal dysplasia is
LIPID ABNORMALITIES: CAUSES
there a true lipid deficiency (Lamberts, 1994B).
• True lipid deficiency only in anhidrotic
ectodermal dysplasia
Lipid deficiency is therefore extremely rare and has
only been described in congenital conditions
• Congenital conditions involving an absence
featuring a lack of Meibomian glands.
of the LG
• Changes to lipid composition: Cases of lipid abnormality are likely to be related to
changes in the composition of the Meibomian
- blepharitis
secretions occurring in various types of blepharitis.
- eyelid inflammation MGD is considered an important form of blepharitis
• Ingression of skin sebum in the absence of (Driver and Lemp, 1996). The bacteria that invade
meibum o incompatibility
97400-214S.PPT
the Meibomian glands secrete lipases that
hydrolyse the normal lipids to produce various types
7L497400-214 of free fatty acids. The latter are very surface-active
and have the capacity to rupture an otherwise stable
tear film on contact.
In the absence of meibum secretion, sebum from
the surrounding skin spreads over the aqueous tear
layer with serious consequences. The polarized
nature of sebum and its lower molecular weight can
cause a complete ‘dewetting’ of the ocular surface.
A more common cause of lipid
abnormality/deficiency is the biochemical changes
that follow inflammation of the eyelids, e.g.
blepharitis. This can increase the polar fraction of
meibum because of the enhanced hydrolysis of the
waxy esters to free fatty acids and alcohols.
However, in such cases, the meibum secretion rate
increases proportionally to offset this rise in the
polar fraction, thereby largely preserving the desired
surface properties imparted by the lipids secreted.
A common reduced lipid availability problem is
MGD. This is detailed in Lecture 7.2 of this module,
was well summarized by Driver and Lemp (1996),
and will not be covered further here.
137 Abnormality of the Lipid Layer
The Meibomian glands are modified sebaceous
LIPID ABNORMALITIES
glands and are located on the margin of the upper
• Absence of Meibomian glands and lower lid. They produce the lipid component of
- Congenital syndromes the tear film including:

- Prader-Willi syndrome x Wax esters.

• Meibomian secretion quality x Sterol esters.

- chronic blepharitis/meibomitis x Triglycerides.
• Increased rate of tear evaporation x Cholesterol.
97400-12S.PPT
x Free fatty acids.
7L497400-12 x Polar lipids.

Absent, non-functional, or malfunctioning glands

produce abnormal lipid that directly affects the
ability of the tear film to resist evaporation.

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

138 Slide 138 shows a patient with Prader-Willi

syndrome in which a feature is the lack of
Meibomian glands on the lid margin (the lacrimal
puncta is visible to the left of the lid margin).

7L40363-97

139
Slide 139 indicates a blocked Meibomian gland. In
cases where a significant number of glands are
blocked, the tear film is likely to be abnormal.

7L40322-9

140
Slide 140 represents Meibomian Gland Dysfunction
MEIBOMIAN GLAND DYSFUNCTION
(MGD) inspired by Tsubota, 1998
diagrammatically. While tear production is normal,
tear evaporation is increased significantly because
of the reduced presence of the lipid layer. The latter
Normal tear
production? Reduced lipid
is due to a decrease in the lipid output from the
Tear output Meibomian glands. This increased tear evaporation
evaporation
reduces the volume of tears on the anterior eye,
and results in an apparent reduction in tear drainage
from the eye.
Drainage

97400-223S.PPT

7L497400-223

141 Lid Surfacing Abnormalities:

Any factor affecting the lids adversely can have an
LID SURFACING ABNORMALITIES
effect on the tear film, its formation, or its properties.
• Any factor affecting the lids adversely Included here are Bell’s palsy, exposure keratitis
- Bell’s palsy secondary to Grave’s disease, orbital/retrobulbar
- Grave’s disease tumours, and surgery, pathology, or trauma
affecting any of the facial nerves.
- orbital/retrobulbar tumours
- surgery Local lid or globe incongruities, or shape
abnormalities can also cause local drying.
- pathology/trauma affecting nerves of
Ectropion, entropion, symblepharon, notched
the face
eyelids, and in some cases, pterygium, can interfere
- shape abnormalities with the ability of the lids to resurface/maintain the
97400-215S.PPT

tear film. Incomplete blinking can result in inferior

7L497400-215 corneal staining (punctate staining). Chronic
keratitis may be the result of nocturnal
lagophthalmos.
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142 Dellen (a German word for a depression) start as

small areas of the cornea that become thinned
LID SURFACING ABNORMALITIES locally. Corneal thinning may be due to any local
• Globe incongruities: ‘elevation’ (e.g. pterygium, pinguecula, a contact
- ectropion lens edge with excessive clearance or thickness)
- entropion that prevents the lid margins from remaining in
- symblepharon close apposition to the anterior eye during the blink,
- notched eyelids or when at rest.
- pterygium (rare) Because of their relative rigidity, the lid margins
• Incomplete blinking bridge the void between the ‘elevation’ and the
• Lid margin rigidity (bridging) anterior eye. The inability of the lids to resurface
• Conjunctivochalasis the epithelium in the bridged void means the ocular
97400-216S.PPT
area underlying the void no longer has the capacity
7L497400-216 to support a complete tear film, and dehydration
ensues.
Dehydration results in further thinning and the
formation of a depression. A shallow crater, the
dellen, develops. While sodium fluorescein dye will
pool in the depression, the epithelium in it is
essentially normal, and does not stain. Dellen are
dealt with more fully in Lecture 7.3: Rigid Gas
Permeable Contact Lens Complications and
Their Management.
Another cause of surfacing abnormalities is
conjunctivochalasis, a condition in which redundant
folds of palpebral and inferior bulbar conjunctival
tissue adjacent to the lid margins, disrupt the tear
meniscus (Tseng, 2001).
A Meibomian gland cyst (a chalazion) can also
disrupt the tear film (Hickson, 1994).
143 Abnormalities in the Lid/Tear Film Interaction
Blinking and movement of the lids across the
LID SURFACING ABNORMALITIES surface of the globe form a vital component of the
• Anatomy tear film structure and its maintenance. Any
- lid condition in which blinking is adversely affected may
- globe cause a disruption of the tear film quality.
• Lid action Anatomical abnormalities of the lids, such as scar
- force of blink tissue, or giant papillary conjunctivitis (GPC) as
- completeness shown in slide 145, may result in poor distribution or
- nerve palsy (Bell's palsy) spreading of the tears over the epithelium.
- nocturnal lagophthalmos
Corneal exposure, resulting in dry eye, can occur in
97400-13S.PPT
cases of upper lid retraction, exophthalmos (such
7L497400-13
as occurs in Grave’s disease), Bell’s palsy (slide
146) and lagophthalmos.
Irregularities on the surface of the globe such as
144 pinguecula and pterygia may make it difficult for the
lid to spread the tear film evenly across the eye.
LID SURFACING ABNORMALITIES This may result in localized ocular surface drying
• Ocular surface irregularities and cell degradation.
- pinguecula The presence of a contact lens on the eye may also
disrupt the even spreading of tears by the lids.
- pterygium
- dellen
- surgery
• Contact lens effects
97400-14S.PPT

7L497400-14

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145

7L4675-91

146

7L40002-99

147 Epitheliopathies:
An intact tear film is dependent on a smooth,
EPITHELIOPATHIES
uninterrupted epithelial surface. Any irregularities
• Corneal ulcers may cause, at best, irregularities of the tear film
and, at worst, local points at which the tear film may
rupture (break-up). Because the primary cause of
• Corneal erosions the irregularity is usually of greater concern than the
ramifications for the tear film, this category of dry
• Corneal scars eye is regarded as being the least important
(Lamberts, 1994B). Resolving the cause of any
irregularity will also resolve the tear film issues that
• Other ensued. Common causes are: corneal ulcers,
97400-217S.PPT
erosions, and scars.
7L497400-217

148 Epithelial Pathology and Tear Film Structure

Structural integrity of the epithelium is a key factor in
EPITHELIAL PATHOLOGY
the formation and maintenance of the tear film. Any
• Dystrophies condition that compromises the epithelium may
cause an abnormal tear layer. Basement
• Degenerations membrane disorders and dystrophies (map, dot,
fingerprint, etc.) usually result in structural
• Irregular surface
breakdown in the overlying tear film (slides 149,
- microvilli and microplicae 150).

- accelerated cell loss

97400-15S.PPT

7L497400-15

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149

7L41104-96

150

7L42919-93

IV.A.I Sjögren’s Syndrome

151 Sjögren’s Syndrome (SS) and Ocular Dryness

This syndrome, originally termed Mikulicz’s Disease
SJÖGREN'S SYNDROME (Morgan and Castleman, 1953, cited in Tabbara,
• Chronic inflammatory disease 1994), later Gougerot-Sjögren’s syndrome
(Tabbara, 1994), and described comprehensively in
• Multisystemic involvement a doctoral thesis by Sjögren in 1933, is a potentially
• Clinical manifestations include: severe, often chronic inflammatory condition. A
chronic autoimmune disorder, it manifests with
- KCS
multi-system abnormalities that can affect many
- xerostomia different parts of the body.
(The term KeratoConjunctivitis Sicca, or KCS, was
- connective tissue disease
also coined by Sjögren)
97400-16S.PPT

It is detailed here because it:

7L497400-16
x Is relatively common.
x It can compound other ocular conditions, and
contact lens wear.
x It is used as one definition of dry eye type, i.e.
those with a tear-deficiency type dry eye may be
classified into Sjögren’s, or Non-Sjögren’s Dry
Eye (NSDE) types (see Lemp, 1995). SDE and
NSDE are apparently separate entities without
conversion from one to the other (Igarashi et al.,
1996).

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

Possible causes of Non-Sjögren’s Dry Eye (NSDE)

include (after Baudouin, 2001):
x Allergy.
x Infection.
x Blepharitis.
x Preserved eyedrops.
As was first recognized by Sjögren, arthritis is also a
major feature of the disease (after Tabbara, 1994).
SS affects primarily women more than men (9:1)
(Tsubota, 1998). In the eye, it is manifested as a
keratoconjunctivitis sicca (of the aqueous tear
deficiency type). Other mucous membranes in the
body are also affected by dryness.
Importantly, the severity of the ocular surface
abnormalities is greater in Sjögren’s syndrome
(Pflugfelder et al., 1990, Tsubota, 1994, Tsubota et
al., 1994). Abnormalities include increased
squamous metaplasia (Pflugfelder et al., 1990B),
and greater Rose Bengal and sodium fluorescein
152 staining. However, since both groups lack basic
tears, desiccation alone cannot explain the
differences in staining between SS (greater) and
non-SS eyes (lesser). This difference is due to the
ability of non-SS cases to produce reflex tears
(Tsubota et al., 1996a, cited in Tsubota, 1998.
Shearn (1971, cited in Tabbara, 1994) found that
about 25% of all rheumatoid arthritis sufferers also
had SS. Tsubota et al. (1997) provides evidence
that systemic immune conditions, e.g. Sjögren’s
syndrome, affect local lacrimal gland function
directly.
Slide 152 shows the effect of Sjögren’s syndrome
7L40307-95
on the tongue (xerostomia, dry mouth).
153 Sjögren’s Syndrome: Aetiology
SS is an autoimmune disorder characterized by the
SJÖGREN’S SYNDROME: AETIOLOGY infiltration of lymphocytes into the lacrimal and
• Autoimmune disorder salivary glands (Fox et al., 1986, cited in Tsubota,
- lymphocytic infiltration of: 1998, Pflugfelder et al., 1990B, Tabbara, 1994).
• lacrimal gland This infiltration leads to the destruction of the ductal
• salivary gland and acinar structures that results in a deficiency of
- destruction of ductal & acinar structures tears and saliva. Although SS can occur in
• deficiencies of tears & saliva isolation, it is often accompanied by other
• Epstein-Barr viral infection ? autoimmune diseases (Tabbara, 1994). Tsubota et
• Congenital abnormality of the suppressor T al. (1993) found that the tissue destruction in the
lymphocyte ? immune-mediated cytolysis in SS was associated
97400-251S.PPT
with both granzyme A and perforin. This suggests
7L487400-251 that a drug suppressing granzyme A and perforin
specifically, may have a role in curtailing the
destruction of the lacrimal gland in SS cases.
Although neither a proved, nor universally accepted
aetiology, several authors have associated SS with
an Epstein-Barr viral infection (Fox et al., 1986,
cited in Tsubota, 1998, Pflugfelder et al., 1990C,
Tsubota et al., 1995, Tabbara, 1994). A single
antigen may be responsible for both lacrimal and
salivary gland disease (Tsubota, 1998). It is
believed that the infiltrating lymphocytes (mainly

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 Module 7: Contact Lens-Related Ocular Complications

helper T cells) cause the destruction of the lacrimal

gland in SS, suppress reflex tears, and deprive the
ocular surface epithelium of critical nutrients and
hydration. When patients lose both reflex and basic
tears, no essential factors can be supplied to the
ocular surface, i.e. in SS, simple desiccation and a
lack of substances essential to epithelial growth are
compounded (after Tsubota, 1998).
It has been suggested that SS is the result of an
inborn abnormality of the suppressor T lymphocyte
(Tabbara, 1994). The association with Epstein-Barr
virus is the subject of further investigation.
154 Sjögren’s Syndrome: Clinical Types

SJÖGREN’S SYNDROME:
The classical clinical triad for SS is:
CLINICAL TYPES x KCS.
Primary x Xerostomia.
• KCS alone x A connective tissue disorder, usually
• KCS & xerostomia rheumatoid arthritis.
A common division into primary and secondary SS
• Hyper gammaglobulinaemia
is now used.
• Antinuclear antibodies
Primary:
• Effects on bronchial & vaginal mucosae ?
x KCS alone, or...
97400-252S.PPT

x KCS and xerostomia.

7L497400-253
x Hypergammaglobulinaemia.
x Antinuclear antibodies.
155
x In some cases, the involvement of the bronchial
SJÖGREN’S SYNDROME: and vaginal mucosae.
CLINICAL TYPES
Secondary (associated with at least one connective Secondary:
tissue disorder)
• KCS alone, or… x KCS alone, or...
• Xerostomia alone, or… x Xerostomia alone, or...
• KCS & xerostomia, but associated with: x KCS and xerostomia but associated with at
- rheumatoid arthritis least one other connective tissue disorder, e.g:
- scleroderma
– rheumatoid arthritis
- sarcoidosis
- Crohn’s disease
– scleroderma
97400-252S.PPT

– sarcoidosis
7L497400-252
– Crohn’s disease.
Several clinical studies (see Tabarra, 1994) have
shown definite differences between primary and
secondary SS using: genetic, immunopathological,
serological, and clinical criteria.
Other autoimmune diseases associated with SS
include:
x Rheumatoid arthritis.
x Systemic Lupus Erythematosus (SLE).
x Progressive systemic sclerosis.
x Hashimoto's thyroiditis.
x Waldenström’s macroglobulinaemia.
Furthermore, several studies have shown that all
SS sufferers have a heightened risk of developing
lymphomas or other lymphoproliferative disorders
(see Tabbara, 1994).

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156 Sjögren’s Syndrome: Signs and Symptoms

Sjögren’s cases have all the symptoms of dry eye
SJÖGREN’S SYNDROME
SIGNS & SYMPTOMS sufferers, as well as changes in the periphery of
• All of the usual dry eye symptoms, especially: their corneas, e.g. approximately 10% of SS cases
- acute redness exhibit infiltration of the corneal periphery.
- pain Complaints may include:
- photophobia, and…
- changes in the corneal periphery x Acute redness.
–10% of SS cases have peripheral
corneal sub-epithelial infiltration x Pain.
• Peripheral corneal ulceration is also possible
x Photophobia.
• Increased blink rate
• Shorter BUTs 97400-254S.PPT
A slit-lamp examination usually reveals single or
multiple peripheral, whitish-grey, subepithelial
7L497400-254 infiltrates with a clear surround. The infiltrates
coalesce rarely, but if they do, they form linear or
arcuate peripheral infiltration. The overlying
epithelium may remain intact, at least initially, but
may break down after a few days leaving a small
peripheral ulcer. Corneal sensation usually remains
intact.
The infiltrates are local deposits of immune
complexes originating from the terminal capillary
loops of the limbal vasculature. It is thought that
chemotactic factors are released from the
capillaries and these lead to local corneal infiltration
by polymorphonuclear leucocytes (PMNs).
These infiltrates respond to topical steroids whose
use should be discontinued as soon as the lesion
‘improves’ (after Tabarra, 1994). Long-term topical
steroid therapy is imprudent.
Peripheral corneal ulceration, corneal thinning, and
even corneal perforation may be observed in either
type of SS, i.e. primary or secondary. Similar
changes may also be seen in rheumatoid arthritis.
Interestingly, Mackie and Seal (1981) assert that in
Sjögren’s syndrome, it is possible to have
xerostomia, and rheumatoid arthritis, without an
apparently dry eye (their italics). A similar
conclusion was reached by Farris et al. (1991).
Krenzer et al. (1999) demonstrated that there is
considerable overlap in the clinical features of dry
eye in SS and MGD patients. This means that a
differential diagnosis needs to be made from either
a detailed history, a careful slit-lamp examination, or
an immunological investigation.
Either the patient may report, or the practitioner may
notice, an increased blink frequency. Prause and
Norn (1987) studied BUT and blink frequency in
normals and Sjögren’s syndrome cases.
They found low blink rates in cases with long BUTs,
and vice versa. In Sjögren’s syndrome cases (short
BUTs), although the blink frequency was high, most
tear film break-ups were prevented by the increased
blink frequency. While break-up was apparently
prevented, Prause and Norn did not rule out the
possibility that just prior to a break-up becoming
apparent, there may still have been changes in the
tear film (e.g. decreased thickness) that the cornea
could sense and use to stimulate a blink.

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157 Sjögren’s Syndrome: Diagnosis

SJÖGREN’S SYNDROME
A simple issue that can be explored clinically is that
DIAGNOSIS of the reduced, or absent, tear reflex to a strong
stimulus in Sjögren’s syndrome. The simple dry eye
• All the usual dry eye tests are applicable usually retains the tear reflex (Tsubota et al. (1994)
• The tear reflex is usually absent (slide 158).
• Tear lysozyme level In addition to the battery of tests applicable to dry
eye (detailed in Section IV.B Clinical Tests for Dry
• Conjunctival impression cytology
Eye in this lecture), other tests are applicable to SS
• Conjunctival histopathology cases specifically.
• Other, non-contact lens-related tests Those not applicable to contact lens practice
97400-255S.PPT
include:
7L497400-255 x Tests for xerostomia. Parotid flow rates can be
determined, and investigations of the accessory
salivary glands (including a biopsy) can be
158
undertaken.
RESPONSE TO A STRONG STIMULUS x Haemotological and serological tests. SS
(E.G. AN ACCIDENTAL POKE IN THE EYE)
patients may show evidence of anaemia and
after Tseng and Tsubota, 1997
leucopenia.
Non-Sjögren’s Sjögren’s
dry eye syndrome x ESR rates may be elevated.
x Binding, or radioassays, of immune complexes.
x Assays of antibodies to nuclear antigens to
investigate the presence of other autoimmune
diseases.
97400-168S.PPT x Tissue typing.
7L497400-168 These will not be dealt with further here.
Tear Lysozyme Levels:
Lysozyme levels are of interest because it is known
that lysozyme concentrations are decreased in SS
and dry eye. In SS, this is thought to be due to the
infiltration of the lacrimal gland.
Conjunctival Impression Cytology:
Early onset cases of SS may show an increased
number of conjunctival goblet cells in cytological
impressions taken from the conjunctiva.
Conjunctival Histopathology:
A conjunctival biopsy may show evidence of
squamous metaplasia (a pathological transition of
non-keratinized, stratified epithelium [secretory or
non-secretory] to non-secretory, keratinized
epithelium, Tseng, 1985), and keratinization of the
conjunctival epithelium. Commonly, lymphocytic
infiltration of the accessory lacrimal glands (Krause
and Wolfring) is also seen.
Reflex Tearing:
Sjögren’s syndrome sufferers loose their reflex
tearing ability whereas NSDE cases can respond to
a strong stimulus with reflex tears (Tseng and
Tsubota, 1997) (slide 158).
Differential Diagnosis:
Chalmers et al. (2002) showed that the Schirmer
test and Lissamine Green were the most useful for
identifying SS cases, and BUT and fluorescein
staining were the most useful in distinguishing dry
eye cases (SS and NSDE) from the study’s
asymptomatic controls.
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159 Sjögren’s Syndrome: Management

SJÖGREN’S SYNDROME Some of the treatment of SS needs to be directed to

MANAGEMENT the dry eye component of the syndrome. However,
• Dry eye problems need addressing other aspects, especially the peripheral corneal
• Peripheral corneal infiltration needs special infiltration, require special care, much of which is
consideration outside the scope of ‘normal’ contact lens practice,
• Many of the other aspects are outside the scope e.g. the treatment of the lacrimal gland infiltration by
of contact lens practice, e.g.
the use of anti-inflammatory, or immunosuppressive
- infiltration of the lacrimal & salivary glands
agents, or both. The salivary gland is also affected
- long-term use of immunosuppressive agents
cannot be justified
by such therapy. However, the use of
• Some experimental treatments have shown
immunosuppressive agents late in the syndrome,
promise cannot be expected to provide any significant
97400-256S.PPT
symptomatic relief, or produce any significant
7L497400-256 improvement in tear production because of the
atrophy and cicatrization of the glands that can
reasonably be expected to have accrued.
Furthermore, the risks and hazards of long-term use
of immunosuppressive agents cannot be justified.
The use of such agents in early or young SS cases
may help delay the onset of the destruction of
tissue, scarring, and fibrosis (this section after
Tabbara, 1994).
Tsubota et al. (1999) showed that autologous serum
(the patient’s own blood serum) could be used as a
safe, ocular, Sjögren’s syndrome treatment when
diluted to 20% with saline. Their 4-week trial
showed significant reductions in ocular surface
staining (by sodium fluorescein and Rose Bengal)
possibly due to up regulation of MUC1 expression
from conjunctival cells.
Avisar et al. (2000) compared diclofenac sodium
0.1% and NaCl 5% in the treatment of filamentary
keratitis secondary to Sjögren’s syndrome. Both
treatments proved to be effective although the
diclofenac compound produced significantly more
rapid results.
More recently, Mathers and Dolney (2000) have
shown that the use of oral pilocarpine (Salagen™,
MGI Pharma Inc.), intended originally to treat the
reduction of saliva found in Sjögren’s syndrome,
also increased tear flow.
Tsubota et al. (2001) used cyclosporin A
successfully in a mouse model of SS. Cyclosporin
A improved tear secretion by preventing
lymphocyte-induced apoptosis of lacrimal gland
acinar cells.
Owens and Phillips (2001) reported that punctal
plugs restored initial tear velocity and stabilization
times in cases of SS.
Even more recently, androgen deficiency found in
many Sjögren’s syndrome patients, especially
women (Sullivan et al., 2000), has been treated
successfully with testosterone cream (3%) applied
topically to the upper and lower eyelids twice daily
for extended periods (Connor, 2004).

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160 Non-Sjögren’s Dry Eye (NSDE)

NSDE is a term that can be used to cover a group
AQUEOUS DEFICIENCY SYNDROMES of local and systemic disorders, excluding Sjögren’s
from Bron, 1994
Unilateral Bilateral Syndrome, that give rise to symptoms and signs of
• KCS dry eye (Bron, 1994). NSDE can be defined as a
• Paralytic hyposecretion • Sjögren’s syndrome disorder of the ocular surface, especially involving,
• Dacryoadenitis
• Sarcoidosis but not confined to, the interpalpebral zone, due to a
• Congenital alacrima
deficiency of tear components, or their distribution.
• Multiple neuromatosis
• Dacryoadenectomy
It occurs in the absence of an autoimmune disease,
• Riley Day syndrome
• Scarring of gland and duct • HIV infection
a feature that characterizes Sjögren’s syndrome.
• ‘Cri du Chat’ syndrome The different forms of NSDE have interpalpebral
• Anhydrotic ectodermal dysplasia
• Graft vs. host disease ocular surface damage in common.
97400-162S.PPT

NSDE can be caused by a deficiency of any of the

7L497400-162 major components of the tears. The following is
after Bron (1994).
Aqueous deficiency:
Usually, this form of NSDE results from a failure of
the lacrimal gland function. This may be due to:
x A congenital absence of the gland.
x Denervation.
x Inflammation and infection.
x Toxicity.
x Trauma.
x Obstruction due to cicatrical changes at the
glandular orifices.
Some autoimmune diseases border on NSDE and
Sjögren’s syndrome, e.g.:
x Graft versus host disease
x The dry eye of HIV infection.
The most common form of aqueous-deficient NSDE
is KeratoConjunctivitis Sicca (KCS) which Bron
defines as an age-related disorder more common in
women. In KCS, the lacrimal gland is infiltrated by
lymphocytes that appear to destroy the lacrimal
acinar, and duct tissue. However, there is also a
normal, age-related increase in round cell infiltration
of the gland and duct tissue. It has been suggested
that KCS may be an exaggeration of this aging
process (Damato et al., 1984). Some causes of
unilateral and bilateral aqueous deficiencies are
presented in slide 160.
161 Goblet Cell (Mucin) Deficiency:

GOBLET CELL DEFICIENCY Mucin is a product of the conjunctival goblet cells

from Bron, 1994 and, according to Dilly (1985) and others,
• Xerophthalmia (hypovitaminosis A) subsurface epithelial vesicles (see slide 31 in this
• KCS lecture for details). Mucin lowers the surface
tension (ST) of tears and helps stabilize the tear
• Mucous membrane pemphigoid
film. Short tear BUTs may imply a heightened ST,
• Erythema multiforme and reduced ocular surface wettability. The main
• Trachoma (cicatrical conjunctivitis) causes of goblet cell deficiency are presented in
slide 161.
• Chemical and thermal burns
• Drug induced (e.g. Practolol™)
97400-163S.PPT

7L497400-163

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

162 Lipid Deficiency:

The main causes of lipid layer deficiencies are listed
LIPID LAYER (MEIBOMIAN) DEFICIENCY
in slide 162. Dystichiasis is a congenital condition in
from Bron, 1994
• Congenital absence which the Meibomian glands are substituted for by a
second row of eyelashes. Further, exposure to
• Dystichiasis PCBs (PolyChlorinated Biphenyls), adrenergic
• MGD drugs, and retinoids may affect the Meibomian
glands adversely.
• Retinoid therapy
Ocular Surface Damage:
• KCS
Any tear component deficiencies can directly or
• Cicatrizing conjunctival disease indirectly, alone or in combination, disturb or
97400-164S.PPT
damage the ocular surface. The means of damage
7L497400-164 include: hyperosmolality of the immediate
environment, mucin deficiency, the products of
163
inflammatory reactions, a lack of lubricity (Ĺ friction),
OCULAR SURFACE DAMAGE and possibly, dehydration.
A deficiency in any tear component can disturb
or damage the ocular surface either directly or
indirectly, alone or in combination with other
factors
The means of damage include:
• Hyperosmolality
• Mucin deficiency
• Products of inflammatory reactions
• Lack of lubricity
• Dehydration (possibly)
97400-384S.PPT

7L497400-384

164 Blepharitis and Dry Eye

Blepharitis is a relatively common eye condition, so
BLEPHARITIS & DRY EYE common in fact, that it often coexists with other
• Blepharitis is relatively common
ocular conditions. Dry eye (KCS) is one such
– often coexists with dry eye (KCS)
pairing. Bowman et al. (1987) stated that, although
– can coexist with other conditions
• Common types of blepharitis:
no causal relationship was proved, the common
– staphylococcal occurrence of KCS in blepharitis cases had
– pure seborrhoeic important implications clinically. They believed that
– seborrhoeic with staphylococcal component there was a complex and dynamic interaction
– seborrhoeic with Meibomian seborrhoea between eyelid surface abnormalities, the host’s
– seborrhoeic with Meibomianitis immune system, and natural immunity involving the
– Meibomian keratoconjunctivitis eyelids and tear film.
97400-257S.PPT

Bowman et al. separated blepharitis into six

7L497400-257 categories. These are:
x Staphylococcal blepharitis. Features include:
– 80% are relatively young women, with a
relatively short history of ocular symptoms
– commonly, the eyelids are inflamed, with
fibrinous scales; collarettes of scales may be
seen around the lashes.
– frequently, there is a significant loss of
lashes (madarosis), along with a chronic
papillary conjunctivitis
– inferior epithelial keratitis (keratitis
associated with KCS tends to be
interpalpebral), catarrhal ulceration, and
phlyctenulosis can also occur
– mucoid filaments
– 50% of cases have KCS
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 Module 7: Contact Lens-Related Ocular Complications

– later changes may include: distichiasis (two

rows of eyelashes only one located
normally), trichiasis (eyelash inversion with
the lashes impinging on the globe),
entropion, ectropion, and eyelid margin
irregularities.
x Pure seborrhoeic blepharitis, i.e. with no other
condition(s) associated. Features include:
– generally, the sufferers are older than those
with the staphylococcal form, and the
symptoms are of longer standing
– usually, the symptoms are constant, and are
infrequently exacerbated by other conditions
– the eyelids are less inflamed, and scaling is
more oily or greasy
– 15% have associated conjunctival and eyelid
changes
– the keratitis involves mainly the lower third of
the cornea
– inflamed bulbar conjunctiva, and eventually,
papillary hypertrophy of the tarsal
conjunctiva
– seborrhoeic dermatitis is likely to be found
elsewhere
– KCS in about 33% of cases.
x Seborrhoeic blepharitis associated with a
staphylococcal component. Features include:
– the hallmark appearance of seborrhoeic
blepharitis with a history of significant
exacerbations, i.e. a number of
events/conditions have, in the past, made
the blepharitis worse
– sufferers have more inflammation than pure
seborrhoeic blepharitis cases, and they
exhibit oily loose scales and flakes of skin,
as well as lash collarettes.
x Seborrhoeic blepharitis with Meibomian
seborrhoea. Features include:
– association with mild anterior eyelid
changes, and mild bulbar injection
– usually, sufferers are highly symptomatic
165 and complain of a burning sensation on
awakening
– excessive Meibomian gland secretion; but
glands are dilated but unplugged
– excessive foam in the tear film (slide 165)
– KCS in about 40% of cases.
x Seborrhoeic blepharitis with secondary
Meibomianitis. Features include:
– mild eyelid changes and mild bulbar injection
97400-326S.PPT
– symptoms are likely to be a burning
sensation on awakening in the morning
7L497400-326
– excessive Meibomian gland secretions,
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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

dilated Meibomian glands, but the orifices

are neither plugged, nor blocked
– excessive foam is often present (slide 165)
– KCS in about 40% of cases.
x Meibomian keratoconjunctivitis. Features
include:
– sufferers have a shorter history (duration) of
symptoms
– frequently, there is an associated
seborrhoeic dermatitis, or acne rosacea
– the eyelids are almost normal, and any
abnormality is likely to involve the Meibomian
glands themselves, e.g. orifice pouting, and
plugging
– papillary conjunctivitis, and an inferior
punctate keratitis are common
– unstable tear film
– KCS in about 33% of cases.
These figures show that the incidence of KCS in
each category does not vary greatly (33-50%).
Importantly, there is a small group of patients with
blepharitis associated with conditions such as atopy
and psoriasis that clinically, do not fit the categories
detailed above.
166 Complications Associated with Dry Eye
While much time, effort, and research have been
COMPLICATIONS OF DRY EYE expended on dry eye and its treatment, it is easy to
• Corneal gloss over the numerous complications of dry eye
left either untreated, poorly controlled by, or
- erosion
unresponsive to, the treatments tried.
- inflammation These complications range from mild to severe and
- ulceration can affect all the anterior segment structures. Slide
168 shows an extreme case of corneal ulceration
- scarring associated with severe dry eye.
- vascularization Dry eye related disease may be accompanied by
97400-58S.PPT
emotional, psychological, and lifestyle disturbances
7L497400-58
that must also be managed, at least partially, by the
practitioner.
Inflammation is a feature of dry eye. The
167 conjunctivae become injected and there are
increased blood serum proteins in the tears (Bron,
COMPLICATIONS OF DRY EYE 1994). Furthermore, leucocytes (PMNs), and
inflammatory mediators such as superoxides or
• Blepharitis
prostaglandins may be detected in the tears of KCS
• Conjunctivitis cases.
It is unclear whether ocular surface damage is a
• Keratinization
result of the inflammatory response of the ocular
• Psychological distress surface to damaging agents, or the outcome of
exposure to the inflammatory products themselves.
• Lifestyle changes Bron (1994) believes that in aqueous or mucin
97400-59S.PPT
deficiencies, the resulting hyperosmolality is the
primary effect, while the loss of conjunctival goblet
7L497400-59 cells is a secondary effect, i.e. an effect of the
adverse change in osmolality on the ocular surface.
Surface damage may then give rise to an

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 Module 7: Contact Lens-Related Ocular Complications

168 inflammatory event that might cause further

damage, leading to a cycle of damage.
Other complications include:
x Sterile stromal ulcers:
– almost all sufferers have rheumatoid arthritis
(slide 169)
– the cause of the stromal melting remains
unknown
– affects men and women almost equally
– although apparently ‘sterile’, progress can be
rapid, and the cornea can perforate
7L41311-95 – the melt is usually oval, without infiltrates,
and located at, or below, the visual axis
169 – the rest of the eye remains quiet and white
– treatment: either a bandage contact lens, or
covering the defect with surgical
cyanoacrylate adhesive
– if perforation occurs, a graft will usually be
necessary.
x Blepharitis (slide 170) and conjunctivitis:
– infections are more common in dry eye cases
– the dry eye’s lowered resistance to infection,
especially by Staphylococcus aureus, may be
a result of:
7L40204-97 – decreased levels of: tear lysozyme, other
bactericidal and bacteriostatic tear
components
170
– tear film stagnation/reduced flow.
x Band keratopathy:
– the development of a band keratopathy
within epithelial defects
– epithelial defects are predisposing factors
that follow the development of dry eye
– cause unknown.
x Keratinization of the corneal and conjunctival
epithelia:
– can follow any condition capable of
7L40329-97 damaging conjunctival goblet cells, e.g.
vitamin A deficiency, burns, pemphigoid,
Stevens-Johnson syndrome, and trachoma
– keratin formation may be associated with
abnormal mucous membranes, and mucus
deficiency
– the altered epithelium results in discomfort
and, possibly, vision loss
– keratinization of the palpebral conjunctiva is
more common
– keratinized epithelia has a distinct pearly,
white sheen, is rougher than normal, and is
slightly elevated
– microscopically, keratinized epithelia lack

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

their normal mosaic pattern of mucin-like

glycoprotein (Watanabe et al., 1997)
– because it wets poorly, the altered corneal
epithelium stain poorly with sodium
fluorescein
– the irritation caused by the surface
roughness can be resolved by the use of a
bandage lens
– usually irreversible except in cases of
vitamin A deficiency.
x Psychological. Because most of the underlying
causes of dry eye are life-long, the problems
they pose to the patient are of concern to them,
have to be accommodated, and/or accepted,
and the lack of a ‘cure’ confronted. These
conditions can lead to a dependence on regular
practitioner consultations. Compassion, as well
as medication, may be required in ‘equal’
quantities. Sufferers can experience periods of
despondency, or even depression, and lifestyle
changes may be required. Although much can
be done for sufferers of the more serious forms
of dry eye, more than just medication is often
indicated (this section after Lamberts, 1994B).
171 Ocular Surface Conditions
Wilson (1991) asserts that, based on unpublished
OCULAR SURFACE CONDITION research data on several animal species including
• Epidermal Growth Factor (EGF) is a tear humans, the lacrimal gland synthesizes Epidermal
component Growth Factor (EGF). EGF was identified as a
• EGF is synthesized by the lacrimal gland component of tears by Ohashi et al. (1989), and van
• EGF may be important to the integrity of the Setten et al. (1989). Van Setten et al. suggested
corneal and conjunctival epithelia because
both have EGF receptors that EGF may be important to the maintenance of
- this suggests that the lacrimal gland the integrity of the corneal and conjunctival
participates in: epithelia.
– the maintenance of the ocular surface
The presence of EGF receptors in the corneal and
– wound healing conjunctival epithelia, and EGF in the tears
97400-258S.PPT

suggests the possibility that the lacrimal gland

7L497400-258 participates in ocular surface maintenance and
wound healing. Wilson postulates that EGF
deficiency may be a factor in a subgroup of dry eye
cases, a group that may respond to the topical
application of EGF. Topical EGF administration
may also have a role in corneal wound healing.
Seal et al. (1986) proposed that the conjunctiva of
the dry eye whose tears lacked lysozyme and
lactoferrin, had an alternative antibacterial
protection mechanism that was a derivative of
serum proteins passing from chronically inflamed
conjunctival blood vessels.

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172 Post-Surgical Dry Eye

Battat et al. (2001) studied the effects of LASIK on
POST-SURGICAL DRY EYE tear production, tear clearance, and the ocular
• LASIK is likely to induce dry eye surface. They reported ocular irritation due to
– reduced surface sensitivity may be altered ocular surface tear dynamics despite a
involved in ocular surface alterations reduction in corneal and conjunctival sensitivity still
– duration of one month or more detectable 16 months postoperatively. Schirmer
– Schirmer result reduced
type I test results were reduced postoperatively (24
mm preop. versus 18 mm at 1 month postop.).
– fluorescein clearance rates were higher
Tear fluorescein clearance rates were greater after
post-surgically, and remained so
surgery, and remained so. Sensory denervation of
• Post-operative artificial tears are suggested the ocular surface was suggested as the cause of
97400-259S.PPT
both the ocular surface alterations, and the
7L497400-259 symptoms.
The effect of LASIK on the eye, with special
reference to the induction of dry eye postoperatively,
was also studied by Toda et al. (2001). They found
that LASIK compromised the tear function for at
least a month after surgery. They recommended
the use of artificial tears postoperatively to prevent
unwanted symptoms, and ocular surface damage.
However, Toda et al. (2002) found that, while safety
and efficacy of LASIK was not affected by pre-
existing dry eye, such dry eye is a risk factor for
severe post-surgical dry eye resulting in lowered
tear function, vital staining of the ocular surface, and
more severe symptoms.
IV.B Clinical Tests for Dry Eye

173 Clinical Diagnostic Tests for Dry Eye

CLINICAL TESTS: GENERAL To obtain the most accurate assessment of the dry
Non-Invasive eye patient, the practitioner should consider testing
• Look, but Do Not Touch the patient on a number of occasions to obtain valid
- use slit-lamp, or other viewing system and useful data. When several tests are to be
- eye to remain undisturbed physically, and applied in one clinical session, the least invasive
physiologically should be undertaken first. In this case, the
Invasive observational tests such as the assessment of the
• Instillation (drugs, stains, drops, etc.)
tear lipid layer and the amount of tear debris, are
• Insertion (contact lens, Schirmer test, PRTT, etc.)
performed first.
• Manipulation (pressure, massage, eversion, etc.)
• Sampling (tear fluid, impression cytology, etc.) The diagnosis of Non-Sjögren’s syndrome Dry Eye
97400-316S.PPT
(NSDE) can follow more than one path (Sjögren’s
syndrome dry eye is treated separately in this
7L497400-316 lecture). Diagnosis of NSDE may be by:
x Assessing tear component deficiency (e.g.
174 Schirmer, PRTT, osmolality determination,
BUTs)
CLINICAL DIAGNOSTIC TESTS
Least invasive (observational):
x Detecting the damaging agents (e.g. impression
• Frothing of the tears cytology, tear protein assays).
• Tear film debris x Disclosing the extent of the ocular surface
• Tear prism (inferior meniscus): damage (e.g. sodium fluorescein, Rose Bengal,
- height Lissamine Green).
- appearance/continuity
• BUT (non-invasive) or MBI Slides 174 to 177 categorize the tests applicable,
• Tearscopes (Keeler™, others) according to their invasiveness. Essentially, the
- lipid layer thickness tests should be applied in descending order. The
– interference patterns order of application within a broad category, e.g.
97400-28S.PPT
least invasive, most invasive, etc. is less significant
7L497400-28
but common sense applies, e.g. tear fluid sampling
required for laboratory analysis, or lactoferrin

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175 testing, should be carried out before a Schirmer

test, PRTT, impression cytology, or other invasive
CLINICAL DIAGNOSTIC TESTS test is attempted.
contd…
Invasive:
• Fluorescein instillation, note:
- spread with first blink
- rate of wash-out
- any staining pattern
- measure tear break-up time (invasive)

97400-29S.PPT

7L497400-29

176
CLINICAL DIAGNOSTIC TESTS
contd…

Invasive:

• Other vital stains:

- Rose Bengal

- Lissamine Green

- sulforhodamine B (?)
97400-30S.PPT

7L497400-30

177
CLINICAL DIAGNOSTIC TESTS
contd…
Most invasive:
• Schirmer test
• Phenol red thread test (PRTT)
• Lactoferrin test (e.g. Lactoplate™)
• Laboratory assays (e.g. mucin, lysozyme,
osmolality)
• Impression cytology
97400-143S.PPT

7L497400-143

IV.B.I Clinical Tests for Dry Eye: Non-Invasive

178 Assessment of the Inferior Tear Meniscus

Height
INFERIOR MENISCUS HEIGHT
The height of the inferior tear meniscus (sometimes
• Guide to tear volume the Tear Meniscus Height (slide 180) [TMH], or
• Lower lid margin
Tear Prism Height [TPH]) provides a guide to the
• Utilize an optic section
volume of tears on the ocular surface. A below-
• Measure (graticule), or grade tear prism
height average height suggests a low tear volume that may
• In dry eye: be a cause of dryness. However, there is not
- p height universal agreement on the correlation between
- n irregularity TMH, tear volume, and tear secretion rate. Some of
- n differences between eyes the dissention among authorities is centred on:
- absence of temporal meniscus
97400-31S.PPT
x The effects of evaporation.
7L497400-31 x Low tear-secretion rates.

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179 x Abnormalities of lid posture/margins.

x Abnormally high drainage rates because of
INFERIOR TEAR MENISCUS HEIGHT abnormally frequent blinking.
EXPECTED VALUES
• Normal: x Abnormally high conjunctival absorption (see
- 0.2 to 0.5 mm data and references in Port and Asaria, 1990).
- 0.28 mm (Tran et al., 2001)
A slit-lamp optic section provides a relatively simple
- >0.1 mm (in 93% of cases) (Lamberts et al., 1979) method of determining the meniscus height.
- elderly: 0.057 – 0.271 (Doughty et al., 2001) Examples of a normal tear prism height are shown
• Dry eye: in slides 180 and 183, and is represented
- <0.2 mm (Craig, 2000) diagrammatically in slides 184 and 185. The ‘dark
- <0.3 mm (Bitton & Sorbara, 2002) line’ shown delineates the junction of the tear
97400-318S.PPT
meniscus and the normal tear film. It occurs
7L497400-318 because of the opposing demands of the relatively
thirsty tear meniscus on one hand (Maragoni flow
180
induced by zones of disparate surface tensions
being in close proximity, i.e. the surface tension
gradients that exist between the tear meniscus, lid
margins, and the bulbar conjunctiva), and the
elasticity of the tear film itself (Maragoni elasticity,
i.e. the resistance of the tear film to stretching).
Adding a very small amount of sodium fluorescein
to the tear film highlights the tear prism (slides 182
and 183). Excess fluorescein invalidates the test as
the tear volume is increased artificially.
Port and Asaria (1990) used an optical pachometer
to measure the tear meniscus height (TMH). They
7L43057-93 reported the following values:
181
x A TMH of 0.18 mm was found in normals.
INFERIOR MENISCUS HEIGHT x A TMH <0.1 mm is suggestive of a tear film
• Technique: volume abnormality, i.e. dry eye.
- thin optic section
x No differences were found in TMHs of the
- primary gaze
sexes, or between young and presbyopic
- middle of lower lid margin
subjects.
- minimize light intensity
- normal blinking x Elevating the eye’s up-gaze position by 15°
• Fluorescein increased the TMH by 0.07 mm.
- highlights prism
- use minimal quantity, excess invalidates x Inhibiting normal blinking also Ĺ the TMH.
test (artificial n in tear volume)
97400-32S.PPT Abnormalities of the tear film and/or the tear volume
are suggested by:
7L497400-32
x Differences between the TMHs of the two eyes
of 0.06 mm.
182
x Irregularities of the tear prisms.
x Absence of the tear meniscus/menisci, or
lacrimal lake(s), temporally.
Topography
More recently, measurement of the topography of
the inferior tear meniscus has been the subject of
renewed interest. For such assessments, the most
common aspect studied has been the tear
meniscus radius, or the TMR. As with the TMH, an
invasive, or non-invasive, technique can be
employed.
7L41627-92 Yokoi et al. (1999) employed non-invasive
photographic and video techniques and concluded
that the radius was 0.365 mm (SD = 0.153mm),
range: 0.128 – 0.736 (n = 45). Mainstone et al.
382 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

183 (1996) gave higher figures of 0.545 ±0.259 mm

using an invasive technique (sodium fluorescein
instillation). Mainstone et al. found lower (steeper)
values for dry eye cases (0.314 ±0.160 mm) using
their technique. Yokoi et al. also found dry eye
TMR to be steeper at 0.25 mm.
Oguz et al. (2000) investigated the relationship
between the radius of the tear meniscus curvature
(TMR, slide 186), and the TMH. The TMH, and
then the TMR (measured with, and without the aid
of sodium fluorescein using a purpose-built video
meniscometer), were measured at the centre of the
lower lid. A second estimate of the TMH was made
from slit-lamp photographs. The values were:
7L40003-99
x TMR: 0.22 ±0.09.
184 x TMH: 0.19 ±0.09.

LID MENISCUS x TMH-Na Fluo: 0.21 ±0.14.

Tear film Cornea x TMH-Na Fluo from photo: 0.24 ±0.09.
Dark line
These results suggest that the addition of sodium
Lower The dark line is a localized
tear thinning of the tear film
fluorescein to the tears increases the apparent
meniscus It is the demarcation between TMH, and photography exaggerates the result.
a ‘demanding’ tear meniscus & Because TMR correlated significantly with all forms
a tear film that is unable to of TMH measurement, and TMR was easier to
Lower lid
supply the meniscus’ demands determine, the authors concluded that
meniscometry (TMR) had a role to play in the
assessment of the parameters of the tear meniscus.
97400-234S.PPT

Mainstone et al. (1996) assessed the efficacy of the

7L497400-234 measurement of TMH, TMR, Tear Meniscus Width
185 (TMW), and cross-sectional area (XSA) in the
diagnosis of dry eye. They used data from
TEAR MENISCUS HEIGHT (TMH) photographic records of tears stained minimally with
Tear film Cornea
sodium fluorescein. TMR and TMH were found to
have good diagnostic accuracy, and correlated well
with other tear assessments, e.g. PRTT, NIBUT,
TMH and ocular surface staining scores. TMH was found
to be the most powerful indicator of tear film
insufficiency, at least for the ‘aqueous deficient’ type
of dry eye.

Lower lid

97400-235S.PPT

7L497400-235

186

TEAR MENISCUS RADIUS: TMR

Tear film Corneal epithelium
Dark line

TMR

Lower lid

97400-321S.PPT

7L497400-321

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187

INF. TEAR MENISCUS: TMR

• TMR is steeper in DE

• TMH & TMR are correlated

• TMR correlates well with other tear tests

• TMR is easier to measure

97400-320S.PPT

7L497400-320

IV.B.II Tear Film Interferometry

188 Tear Film Interferometry

Thin-film interference from the tear film was an early
TEAR FILM INTERFEROMETRY slit-lamp observation (Marx, 1921, Vogt, 1921,
Meesman, 1927, all cited in Guillon and Guillon,
The clinical application of
1994).
Thin-film interference (TFI, see next topic Thin-Film
thin-film interference to Interference (TFI)) has been the basis of many
instruments over the years, e.g.:
the pre-corneal, and pre- x Norn (1979, cited in Guillon & Guillon, 1994).
x Hamano et al. (1979, 1982) both cited in Hamano
lens, tear films
97400-324S.PPT
and Kaufman (1987).
7L497400-324 x Hamano et al. (1980).
189 x The Tearscope™ by Guillon (1986, cited in
Guillon & Guillon, 1994).
INTERFEROMETRY: TEARSCOPE
WIDE-FIELD SLIT-LAMP TECHNIQUE x Guillon & Guillon (1988).
x Doane (1989).
S/L Microscope
Retro
Internal Illumination The designs of most of these fall into either of the
Illumination two categories illustrated in slide 189. The main
difference relates to the location of the illumination
Hemispherical Hemispherical
bowl bowl systems, i.e. internal (reflective bowl), or from
(reflective)
Cold-cathode or
(translucent) behind (retro-illuminated translucent bowl).
fluorescent tubes
Anterior eye Anterior eye Most instruments have a hemispherical (or similarly
97400-328S.PPT
shaped) bowl with an axial opening. Through this
opening, a magnifier or slit-lamp microscope can be
7L497400-328
used to observe the tear film illuminated broadly by
the bowl acting as a broad, extended, uniform light
source. To reduce any induced tear fluid
evaporation, the light sources used must run cool.
When viewing the whole cornea, only a low slit-lamp
magnification can be employed. In some
instruments, the size of the circle of illumination may
limit just how much of the cornea can be observed
at any one time.
Whole-cornea views will often demonstrate more
than one pattern because of the differing conditions
existing around and over the cornea during the
observation.

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190 Thin-Film Interference (TFI)

THIN FILM INTERFERENCE Interference occurs when two light waves interact.
LIGHT RAYS In thin films, the two interacting rays are the
In
reflection from the front surface of the film, and the
y y
cid ra ra reflection from the next (deeper) optical interface
en d ed
tr c te ct
ay ef
le fle within the film. This source also undergoes two
st R Re
1 2
nd refractions (see slide 190).
Tear film Air

Optically, the deeper surface must involve a

physical junction that delineates an interface
between optical media of differing refractive indices.
As was shown in Module 2, Lecture 2.3, Section IX
97400-140S.PPT
Light Loss by Reflection, only some of the
incident light is reflected at such an optical interface.
7L497400-140
The amount reflected can be calculated from
Fresnel’s formula but such a calculation is only
191 applicable to normal, or nearly normal, angles of
incidence. Generally, the greater the refractive
THIN FILM INTERFERENCE index difference that exists across the interface, the
LIGHT WAVES
greater the amount of light reflected.
In the eye, these interfaces may be between the
lipid-aqueous layers (lipid has the higher refractive
See
next index), the aqueous-mucin layers, the tear film and
Tear film Air

slides the corneal epithelium. However, the irregular

nature of the microvilli of the epithelium means that
it does not present a smooth and regular reflecting
surface. This irregularity is compensated for, at
least partially, by the tear mucin layer that covers
97400-139S.PPT
the microvilli.
7L497400-139 When the mucin is hydrated fully, the refractive
index difference between the aqueous and mucin is
small enough to be inconsequential optically,
resulting in no specular reflection from this
‘interface’ (after Guillon and Guillon, 1994). This is
a case of an interface existing physically but not
optically, because the refractive indices on either
side are the same, or very nearly so. No second
reflection occurs.
In the eye therefore, interference is more likely to
occur from the lipid layer, or in the case of a thinned
aqueous layer, the whole tear film, i.e. its front and
back surfaces.
To gain an understanding of the ‘colours’ observed,
an analysis of the light waves involved, and their
interference, is required (slide 191).
192 Thin-Film Interference: Constructive and
Destructive
CONSTRUCTIVE INTERFERENCE The interaction of the two light rays can be either
(for simplicity monochromatic light assumed)
constructive (same or similar phase relationship,
see slide 192) or destructive (out of phase or nearly
so, slide 193). While intermediate wave
x
relationships exist, for simplicity only the two
Amplitude

-x 2x
extreme cases are presented here, i.e. exactly in
x -2x phase (slide 192), or exactly out of phase (slide
-x
193).

97400-138S.PPT

7L497400-138

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193

DESTRUCTIVE INTERFERENCE
(for simplicity monochromatic light assumed)

x
-x

x Amplitude
x-

97400-137S.PPT

7L497400-137

194 Thin-Film Interference: Colours

The treatment of colours in interference is more
INTERFERENCE COLOURS complex than is presented here. A simplistic
Tear film thickness dependent
Assume ‘greenish’ wavelengths interfere destructively example is presented in slide 194. Basically, as
Coloured fringes will appear to be light waves of various wavelengths approach
White incident light
‘purplish’ ( red + blue)
conditions of constructive interference, their region
Red Blue ‘Purplish’
of the visible spectrum is reinforced (enhanced).
Amplitude

Green
On the other hand, as the conditions of destructive
Gr
ee
n

interference are approached, that part of the

d

Green
Blue

Blue
Re

Red

Green
The ‘reds’ interfere constructively
spectrum involved is suppressed (dimmed). In this
The ‘greens’ interfere destructively
The ‘blues’ interfere constructively
way, a characteristic hue is created that is film-
Film thickness
determines the colour(s)
thickness dependent.
97400-133S.PPT (Simplified treatment)
As conditions are seldom ideal in a real tear film
7L497400-133 and many thicknesses may be present, the
195 existence of multiple colours is both predictable and
expected (see slide 195).
INTERFERENCE COLOURS
• Incident light is assumed to be ‘WHITE’
• At any instant in time, tear film has
different thicknesses at different
locations (orderly & random differences)
• Interference minima (destructive
interference) can only affect a particular
wavelength under particular conditions
• Adjacent wavelengths affected to a
lesser extent under these circumstances
• All other wavelengths reinforce
(constructive interference) to varying
degrees, i.e. slightly to maximally
97400-136S.PPT

7L497400-136

196 Interference Patterns

INTERFERENCE PATTERNS An important issue is: which layer, or layers, is/are

(after Forst 1988) responsible for the generation of the patterns and
Tear film interference patterns (coloured coloured fringes observed?

fringes) can indicate the different

Usually, the lipid layer is responsible for any
coloured fringes seen. However, should the lipid
thicknesses of the component layers layer be thinner than about 60 nm, only ‘white’ light
patterns and reflections are seen, i.e. no coloured
phenomena are observed (after Korb et al., 1996B).
Usually, the lipid layer is responsible
Should the thickness of the whole tear film be
for the coloured fringes seen
reduced so much that it becomes ‘thin’ in an
97400-141S.PPT
interferometric sense (implying a significant loss of
7L497400-141 the aqueous, i.e. the bulk of the film volume),
coloured fringes may be seen. These are observed
most commonly just before, and in the region of, a
rupture of the tear film, such as occurs during BUT

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

197 assessments.
Similar effects may be observed during drying of the
INTERFEROMETRY pre-lens tear film in situ, especially on contact lens
CLINICAL OBSERVATIONS surfaces that wet poorly.
• Lipid layer patterns commonly colourless
The visibility of the aqueous layer also has clinical
- layer too thin for interference (<60 nm?) implications. A classification system appears as
• Any aqueous layer pattern is ‘swamped’ by slide 198. When coloured fringes appear in the
the tear film’s specular reflex aqueous layer, they are counted, or their number
- except when lipid layer is very thin
estimated. The layer thickness can be estimated
from the data in the table in slide 199.
• Pre-lens coloured fringes probably due to
thinning aqueous
97400-323S.PPT

7L497400-323

198
AQUEOUS LAYER PROPERTIES
VISIBILITY
from Guillon & Guillon, 1994

Classification Implication

• High • Very thin or absent lipid layer

• Moderate • Thin lipid layer

• Poor • Normal

• Not visible • Normal to thick lipid layer

(& swamping by tear film reflex)
97400-161S.PPT

7L497400-161

199
AQUEOUS LAYER THICKNESSES
from Guillon & Guillon, 1994

Classification Estimated thickness Pm

• Fewer than 5 fringes • <1.0

• 5 - 10 • 1.0 - 1.8

• >10 fringes • 1.8 - 3.5

• Present, no fringes visible • >3.5

97400-160S.PPT

7L497400-160

200 Colours and Patterns versus Lipid Layer

Thickness
COLOURS vs FILM THICKNESS
Colours Observed
• Interference colours usually limited to:
Many authors (see Guillon and Guillon, 1994) have
- yellow, brown, blue, and purple (Guillon &
Guillon, 1994) reported that lipid layer reflections result most
— yellow 90 nm commonly in colourless patterns. This is because
— brown 140 nm the layer thickness is below the minimum to
— blue 220 nm
produce interference fringes, i.e. the phase shift
resulting from the passage into, and out of, the thin
• Coloured areas represent the thickest film is too small to produce any significant colour
zones of the lipid layer (n phase shift)
effect (enhancement). Korb et al., 1996B reported
• Grey zones are thinner, ono pattern an absence of spectral colours for tear films whose
97400-126S.PPT

lipid layers were <60 nm in thickness.

7L497400-126
However, various authors have produced tables of
colours versus lipid film thickness, e.g. Guillon and

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 Module 7: Contact Lens-Related Ocular Complications

201 Guillon, 1994 (slide 200), Forst, 1988 (slide 201),

and Korb et al., 1996B (slide 202).
COLOURS vs FILM THICKNESS Patterns Observed
after Forst, 1987-89
Although many terms have been used to describe
• Grey-Blue 50 nm
the patterns seen in light reflected from the lipid
• Pale Straw Yellow 90 nm layer, or the tear film in general, most authors have
settled on a six-classification naming convention
• Brown-yellow 140 nm that in now in popular use. This classification
system is the outcome of the works of McDonald,
• Violet 190 nm
1969, Hamano et al., 1979, 1980, and Guillon &
• Sky Blue 220 nm Guillon, 1986, 1988 all cited in Guillon and Guillon,
1994).
97400-127S.PPT

These lipid pattern descriptions are (after Guillon

7L497400-127
and Guillon, 1994):
202
x Marmoreal (marble-like, marbled). This pattern
is seen in about 90% of normal eyes (Hamano
COLOURS vs FILM THICKNESS
after Korb et al., 1996 and Kaufman, 1987):
• White 30 nm
• Grey-White 45 nm
– open, or open meshwork. The appearance is
• Grey 60 nm grey, and marble-like. This pattern of bright
• Grey-Yellow 75 nm and dark regions is due to thicker, local lipid
• Yellow 90 nm areas over a thin, lighter coloured, underlying
• Yellow-Brown 105 nm
• Brown-yellow 120 nm main layer. The mesh-like pattern is open,
• Brown 135 nm relatively sparse, and relatively stable. This
• Brown-Blue 150 nm pattern corresponds to the thinnest lipid layer
• Blue-Brown 165 nm
• Blue 180 nm visible. Craig (1994) advised against fitting
97400-158S.PPT contact lenses to people showing open
meshwork or coloured fringe-type patterns
7L497400-158
when examined with the aid of a Tearscope™
because they showed reduced BUTs.
203 – closed, or closed meshwork. Again, the
appearance generally is a grey, marble-like
LIPID PATTERN CLASSIFICATION pattern. However, this pattern is closed and
from Guillon & Guillon, 1994
tight but, like open meshwork, is relatively
Description (Incidence [%]) Estimated thickness
stable. This pattern corresponds to a thicker,
• Open meshwork 21 • | 15 nm more stable, more visible lipid layer than the
• Closed meshwork 10 • |30 nm open meshwork type.
• Flow 23 • |30 - 80 nm x Flow (wave or wave-like). This pattern is wavy
• Amorphous 24 • 80 nm and changing constantly during the interblink
period. It is the marmoreal pattern encountered
• Colour 15 • 80 - 370 nm
most commonly. The likely cause is poor
• Other 7 • Variable mixing of tear lipids. The constantly changing
97400-159S.PPT

pattern differentiates flow from meshwork

7L497400-159 (marmoreal) patterns. The shapes formed by
204 the pattern tend to be rounder than the
meshwork varieties.
INTERFEROMETRY
CLINICAL IMPLICATIONS x Amorphous. This pattern has a bluish-whitish
• Open meshwork after Guillon & Guillon, 1994 appearance due to a thick, well-mixed lipid
- thin lipid layer opossible CL drying problem layer. It is the normal pattern seen in non-
• Closed meshwork
- stable tear film, ogood for CLs contact lens wearers.
• Flow/wave pattern
- stable tear film, CLs possible, n lipid deposits? x Colour fringe patterns. The colours are the
• Amorphous pattern result of thin-film interference as detailed
- very stable tears, good for CLs, greasing problem? earlier. Usually, the colours are confined to
• Colour fringe pattern
- very thick lipid, CLs possible, lipid contamination? yellow, brown, blue, and purple, or variations of
• Other patterns, with mucus strands? these, or combinations of these. The coloured
- pathological?, no CLs zones represent areas over which the thickest
97400-329S.PPT

lipid layers are present. The grey background is

7L497400-329 due to the thinner zones of the lipid layer that
are not producing thin-film interference colours
(because they are too thin to do so).
388 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

205 x Other. Some lipid layer-produced patterns can

be difficult to classify. They are often highly
variable coloured patterns that may include
mucus strands. Usually, they can be regarded
and treated as pathological. Generally, they are
regarded as a contra-indication to contact lens
wear.
x When the whole of the cornea is viewed at
relatively low magnification (7X –10X) it is
common to observe more than one pattern type
concurrently. A particularly common
combination is that of a closed meshwork with
areas of flow. Other combinations are relatively
common, e.g. amorphous with coloured fringes.
In the case of the latter, the colours are usually
yellow and brown, occasionally blue, that
correspond to lipid layer thicknesses of 90, 140,
and 220 nm respectively. The properties of
combinations of lipid layers relate to the
properties of the components.
Slide 203 presents the classifications, incidences
and lipid layer thicknesses of the common patterns.
Slide 204 correlates the patterns seen with their
clinical implications including their significance to
possible contact lens wear.
Other lipid layer interference pattern grading
systems have been proposed. One such system
proposed by Yokoi et al. (1996) grades by colour
and uniformity of distribution of the pattern. The
7L40070-98
grades are:
206 x 1: Somewhat grey, uniform distribution.
x 2: Somewhat grey, non-uniform distribution.
x 3: A few colours, non-uniform distribution.
x 4: Many colours, non-uniform distribution.
x 5: Corneal surface exposed partially.
Good agreement (84%) was claimed for this
grading system among the raters. Good agreement
was also found between this rating system and the
results of other tests for dry eye including sodium
fluorescein staining, Rose Bengal staining, and
BUT. Yokoi et al. (1996) concluded that
7L40117-93 (FLOW) interference patterns were highly correlated with the
severity of dry eye.
A clinical routine for the use of tearscopes,
207
especially his Tearscope™, was presented by
Guillon (1998).

7L40507-93 (COLOURED)

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208 Thickness of the Lipid layer

Uniformity of the lipid layer is a guide to the overall
LIPID LAYER THICKNESS quality of the tear film.

• Uniformity of lipid

• Appearance of coloured fringes

• Excess lipid

97400-35S.PPT

7L497400-35

209 The typical marmoreal pattern (slide 209) seen in

the lipid layer is absent in the dry eye.

7L40381-92 (COLOURED)

210
Coloured fringes (slide 210), indicating a thicker
lipid layer, are usually more visible in dry eye. This
is often accompanied by the appearance of excess
debris in, and more likely on, the tear film.
Estimated thickness of the various lipid layer
patterns are presented in slide 200 (after the data of
Guillon and Guillon, 1994):
Eyes that have BUTs of <10 seconds mostly exhibit
an amorphous pattern

7L40534-98 (OPEN MESH)

211 Non-Invasive Tear Break-Up Time Measurement

(NIBUT)
TEAR BREAK-UP TIME
NON-INVASIVE TECHNIQUE (NIBUT) The limitations of an invasive fluorescein technique
(detailed in the next section of this lecture) are
• Assesses tear film stability non-invasively
circumvented to some degree by the use of non-
• No dye instilled invasive methods of measuring the tear BUT
• Variety of methods (Mengher et al., 1985, Tiffany, 1994).
- keratometer Generally, non-invasive BUTs (NIBUTs) tend to be
- grid pattern higher (longer) that the equivalent invasive (sodium
- tearscope (including Tearscope™) fluorescein instilled) values (slides 216 and 217).
• Can assess a pre-lens tear film BUT
Because some normal NIBUTs can be up to 60
97400-40S.PPT
seconds or more, Guillon and Guillon (1994)
suggest that tests be stopped at the 45-second
7L497400-40
mark. Tonge et al. (1991) gave a median NIBUT
time of 62 seconds. Invasive BUTs range from 10
to 34 seconds according to the same authors.
390 IACLE Contact Lens Course Module 7: First Edition
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212 Tonge et al. were unable to provide a mean value

for NIBUT because of an inability of some subjects
to withhold a blink for extended periods despite
there being no apparent rupture of the pre-corneal
tear film. Their conclusion was that normal NIBUTs
ranged between 40 and 60 seconds. Dry eye cases
demonstrated shorter NIBUTs (25 to 32% of the
normal values).
Generally, while the NIBUTs found in normals
varied widely, those in dry eye cases were less
variable (between subjects, as well as between the
eyes of the same subjects). Continuous video
game playing has also been shown to decrease
7L40135-93 BUT by up to 15 seconds (Suber et al.,2001).
Unlike invasive BUT data, NIBUT data fails to show
any differences between the sexes.
213
The longer NIBUTs suggest that the addition of a
dye (e.g. fluorescein) to the tear film alters the
stability of the tear film adversely, thereby producing
an artificial, and less stable, anterior eye
environment. This increased instability has already
been confirmed by Mengher et al. (1985B). This
means that tear film stability is underestimated by
invasive techniques using instilled sodium
fluorescein dye.
Interestingly, Mengher et al. (1985) reported that
discomfort was experienced before the pre-corneal
tear film broke up, leading them to suggest that
7L40007-99
blinking is stimulated by a breakdown of the tear
film over the bulbar conjunctiva rather than the
214 cornea.
Technique
The basic technique does not require the use of an
added dye such as sodium fluorescein. A variety of
instruments, e.g. a keratometer (slide 212), a
modified keratometer (slide 213), a tearscope (slide
214), or a Tearscope™ (slide 215) allow the
practitioner to observe the optical effects of changes
in the tear film on the cornea or contact lens after a
blink.
The non-invasive instrument developed by Mengher
et al. (1985), based on the work of Lamble et al.
7L41322-93 (1976, cited in Mengher et al., 1985), used a black
hemispherical bowl on which a regular grid of white
lines was inscribed. This bowl (radius 20 cm) was
215 mounted around a slit-lamp microscope and was
illuminated internally by a circular fluorescent tube.
The reflection of the white grid in the whole pre-
corneal tear film was monitored through the slit-
lamp for the irregularities or distortions that
accompany a thinning or rupture of the tear film.
Non-invasive methods are not flawless and are
open to interpretation. For example, the
keratometer can measure the time until the tear film
changes (such as a thinning of the tears), but it
cannot determine the precise time to a full break in
the tear layer.

7L47400-6
In the case of the so-called marginally
(questionably) dry eye, a NIBUT determination may

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 Module 7: Contact Lens-Related Ocular Complications

216 be useful in differentiating normal from marginal.

Guillon and Guillon (1993) presented the following
TEAR BREAK-UP TIME summary:
NON-INVASIVE TECHNIQUE (NIBUT)
x NIBUT < 10 seconds – a marginally dry eye that
NIBUT times > BUT (invasive)
may be prone to contact lens intolerance.
• NIBUT:
x NIBUT of 10 – 20 seconds – borderline
- 20 – 45+ sec (Guillon & Guillon, 1994)
marginally dry eye, may be more prone to lens
- normal averages 40 sec (range: 20 - 62, Tonge et al., 1991) deposits than normals.
- dry eye averages 12 sec x NIBUT > 20 seconds – stable tear film, normal.
• BUT:
However, because of its borderline nature, the
- 10 – 34 sec (Tonge et al., 1991) questionably dry eye poses a challenge clinically,
e.g. Tiffany et al. (1989) found a significant negative
97400-41S.PPT

7L497400-41 correlation between surface tension (ST) and

217 NIBUT in both dry eye cases and normals.
Inatomi et al. (1999) divided non-invasive break-ups
NIBUT (NIBUs) into two categories:
Mengher (1985)
100
x Type 1 (more common, 89% of cases) involved
film ruptures not associated with any superficial
80
punctate epitheliopathy.
NIBUT (Second)

60 48 + 5
x Type 2 showed deep and reproducible tear film
40 (p<0.001)
break-ups over regions of dense staining and was
20
12 + 2
thought to be associated with poor interaction
between mucus and the epithelial cell
0
Normal Dry Eye membranes.
97400-75S.PPT

7L497400-75

218 Infrared Thermography

Mori et al. (1997) evaluated the tear film with a high
CLINICAL TESTS: NON-INVASIVE speed, high resolution, infrared radiation
INFRARED THERMOGRAPHY
thermographer. The rate of change of corneal
temperature, an analogue of the tear film
Can assess: evaporation rate (because evaporation produces
cooling), was measured.
• Tear stability non-invasively
They confirmed that dry eye cases experienced a
• The general status of the tear film lower evaporation rate than did normal subjects
(possibly because there is less tear fluid to
evaporate). Because the apparatus was sensitive
97400-331S.PPT
and responsive enough to ascertain the corneal
temperature fluctuations between blinks with only a
7L497400-331 1 second delay, Mori et al. were able to show that in
dry eye cases, the temperature decline was slower
because of the reduced tear film evaporation rates.
219
Mori et al. proposed that thermography be
CLINICAL TESTS: NON-INVASIVE considered a viable, non-invasive method of
INFRARED THERMOGRAPHY assessing the stability and general status of the tear
film.
• Infrared thermograms confirm:

- dry eyes have lower evaporation rates

- corneal temperature fluctuates between

blinks (an effect of evaporation)

- dry eyes have slower between-blink cooling

(reduced evaporation)
97400-330S.PPT

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IV.B.III Clinical Tests for Dry Eye: Invasive

220 Clinical Test: Invasive Tests

One of the common ways of assessing the tear film
CLINICAL TESTS: INVASIVE and evaluating the integrity of eye’s anterior surface
• Often involve the use of stains (dyes): (slide 222), is by the instillation of a dye or stain, e.g.
sodium fluorescein, or Rose Bengal, to make the
- sodium fluorescein tear film, or any ocular surface damage, more
visible to an observer.
- Rose Bengal Among other difficulties, one of the most overlooked
issues is that of ‘swamping’. Given that the volume
- other stains (e.g. Lissamine Green, of tears present on the anterior surfaces of the eye
sulphorhodamine B)
is about 7 to 8 µL, the arrival of an additional 20 to
97400-332S.PPT
30 µL of dye (Tonge et al., 1991), constitutes an
abnormal, and unrealistic, set of circumstances.
7L497400-332 Further, impregnated paper dye strips can contain
221 preservatives, e.g. benzalkonium chloride, a
cationic surfactant. Consequently, the effects of the
CLINICAL TESTS: INVASIVE dye, its preservative, or their combination, can affect
CONSIDERATIONS BUT determinations by their effect(s) on tear film
• ‘Swamping’ an issue, e.g. 7-8 PL of tears is stability (Tonge et al., 1991). These considerations
‘diluted’ by 20-30 PL of dye-containing saline are not relevant when the intention is to stain the
or other suitable dye vehicle eye’s surfaces.
• Impregnated paper dye strips may include If the tear film is dyed before contact lenses are
preservatives with surfactant properties inserted, the dye may stain SCLs. In this situation,
lens insertion should be delayed, or the anterior eye
- tear film characteristics may be altered
irrigated before lens insertion.
• Some SCL materials may imbibe dye
97400-333S.PPT

7L497400-333

222
DRY EYE
OCULAR SURFACE DAMAGE
Usually demonstrated by vital staining:
• Rose Bengal
- rating system exists (van Bijsterveld, 1969)
• More recently, Lissamine Green used
- better tolerated
• Sodium fluorescein also has a role
- observe with yellow barrier filter (W12, OG515)

97400-112S.PPT

7L497400-112

223 Evaluating the Ocular Surface

Epithelial Staining: Rose Bengal
ROSE BENGAL STAIN
WHAT IS IT? Rose Bengal, once thought to be a vital stain,
assists in the differentiation of dead cells and
• Class: Fluorone damaged, but viable cells in the epithelium.
However, Feenstra and Tseng (1992, 1992B)
• C20H2O5I4Cl4Na2
studied sodium fluorescein and Rose Bengal
• M.W. : 1017.686 staining and found that Rose Bengal was not a vital
stain in that it caused epithelial cells to loose vitality.
• 4,5,6,7-tetrachloro-2,4,5,7-tetraiodo Their finding was that Rose Bengal stained cells
fluorescein sodium whose protection by the preocular tear film was
defective or poor. Dry eye cases are more likely to
97400-147S.PPT
have greater numbers of dead or affected cells.
7L497400-147 Typically, the conjunctival staining pattern observed
with Rose Bengal is V-shaped, with the principal

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224 zones located within the palpebral aperture. The

corneal epithelium may also take up the stain (see
ROSE BENGAL STAINING slides 224, 225).
Rose Bengal is best applied using the strip form. In
• Considerable discomfort on instillation
this way, the amount of Rose Bengal instilled is
• Application by strips or solution better controlled (than when applied as drops), and
the amount of discomfort and stinging is minimized.
• Corneal and conjunctival
Lee and Tseng (1997) used Rose Bengal to stain
• In dry eye: those anterior eye areas not normally exposed to
- interpalpebral conjunctiva shows typical the atmosphere. In dry eye, they found that the
changes characteristic of tear lipid deficiency (lytic
V-shaped staining pattern
[disrupted cell-cell junctions] changes without
squamous metaplasia) could be differentiated from
97400-36S.PPT

7L497400-36 changes due to an aqueous deficiency. Aqueous

deficient eyes usually stain with Rose Bengal in the
interpalpebral (exposed) zones with an intensity that
225 correlates well with the severity of the squamous
metaplasia.
Further details of Rose Bengal, and an established
grading system, are presented in slide 223.

7L41885-92

226

7L41175-96

227
ROSE BENGAL STAIN
ISSUES
• Normal eyes should exhibit no RB staining,
but…
- Rose Bengal may cause epithelial cells
to lose vitality
• Thought to differentiate vital cells from dead
cells and mucus but…
- RB can stain normal epithelial cells,
especially if preocular tear film is
defective (see Feenstra and Tseng, 1992)
97400-144S.PPT

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228 The grading scale proposed by van Bijsterveld

(1969) is presented diagrammatically in slide 228.
GRADING SCHEME Essentially, the anterior eye is divided into the
FROM: van Bijsterveld, 1969
• Areas: corneal zone, and the three zones of exposed
Zones conjunctiva.
- Cornea, N, T, I conjunctivae
• Ratings:
- 0 = no punctate staining Nasal Corneal Temp.

- 1 = small (readily countable)

Inferior
- 2 = numerous (uncountable)
- 3 = confluent or nearly confluent Conjunctivae

97400-153S.PPT

7L497400-153

229 Evaluating the Ocular Surface

Epithelial Staining: Fluorescein
SODIUM FLUORESCEIN
How:
• A vital stain
Sodium fluorescein is a vital stain that is taken up by
• Stains altered epithelial cells revealing:
epithelial cells that are damaged or disrupted.
- cell damage (adheres to devitalized cells)
- surface disruptions (‘pools’ in the defect & Wilson et al. (1995) showed that fluorescein is
stains the damaged cells surrounding it) taken up by damaged cells and is not related to
- penetrates in & under the epithelium, entering
via surface disruptions drop-out of cells, pooling, or filling intercellular
– halo of fluorescein forms ‘around’, but is spaces. However, Schwallie et al. (1998)
actually under, areas of disruption postulated that the low-grade bulbar conjunctival
– disruption appears as the ‘nucleus’ of the staining they saw when assessing day-to-day
halo (because of staining & pooling)
97400-37S.PPT
variations in staining was physiological and probably
related to epithelial cell desquamation. This is
7L497400-37
consistent with Tabery (1997) who suggested that
micropunctate fluorescein staining probably
230 discloses disruptions of intercellular junctions during
the early phase of the exfoliation process.
SODIUM FLUORESCEIN STAIN A possible complication in some pathological states
is the adherence of sodium fluorescein dye to
• Class: Fluorone diseased epithelial cells as demonstrated by Tabery
(1992). Conditions known to exhibit this
• C20H10O5Na2 phenomenon include herpes zoster ophthalmicus
• M.W. : 376.282
and dry eye.
Interestingly, Tabery found that the staining pattern
• Alternatively: Fluorescein, Uranin, Acid resulting from fluorescein adherence matched
yellow 73 closely that found with Rose Bengal. This should
not be surprising since both Rose Bengal and
97400-146S.PPT
sodium fluorescein are fluorones, i.e. chemically,
7L497400-146 they are closely related and can be expected to
231 have some properties in common. Fluorescein
therefore has a dual function, it penetrates into, and
FLUORESCEIN STAINING under, defective epithelia that it discloses by
TECHNIQUES fluorescence, and it adheres to devitalized surface
• Apply to inferior, or superior-temporal bulbar cells.
conjunctiva
• Discloses corneal and conjunctival staining Clinical Considerations:
• However: Korb and Herman (1979) studied sodium
- alters tear film stability fluorescein staining after both a once-only
- often ‘tattoos’ bulbar conjunctiva at point of application, and a sequential instillation. In 200
application corneas they found 19% showed staining after only
- pools in bulbar conjunctival folds
one application and an additional 23% after six
- fills ‘valleys’ of the palpebral conjunctiva in
cases of CLPC additional instillations at 5 minute intervals, i.e. a
97400-335S.PPT total of 42% showed staining after all the fluorescein
7L497400-335
had been instilled. They also found a correlation
between severe staining and contact lens
intolerance.

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232 Korb and Herman believed it is possible that the

susceptibility of the cornea to staining related to the
FLUORESCEIN STAINING integrity of the epithelium and/or the tear film.
Other issues: (after Schwallie et al., 1997/1998) A study of daily sequential staining (7 instillations, 3-
• Usually, right = left eye minute intervals at the same time each day) was
• Examiners graded staining comparably carried out by Caffery and Josephson (1991) on
• Duration of mild staining: about 1.2 days
female subjects over 30 days. They found no
- more severe grades: about 2 days
predictable pattern, intersubject variability, and
• Most common sites:
- inferior cornea (most exposed) 50%
staining that varied from day to day. As a result of
- nasal 20%
the study outcome, the authors questioned the
• Some staining is physiological - desquamation? wisdom of reliance on a single stain instillation for
prediction of contact lens success, various epithelial
97400-336S.PPT
anomalies, or diagnosis of marginally dry eye.
7L497400-336
A fine punctate staining pattern may be widespread
over the cornea and conjunctival epithelium but,
233 typically, a focus of staining is visible in the inferior
corneal region (slide 234). The presence of
CORNEAL STAINING WITH AGE fluorescein staining becomes more common in
older age (Norn, 1982, see slide 233).
Norn (1982)
25
21 Fluorescein staining of the cornea of normal non-
PATIENTS WITH STAINING (%)

20
19
18 contact lens wearers has been evaluated by
15
Schwallie et al. (1997). Their results showed:
12

10 x Little difference between the eyes.

4
5 x Good consistency between examiners.
0
<40 >40 >50 >60 >70 x An average grading of about 0.5 (scale 0 to 4).
(YEARS)

97400-74S.PPT x Staining endured for about 1.2 days.

7L497400-74 x The most prevalent location was the inferior
234 region (50%), followed by the nasal region
(20%).
The authors asserted that their study was useful in
establishing the normality of suspect sodium
fluorescein staining and its expected duration.
In a later study, Schwallie et al. (1998) examined
the day-to-day variation in bulbar conjunctival
surface staining. They reported:
x Little variability between right and left eyes.
x Consistency between clinician’s ratings of what
they saw despite a lack of any procedure to
standardize them.
7L42125-95
x Staining above a 0.5 rating persisted for an
235 average of 2 days.

FLUORESCEIN STAINING
GRADING SCALE: CORNEAL Several staining grading scales have been
TYPE DEPTH EXTENT produced. One such scale appears in slide 235.
• None • Superficial (no • % of sector
Stromal Glow [SG]) area Another is presented in Efron (1999).
• Micropunctate Corneal sectors
• Delayed SG
• Macropunctate (local) S
• Coalescent areas • Immediate SG N C T
(local)
• Patch
• Immediate SG with I
sub-epithelial Cornea
diffusion
97400-337S.PPT

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236 Evaluating the Ocular Surface

Other Stains
LISSAMINE GREEN STAIN Other stains have been used to assess the integrity
• Class: Triarylmethane of the eye’s anterior surface. Some of these follow.
• C37H34 N2O9S3Na2 Lissamine Green is marketed as a substitute for
• M.W. : 792.875 Rose Bengal. Like Rose Bengal, it stains
degenerate and dead cells, and mucus.
• Alternatively: Lissamine Green SF,
Sulforhodamine B, a fluorescein-like compound, has
FD&C Green #2, Light green
been used as a substitute for sodium fluorescein
• Marketed as a substitute for Rose Bengal because it:
• Stains: degenerate and dead cells, mucus
97400-145S.PPT
x Resolves the problem of distracting scleral
fluorescence that normally makes bulbar
7L497400-145 conjunctival and tear film staining difficult to
discern (Eliason and Maurice, 1990). This dye
requires a green exciter light and fluoresces in
237
the orange wavelengths, thereby providing
better staining contrast than sodium fluorescein.
SULFORHODAMINE B STAIN
x Shows more conjunctival staining than sodium
• Class: Fluorone ?
fluorescein, at least in Sjögren’s syndrome
• C27H29N2O7S2Na cases. Eliason and Maurice concluded that
sulforhodamine B was more capable of
• M.W. : 559 or 580.69 revealing subtle surface abnormalities, cf.
sodium fluorescein and Rose Bengal, for
• Alternative names: Acid Red 52, Xylene
disclosing the effects of dry eye and epithelial
Red B, Lissamine Rhodamine healing.
(also spelt: Sulphorhodamine B) Suitable filters are: exciter: band-pass interference
97400-149S.PPT
filter 520-550 nm (blue), as used in most slit-lamps;
7L497400-149 barrier: Kodak Wratten #22, or equivalent.
These stains are detailed in the slides opposite.
238 Invasive Tear Break-Up Time Measurement
DRY EYE: Tear Break-Up Time (BUT or TBUT) is still the only
TEAR INSTABILITY
measure of tear film stability (Tiffany, 1994). It can
Measure Break-Up Time (BUT)
be done with (invasive) or without (non-invasive) the
• Used as a test for film stability
addition of a tear film dye.
A measure of tear film stability is achieved by
• BUT depends on tear surface tension adding sodium fluorescein to the tears (slide 241
and then determining the length of time from a blink
• Shorter BUTs result from a rise in tear to the first appearance of a localized disruption (or
surface tension (due to lowered mucin break). Slide 244 demonstrates the pattern after a
levels) considerable amount of tear break-up has occurred.
97400-113S.PPT

This technique is a useful guide for the practitioner

7L497400-113 but it is not a definitive assessment. The suspicion
that the invasive nature of tear BUT measurements
using instilled fluorescein destabilizes the tearfilm
239 was confirmed by Patel et al. (1985). They found
DRY EYE the Tear Thinning Time (TTT) was reduced from 18
TEAR INSTABILITY to 14.4 seconds by sodium fluorescein. NIBUT in
• Tear mucin reduced by: the same study was higher at 22.7 seconds. TTT
–decreased conjunctival goblet cell was ascertained using alterations to the anterior
density tear film reflection (Purkinje-Sanson Image #1) with
and without sodium fluorescein while being
– occurs in disorders of the lacrimal
and Meibomian glands monitored with the aid of a one-position
keratometer.
• The relative contributions to BUT of
ocular surface mucins and goblet TTT is not the same as BUT as the latter is a failure
cell mucin are unknown of the tear film, the former is probably a precursor to
97400-114S.PPT such a failure. Interestingly, subjects reported
discomfort just before the TTT was determined,
7L497400-114

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240 suggesting that ocular surface condition and tear

stability issues were involved in blink stimulation.
TEAR BREAK-UP TIME See Factors Affecting Blinking opposite slide 53
INVASIVE TECHNIQUE of this lecture. In a subsequent paper (Hirji et al.,
Using instilled sodium fluorescein: 1989), a novel grid-pattern keratometer mire (the
• Black ‘areas’ in the fluorescein layer Hir-CAL Grid) was developed and used to study a
- result of tear film thinning new measure of tear film stability non-invasively (i.e.
- measure time taken to appear no sodium fluorescein was used), the Tear film Pre-
after a blink Rupture Phase Time (TP-RPT). TTT and TP-RPT
• An invasive assessment are one and the same. No difference was found
- alters the tear film between the eyes and a normal figure of 18 to 19
- can induce reflex tearing seconds was found, i.e. the same result as Patel et
97400-38S.PPT
al. (1985).
A very rapid tear BUT is a useful predictor of dry
7L497400-38
eye. However, the wide range of normal values
241 using this technique makes it of limited value in
determining the marginal dry eye patient. (slide
242). Slide 243 shows some of the published
‘normal’ BUTs.
More recently, Korb et al. (1999) demonstrated that
a new fluorescein strip intended to standardize the
fluorescein dose for BUT determinations, gave
more reproducible results.

7L40006-99

242
TEAR BREAK-UP TIME
INVASIVE TECHNIQUE
• Wide range of normal responses possible

• Measurement times:

- < 5 sec indicates very dry eye

- 6 - 10 sec suggests marginal dry eye

- > 10 sec is normal

97400-39S.PPT

7L497400-39

243
FLUORESCEIN TEAR BUT
WIDE RANGE OF NORMAL VALUES
30 27

25
BUT (Second)

20
15
13
15
10
10

0
Norn Kame Shapiro Cho

97400-77S.PPT

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244

7L40658-98

245 Schirmer Test and Dry Eye

SCHIRMER TEST: TECHNIQUE The Schirmer test (slides 246) is a loose measure
• Indicates tear volume and tear production of tear volume and tear production.
• Strip of absorbent paper, held by lower lid Some confusion exists about the various methods
• Performed: of administering this test. Schirmer’s original
– without anaesthetic (Schirmer I) variations, labeled type I and type II, involved the
– with anaesthetic & reflex tearing [nasal use of his strips without anaesthesia (type I) and
mucosa stimulation] (Schirmer II) with topical anaesthesia and camel hair brush
– with anaesthesic & reflex tearing [glare stimulation (irritation?) of the nasal mucosa.
source stimulation] (Schirmer III)
However, in the normal eye, reflex tearing induced
• Measurement of the ‘wet length’
by such provocation usually results in a large
– fixed time, 5 minutes (Schirmer I)
97400-42S.PPT
volume of tears being produced immediately.
7L497400-42 Schirmer also used a type III test (Lupelli,1986) in
which a bright glare source was used in place of
246 nasal stimulation.
Common usage now describes the two tests as
being with (type II), and without (type I) anaesthesia.
This is incorrect. Lamberts suggested the use of
the descriptors ‘with’ and ‘without’ rather than I and
II unless the tests are applied as described originally
by Schirmer.
Usually, the Schirmer filter paper is notched at the 5
mm mark to ensure the strips are always inserted in
a repeatable and standardized manner. The strip is
bent at this point to form a hook used to suspend
the strip from the lower fornix. Care is required to
7L47400-5
avoid the central lid region because the adjacent
cornea can be abraded by the strip in most normal
eye positions.
247 It has been estimated that a Schirmer test strip has
SCHIRMER TEST a maximum absorption rate of 11.4µL/min at the
CLINICAL CONSIDERATIONS one minute estimation allowing for evaporation
• Unreliable measure (Holly et al., 1982). This suggests that in just one
- ocular irritation minute, a Schirmer test strip has the ability to
absorb more than 1.5X the volume of tears believed
- unwanted reflex tearing
to be resident on the anterior eye of a normal
• Not qualitative subject. Therefore, the absorbency of the strip is
• Confirms extreme dry eye cases unlikely to be a limiting factor in its performance.
- < 5 mm of wetting Lamberts et al. (1980, cited in Lamberts, 1994B)
• Correlation with results of other tests is ? found no statistical difference between the Schirmer
97400-43S.PPT
test applied to the open or closed eyes. A
difference due to the order in which the tests were
7L497400-43 applied was found. The test applied second was
highly likely to show less ‘wetting’ (some tear fluid

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 Module 7: Contact Lens-Related Ocular Complications

already removed by the first test?).

Lamberts’ summary of the Schirmer test
summarizes the present situation succinctly: “In
spite of its notorious variability, the Schirmer test
remains the most commonly performed clinical test
for sicca”. Cho and Yap (1993) believed the
continuing acceptance of the test is possibly due to
its simplicity, speed, and low cost.
In a related study of the test’s repeatability (Cho and
Yap, 1993B), the authors found it inconsistent and
concluded that it was unreliable and of little use.
Further, Lucca et al. (1990) found the Schirmer test
lacked sensitivity to detect KCS
Dry eye versus normal
A broad classification of the Schirmer test results is
as follows:
x Normal >10mm wetting in 5 min (with or without
anaesthesia).
– •20 mm without anaesthesia
– •12 mm with anaesthesia.
x Borderline dry eye 5-10 mm wetting in 5 min.
x Pathological dry eye < 5mm wetting in 5 min.
A shortcoming of the Schirmer test is the difficulty of
controlling reflex tearing. This means the results
cannot be assessed in isolation when attempting to
make a definitive diagnosis of dry eye.
Lamberts speculated that the first 5 minutes of
Schirmer-induced tear flow be discarded because of
its predominantly reflex origin and the second 5
minutes’ results be used as the Schirmer measure.
Clinch et al. (1983) found that the initial reflex
tearing could be reduced, but not eliminated, by the
use of a topical anaesthetic. They concluded that
any Schirmer test is incapable of measuring basal
tear levels independent of reflex components.
Bowers et al. (1999) found the Schirmer test
reached a ‘steady state’ with stable tear production
after 3 minutes of testing.
Tsubota et al. (1999) found vital staining (Rose
Bengal and sodium fluorescein) correlated best with
the Schirmer type II test. Of these, Rose Bengal
staining correlated better. However, the Tear
Clearance Rate (TCR) and BUT correlated better
with sodium fluorescein staining. Macri and
Pflugfelder (2000) studied the correlation between
Schirmer I and the fluorescein stain-clearance test
in normals, MGD cases, and aqueous tear
deficiency. They found that the clearance data
correlated better with symptoms of ocular irritation
than Schirmer I. However, a correction factor based
on the Schirmer I data the authors developed, was
found to improve the correlation further.
Mackie and Seal (1981) suggested a modification to
the Schirmer test to assist in the diagnosis of the
questionably (marginally?) dry eye, i.e. an eye with
at least one feature of dryness in a symptomatic
patient. They observed that patients with
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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

significantly lower Schirmer results had particulate

matter in the tear film, and low tear enzyme
concentrations. They suggested that if no fluid
diffuses along the Schirmer strip within 2 minutes,
the strip be moved to another site within the same
fornix, and the timing recommenced.
248 Phenol Red Thread Test (PRTT) Measurement in
Dry Eye
PHENOL RED THREAD TEST (PRTT)
The phenol red thread test provides an assessment
• Assesses basal tear volume of the basal tear film volume. It is similar to the
• Two-ply cotton thread Schirmer test but has the major advantage of being
much less invasive, thus reducing the risk of reflex
- impregnated with a pH sensitive dye
tearing (slide 250).
– phenol red (phenolsulphophthalein)
The basis of the PRTT was proposed by Kurihasi et
– changes to red (from yellow) when wet al. (1975, cited in Kwong and Cho, 1998) and
• Thought to be less ‘invasive’ (less stimulating?) developed further by Hamano et al. (1983). It uses
than a Schirmer test
a 70 mm long cotton thread impregnated with
97400-45S.PPT
phenol red (phenolsulphophthalein), a pH-indicating,
non-toxic chemical (C19H14O5S MW = 354.4).
7L497400-45
Hamano et al. (1983) give the average ‘wet length’
249 as 16.7 mm.
PHENOL RED THREAD: TECHNIQUE

• Placed in inferior temporal fornix

• Left in situ for 15 sec (longer recommended

periods appear in the literature)

• ‘Wet length’ measured with a rule

– measurement made immediately after removal

as tear fluid continues to travel along thread
97400-44S.PPT

7L497400-44

250

7L41078-92

251

7L47400-7

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252 Bennett et al. (1992) and Sakamoto (1993)

evaluated the PRTT and found ethnic differences
PHENOL RED THREAD TEST between Japanese and American subjects (the
Hamano (1983)
Japanese wet length was shorter, suggesting their
n = 3780 basal tear volume was lower). Kwong and Cho
(1998) found similar differences between Chinese
Average thread wet length and Caucasian subjects, but no differences
between Chinese and Japanese subjects.
16.7mm
Not all the literature is supportive of the PRTT.
Holly and Lamberts (1984), Lupelli (1988), Lamberts
< 9mm is diagnostic of dry eye (1994B), and Tomlinson et al. (2001) have all
criticized the test while accepting that it stimulates a
97400-79S.PPT
minimum of reflex tearing.
7L497400-79 Others have made PRTT-like tests of their own, e.g.
253 Blades and Patel (1996), and Cho and Kwong
(1996). Blades and Patel concluded that a PRTT
PHENOL RED THREAD TEST may be more useful differentiating between dry and
ETHNIC DIFFERENCES normal eyes than a Schirmer test. Subsequently,
Sakamoto (1993)
50 Patel et al. (1998) found they could differentiate
40 between aqueous deficient and non-aqueous
WET LENGTH (mm)

30 24 25
deficient dry eye, using their clone of the PRTT.
23
20
18 However, Cho and Kwong (1996), and later Kwong
20 15
and Cho (1998), suggested neither test (PRTT, nor
10
a clone) performed well in dry eye patients.
0
USA Japan In relation to researcher-made PRTTs, the issue of
Mean Male Female
phenol red purity from commercial suppliers was
97400-78S.PPT
raised by Hay and Stevenson (1996) who advised
7L497400-78 that it be purified before thread impregnation.
254 Cho et al. (1996) evaluated the effect of applying
the PRTT before and after a NIBUT determination
PHENOL RED THREAD TESTS to ascertain whether the PRTT had any effect on
CLINICAL CONSIDERATIONS tear film stability and/or the location of tear film
• Thread has limited ‘carrying’ capacity
defects that occurred during the NIBUT
• Thread properties, e.g. absorbency, affect results measurement. They found that the PRTT had no
• Tear fluid travel along thread continues after effect on NIBUT, or the location of the breaks in the
removal from eye tear film. Interestingly, Cho et al. found that the
• Ability to differentiate between: locations of the breaks were not random and they
- normal and dry eye? occurred more frequently in the inferior corneal
- aqueous, and non-aqueous, deficient dry eye? periphery.
• In clone PRTTs, purity of phenol red an issue The PRTT is manufactured by Showa of Japan, and
97400-338S.PPT
has been marketed as Zone-Quick™ in some
7L497400-338 countries.
255 The Tear Function Index
The Tear Function Index (TFI) was introduced by
CLINICAL TESTS: INVASIVE
Xu et al. (1995) while developing an efficient way to
THE TEAR FUNCTION INDEX
evaluate tear dynamics.
Schirmer wet length (anaesthetized) The TFI is the value obtained from dividing the
TFI = Tear Clearance Rate (TCR) value of the Schirmer test with anaesthesia, by the
Tear Clearance Rate (TCR). The motivation for the
TCR is a coloured, visual comparison scale new test was the realization that a Schirmer Test
(256 steps) against which the stained
Schirmer test strip is compared.
not only reflected tear production but also tear
1 = Dark drainage. Xu et al. found that the TFI was both
256 = Almost imperceptible more specific and sensitive that either a Schirmer
97400-262S.PPT
Test, or tear clearance rate assessments alone.
7L497400-262 The steps in determining a TFI result are detailed in
slide 256. Once a Schirmer result is to hand the
Tear Clearance Rate (TCR) is required.
The TCR is graded visually by comparing the

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256 intensity of the staining (by the instilled sodium

fluorescein) of the Schirmer Test strip with a
THE TEAR FUNCTION INDEX standard colour plate created for the purpose (Xu
TECHNIQUE and Tsubota, 1995). The rating scale ranged from
• Anaesthetize the eye 1 (dark) to 1/256 (almost imperceptible). Thus:
• Wait 5 minutes TFI = Schirmer wet length/TCR rating, e.g.

• Apply Schirmer for 5 minutes

Wet length = 10 mm
TCR = 1/8
• Measure Schirmer wet length
TFI = 80 (i.e. 10/(1/8))
• Grade TCR using 256-step grading scale
The higher the TFI value the better is the condition
created specially for the purpose
97400-339S.PPT
of the ocular surface, e.g. values below 96 are
suggestive of a dry eye condition existing, values
7L497400-339 below 34 were highly associated with Sjögren’s
257 Syndrome dry eye.
The tear clearance rate (TCR) is correlated with the
THE TEAR FUNCTION INDEX basal tear turnover and the tear flow (Xu and
RESULTS Tsubota, 1995). Age was not correlated with either
basal tear turnover, tear volume, tear flow, or the
• The higher the TFI the better TCR.

• TFI < 96 suggestive of dry eye

• TFI < 34 suggestive of Sjögren’s syndrome

97400-340S.PPT

7L497400-340

258 Collecting Tears

Primarily, the aim of any tear collection system is to
COLLECTING TEARS
(after Jones et al., 1997) sample tears without stimulating the production of
The ideal tear collection system would: reflex tears. It is probable that such a goal is never
• Permit rapid collection without ocular irritation achieved.
- thereby making differentiation between The ideal tear collection system is detailed in the
basal & reflex tear-protein levels possible slide opposite (after Jones et al., 1997).
• Allow efficient & reproducible recovery of low
& high-abundance proteins Regardless of the sampling technique used, the eye
• Lend itself to sensitive, quantitative protein must be approached intimately. Therefore, care
assays, e.g. ELISA must be taken to allay the subject’s fear of having
• Be readily useable in a clinic setting their eye touched, or harmed in any way. The use
97400-269S.PPT
of glass capillary tubes to collect tear fluid for
7L497400-269 example, does little to allay such concerns. The
Schirmer and Phenol Red Thread Tests fare a little
better, but are probably more stimulating.
259
COLLECTING TEARS
• Aim: CLINICAL CONSIDERATIONS
- allay patient fears
- prevent reflex tearing if at all possible
– impossible to collect undisturbed tears?
• Sampling techniques often disturbing:
- eye is touched, practitioner is too close ?
- ‘tools’ appear threatening (dry paper, glass
capillary tubes, and porous rods)
- collection techniques often slow, requiring
patience from both subject and practitioner
97400-341S.PPT

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260 Conventional sampling methods are presented in

slide 260.
COLLECTING TEARS
SAMPLING TECHNIQUES Jones et al. (1997) developed a user-friendly
• Filter paper strips of the Schirmer test technique using porous polyester rods and found
they collected tears some 3.9X faster than did the
- these also bind tear proteins conventional glass capillary method.
• PRTT
• Cellulose sponges
• Glass-capillary micropipettes
• Porous polyester rods (3.9X faster than
glass-capillary micropipettes)
97400-342S.PPT

7L497400-342

261 Tear Drainage Tests: The Drop Test

Shalin and Chen (1996) developed a tear drainage
CLINICAL TESTS: INVASIVE
THE DROP TEST
test, the Drop Test, in which 10 µL drops of
lukewarm (37°C) normal saline were instilled
• A test of tear drainage repeatedly into the conjunctival sac for three
• A quantitative measure of lacrimal pump minutes. The feed rate was tailored to ensure an
excess of saline (but without spillage) was
function
maintained in the eye and the total volume instilled
• Influenced by: noted. After three minutes, the excess saline
- gravity (head position/posture) solution was removed from the tear film with a
capillary tube and the volume removed noted. The
- blink rate
difference between the volume instilled, and the
97400-263S.PPT
excess removed, denotes the volume that was still
7L497400-263 on the eye or had drained into the nose (the small
amount that may have evaporated is ignored). The
removal of all excess tear fluid by the capillary tube
262 leaves the on-eye tear volume at its normal pre-test
level, nominally 7 µL.
THE DROP TEST
TECHNIQUE Shalin and Chen concluded that, in the normal eye,
• 10 PL drops of lukewarm (37°C) saline the drainage system has a much greater potential
instilled repeatedly for 3 min capacity to remove tears than is required (50 µL/min
- this gives an excess of saline without versus 1 µL/min). In a subsequent paper utilizing
spillage (epiphora) the drop test (Sahlin and Chen, 1997) showed that,
• At 3 min, excess saline solution is removed in young individuals at least, drainage capacity was
from the tear film with a capillary tube (i.e. affected significantly by both gravity and blink rate,
eye’s tear volume is returned to ‘normal’) and that the drop test could measure lacrimal pump
• The tear volume in the capillary tube is function quantitatively.
ascertained (=Removed)
97400-343S.PPT

7L497400-343

263
THE DROP TEST
RESULTS
• Calculate volume instilled over 3 min (This is
the Instilled figure)
• Volume of excess tears removed with the
capillary tube is ascertained
- This is the Removed figure
• Instilled – Removed = Drained (+ evaporation
which is ignored)
- i.e. Difference = Drained
97400-344S.PPT

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264 Impression Cytology

CLINICAL TESTS: INVASIVE Egbert et al. (1977) is credited with introducing the
IMPRESSION CYTOLOGY concept of conjunctival impression cytology (Connor
• Introduced by Egbert et al., 1977 et al., 1991). It can be used for assessing many
• Usually, conjunctival only conditions, some of which appear in the slide
• Assesses:
– goblet cell density
opposite. It may also have a role in the diagnosis of
– epithelial cell morphology in: mucopolysaccharidoses, infectious diseases, and
– KCS allergic disorders.
– xerophthalmia
– ocular pemphigoid Impression cytology is a rapid and simple diagnostic
• Differentiate between types of dry eye? procedure that causes minimal discomfort. Nelson
(Nelson, 1988)
• Useful in ocular surface disorders, especially (1988) and Cakmak et al. (2003) described it as
conjunctival squamous metaplasia (Tseng, 1985) non-invasive but few would agree that a technique
97400-264S.PPT

that is in effect harvesting cells from living tissue, is

7L497400-264 non-invasive.
265
IMPRESSION CYTOLOGY Technique
APPLICATOR
• Table tennis bat-shape An applicator must be fashioned from a suitable
material. Suitable materials include Millipore VSWP
• Rectangular
(0.25 µm pore size) or HAWP (0.45 µm pores)
• Asymmetric (helps identify underside) ‘paper’ [actually the material is a polymer, cellulose
• Millipore 0.25Pm or 0.45 Pm polymeric filter acetate] but it is likely that Whatman and others
‘paper’, or equivalent manufacturers also have suitable filter ‘papers’
• Diameter/width 5 to 6.5 mm (after Connor et al., 1991).
• Apply matte surface Shapes used include:
• Press with a rod 97400-346S.PPT
x Table tennis bat (Connor et al. 1991)
7L497400-346
x Rectangular strips (Nelson et al., 1983, Keenum
et al., 1990).
266 x Asymmetrical shape for orientation or side-of-
IMPRESSION CYTOLOGY application control (Tseng, 1985).
TECHNIQUE The basic technique is described in slide 266.
• Anaesthetize the eye topically
• Apply matte surface of applicator to bulbar Generally, repeated applications increase the
conjunctiva number of cells harvested. Once is almost never
• Press applicator onto eye using a suitable enough but a fourth application does little to
clean tool (rounded plastic or glass rod) increase cell numbers, and often leads to greater
• Maintain contact for 2 sec patient discomfort.
• Remove applicator using peeling motion Frequently, harvesting success can be judged by
- easy removal = fewer cells harvested monitoring the apparent adhesion of the paper to
• Repeat at least twice (prefer 3X) - same area the conjunctiva. Paper that needs to be ‘peeled’
almost guarantees an adequate number of adherent
97400-345S.PPT

7L497400-345 cells. Easy removal (little adhesion) indicates the

likelihood of a poor harvest, and the probable need
for a repeat application. This is almost certainly due
267 to an eye that is too ‘wet’. Gently pulling the lower
IMPRESSION CYTOLOGY lid away from the globe and allowing the tears to
RESULTS evaporate for a few seconds, may improve the cell
(after Nelson et al., 1983)
In cases of KCS: harvest. As the fluid-absorbing capacity of the
• Bulbar conjunctival epithelial & goblet cells show applicator’s material is limited, excess tear fluid can
‘substantial’ abnormalities not be removed from the anterior eye by dabbing
In cases of primary ocular surface disorders: with the applicator.
• Both bulbar & palpebral surface cells are abnormal
• Drying effects on exposed surfaces (i.e. eye areas
Nelson et al. (1983) and Refaat and Allan (1990)
exposed between blinks) implicated in abnormalities found that the matte side of filter paper was more
seen effective in removing cells from the eye.
- areas protected by lids, and lids themselves largely
unaffected Once a suitable cell harvest has been achieved, the
97400-348S.PPT
working end of the applicator is mounted on a
7L497400-348
microscope slide. The slide is stained using Schiff’s
reagent, haematoxylin, and lithium carbonate. The

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268 result is inspected with a microscope and the types

and numbers of stained cells in the harvest are
IMPRESSION CYTOLOGY noted. Special attention is given to the morphology
RESULTS: ASYMPTOMATIC ‘NORMALS’ of the cells seen and an assessment of whether
(after Nelson, 1993)
• Can show epithelial squamous metaplasia of they are normal or abnormal.
the conjunctiva
• Postulated that as a physiological response : Results
- stressful environment op goblet cells & n
squamous metaplasia of the epithelium Using impression cytology, Nelson et al. (1983), and
• Changes can occur independent of: later Nelson (1993), found various changes to the
- symptoms external eye in cases of KCS, and asymptomatic
- observable pathology
- BUT changes ‘normals’. These are summarized in slides 267 and
- surface tension changes 268. Dry eye patients may also show decreased
- staining (sodium fluorescein, Rose Bengal)
97400-349S.PPT
epithelial cohesion. This may affect (increase) the
number of cells harvested.
7L497400-349
Blades et al. (1998) used impression cytology to
assess quantitatively the surface area of bulbar
conjunctival cells. In the normal eye, they found the
average cell size to be considerably smaller than
2
reported previously (108 versus 585 µm ). Eyes
with borderline dry eye were found to have a higher
proportion of larger cells (thereby increasing the
‘average’ cell area). Interestingly, cases of
squamous metaplasia had average cell areas of
2
543 µm , a figure close to that for normals in
previous literature.
269 Laboratory Testing for Dry Eye

LABORATORY DIAGNOSTIC TESTS A number of laboratory-based tests are available for

• Mucin measurement the assessment of dry eye. In some cases, these
tests may be applicable to a clinical setting.
• Goblet cell counts
- impression cytology Some tests and their results in dry eye (DE) are
– p density summarized in the slides opposite.
• Epithelial cell size Mackie and Seal (1984) generated tear protein
n profiles that were characteristic for each of KCS,
• Tear osmolality questionably dry eye, and ocular pemphigoid. Their
- increased (> 312mOsm/L indicative of DE) work suggests protein profiling as a way of
- high sensitivity
differentiating various dry eye subtypes.
97400-46S.PPT

Another test is the Lactoplate™ Immunoassay Test

7L497400-46 (a simple tear lactoferrin assay test supplied as a
kit). This method allows an earlier diagnosis of dry
eye problems, and the prevention of potential
270 contact lens problems, according to MacKeen
(1986). An opposite view was presented by Yolton
LABORATORY DIAGNOSTIC TESTS
et al. (1991, see slide 272). This test uses a
• Refractometry of tear fluid standardized 4 mm diameter sterile disc of filter
paper. The steps are detailed in slide 271.
- p n in DE with p lacrimal secretory proteins
(Golding and Brennan, 1991)
Upon removal, the disc is blotted on the paper
• Lactoferrin level supplied and then pressed onto an agarose test
- reduced surface (also supplied). The discs are enclosed to
reduce evaporation and allowed to stand for three
- immunologic assay days at room temperature. The diameter of the
resulting white circle (resulting from the reaction
- protein concentration
97400-47S.PPT
between lactoferrin from the tears, and its antibody
in the test disk) is measured and the tear
7L497400-47 concentration of lactoferrin determined from a table
supplied as part of the kit.
Dunsky (1990) suggested that the Lactoplate™ test
could be applied with or without topical anaesthesia
because he found that a local anaesthetic had no
adverse effect on the test.

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271 Although they reported favourably on the Lactoplate

test for diagnosing dry eye, Lucca et al. (1990)
THE LACTOPLATE• IMMUNOASSAY TEST preferred a good clinical history combined with tear
A LACTOFERRIN TEST
osmolarity as their ‘gold standard’ for dry eye
• Measures tear lactoferrin content reliably diagnosis.
– lactoferrin: antibacterial glycoprotein
Clinical considerations presented by Yolton et al.
– lactoferrin: secreted by the lacrimal gland
(1991) originally, are included in slide 272.
• Performed with or without topical anaesthetic
• Paper discs in lower conjunctival sac for 5 min
They concluded that lactoferrin concentration alone
was insufficiently sensitive or specific to be used as
• Test capability: 0.25 – 2.7 mg/mL
a stand-alone test for dry eye, except in moderate to
– > 0.9 mg/mL is considered normal severe cases.
• Not a stand-alone test for DE
97400-128S.PPT

7L497400-128

272
THE LACTOPLATE• IMMUNOASSAY TEST
CLINICAL CONSIDERATIONS
• Not well correlated with: (Yolton et al., 1991)

- BUT
- Rose Bengal staining
• Will only detect DE if lacrimal gland
dysfunction is the cause
• Not sensitive enough for mild to moderate DE
• Signs & symptoms are manifest before
lactoferrin changes are detected
• Lactoferrin changes occur only in reflex tears,
not basal tears
97400-350S.PPT

7L497400-350

273 Miscellaneous Tests:

Lacrimal Protein Content (slide 273).
LACRIMAL PROTEIN CONTENT
(Dohlman, 1976)
• Can vary between 3 & 20 g/L (3 in reflex Tear Osmolality (or Osmolarity)
tears, 20 in basal tears) Using ultra small-volume osmometry, it is possible
• Sampling techniques: to determine the osmolality of the tears. Usually,
- polyacrylamide gels the freezing point-depression technique is used.
- filtering
Unfortunately, nanolitre micro-osmometers are
uncommon in general laboratories, are relatively
- cellulose acetate membranes
difficult to use for routine testing, and require
• Assayed using electrophoretic separation fastidious maintenance if the results are to be
• Some assays may be for specific proteins, reliable with such small sample volumes. Wood et
e.g. lysozyme 97400-351S.PPT
al. (2002) concluded that osmalarity is the best
7L497400-351
prredictor of both self-reported dry eye, and ocular
surface damage as characterized by fluorescein
274 and Lissamine Green staining.
LABORATORY DIAGNOSTIC TESTS Tear Mucous Ferning
• Tear lysozyme Tear samples prepared as films that are allowed to
dry, crystallize in fractal-like patterns that resemble
measurements: the fronds of a fern. It is difficult to assess the
- reduction is suspicious different patterns quantitatively, but qualitatively it is
possible to assess the abundance and uniformity of
• Tear ferning test: ferning, the dimensional extent of the ferning, the
completeness of the pattern, the absence of ferning,
- ill-defined etc. For a comprehensive review, see Golding and
- significance ? Brennan (1989).
97400-130S.PPT

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275 Dry Eye Testing/Clinical Signs: Epilogue

DRY EYE: McCarty et al. (1998) studied the epidemiology of
WHAT IS THE PREVELANCE? dry eye in an Australian capital city. Several tests
were applied as part of the study.
Difficult to determine:
The Venn diagram opposite (slide 277) plots the
test results of 635 cases that underwent all four of
• Definition dependent
the clinical tests used in the study to assess dry eye.
• Age-related In such a diagram, the size of the overlapping areas
is proportional to the number of subjects diagnosed
• Gender related as having dry eye by all the tests whose colour
coded areas overlap.
• Influenced by environment
97400-175S.PPT
From this diagram, it can be readily seen that the
agreement between several common clinical tests
7L497400-175 for dry eye is relatively poor, e.g. only one case was
276 diagnosed by all four tests and four cases by three
of the tests.
DRY EYE: EPIDEMIOLOGY Once again, the Schirmer test was found to have
poor discrimination, a finding that supports the
conclusions of many others. Best agreement
Prevalence varies between tests was given by the combination of
Rose Bengal staining and BUT (27 of the 635
by cases, see overlap in diagram).
This diagram discloses just some of the difficulties
signs and symptoms many/most practitioners experience when
assessing dry eye. It has rarely, if ever, been
quantified and depicted in such an effective manner.
(Diagram reproduced with permission of Dr C
97400-170S.PPT

7L497400-170 McCarty et al., and Elsevier Science.

Reprinted from McCarty C et al. (1998). The
epidemiology of dry eye in Melbourne, Australia.
277 Ophthalmology, 105(6): 1114 – 1119.
CLINICAL TESTS FOR DRY EYE ©1998 Elsevier Science).
HERE IS PART OF THE PROBLEM
Albeitz (2000) showed a dry eye incidence of 10.8%
for a large population sample (n=1584). She found
NB: The original of this diagram is in colour

the prevalence of dry eye to be greater in subjects

Reproduced with permission:
McCarty C et al., 1998 40 years and older.
© Ophthalmology
Elsevier Science
The dry eye subtypes more prevalent in older
people were found to be Lipid Anomaly Dry Eye
(LADE) and Aqueous Tear Deficiency (ATD) types.
Dry eye is more prevalent in post-menopausal
women. This suggests female hormone deficiency
97400-270S.PPT
as a possible aetiology (Guttridge, 1994).
7L497400-270 Schein et al. (1997) found that, although symptoms
of dry eye are common among the elderly, there is
minimal overlap between individuals identified by
278 questionnaire, Schirmer test, and Rose Bengal
DRY EYE: EPIDEMIOLOGY staining. This is confirmed by McCarty et al’s Venn
• Melbourne, Australia diagram (slide 277) and study findings (slide 278).
• 926 responses, 40-97 years old Schein et al. also found that the signs and
• 53% Female, 47% Male symptoms of dry eye were not associated with age,
• DE diagnosed (6 = 50%): race, or sex in the elderly population studied.
– 11% by Rose Bengal An overview of the thrusts of clinical tests for dry
– 16% by Schirmer eye and related issues is presented in slide 281.
– 9% by BUT
Following two surveys of eyecare practitioners, Holly
– 2% by sodium fluorescein
(1989) reported that there was clearly an
– 7% by two or more signs
overwhelming need for improved diagnostic tests for
– 6% with any severe symptoms 97400-174S.PPT
dry eye. Despite the volume of research carried out
7L497400-174
and reported in the interim, it is likely that such a
plea remains applicable.
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279

DRY EYE: PREVALENCE ?

Influenced by:

• The test(s) used to assess

• The practitioner

• The patient’s tolerance

• The time of day

97400-171S.PPT

7L497400-171

280

DRY EYE: CONCLUSIONS

• Avoid diagnoses based on a single test

• A combination of tests will give the

practitioner valuable information

• Avoid disturbing the tear film (non-invasive)

97400-131S.PPT

7L497400-131

281
NSDE: DIAGNOSTIC CRITERIA
Bron, 1994
Primary
Primary Primary Secondary
Disease Damaging
Deficiency Test Test
Agent
BUT
Schirmer
Lacrimal Hyperosmolality Osmolality
KCS Tear lysozyme
secretion RB staining Meibometry
Tear lactoferrin
Tear ST
Meibomian Hyperosmolality BUT
MGD Meibometry
lipids RB staining Osmolality
Tear ST
Vitamin A Goblet cell
Tear mucin Mucin deficiency Bitot's spots
deficiency density
Vitamin A levels
Blink Hyperosmolality BUT
Tear film Blink interval
deficiency RB staining Osmolality

Surface Hyperosmolality Impression

Ocular surface
abnormality RB staining cytology

97400-226S.PPT

7L497400-226

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V Management of Dry Eye

282 Management of Dry Eye
MANAGEMENT OF DRY EYE Treatment of dry eye can be intended to either
KEY FACTORS improve the quality of the tear film, or increase the
• Identify cause (often difficult) volume of the abnormal tears present to improve
ocular surface wetting (Tickner, 1997).
• Treat the cause, not just the effect
• Many possible treatment regimens While many treatment regimens are available for
• Individualize the treatment regimen, consider
dry eye cases, a key factor in treatment is the
patient’s needs & circumstances correct diagnosis of the cause of the condition.
However, this can be very difficult to achieve for all
• In most cases, only palliative treatment possible
patients.
• Treat promptly if eye’s anterior surface is to be
protected (Xu et al., 1996) Importantly, given the current state of our
97400-48S.PPT
knowledge, dry eye cannot be cured. Therefore,
7L497400-48 any treatment regimen must be regarded as being
palliative only.
Lemp’s (1987) grading and management systems
283 are presented in slides 283 and 284.
GRADING DRY EYE: LEMP, 1987 Tseng and Tsubota (1997) stress that, because the
Rose Bengal
(Staining Grade) X ocular surface epithelia and the preocular tear film
0 1 2 3

function as a unit, several corneal and external

1 diseases can be categorized as disorders of the
6 - 12 15
Schirmer (mm wet)

BUT (seconds)

ocular surface and tears. This concept has

2
3-5 10 - 15
ramifications for the management and treatment of
1-3 5 - 10 dry eye.
Tseng and Tsubota’s basic concepts of treatment
X 1 3 5
X are:
280 - 300 300 - 315 315 - 345 345
Tear Osmolarity
97400-201S.PPT
X x Ocular surface health is ensured/maintained by
a close relationship between the surface
7L497400-201 epithelia and the preocular tear film.
x A stable tear film is maintained inherently by the
284 external adnexae.
TREATMENT BY GRADE: LEMP, 1987 x The intact protective mechanism is controlled
Grade 1 by effective neuroanatomic integration.
X Artificial tears
Lubricating ointment x Corneal epithelial stem cells are located at the
1 Grade 2
Artificial tears
corneoscleral limbus.
Lubricating ointment
2 Tear inserts
x Ocular surface epithelial cell function is
supported by stromal fibroblasts, and the
(controlled-release)
Mucolytic agents stromal matrix.

X
3 X
Grade 3
Punctal occlusion Epithelial changes in dry eye are probably not
Bandage lenses simply due to the hyperosmolality of the tears
X Oestrogens
97400-202S.PPT Moist chambers because Wilson (1996) has shown that osmolalities
in the range normally encountered in dry eye are
7L497400-202
insufficient in themselves to increase epithelial
shedding rates. This means that simply maintaining
the tear osmolality is unlikely to be a successful dry
eye management strategy.
Efficacy of Treatment
Kozma et al. (2000, cited in MacKeen, 2001)
reported that 76% of dry eye sufferers rated their
condition as being the same or worse than the
previous year despite treatment.
Some dry eye patients find that they can tolerate
brief periods of abstinence from their dry eye
treatment reasonably well, some stating that they
feel better when abstaining. In that case, a longer

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Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

period without treatment can be trialled because this

finding suggests an association between their
symptoms and their medication rather than with
their eye condition (after Farris, 1991).
Generally, Farris recommended a staged therapy in
which the treatment is individualized and which
mirrors the severity of the condition with appropriate
monitoring of the effects of the treatment being
given at each stage. He believes this also reduces
the likelihood of complications from the
medication(s) used.
MacKeen observed that despite the greater rate of
patenting, and more publications about treatments,
the efficacy of dry eye treatments generally has not
kept pace.
Evidence suggests strongly that a sufficient intake
of dietary vitamin A and protein are essential to the
health of the tear film and ocular surface. Protein is
necessary for the delivery of vitamin A to the ocular
surface. However, until sound evidence is provided,
specific dietary recommendations aimed at
altering/improving the tear film, its properties, or the
balance of its components, cannot be made (after
Caffery, 1991). Caffery’s recommendations are
similar to most general dietary recommendations
and included:
x Reduce protein, total fat and cholesterol
intakes.
x Increase complex carbohydrate intake.
x Increase vitamin A intake by consuming more
red, orange, yellow and dark green vegetables.
Caffery (1990) reported that vitamin A applied
topically may have some benefit in the more
advanced cases of dry eye, i.e. those eyes in
which ocular surface damage was already
present. However, such treatment played no
significant role in prevention, or treatment, in the
early phases of the disease.
x Increase zinc and folate intake by eating whole
grains, legumes, and raw vegetables, especially
spinach.
+
x Ensure adequate B6 and K intake by eating
nuts, bananas, and beans.
x Ensure vitamin C intake by eating citrus fruits.
x Eliminate alcohol and caffeine from the diet.
x Reduce sugar and salt intakes.
x Increase water consumption to 6-8 glasses per
day.
Patel et al. (1994B) studied the effect of ingesting
vitamin and trace element supplements on the
stability of the pre-corneal tear film in normal
subjects. The rationale was the possibility that
marginally dry eye cases in otherwise normal
subjects may be due to sub-clinical marginal dietary
imbalances.
Somewhat surprisingly, a 10-day course of 1 gram
of vitamin C daily improved the stability of the tear

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film significantly in normals by almost 6 seconds.

Those subjects that took a multi-vitamin and trace
elements tablet under a similar regimen showed a
slightly greater improvement of 6.15 seconds. Tear
stability was assessed by the tear thinning time
(TTT) method in which tear film changes are
monitored with a one-position Sutcliffe-type
keratometer.
The consumption of water was highlighted by
Bowden and Harknett (2001) who found that those
who were water drinkers were less likely to have
symptoms of dryness than tea or coffee drinkers.
285 Managing a Dry Eye with Tear Substitutes or
Additives
MANAGEMENT OF DRY EYE The most common form of treatment of dry eye is
still the provision of a tear substitute or replacement
• Tear substitutes/additives therapy (slide 286). This is usually in the form of
drops, ointment (resides on the eye longer), or
- drops inserts, and are designed to:

- inserts
x Provide short-term relief of symptoms.
x Reduce risk of epithelial desiccation.
• Lubricating ointments
x Aid the repair of damaged epithelium.
97400-49S.PPT
Artificial tear drops are still the mainstay of
treatment for KCS (Holly, 1988, Roberts, 1991,
7L497400-49
Abelson and Knight, 1994, Korb et al., 1996).
286 These play the role of symptom ‘treatment’ rather
than a ‘curative’, or a ‘restorative’ role.
Time On the Eye (Stay-Time)
A clinic issue for tear substitutes is the known
brevity of their on-eye stay times, especially with
liquids of low viscosity. Some have half-lives
measurable in seconds and only offer a transient
effect. Some published results are summarized
here:
Saline:
x 2-3 blinks (Cho and Brown, 1998).
x 4 minutes (MacKeen, (2001).
7L41692-91
Other Solutions:
x A surfactant-containing solution, 4-6 blinks (Cho
287 and Brown, 1998).
MANAGEMENT OF DRY EYE x No tear substitute tested provided long-term
CLINICAL CONSIDERATIONS: TEAR SUBSTITUTES tear film stability (>30 minutes) (Carney and
• Most treat symptoms, not cause Jacobs, 1999).
• Brevity of on-eye stay times
x Sodium hyaluronate (SH)(0.2%) had a mean
• Higher viscosities intended to n time on eye
half-life (time out to which at least half the
• Mimic tears: concentration remained) on the ocular surface
– especially K+, Cl–, (HCO3)– ions of 321 seconds (Snibson et al., 1992)
• More recently, mucomimetic technology used
(binds to epithelium)
x Hydroxypropylmethylcellulose (HPMC)(0.3%)
had a half-life of only 44 s (Snibson et al.,
• Difficult to lower osmolality for sustained periods
1992). Somewhat paradoxically, a 0.5%
97400-352S.PPT
HPMC-based dry eye treatment was shown to
7L497400-352 be effective by Toda et al. (1996) and was
found to provide ‘sustained’ coverage of, and
protection for, the ocular surface.
x Polyvinyl alcohol (PVA)(1.4%) had a half-life of
only 39s (Snibson et al., 1992).

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288 Physical and Chemical Properties:

A difficulty facing artificial tear formulators is
MANAGEMENT OF DRY EYE selecting a suitable viscosity. Too low a viscosity
TEAR SUBSTITUTES may reduce the stay time, too high may stay longer
• Numerous formulations include: but with reduced comfort and reduced vision (Holly,
- cellulose derivatives (e.g. methyl cellulose) 1978).
- dextrans The use of solutions of widely differing osmolality is
- polyols
probably a pointless exercise because Holly and
Lamberts (1981) found it took only seconds for the
- polyvinyl alcohol (PVA) tears to restore their osmolarity following the
- povidone instillation of non-isotonic solutions, provided the
- carbomer instillation was not continued. This means that,
97400-50S.PPT
while lowering the tear film osmolality decreases the
7L497400-50
clinical signs of ocular surface disease and
improves patient comfort, some way of achieving
this effect other than eyedrops is required (after
289 Gilbard, 1985).
Ideally, an artificial tear solution should mimic the
ARTIFICIAL TEARS composition of human tears. Some of the chemistry
inspired by Tsubota, 1998
included in tear substitutes is listed in slide 288.
Tear
evaporation
Artificial While the use of liquids with higher viscosities can
Tear
production
tears
be traced back to 1945, more recent innovations
include formulations that are mucomimetic (as first
suggested by Holly, 1978), i.e. they bind to the
epithelium at multiple sites to form a hydrophilic
layer (Lamberts, 1994B).
Tear
drainage The efficacy of carbomer gel, an ingredient in dry
97400-222S.PPT eye products on the market worldwide, was
compared with a placebo in moderate to severe dry
7L497400-222
eye patients by Sullivan et al. (1997) and found to
offer greater efficacy with safety.
290 Carbomer is a polymer resin that is claimed to
maintain the tear film in contact with the eye for
SOLUTION PRESERVATIVES extended periods of time.
• Sensitivity reactions
No reduction in secondary subjective symptoms
• Other adverse effects on a compromised eye: such as tearing, itching, scaling, conjunctival
– n conjunctival inflammation discharge, palpebral and conjunctival redness,
– p goblet cell density conjunctival lustre, relief of discomfort, ease of use,
• Preservative-free artificial tears may not be and overall acceptability were found. Furthermore,
efficacious either Schirmer test results, and sodium fluorescein
staining did not improve with either the placebo, or
– treat the underlying cause rather than the
overt effect, e.g. control inflammation
the carbomer gel.
rather than the tear deficiency
97400-319S.PPT
Ointments still tend to be based on liquid paraffin
but their adverse effect on vision quality often
7L497400-319 relegates their use to before-sleep periods rather
than when quality vision is required. Eyedrops can
also have similar disadvantages, e.g. Shimmura et
al. (1998) found that artificial tears caused an
uneven thickening of the tear film, particularly over
the superior cornea. This film irregularity reduces
vision quality.
Lehman et al. (2002) found that two common tear
substitutes (Tears Naturale and Refresh) did not
alter tear film stability or symptoms significantly.
An alternative to a liquid or a gel is a lacrimal insert,
in the form of a small 5 mg pellet of hydroxypropyl
methylcellulose placed into the lower fornix, which
dissolves slowly over a 6-12 hour period.

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291 The Use of Preservatives

Compounds containing preservatives should be
MANAGEMENT OF DRY EYE used with caution due to the risk of developing a
COMPLIANCE sensitivity reaction to the preservative, or adverse
• As with health care generally, compliance effects on the already compromised eye. Users of
warrants careful monitoring such solutions must be warned of these risks,
• Many dry eye sufferers vary treatment based on
especially when used for extended periods of time.
a day-to-day assessment of their own needs Albeitz and Bruce (2001) confirmed that conjunctival
– consequently, some practitioners are inflammation, and reduced goblet cell density, in dry
reluctant to issue specific regimens eye is exacerbated by the use of preserved topical
— recommendations made on a case-by-
agents. They also reported that preservative-free
case basis artificial tear supplements did not improve the ocular
97400-386S.PPT
surface conditions significantly, and they
7L497400-386
recommended that therapy be directed towards
increasing goblet cell density, and controlling ocular
surface inflammation, i.e. treat the underlying issues
rather than the overt effects (e.g. tear deficiency).
Interestingly, Tomlinson and Trees (1991) showed
that artificial tear solutions that were either
unpreserved, or preserved with benzalkonium
chloride (0.004%) or chlorobutanol (0.5%), did not
induce any differences in the tear evaporation rate
when applied to the eye. It was suggested that at
these concentrations at least, the lipid layer of the
tear film was not affected by the solutions applied.
However, Holly (1978B) found that benzalkonium
chloride has the most deleterious effect on the lipid
layer stability.
Geerling et al. (2001) studied the toxicity of various
substances used in KCS therapy, on a culture of
human epithelial cells. Using cellular ATP as their
measure, they found that isotonic saliva and serum
offered greater therapeutic potential than did the
pharmaceutical tear substitutes.
If prolonged use of an artificial tear solution is
envisaged, it is probable that a preservative-free
product should be considered and this is Snyder’s
(1999) recommendation in cases of severe dry eye.
However, the incorporation of modern, less toxic
preservatives in tear supplements may mean that
the conservative and expensive approach of unit-
dose, unpreserved solutions may no longer be
justified except in special cases.
Compliance
Swanson (1998) examined the compliance with,
and typical use of, artificial tears in dry eye sufferers
and found that most patients varied their use of
prescribed products according to their own
assessment of their condition on a day-to-day basis.
In view of this finding, Swanson saw little reason to
prescribe a particular dosage regimen for the
majority of patients.

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292 Dry Eye Treatments: Drugs and Others

MANAGEMENT OF DRY EYE New treatments are always under development.
SYSTEMIC DRUGS Strategies include topical anti-inflammatory drugs,
• Stimulation of tear production by drugs and immunomodulatory agents such as cyclosporin
• Treatment of MGD, e.g. pilocarpine, IBMX A (Foulks et al., 1996, Helms, 1996, Moore et al.,
• Antibiotics: 1999, Stevens et al., 2000, Turner et al., 2000,
- tetracycline / doxycycline Calonge, 2001).
– softens secretions, stabilizes lipid production
• Mucolytic agents: Moore et al. found that cyclosporin A enhances
- acetylcysteine conjunctival mucin production, at least in the canine
– breaks down the filaments animal model. More recently (2003), a cyclosporine
– relieves blink-induced pain (dragging filaments) emulsion (0.05%) has been relased (Restasis™ by
97400-55S.PPT
AMO) for use by patients with chronic dry eye
(OptiStock News, 2003).
7L497400-55
Systemic Drugs:
Although originally thought to help maintain the
293 condition of the ocular surface in post-menopausal
women (e.g. Lemp, 1987), a recent study
HRT & DRY EYE (Schaumberg et al., 2001) of the use of Hormone
Schaumberg et al., 2001
Replacement Therapy (HRT) in a large sample of
• Women on oestrogen-only therapy were 69%
MORE likely to be diagnosed with dry eye such women found the opposite may be true. The
study’s results are summarized in slide 293.
• Those on oestrogen-progesterone, or
oestrogen-progestin, only 29% MORE likely In Meibomian gland disease, drugs such as
to be diagnosed with dry eye tetracycline may improve the tear film by stabilizing
• The longer HRT is used, the greater the risk the lipid production in the glands, and softening the
of dry eye secretions. This has the effect of producing a
• Postulation: sex hormones may influence the higher quality tear lipid layer. For contact lens
Meibomian glands, affecting their lipid output wears who suffer MGD dry eye secondary to sub-
97400-356S.PPT
clinical Staphylococcal infection, Seger (2001) has
7L497400-356 suggested the use of doxycyline (50 mg, twice daily
for 30 days) to improve lens tolerance especially if
they are RGP lens users exhibiting 3 & 9 o’clock
staining.
Oral flaxseed oil has been shown to be successful
294 in a 3 year, 200 patient trial by Boerner (2000).
Topical Drugs:
MANAGEMENT OF DRY EYE
TOPICAL DRUGS A number of drugs may be useful for the treatment
of dry eye or associated conditions. Certain drugs,
• p osmolality, or... such as pilocarpine, are capable of stimulating the
• n tear volume production of tears by the lacrimal system.
• VIP, cAMP, cGMP (n tear production) Gilbard et al. (1990) found several pharmacological
agents that increased tear volume and/or decreased
• Bromehexine (n tear flow) tear fluid osmolarity. These included VIP, cAMP,
• IBMX (n tear production) and two cGMP analogs. Forskolin (increases
cAMP) increased tear volume significantly. The
• Sodium hyaluronate (maintains epithelium)
97400-354S.PPT
authors concluded that agents that increase either
cAMP or cGMP levels pharmacologically, stimulate
7L497400-354 tear production when applied topically.
Corneal filaments that form in some dry eye patients
(slide 295) can be broken down by the use of
mucolytic agents such as acetylcysteine (as a 10 or
20% aqueous solution. This can provide some
symptomatic relief from the pain associated with
blinking and the resultant dragging of the filaments
by the lid.
Although sodium hyaluronate eyedrops were not
found to offer any advantages over conventional
tear substitutes, Shimmura et al. (1995) thought that
it might play a role in maintaining a healthy corneal
epithelium. However, Condon et al. (1999)
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 Module 7: Contact Lens-Related Ocular Complications

295 demonstrated ‘clear benefits’ of sodium hyaluronate

over saline, both subjectively and objectively, in dry
eye syndromes.
Benitz del Castillo et al. (1999) showed that
Carbopol 974P, a carbomer, was beneficial to a
reduction in corneal epithelial permeability in KCS.
Trials have been done using INS365 a P2Y(2)
receptor agonist that stimulates the release of salt,
water, and other natural tear components that
lubricate the eye’s surface (press release, 2001).
Avisar and Savir (1980) found that bromehexine
(Solvex™) increased tear flow in 70% of KCS cases
along with an increase in tear lysozyme content.
7L42012-93
Ousler et al. (1999) found lubricating eye drops
were successful in Computer Vision Syndrome
(CVS).
Connor and Karkkainen (2001) extended the BUT
and improved the Schirmer result using a topical
tear substitute dosed with a steroidal androgenic
hormone (DHEA).
Experimental drug therapy aimed at stimulating tear
production (by the accessory lacrimal glands) has
been tried successfully in the rabbit model using
IBMX (3-isobutyl-1-methylxanthine) (Gilbard and
Rossi (1991, 1993). Progress of the resulting ocular
surface disease was reversed following IBMX
treatment.
A New Drug Application (NDA) has been filed with
the US FDA for an ophtalmic solution containing
diquafosol tetrasodium for the treatment of dry eye
(Optistock, 2003B)
Combination Topical and Systemic Treatments:
Toda et al. (1995) disclosed details of an
experimental treatment for dry eye consisting of a
topical anti-histamine and a low-dose steroid. Its
use was suggested in dry eye cases that did not
respond to conventional dry eye therapies,
especially cases of allergic conjunctivitis.
Current thinking on potential dry eye treatments is
summarized in MacKeen (2001B, 2001C)
296 Treatments for Dry Eye: Unconventional
DRY EYE TREATMENTS: Various less conventional, or even unconventional,
UNCONVENTIONAL treatments for dry eye have been reported over the
• Vitamin A years.
- normal, or…
Holly (1990) reported on the use of vitamins and
- transretinoic form polymers in the treatment of ocular surface
• Vitamin B12 disorders. Treatments included:
• Vitamin C x Lacrophilic artificial tears. Various eye
• Multivitamin preparations preparations that have ingredients intended to
• Lacrophilic artificial tears (hypertonic?) resist corneal swelling are available. Usually,
• Jet-of-air stimulators this resistance is achieved by the incorporation
97400-267S.PPT
of various polymers at relatively high
7L497400-267 concentrations (i.e. they are hypertonic).
x Vitamin A, or one of its forms, transretinoic acid
(also called tretinoin), is included in some
artificial tear preparations. Vitamin A is
combined with another compound as a
416 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

complexant to overcome the difficulties of

dissolving vitamin A in an aqueous solution.
Vitamin A, has been found to have a healing
effect on the ocular surface, especially if
squamous metaplasia is present (Tseng, 1987).
Westerhout (1991) also reported advantages to
retinoic acid use in dry eye and found a
subjective improvement in symptoms in 61% of
vitamin A drop patients compared with 15% of
patients using an artificial tear compound.
However, the use of vitamin A is still
controversial. Paradoxically, the use of
excessive vitamin A is known to induce dry eye
(Lamberts, 1994B).
x Artificial tears containing nutrients are also
available. Vitamin B12 is one constituent of such
solutions probably because of its known role in
epithelial cell growth. Its efficacy in humans
when used topically remains unclear.
Schwab et al. (2000) transplanted successfully
bioengineered tissue replacement in patients with
ocular surface disease. The replacement tissue
was derived from cultured epithelial stem cells
seeded onto an amniotic membrane-derived matrix.
Such a combination of microsurgical technique and
limbal stem cell-derived cultured tissue was also
supported by Holland and Schwartz (2000).
Toi and Dumery (1997) reported a partial reduction
in dry eye symptoms among computer monitor
users when increased blink rates were achieved by
either a jet of air stimulus every 10 seconds
(resulted in partial relief), or by the automatic
instillation of normal saline every minute (this
prevented dry eye symptoms recurring).
297 Managing Dry Eye by Reducing Tear Excretion:
An Environmental Approach
MANAGEMENT OF DRY EYE An assessment of the role of the environment in dry
eye problems may reveal factors that exacerbate
• Environmental considerations the condition. Alterations to, or removal of, these
factors are likely to improve the lot of dry eye
- temperature
patients.
- humidity A number of the dry eye treatments are designed to
minimize the loss of tears from the ocular surface,
- drafts, wind
e.g. goggles, spectacles with side-shields, or
- pollution prevent the evaporation of the tears into the
97400-57S.PPT
atmosphere (Kornfeld et al., 2001, Paugh et al.,
2002). Humidifiers maintain the eye in a moist
7L497400-57
environment though this is not a convenient option
for most patients.
Nakamori et al. (1997) argued that, since the area
of the anterior eye exposed to the atmosphere (see
Tsubota and Nakamori, 1995) affects the blink rate
and tear film dynamics, it may be prudent to
consider simple measures that reduce the area
exposed. For example, placing computer monitors
and gaming machines at a lower than normal
position so that with normal posture the upper eyelid
covers more of the external eye.
More extensive intervention in dry eye cases

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298 includes the deliberate closing or narrowing of the

palpebral aperture by taping or surgery.
DRY EYE MANAGEMENT
ENVIRONMENTAL
Environmental considerations in the treatment of dry
eye include the following:
• Reposition VDUs lower (lowers the upper
eyelid to parea of the anterior eye exposed)
x Temperature: higher ambient temperatures are
more likely to induce tear film evaporation and
• n RH by: exacerbate the dry eye condition.
– p air-conditioning, or installing a humidifier x Humidity: lower humidity levels (arid regions)
may promote tear film evaporation.
– goggles, or side shields on spectacles
x Pollution: excessive pollution may cause ocular
– taping lids closed, or reducing PAS
irritation and alter the tear film constituents.
97400-266S.PPT

x Exposure to drafts, wind, air-conditioning

7L497400-266
system outlets.
Other approaches to the problem of dry eye include
299 the artificial elevation of the relative humidity (RH) of
the environment. Suggestion tried include
DRY EYE MANAGEMENT
ENVIRONMENTAL swimming goggles, shrouds and side-guards added
to the sufferer’s existing spectacles (Tsubota et al.,
• Punctal occlusion 1994), eyelid taping, and manual or automatic
artificial tear-injecting, modified spectacles (with
• Spectacles with injection of artificial tears
solution reservoirs in the frame’s temples [sides]).
• Remove sources of air pollution Fujishima et al. (1997) showed that cooling artificial
tears before instillation to 4°C provided relief by
• Lower ambient temperature without reducing corneal and conjunctival sensation.
lowering relative humidity Mori et al. (1999) studied the relationship between
97400-387S.PPT BUT and ocular discomfort during treatment with an
experimental eye warming device (infrared-based).
7L497400-387
While there was an improvement in BUT from the
treatment, only a tendency for the symptoms to
improve was found.
300 Punctal Occlusion for Dry Eye
Occlusion of the puncta (presented
PUNCTAL OCCLUSION
inspired by Tsubota, 1998 diagrammatically in slide 300, and illustarted in
slides 303 to 305) is the most effective method of
Tear
Tear reducing tear excretion and thereby maintaining a
evaporation
production greater volume of tears on the eye.
Punctal occlusion (PO) usage is largely country
dependent, e.g. PO is more popular in the US than
other countries (Golding and Brennan, 1992).
Plugged
drainage Punctal occlusion is a simple and reversible means
of preserving and extending the role of those tears
97400-220S.PPT
that already exist in the eye.
7L497400-220 Blocking the drainage system may provide some
relief from dry eye symptoms, however concurrent
use of artificial tears may also be required.
Occlusion of the puncta can be achieved in a variety
of ways.
A short-term evaluation of the effects of occlusion
on a dry eye condition can be made using collagen
plugs that swell to twice their original diameter when
wet, and dissolve over a few days. New plugs are
then required if the trial is to continue. Currently,
this is a practitioner-only procedure. For a long-
term solution, silicone plugs are used. They do not
swell or expand in situ. Other types exist, e.g.
Hamano et al. (1985) described a polymer punctal

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301 plug that shrank to a third of its original size when

dried to make insertion easier.
PUNCTAL OCCLUSION Total and permanent occlusion, i.e. a surgical
• Collagen plugs approach, is usually the final option (last resort?)
- swell to 2X size in situ taken to maintain the tear volume. Generally,
- easy to insert occlusion is performed if collagen or silicone plugs
- soluble over 7 days indicate that some improvement in the ocular health
- enables short-term is achievable.
assessment Despite a propensity for silicone punctal plugs to
- look for signs of dislodge, silicone plugs were found to be an easy
improvement and efficient method of treating dry eye (Balaram,
- upper and lower puncta 1999).
97400-52S.PPT

Giovagnoli and Graham (1992) reported a 34.6%

7L497400-52
increase in wearer comfort following the insertion of
permanent punctal plugs.
302 The gauge of the punctal plug to be inserted must
be ascertained. Calibres available range from 0.2
PUNCTAL OCCLUSION to 0.6 mm, in lengths of 1.6 to 2 mm. Usually, plugs
• Silicone plugs are inserted using special tools that are an integral
- removable part of a punctal plug system (slides 303 and 304).
- long lasting The puncta may be plugged either at, or near, the
- one puncta first orifice (slide 306), or intracanalicular plugs may be
• Supplementary lubrication used (slide 307), i.e. plugs that are inserted some
distance into the canaliculi. Silicone canalicular
• Assess improvement in:
plugs were used successfully in trachomatous dry
- signs of dry eye eyes by Guzey et al. (2001). A decreased need for
- symptoms artificial tears was also noted.
97400-53S.PPT

Ward (2001) found that plugging either punctum,

7L497400-53
i.e. superior or inferior, produced equivalent results
while Sharpe and Connor (2001) found no
303 advantage in plugging the superior puncta only.
Clinical Considerations:
Use of punctal plugs may be associated with side
effects such as epiphora, discomfort, and accidental
loss.
Contraindications include (from Tickner, 1997):
x Allergy to the plug’s material.
x Infective ocular surface disease.
x Dacryocystitis.
x Blepharitis.
x Epiphora.
7L47400-4

304 For an update on the various design and patents

relevant to punctal plugs and punctal occlusion refer
to MacKeen (2001).

7L47400-2

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305

7L47400-1

306

7L4002CWG-03

307

7L4003CWG-03

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308

PUNCTAL OCCLUSION
• If no improvement with other methods...

• Permanent occlusion

– electrocautery

– argon laser

– all irreversible

– final option (?last resort)

97400-357S.PPT

7L497400-357

309
PUNCTAL OCCLUSION
CLINICAL CONSIDERATIONS
• Discomfort
- mechanical
- mucus build-up
• Inadequate blockage
- tear supplements required
• Epiphora
• Accidental loss of small inserts
• Allergy to plug material
97400-54S.PPT

7L497400-54

310 Lid Hygiene

Forceful expression of lipids from the Meibomian
DRY EYE: LID HYGIENE glands, and the daily treatment of the lid margins by
• Warm compresses (wet face washer applied at
the highest tolerable temperature) lid scrubbing, often alleviate the symptoms of dry
- reduces viscosity of Meibomian gland eye or contact lens intolerance (after Doane, 1994).
secretory products Lid scrubbing using a cotton bud (cotton tip) or
• Gentle expression of the Meibomian gland’s lipid special purpose pad with or without special purpose
content
solutions, or simply using sterile saline, is usually all
• Lid margin ‘scrubs’:
- with cotton bud (cotton-tipped applicator)
that is required.
- with special applicator pad Firstly, apply warm compresses to the eye before
- with normal saline any expression or scrubbing. A cloth dipped in hot
- with special-purpose lid-care solution water and applied at a temperature that is just
97400-265S.PPT

tolerable, should be used on the whole of the closed

7L497400-265 eye and left in place until cooler. This step may be
repeated. This will not only decrease the viscosity
of the Meibomian secretions (thin them) making
them more expressible, but will also increase the
blood circulation to the general area and possibly
increase the output of the lacrimal and Meibomian
glands.
As the lid margin environment, i.e. the lashes, the
Meibomian glands, and the skin, plays an important
role in the production and maintenance of the tear
film, it is useful to have the dry eye patient maximize
their lid hygiene by instituting scrubs, massaging,
and the application of warm or hot, or alternating hot
and cold compresses.
Korb and Greiner (1994) increased the thickness of
the lipid layer by treating the underlying MGD of trial
subjects using a combination of office and self-
administered (daily) Meibomian gland expression

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and lid scrubbing, supplemented by warm

compresses. Self-reported symptoms also
improved.
311 Management of Dry Eye: Contact Lenses
MANAGEMENT OF DRY EYE Somewhat paradoxically, contact lenses can also
CONTACT LENSES have a role in KCS care. They are helpful in:
• Therapeutic contact lens x Filamentary keratitis (SCL usage brings almost
• Choice of material immediate and sustained relief as long as lens
wear continues).
• Supplementary hydration
x Mucin-deficient dry eye with adequate aqueous
• Risk of ocular infection phase.
• Frequent patient examination x Exposure keratitis.
• GP sclerals (stock or custom) Bandage lenses need to be kept moist and usually
97400-82S.PPT
require the concurrent use of artificial tears. The
7L497400-82 use of contact lenses in dry eye has an attendant
increased risk of infection and the use of
prophylactic antibiotic drops (e.g. chloramphenicol
drops twice daily) is recommended (Lamberts,
1994B).
Gasset and Kaufman (1971) used the Griffin
Bionite™ 55% lens successfully in 29 cases.
However, many of these cases were of dry eye
secondary to other more serious underlying
conditions such as Stevens-Johnson syndrome, and
ocular pemphigus.
Romero-Rangel et al. (2000) reported on their use
of gas-permeable scleral lenses as therapy for
ocular surface disease. From their results, they
believed that GP scleral lenses offered an effective
strategy that managed the surface problems of
complex debilitating ocular surface diseases, as
well as rehabilitating the wearer visually. A similar
report was made by Tappin et al. (2001).
Advantages included:
x Ease of handling.
x Ease of lens care.
x Physical and physiological protection of the
eye’s surface in complex ocular surface
conditions.
x The tear lens neutralizing irregular corneal
astigmatism.
Highly permeable scleral lenses were a possibility
for overnight wear on an as-needed basis.
However, nobody in the literature has suggested
RGP sclerals be the lenses of first choice, rather
they were a possible solution to complicated ocular
surface problems.

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

312 Dry Eye Therapy: Summary

The accompanying slides summarize briefly the
DRY EYE THERAPY
from Farris, 1987
most common treatment options under headings
Tear volume abnormality: related to aetiology rather than symptoms or overt
• Increase humidity effects.
• Avoid anticholinergic drugs
• Control air currents (wind, air-con., etc.)
• Artificial tears
• Lacriserttm
• Punctal plugs
97400-196S.PPT

7L497400-196

313
DRY EYE THERAPY
from Farris, 1987

Tear mucin abnormality:

• Artificial tears

• Acetylcysteine

• Physical removal of mucus

97400-197S.PPT

7L497400-197

314
DRY EYE THERAPY
from Farris, 1987

Tear lipid abnormality:

• Eyelid hygiene

• Topical antibiotics

• Systemic tetracycline

97400-198S.PPT

7L497400-198

315
DRY EYE THERAPY
from Farris, 1987
Surfacing abnormality:
• Tape eyelids shut
• Tarsorrhaphy
• Artificial tears
• Ointments
• Plastic surgery of the eyelids
• Scleral shell
97400-199S.PPT

7L497400-199

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 Module 7: Contact Lens-Related Ocular Complications

316
DRY EYE THERAPY
from Farris, 1987
Tear base abnormalities:
• Epithelial scraping
• Microperforations (cautery) of
Bowman’s layer
• Therapeutic SCLs
• Corneal graft
97400-200S.PPT

7L497400-200

317 Dry Eye: Conclusions

DRY EYE: CONCLUSIONS The slides opposite present the key steps to be
followed when assessing a suspected case of dry
• Important to establish aetiology
eye. Unfortunately, as was established earlier in
• Correlate patient history and this lecture, there is no accepted single test that
symptoms delivers a definitive answer to the question: Is this a
case of dry eye?
• Physical examination a key factor

• The diagnosis of dry eye should be

based on specific tests to determine
its pathogenesis. A single test is
not definitive
97400-122S.PPT

7L497400-122

318
DRY EYE: CONCLUSIONS
• Dry eye questionaire (e.g.
McMonnies)
• Assessment of lids - condition?
• Biomicroscopy - Meibomian glands,
conjunctiva, corneal, epiphora, etc.
• Tear quantity and quality
• Laboratory tests
97400-123S.PPT

7L497400-123

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

VI Contact Lenses and Dry Eye

319 Contact Lenses and Dry Eye: Symptoms

THE ‘TRILOGY’: Dryness is the most frequently reported symptom

among soft contact lens wearers (McMonnies and
THE 3 DISCOMFORT ISSUES
Ho, 1986, Brennan and Efron, 1989). The latter
Symptoms Specs(%) SCL (%) RGP (%) paper reported than only 25% of HEMA SCL
n=664 n=171 n=48
wearers had never reported experiencing symptoms
Dryness 3 13** 23**
Redness 7 16* 20* of dryness.
Grittiness 1 3 9* Pritchard et al. (1999) reported that the primary
(Vajdic, 1996)
reason for contact lens wear discontinuation was for
discomfort, dryness, and red eyes.
Some issues relevant to contact lens wearer are
97400-118S.PPT
* Sig Differences
presented in slides 320 and 321.
7L497400-118 It is not always known whether a reduction in tear
quality, quantity, and blink efficiency during lens
wear leads to wearing difficulties (after McMonnies,
320 1996).
SOFT CONTACT LENSES Tomlinson et al. (2001) found no significant
(Fonn et al 1998, B&L Survey 1995, etc.) differences between non-lens wearing and lens-
Discomfort wearing females using oral contraception.
However, Brennan and Efron (1989) reported that
• Over 50% of all contact lens wearers using oral contraceptives
wearers cease reported experiencing dryness at some time, versus
wearing contact 63% of those not using oral contraceptives.
lenses because However, 76% of male lens wearers also had
of chronic low symptoms of dryness. This suggests that the belief
levels of that women are more likely to be affected by dry eye
discomfort problems may not be true, at least for contact lens
97400-116S.PPT

wearers.
7L497400-116
Puffer et al. (1980) found no significant differences
in tear elimination rates between contact lens
321 wearers and non-wearers. Their findings showed
that 15% of the tear volume was eliminated every
CONTACT LENSES & DRY EYE minute (range with 95% confidence: 5 – 30%/min).
Patel et al. (1994) measured the refractive index of
20-50% of contact lens wearers
tears using two methods and compared the tears of
‘experience’ (Nichols, 2000): normals with those of SCL wearers. They found no
- Dryness statistical difference between groups.
- Irritation
When McCarty et al. (1998) removed the 2.27% of
- Mild burning their study sample that wore contact lenses, their
- Stinging data, and their conclusions, remained unaltered.
- Foreign body sensation
The relative humidity in aircraft can range from 4%
97400-117S.PPT to 27% (Rocher and Fatt, 1995) and these low
7L497400-117
values can be expected (and usually do) result in
significant discomfort for contact lens wearers,
especially SCL wearers.
Chalmers et al. (2001B) found that contact lens
wearers report symptoms of dryness differently from
those reported by non-wearers. The difference was
greatest late in the day when wearers reported the
greater symptoms.
Prevalence data and some of the effects of contact
lenses on the tears and the anterior eye are
summarized in slides 322 to 325.

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 Module 7: Contact Lens-Related Ocular Complications

322
DRY EYE: PREVALENCE
SUMMARY OF CL WEARERS

• 51% • Bowden et al., 2001

• 40% (VDU) • Bowden & Harknett, 2001

• 60% (air-con) • Bowden & Harknett, 2001

• 39% (aircraft) • Bowden & Harknett, 2001

• 15% • Schaumberg et al., 2000

97400-178S.PPT

7L497400-178

323
CONTACT LENSES & DRY EYE
Contact Lens wear:
• Induces or exacerbates dry eye conditions
- medications compound the problem
• Is a provocative test for dry eye?
• Exacerbating factors:
- low RH
- concurrent eye conditions
- lens care preservatives
97400-115S.PPT

7L497400-115

324

CONTACT LENSES AND DRYNESS

Contact lenses:
• Disturb the interactions between tear
components
• Add interactions between themselves
and the tear components (Tiffany, 1988)
• Affect the:
- ocular surface
- tear film components
– p quality & quantity
• Lose water
• p blink efficiency
97400-60S.PPT

7L497400-60

325

CONTACT LENSES AND DRYNESS

McMonnies, 1990

“The high prevalence of symptoms (of

dryness) among contact lens wearers
suggests that contact lens wear acts like a
provocative test for tear function, causing
marginal or incipient tear dysfunction to
become apparent.”

97400-61S.PPT

7L497400-61

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

326 Contact Lens or Eye-Related Dryness?

After a few hours of lens wear, some wearers may
LENS OR EYE-RELATED DISCOMFORT?
report the onset of symptoms of ocular and/or lens
• Concurrent ocular pathology dryness that become worse the longer the lenses
are worn (light sensitivity is a possible exception).
• Unilateral or bilateral Initially, lens wearers may not present with obvious
signs of dry eye. However, when burdened with the
• Effect of lens removal
additional stress of contact lens wear, they may find
• Effect of swapping lenses
it necessary to reduce their wearing time, or
discontinue lens wear altogether, because of the
• Effect of ocular lubricants symptoms of dryness, redness, burning, itching,
97400-80S.PPT
grittiness, and foreign body sensation (Orsborn,
1989).
7L497400-80
Efron and Brennan (1989) have shown that SCLs
327 are more likely to induce complaints of dryness.
NIBUT: However, their finding that symptoms are more
CORNEA vs SOFT LENS likely to be reported in cases involving greater
100 Pre-Lens Tear Film dehydration, is opposite to that of Fonn et al. (1999).
CCLRU data
Pre-Corneal Tear Film
80 Begley et al. (2000) surveyed the symptoms of
60 contact lens wearers and found ocular dryness and
60 50
BUTs in SECONDS discomfort were relatively common among lens
40 wears and that, as is often reported, these
25 25
15
symptoms worsen towards the end of the day.
20 10
0
5
0 0
5 5 Begley et al. suggested that contact lens
0 practitioners examine contact lens wearers later in
0-4 5-9 10-14 15-19
97400-172S.PPT
20-24 25-30
the day to better identify the symptomatic ones.
7L497400-172 Caffery (2000) used a questionnaire to ascertain
what dry eye patients feel.
Contact lens wearers reported more frequent:
328
x Ocular discomfort.
PHENOL THREAD AND CONTACT LENSES
x Dryness.
Hamano (1983)
100
x Visual changes.
CASES WITHOUT SYMPTOMS/SIGNS (%)

82
74
80
x Soreness.
60
x Redness.
40 25 27

20
However, non-contact lens wearers reported more:
0
RGP SCL
x Burning.
Wet Length >20 mm Wet Length <10 mm
x Stinging.
97400-76S.PPT

x Light sensitivity. This is somewhat surprising

7L497400-76 since photophobia has been viewed traditionally
as a problem of contact lens wearers, especially
rigid lens wearers. However, Chalmers et al.
329
(2001) found photophobia to be the least useful
DRYNESS CORRELATIONS symptom when trying to differentiate tear-
deficient dry eye patients from normals (all non-
Dryness symptoms correlate with various wearers).
clinical tests:
x Itching.
• ? NIBUT (results are mixed)
The data suggested that discomfort was more
• p PRTT
prevalent than redness, burning, and itching, and
• p lactoferrin that discomfort may be a unique sensation, despite
• n staining the usually nebulous descriptions most provide.
• ? TMH (results are mixed) Correlation with Clinical Tests
97400-359S.PPT Guillon et al. (2000, cited in Nichols, 2001) analyzed
the lipid layer of the pre-lens tear film in a group of
7L497400-359
SCL wearers and found an excessive level of

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 Module 7: Contact Lens-Related Ocular Complications

330 cholesterol indicated an unstable tear film and

symptomatology during lens wear.
Fonn et al. (1999) reported on SCL hydration, and
AETIOLOGY OF DRY EYE SYMPTOMS
subjective comfort and dryness ratings, in lens
• Exposed bulbar conjunctiva wearers with and without symptoms.
Disappointingly, no correlation was found between
- NOT interactions between lens & tarsal
lens dehydration and subjective dryness and
conjunctiva comfort. This means that it is impossible to
• Associated with allergy correlate lens hydration factors with dry eye
symptoms because some wearers without
- but mediated immunologically
symptoms had significant dehydration while some
• Associated with n dehydration ? with significant symptoms had little dehydration.
97400-360S.PPT The lack of correlation between dryness and NIBUT
means that the clinical significance of reduced pre-
7L497400-360
lens NIBUT to the diagnosis of dry eye is
questionable.
331 A previous study showed that reduced BUTs were
DRY EYE SYMPTOMS
associated with measurably reduced comfort, and
EFFECT OF LENS MATERIALS increased dryness ratings (Lowther, 1993).
• No correlation between lens dehydration and However, Bruce et al. (1995) failed subsequently to
subjective dryness or discomfort (Fonn et al.,1999) demonstrate this association. Bruce et al. assessed
• Lenses that dehydrate less ‘on eye’ exhibit: symptoms in SCL wearers to better understand the
– less spoilage (Young et al., 1997B) origins of the dryness reported. They concluded
– greater comfort that discomfort did not arise from tear film stability,
or interaction between the lens and tarsal
– fewer symptoms
conjunctiva. Rather, they felt that discomfort may
– less fluorescein staining (Lemp et al., 1999)
arise from the exposed bulbar conjunctiva (i.e. the
• Modern materials and designs produce fewer conjunctiva not covered by either the lens or lids).
symptoms (Reeder et al., 1999)
97400-388S.PPT

Fonn et al’s study used two different lens types

7L497400-388 (etafilcon A and omafilcon A). Omafilcon A had
already been shown to demonstrate less
dehydration (Young et al., 1997) but claims that ‘a
lens that dehydrated less was more comfortable’
were not supported by the results of Fonn et al’s
study. Young et al. (1997B) reported that omafilcon
A lenses exhibited less spoilage than comparable
lenses but, because Fonn et al’s study was a non-
dispensing study, it is impossible to make further
comparisons between these studies, or the lenses
used.
Despite these findings, Lemp et al. (1999) [Young
was a co-author] did find greater comfort, fewer
symptoms, less on-eye dehydration, and less
sodium fluorescein staining in cases of mild to
moderate dry eye when omafilcon A lenses were
worn. Reeder et al. (2000) found no difference
332 between alphafilcon A and omafilcon A when worn
by symptomatic dry eye patients but both lenses
THE EYE IN AIR-CONDITIONING
inspired by Tsubota, 1998 produced fewer symptoms than their previous
Normal tear
production?
earlier generation lenses. The authors suggested
Tear Drafts,
Wind,
that newer lens designs may offer greater comfort.
evaporation
Forced convection
er
ed A study by Hamano (1983) using the phenol red
w H
Lo R thread test to measure basal tear volume, indicated
that patients with a low measurement are more
Slowed drainage? likely to experience dryness.
Albietz (2001) concluded that mechanical influences
are responsible for the squamous metaplasia that
97400-221S.PPT
occurs in contact lens wear. Further, she concluded
7L497400-221 that dry eye in contact lens wear is associated with
allergic and immune-mediated inflammatory

428 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

processes. Tsubota (1995) believes that as long as

the tear reflex is present, even if reduced,
squamous metaplasia will not occur, and Rose
Bengal and sodium fluorescein staining of the
ocular surface will not be seen.
Little and Bruce (1993) studied the post-lens tear
film and found that dryness, or other common
symptoms, was not associated significantly with the
appearance of the post-lens tear film.
333
Clinical Tests
DRY EYE & CONTACT LENS WEAR Nilsson and Andersson (1986) studied the effects of
CLINICAL ISSUES
contact lens wear in dry environments. They
• In low relative humidity:
reported that when RH was < 30%, BUTs were
– p BUTs shortened significantly, and the lenses deposited
– n lens deposits more. Discomfort was also greater in low RH
– p comfort conditions when BUTs were <20 seconds.
• Water content may affect tear characteristics
Conventional refrigerated, or reverse-cycle, air-
conditioning reduces the RH significantly.
• Contact lenses are more likely to induce
symptoms of dryness than the effects of Young and Efron (1991) determined that high water
either age or gender lenses carried a thicker PLTF (both lipid and
97400-389S.PPT
aqueous phases). NIBUTs with these lenses were
7L497400-389 also found to be longer. Lens dehydration was also
measured with a hand-held Abbe-type refractometer
but the dehydration determined was not associated
with the PLTF characteristics found. The finding
that high water lenses carried thicker tear films has
been described as being ‘too simplistic’ by Guillon
and Guillon (1994).
Lowther (1993) surveyed symptomatic and
asymptomatic SCL wearers and found that those
with symptoms (McMonnies questionnaire) also had
dry eye signs (shorter BUTs, decreased lactoferrin
levels, and more sodium fluorescein staining).
However, he found no difference between the
groups for the TMH measurements.
DuToit et al. (2001) reported that the wearing of
contact lenses was more likely to induce dry eye
symptoms than either age or gender.
334 Signs: General Effects of Contact Lenses on the
Tear Film
CONTACT LENS EFFECTS
Minor deficiencies in the tear film may not result in
• Contact lenses disrupt any symptoms. However, the wearing of contact
the tear film
lenses may result in symptoms (Holly, 1980,
• Alter mucus production Orsborn and Robboy, 1989, Nichols, 2001).
• Increases evaporation
of the tear film This may be because of their effect on the tear
• Render the tear film composition (Farris, 1986) which in turn may cause
hypertonic tear components to bind to lens surfaces
• Exacerbate Meibomian (McMonnies, 1990).
Gland Dysfunction?
- increased lipid deposits Some of the known effects a contact lens has on
on lenses? 97400-119S.PPT
the tear film (after Korb (1994) include:
7L497400-119 x Alterations to the menisci along the upper and
lower lid margins.
x The establishment of a lens-edge tear
meniscus that interacts with the pre-existing lid-
anterior eye menisci.
x Tear film is destabilized (Cedarstaff and
Tomlinson (1983). Shorter BUTs can result.

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335 x In SCLs at least, shortened BUTs may lead to a

decrease in vision quality through premature
EFFECTS OF CLs ON TEAR FILM failure of the pre-lens tear film and/or surface
TEAR FILM ITSELF
after Korb, 1994
deposits. Decreased visual acuity can be best
• Tear film is destabilized detected by the use of a low-contrast chart
• p BUTs (especially with RGPs?) (Snellen-type, sine-wave grating, etc.).
• Limited anterior eye tear volume may be Preocular NIBUTs of at least 20 seconds were
insufficient to cover CLs adequately recommended by Guillon and Guillon (1993) as
• Lipid layer of pre-lens tear may be very thin the probable minimum acceptable for
or absent successful contact lens wear.
• CLs may cause stagnation of the post-lens
tear film x More frequent blinking is usually required to
• ntear evaporation rate (esp. SCLs) resurface the eye and lens when the tearfilm is
97400-362S.PPT
less stable.
7L497400-362
x Especially when RGP lenses are worn, the blink
336 amplitude may be altered. The change is often
from a normal blink to an incomplete blink or, in
EFFECTS OF CLs ON TEAR FILM extreme cases, a flutter of the lids with no
LIDS after Korb, 1994
serious attempt to routinely bring the lids
• Alters the menisci along both lid margins
• The introduced lens-edge meniscus interacts together.
with the pre-existing lid-anterior eye meniscus
• Usually, more frequent blinking required to
x Conformance of the lids to the anterior eye may
resurface the eye & the less stable pre-lens film be impossible with a lens in situ, leading to
• The blink amplitude may be altered effects like 3 & 9 o’clock staining in rigid lenses.
(oincomplete?) Lens adherence may result from pressure-
• In RGP lenses, lid conformance to the eye may induced excessive thinning of the post-lens tear
be impossible o3 & 9 staining
• Action of lids on epithelium thwarted by CLs - film.
ramifications for ocular surface wettability ?
97400-361S.PPT x The limited volume of tears on the anterior eye
may be insufficient to cover a contact lens
7L497400-361
adequately.
x The lipid layer of the pre-lens tear film may be
337 either very thin or absent.
EFFECTS OF CLs ON TEAR FILM x Lenses may cause stagnation of the post-lens
TEAR FILM COMPONENTS
after Efron, 1998 tear film by restricting the exchange of tears
• p tear film osmolality @ insertion - reflex from under the lens.
tears
• ' pH ? x All contact lenses prevent the direct action of
• n plasmin (Virtanen et al., 1994) the lids on the epithelium situated under them.
During adaptation: This may have ramifications for the ocular
• n serum-derived proteins (albumin, sIgG, surface’s wettability in the short or long term.
sIgE, transferrin
• n Na+, Cl–, K+ x The tear evaporation rate is increased.
• n cholesterol
• Adaptation results in a return to baseline
Unfortunately, as pointed out by Korb and others,
97400-363S.PPT
the results of studies of the effects of contact lenses
7L497400-363 on the tear film are frequently conflicting. Korb
concludes that the tear film of many individuals is
inadequate to support the increased evaporation
encountered in contact lens wear. Contact lens
surfaces with improved properties that more closely
mimic those of the ocular surface are one possible
direction for future improvements.
Glasson et al. (1999) studied the tear films of
tolerant and non-tolerant contact lens wearers.
Self-reporting of tolerance was combined with a
McMonnies questionnaire and a NIBUT
determination. Tear samples were taken and
subjected to an electrophoretic gel analysis. Their
data suggested that biochemical profiles of the tears
could differentiate the tolerant from the intolerant.
Not surprisingly, the reflex tearing that follows lens
insertion renders the tears relatively hypo-osmotic.

430 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

This has been confirmed in rigid lenses by Terry

and Hill (1977) and in SCLs by Martin (1987).
Martin also studied the contralateral effects of
monocular contact lens wear and found symmetrical
osmolality changes. Studies of changes to tear fluid
pH that follow contact lens wear are ambiguous
(Efron, 1998).
Some tear components that show increased levels
early in the adaptation process include:
x Serum-derived proteins:
– albumin. However, Farris (1986) found that
albumin, lysozyme, and lactoferrin levels did
not change with long-term RGP or hydrogel
lens wear, or in aphakic subjects (Farris,
1986B).
– IgG. Serum IgG is higher in SCL wearers
than RGP lens wearers and non-wearers
(Sengör et al., (1990).
– IgE . Serum IgE levels are higher in contact
lens wearers (both types) than in non-wearers
(Sengör et al., 1990).
– transferrin.
+
x Na ions.
–
x Cl ions.
+
x K ions.
x Cholesterol.
All return to baseline levels following adaptation.
Much of this section after Efron (1998).
Plasmin, a tear protein, is normally in low
concentrations except in cases of corneal disorders
and during contact lens wear. After measuring tear
fluid plasmin activities, Virtanen et al. (1994)
concluded that the elevated tear fluid proteolytic
activity they found may be related to pathological
changes induced by contact lens wear.
338 Signs: Effects of SCLs on the Tear Film

THE PRE-LENS TEAR FILM The following are some of the known effects of
SOFT LENSES SCLs on the tear film (after Korb (1994):
Numerous fringes occur:
• lipid thin or absent x Generally, because of lens deposits and the
effects of tears drying on the front surface, SCL
• poor mucous coverage
wearers exhibit greater vision reduction than do
• low water lens RGP lens wearers (Timberlake et al., 1992).

Few fringes occur:

x In SCLs with relatively high rigidities, problems
due to the physical properties of the lens
• thick tear film
materials, e.g. SEALs, may be induced by
• high water lens excessive local thinning of the post-lens tear
97400-121S.PPT
film. These subjects are covered in more detail
7L497400-121 in Lectures 7.2 and 7.3 of this module.
x SCLs may encourage desiccation of the
epithelium if fabricated from high water
materials and made very thin (pervaporation
staining). This staining is believed to be due to
a thinning or disappearance of the anti-
evaporative lipid layer of the tears over the lens.

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 Module 7: Contact Lens-Related Ocular Complications

339 x The tear evaporation rate is increased. The

rate of evaporation is not related to the initial
EFFECTS OF SCLs ON TEAR FILM water content of the lens and the water lost
DESICCATION from the lens made only a relatively minor
• Pervaporation oepithelial desiccation if SCL: contribution to the increased evaporation from
the eye during lens wear (Cedarstaff and
- too thin
Tomlinson, 1983).
- high water content
Faber et al. (1991) studied the effects, including the
• High water lenses associated with: temporal effects, of hydrogel lenses on tear film
- destabilized PLTF stability. They found that:
- thinning of the lipid layer x The stability of the pre-lens tear film was
97400-364S.PPT
reduced by lens wear as shown by a NIBUT of
the pre-lens (lens in situ) and pre-ocular (before
7L497400-364
lens insertion) tear films (Albarrán et al. (1997).
340
x The lens type (high or low water) was
EFFECTS OF SCLs ON TEAR FILM unimportant in all outcomes.
• n evaporation NIBUT
• ptear film stability, both:
x Tear film instability remained well after the lens
- pre-lens tear film (PLTF) was removed. The cause is unknown.
- pre-ocular tear film (POTF) However, 95% recovery was complete by 25.8
– POTF has altered structure minutes.
- effect remains some time after lens removal
– disrupted epithelial mucin coating suspected x A disruption of the mucin coating of the corneal
• Results < 6 sec not uncommon epithelium was suspected as a possible
• 6 months of SCL wear: explanation of their findings.
- pBUT by 3 sec, and...
- nDE incidence from 28% (before SCLs) From a large sample (1,478 eyes), Guillon and
o68% (after SCLs)
97400-365S.PPT Guillon (1993) found a PLTF NIBUT average of 8.2
7L497400-365
seconds during the day, and only 5.9 seconds and
very unstable on awakening, in a sub-set of 210
eyes.
341 Guillon and Guillon found not only was the pre-lens
EFFECTS OF SCLs ON TEAR FILM tear film (PLTF) less stable than the normal
LIPID LAYER (LL) preocular film (POTF) but it also had a different
• Thinning, or absence, of LL is known structure. The lipid layer is thinner and, in some
• Overnight wear o no, or contaminated, lipid phase cases, absent. Such an absence could explain the
Tearscope patterns: increased evaporation and spoilage rates reported
by many authors (e.g. Guillon et al., 1990).
• Usually, meshwork or flow pattern seen
- open meshwork = thin LL When SCLs are worn overnight, the PLTF is
- closed meshwork & flow = thicker, more stable abnormal on awakening. Most commonly, a dried
LL mucus-covered lens front surface is seen with no
- amorphous = thick, very stable LL aqueous phase apparent, and either no lipid phase,
97400-366S.PPT
or a highly contaminated lipid phase. The
commencement of blinking rehydrates the mucus
7L497400-366 cover and a thick, stable tear structure forms. The
latter is demonstrated by the high incidence of
342 colour fringes in the lipid layer.
PLTF NIBUTs must be longer than the interblink
EFFECTS OF SCLs ON TEAR FILM
period and should be of at least 10 seconds.
AQUEOUS LAYER (AL)
Unfortunately, this is often not the case and BUTs of
• Only visible when LL is thin (open meshwork) about 6 seconds are common.
• Blue & red fringes likely to be seen in AL
The following is a summary by Guillon and Guillon
- if easily visible = AL is thin
(1993) of the PLTF in SCL wear:
- if fainter = thicker & more stable AL
• When AL invisible, LL > 90 nm thick Lipid layer:
- amorphous pattern, or coloured fringes seen x Usually, meshwork or flow patterns.
- no conclusions about AL thickness possible – open meshwork indicates the presence of a
97400-367S.PPT
thin lipid layer
7L497400-367 – close meshwork or flow indicates a thicker,
more stable lipid layer

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

– occasionally, an amorphous pattern is seen

and this indicates a thick, very stable lipid
layer.
Aqueous layer:
x Only visible when the lipid layer is thin (open
meshwork).
– blue and red fringes are likely observations
within the aqueous layer, they are either
– easily visible, indicating a thin aqueous
layer (2-3 µm thick). This film tends to dry
up, or...
– they have faint patterns that correspond to
a thicker (3 µm) and more stable aqueous
layer.
x When the aqueous layer is not visible the lipid
layer is > 90 nm. This appears as either an
amorphous pattern or a coloured fringe pattern.
Under these conditions, no conclusion can be
reached about the thickness of the aqueous
layer or its stability, but it is assumed to be
adequate.
Desiccation
Guillon et al. (1990) concluded that corneal
desiccation staining in high water SCLs was due to
a destabilized PLTF and a thinning of the lipid layer.
This conclusion was reached after it was found that
despite differences in tc (0.08, 0.10. 0.12 mm) the
staining with each lens thickness was not
significantly different. Overall, their opinion was that
desiccation staining was due, at least partially, to
excessive evaporation from the contact lens’ front
surface.
Du Toit et al. (2001) showed that 6 months of SCL
wear decreased BUTs by an average of 3 seconds.
Twenty eight percent of the group studied
experienced symptoms of dryness before contact
lens wear but this rose to 68% when contact lenses
were worn.
Nichols and King-Smith (2003) concluded that eye
closure while wearing siloxane hydrogels (balafilcon
A) thinned the PLTF rapidly such that by 30
minutes, the thickness was less than 1 µm.
343 Signs: Effects of RGP Lenses on the Tear Film

EFFECTS ON THE TEAR FILM: RGPs Some of these effects have already been presented
• Lids unable to conform to shape of lens-anterior eye: (see opposite slide 343). The following are some of
- o 3 & 9 staining the known effects of RGP lenses on the tear film
- o lens adherence (mostly after Korb, 1994):
• May cause post-lens tear film stagnation by restricting
tear exchange x An inability of the lids to conform to the shape of
• Tear film continuity more difficult to maintain
- greater edge clearance
the anterior ‘eye’ with a rigid lens in situ, can
- thicker edges lead to effects like 3 & 9 o’clock staining.
- greater lens mobility Further, lens adherence may result from
• Foreign bodies & film contaminants move and pressure-induced, excessive thinning of the
destabilize tear film more
• Lipid layer not always present and/or disappears rapidly
post-lens tear film.
after a blink 97400-268S.PPT
x Lenses may cause stagnation of the post-lens
7L497400-268 tear film by restricting the exchange of tears
from under the lens.

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344 Guillon and Guillon (1993) assert that RGP lenses

create a much more difficult set of circumstances
for tears to maintain a continuous film over the lens
than do SCLs. Lens geometry, and the greater
amount of lens movement they exhibit, is the most
significant factors in the differences.
A major contributing factor is the difference in edge
clearance of an RGP lens (80-100 µm lens to
cornea) whereas with SCLs the edge is in close
apposition to the conjunctiva. SCL edges tend to be
thinner as well.
The significance of the ‘black line’, a thinning of the
tear film just beyond the boundary of the lens edge
7L41783-93 meniscus (see McDonald and Brubaker, 1971 for
details) is unclear. It probably indicates a limit to the
volume of tears available to the meniscus and the
PLTF, i.e. the edge meniscus could carry a greater
volume of tear fluid if it was available.
Furthermore, an RGP lens moves more on the eye
and the movement (displacement) of foreign bodies
by the lens can also destabilize the tear film.
PLTF patterns on the front of RGP lenses move
rapidly. Their dynamic nature necessitates the
preconditioning of the environment before
assessing the PLTF. To achieve this, the wearer
should be asked to close their eyes fully, open
them, and start to blink normally. The pattern
should be assessed during the early stages of this
normal blinking.
Following a blink, a lipid layer is occasionally
present but disappears rapidly. The aqueous layer
thins by drainage and evaporation. This thinning
results in interference fringes becoming visible
within the aqueous. By counting their number at
eye opening, it is possible to assess the thickness
of the aqueous layer and its stability:
x A thin aqueous layer (<1 µm) has wide bands of
colour fringes of high intensity moving rapidly on
the lens surface.
x A medium thickness aqueous layer (1-2 µm)
has 5 or more faint, narrowly spaced fringes
that move at average speed.
x A thick (>2 µm) aqueous layer has 10 or more
narrowly spaced fringes that move slowly.
When timing and observing tear film breaks, the
type, location, and repeatability of location should be
recorded. With RGP lenses, an additional
measurement is possible – the Non-Invasive
Drying-Up Time (NIDUT) (slide 344). This is the
time in seconds after a blink that the disappearance
of the aqueous phase first occurs. The lens’
mucous coating can then be assessed.
RGP lens PLTF break-up usually occurs as a band
superiorly (Guillon et al., 1990). The proximity of
this zone to the upper lid margin may be a factor in
the instability that leads to the film breaking in this
area. Guillon et al. reported that the PLTF was
thinnest, and the least stable, at the tear meniscus

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

border.
The NIBUT is very short (92% are under 5
seconds). NIDUT values are usually of the order of
20 seconds.
NIBUT values change little over a 6-month wearing
period.
Temel et al. (1990) found that IgA levels were
higher in rigid lens wearers and postulated that
continuous mechanical stimulation of the
conjunctiva was the cause. Temel et al. also
reported that, regardless of lens type, IgG levels
tended to reflect the number of years contact lenses
had been worn.
345 Signs: Tear Film Thickness in Contact Lens
Wear
TEAR FILM THICKNESS IN CL WEAR
The data pertaining to the thicknesses of various
• Non-wearers: 4.5 Pm between, 10 Pm
immediately after, blink tear films with differing lens types is presented in
• Pre-lens film: 2.35 to 2.7 Pm (range 1.4 – 3.9) the slide opposite. The references used include:
- post-lens tear film: 2.45 Pm (other studies up Ehlers (1965, cited in Korb, 1994), Guillon and
to 12 Pm) Guillon (1994), Fogt and King-Smith (1998), Creech
• SCLs: 2.3 to 6.5 Pm et al. (1998), Nichols and King-Smith (2000, cited in
• PLTF: Nichols, 2001).
- RGP: 1 to 5.8 Pm
- PMMA: 2.5 Pm (3.5 Pm with wetting solution)
Creech et al. (1998) showed that with the eye only,
and when wearing RGP or hydrogel lenses, the
97400-248S.PPT
measured thickness of the POTF/PLTF correlated
7L497400-248 with differences in tear film stability.
346 Causes of Dry Eye with Contact Lenses

CAUSES OF DRY EYE WITH Many contact lens wearers experience symptoms of
CONTACT LENSES ocular and/or lens dryness. The exact mechanism
• Reduced blink efficiency for the sensation of dryness is not well understood.
- frequency However many possible causes of dry eye related to
- completeness contact lens use have been proposed. Many are
- conformity presented in the slides opposite.
• Build-up of deposits
- reduced wettability
• Material dehydration
- fitting changes
- epithelial staining
97400-368S.PPT

7L497400-368

347
CONTACT LENS EFFECTS ON THE
TEAR FILM
• Mucus
– increased production
– inadequate surfacing
– mucin layer degradation
• n tear evaporation
– thinned or poor lipid layer
– n tear osmolarity
• n lysozyme and lactoferrin
97400-63S.PPT

7L497400-63

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 Module 7: Contact Lens-Related Ocular Complications

348 Slides 348 and 349 show hydrogel lens surface

deposits and surface dehydration (infrequent
blinking?) respectively. Note the disturbance to the
pupil’s appearance (ignoring the fact that they may
be out of focus) when viewed in retro-illumination
through well-used lenses.

7L40297-98

349

7L41570-95

350

CONTACT LENSES AND DRYNESS

• Need to rule out:

- poor fitting

- manufacturing problems

97400-65S.PPT

7L497400-65

351 Wearer Selection

Guillon and Guillon (1993) presented the wearer
WEARER SELECTION selection criteria that appear in the slide opposite,
Guillon & Guillon, 1993
• Eliminate: without regard to the type of contact lens envisaged.
- those with marked tear instability
- the deposit prone
- those with tear-related intolerance
- NIBUT < 10 seconds
• Be wary of NIBUTs between 10 & 20 s
• Fit those with NIBUTs > 20 s
97400-246S.PPT

7L497400-246

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 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

352 Contact Lens Wear In Dry Eye

LENS SELECTION AND WEAR

When considering the possibility of fitting a dry eye
patient with contact lenses, the issues listed in the
• Patient history slide opposite warrant consideration.
• Types of lenses
Slide 353 illustrates a case of pervaporation staining
• Lens wear modality due to the use of a thin, high water lens. This is
• Wearing schedule only likely to be exacerbated in a wearer who also
• Environmental considerations suffers from dry eye.
• Compliance McNally et al. (2001) showed that symptoms of
• Lens care products dryness were less frequent in siloxane hydrogel
• Re-wetting drops wearers than in wearers of conventional high water
97400-68S.PPT
SCLs. Furthermore, fewer discontinuations and
7L497400-68 unscheduled removals for dryness, were reported in
the siloxane hydrogel group.

353

7L40082-99

354 SCL Fitting in Dry Eye

MANAGEMENT OF DRY EYE Although Efron and Brennan (1989) have shown
WITH SCLs that SCLs are more likely to induce complaints of
• Reduce evaporation & pervaporation dryness, Businger (1998) recommended SCLs for
• Optimal choice of: marginally dry eye patients.
– material (ionic if replaced regularly, Regardless, fitting SCLs on a dry eye patient can be
otherwise non-ionic) problematic. Selection of optimal lens
– lens thickness (thicker) characteristics increases the chance of achieving a
– water content (low, but patient-dependent, successful outcome. Lenses that minimize the
high water should be tried as a last resort) effects of evaporation and pervaporation are likely
– wearing schedule (minimal)
to perform better on a dry eye patient. Further,
97400-71S.PPT
lenses should be replaced frequently. Front-surface
lens deposits disrupt the tear film and lead to short
7L497400-70 BUTs. Regular replacement solves much of this
problem.
355 Daily disposal is the logical endpoint to the
replacement schedules but no conclusive support
MANAGEMENT OF DRY EYE
WITH SCLs has been given to the notion that daily disposal is
‘better’. However, Macri et al. (1997) found that
• Lubrication (unpreserved)
different wearing and replacement strategies had
• Preservative-free lens care products little effect on ocular surface parameters. In
general, they found that all disposable lenses
• Refit with RGP lenses if unsuccessful
induced a deterioration in tear film-related signs.
• Replace frequently to: Loveridge et al. (1996) studied the possible role
– p deposits netrafilcon A (66%) SCLs had in dry eye and
previously unsuccessful SCL wearers. They found
– n BUTs that such lenses were successful in 62% of those
97400-390S.PPT
wearers who completed the study.
7L497400-390 When selecting SCLs, Guillon and Guillon (1993)

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 Module 7: Contact Lens-Related Ocular Complications

suggested determining the NIBUT after 15-30

minutes of trial lens wear and rate the stability of the
PLTF.
x PLTF NIBUT < 5 seconds. Poor on-eye
wettability.
x PLTF NIBUT 5 to 10 seconds. Acceptable on-
eye wettability.
x PLTF NIBUT > 10 seconds. Good on-eye
wettability.
356 RGP Fitting in Dry Eye
The major advantages of RGP lenses over SCLs for
MANAGEMENT OF DRY EYE
WITH RGP
the dry eye patient are their greater tear exchange
• Advantage over SCLs: with blinking, and the maintenance of a more
normal mucin layer on the epithelium.
- tear exchange
- mucin resurfacing Potentially, 3 & 9 o’clock (sometimes 4 & 8 o’clock)
- no pervaporation staining staining is a serious complication that can occur
• Need to minimize 3&9 staining
when a dry eye patient wears RGP lenses. Steps
should be taken to minimize the risk of 3 & 9
- centration (higher riding)
staining by achieving optimal fitting and lens design
- total diameter (larger)
characteristics. Frequent after-care of such patients
- edge thickness (minimal) is mandatory.
97400-71S.PPT

7L497400-71 Guillon and Guillon (1993) recommended the

following guidelines for RGP lenses:
x PLTF NIBUT < 3 seconds. Poor on-eye
wettability.
x PLTF NIBUTs of 3 to 5 seconds. Acceptable
on-eye wettability.
x PLTF NIBUT > 5 seconds. Good on-eye
wettability.
If a decision is made to fit RGP lenses, it is
advisable to:
x Reduce lens mobility.
x Increase TD to achieve a more uniform front
surface film, and reduce the effect of tear film
discontinuities adjacent to the lens edge.
x Decrease lens edge clearance (§ 60 µm).
357 Choice of Lens Wear Modality and Lens
Replacement Regimen in Dry Eye
DRY EYE & CONTACT LENS WEAR: Having made a choice to start, or continue, contact
LENS WEAR MODALITY lens wear, and having selected a lens type (RGPs,
• Generally, EW contra-indicated unless SCLs, or siloxane hydrogels), a choice of wear
‘bandage lens’ effect is required modality needs to be made. In some cases, EW
may be desired as a ‘bandage’. However, the
• Regular replacement programme greater physiological stresses applied to the anterior
desirable eye by EW in any lens type probably contra-
• Daily lens disposal not confirmed to be indicates EW.
better Some form of regular lens replacement is highly
97400-245S.PPT
desirable for all contact lens wearers, but in ocular
surface diseases in which tear stability and surface
7L497400-245 deposits are usually issues, regular lens
replacement is probably mandatory. Daily disposal
of lenses, while appealing intuitively, has not been
shown to be ‘better’ conclusively.

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358 Choice of Lens Care Products in Dry Eye

DRY EYE & CONTACT LENS WEAR: Having chosen the type of lens and the wear mode,
CHOICE OF LENS CARE PRODUCTS the remaining decision is that of the lens care
• Avoid using products containing older- products to be used.
generation preservatives/disinfectants:
Traditionally, discomfort and dryness have been
- thimerosal associated with the use of older-generation
- chlorhexidine preservatives in lens care products, e.g. thimerosal
- benzalkonium chloride and chlorhexidine-based chemistries. The current
• Choose those with lubricating/re-wetting generation of products and hydrogen peroxide-
function incorporated based systems appear to have fewer problems.
• Avoid any that alter the tear film stability on The reputation of so-called cold chemical systems
lens insertion has yet to be ‘restored’. Efron (1998) believes that
97400-244S.PPT

the use of care systems with integral re-wetting or

7L497400-244 lubricating agents help alleviate dry eye symptoms.
The use of contact lens re-wetting drops (also
359 referred to as confort drops, lens lubricant, lens
lube, artificial tears for lens wearers, etc.) has been
RE-WETTING DROPS shown to be beneficial for about five minutes
• Benefits last only up to 5 minutes (Golding et al., 1990) in that they stabilized the pre-
- tear film stabilized for 5 min lens tear film for this period of time. Surprisingly,
- n Tear Evaporation Rate (TER) normal saline performed similarly in their study and
- no effect on lens hydration the levels of ‘relief’ provide by saline was also
• Normal saline has a similar effect similar to that provided by the special formulations.
• Use unpreserved products where possible Golding et al. concluded that re-wetting drops were
- usually preferred by users not a suitable basis for prolonged symptomatic
- BAK, etc. injurious to the cornea relief.
- long-term effects of preservatives on the
cornea?
None of the solutions tested by Efron et al (1991)
97400-369S.PPT
appeared to alter the hydration characteristics of the
7L497400-369 lenses.
Tomlinson and Trees (1991) demonstrated that
both BAK (0.004%) and chlorbutanol (0.5%) did not
affect the stability of the tear fluid layer, as indicated
by an unaltered tear evaporation rate (TER).
Trees and Tomlinson (1990) compared the TER
following the addition of saline and two artificial tear
preparations. All three solutions increased the TER.
However, there was no convincing evidence that
the return to baseline values was faster with the
artificial tears.
Efron (1998) surmised that the perceived benefits of
re-wetting drops whose effects exceeded five
minutes, may be due to a placebo effect.
Caffery and Josephson (1990) evaluated a range of
re-wetting drops and found little difference between
products, although a preference for preservative-
free products was expressed.
As dry eye is usually an ocular surface disorder it is
uncommon to find modern products that use
preservatives at all, or use preservatives with known
cytotoxic effects. These are especially important
issues for dry eye cases as there is a strong
possibility that extended periods of use, or even life-
long usage, is a possibility. Because benzalkonium
chloride (BAK) is known to produce problems of
lens wetting, and be injurious to the cornea, any
products containing BAK should be avoided (most
modern formulations do not contain BAK). Kramer
et al. (1999) showed that intensive dosing of the eye
with artificial tear solutions causes epithelial
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 Module 7: Contact Lens-Related Ocular Complications

damage. However, there was less damage when

the solution used did not contain BAK.
Tsubota et al. (1999) demonstrated that a
petrolatum-based calcium ointment applied to the
skin of the lower lid improved the symptoms, tear
dynamics, and ocular surface staining in dry eye
significantly. They believed that some of the effect
may have been due to the lipids in the petrolatum
vehicle.
360 Management of Dry Eye in Contact Lens
Wearers
MANAGEMENT OF DRY EYE IN
CONTACT LENS WEAR Should a contact lens wearer develop a dry eye, or
• If a CL wearer develops a dry eye, or start reporting symptoms of eye irritation and
reports symptoms of eye irritation or discomfort, a decision is required on whether lens
discomfort: wear should cease, and what tests should be
– assess case-by-case performed to ascertain whether or not the contact
– is lens wear to cease? lenses are the cause.
– will comfort drops suffice ? Cessation of lens wear in isolation is inadequate
because a marginally dry eye may be the underlying
– should a different lens/wear
problem. While no lens wear may resolve the
modality/schedule be trialled ?
97400-247S.PPT
immediate problem of symptoms, it cannot be
claimed that lens wear was the cause.
7L497400-247 Management of this problem is uncertain and
difficult (Farris (1987). Farris also suggests the
trialling of different types of lenses, although he
361
admitted that no specific lens type has been shown
MANAGEMENT OF DRY EYE IN to be especially beneficial.
CONTACT LENS WEAR
• If a CL wearer develops a dry eye, or Finnemore (1990) asserted that dry eye sufferers
reports symptoms of eye irritation or should not be excluded automatically from contact
discomfort: lens wear and that contact lenses pose little risk in
– is the eye ‘marginally dry’ ? most cases. If an underlying cause can be
– what tests are appropriate? identified, a solution to the problem can often be
found. He claimed that the use of blinking
– regardless, management is difficult
exercises, re-wetting drops, or lens design/material
• If ocular surface is compromised – cease changes may often be all that is required. This
wear
general philosophy was also postulated by Farris
• SCLs pose a greater risk (1987) who suggested a case-by-case approach be
97400-391S.PPT

taken to decide those dry eye sufferers who might

7L497400-391
be suitable contact lens candidates.
A counter view was presented by Lemp (1990) who
362 stated that SCL wearers were at greatest risk
because of the poorer post-lens tear circulation.
DRY EYE & CONTACT LENS WEAR:
This resulted in greater risks of conjunctivitis,
MANAGEMENT
blepharitis, and sterile corneal infiltrates.
• Most management is the same as for
Many of the treatments and strategies used to
non-wearers resolve or reduce dry eye in non-contact lens
wearers can also be applied to lens wearers with
• Permanent punctal plugs? the probable exception of solutions, e.g. artificial
tears that are preserved with chemical entities that
• Refractive surgery ??? are incompatible with contact lens materials.
Punctal plugs (see earlier) are also a viable option.
• More frequent after-care is essential
Lowther and Semes (1995) inserted temporary
dissolving punctal plugs in symptomatic SCL
97400-243S.PPT

7L497400-243 wearers uniocularly, and performed a ‘sham’

procedure in the contralateral eye. Both eyes
‘improved’ again, suggesting psychological
overtones to the steps taken to alleviate their
problems (a placebo effect?). However, Slusser
and Lowther (1998) found a lessening of the
benefits over time with plugs, leading them to
440 IACLE Contact Lens Course Module 7: First Edition
 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

363 suggest the concurrent use of rewetting drops to

further increase the benefits of the plugs.
DRY EYE & CONTACT LENS WEAR
MANAGEMENT
After commencing lens wear, additional treatment
may be required such as the use of artificial tears or
• Some treatments have a placebo effect punctal plugs to increase the tear volume and
• Punctal plugs o 35% n in comfort, but... improve lens wettability. Nilsson and Andersson
- benefits pover time
(1986) suggested enzymatic cleaners, frequent lens
replacement, and loose fits as ways of lessening
• Use cleaner if beneficial, however... discomfort and minimizing problems associated with
- frequent replacement, or more frequent lens deposits.
replacement, is necessary to prevent
Toda et al. (1996) evaluated the role
deposits
PhotoRefractive Keratectomy (PRK) might have in
treating highly myopic eyes that were intolerant of
97400-370S.PPT

7L497400-370 contact lenses because of dry eye, with specific

364 reference to the visual outcome and epithelial
wound healing. They concluded that PRK was a
MANAGEMENT OF DRY EYE IN viable treatment option but they expressed
CONTACT LENS WEAR reservations about predictability, and the possibility
• After recommencing CL wear, additional of complications.
‘treatment’ may be required. ‘Treatment’
may include: Regardless of the cause, both the practitioner and
– artificial tears the wearer must accept that more frequent after-
– punctal plugs care visits and a more concerned attitude by both
– enzymatic cleaners parties, are required if lens wear is to continue, or
– frequent lens replacement the possibility of more serious problems is to be
– a looser fit reduced.
– more frequent after-care visits
97400-392S.PPT

7L497400-392

365 Preventing Problems Associated with Contact

Lens Wear in Dry Eye Patients
PREVENTING PROBLEMS
A facetious answer to this issue is to cease contact
• Identifying borderline contact lens candidates lens wear altogether. However, the motivation of a
wearer with a high Rx in social or sporting
- predictive testing circumstances is very high, and many persevere
- history against odds that, to many, would be overwhelming.
• Treating conditions in advance Compounding the problem is the variation of
symptoms that occurs across a wearing period, e.g.
- meibomitis/blepharitis
most SCL wearers report worsening symptoms
- underlying cause towards the end of their normal wearing period.
97400-72S.PPT
This can lead some wearers to exceed prudent
levels of discomfort because the lens is ‘better’ at
7L497400-72 other (earlier) times, therefore the lens must be
acceptable. If it is accepted that symptoms are
indicative of untoward effects on the eye, this
366
exceeding of ‘limits’ can lead to deleterious effects
on the external eye.
PREVENTING PROBLEMS
• Tear supplements The practitioner’s major concern with dry eye
patients should be to prevent the occurrence of
• Punctal plugs problems both before and during wear.
• Adapting to circumstances
Identification of the higher risk candidates during
- patient expectations history taking and preliminary testing helps to
- environmental changes minimize potential adverse effects of wearing
• Lens replacement contact lenses.
- optimal schedule In many cases, the marginal dry eye patient should
97400-73S.PPT
be treated in advance of lens fitting. Conditions
such as Meibomian gland disease and blepharitis
7L497400-73 can cause contact lens-associated problems if they
are allowed to progress unchecked.

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367 If MGD is the root cause of dry eye problems in

contact lens wear, the only common forms of
PREVENTING PROBLEMS treatment are lid scrubs, hot (or hot and cold)
Dry eye patients should have reduced compresses, and Meibomian gland expression.
CL wearing time expectations. Even if they do not eliminate the problems, they can
be expected to bring some relief.
• Consider:
If blinking and completeness of blinking are an
– part-time wear, and/or... issue, Collins et al. (1987) found that blink patterns
– shorter wearing periods in SCL wearers can be altered with training. Many
practitioners find only limited success with their own
– CL wear as being need-driven rather training endeavours.
than routine In most cases, a dry eye patient wearing contact
97400-393S.PPT

lenses should have reduced expectations in terms

7L497400-393 of lens wearing time. Part-time, or reduced wearing
time, may be required to maintain ocular health and
to maximize contact lens performance and patient
satisfaction. Compromises between the effects of
continued lens wear, and cessation of lens wear
are, obviously, reduced lens wearing times, fewer
days of lens wear per week (or intermittent, need-
driven lens wear), or both.
368 Contact Lens Problems in Existing Dry Eye
Numerous problems can occur when fitting a dry
CL PROBLEMS IN EXISTING DRY EYE eye patient with contact lenses. More advanced
• Increased risk of infections cases of dry eye are a contra-indication for lens
fitting due to the high risk of further compromising
due to poor tear exchange
ocular health.
• Lens fitting problems Potential problems with contact lens wear include:
- decentration x Increased risk of ocular infection due to poor
- excess movement
tear exchange, increased cellular exfoliation,
and reduced antibacterial protein levels in the
- adherence tear film.
97400-66S.PPT

x Upper palpebral conjunctival changes such as

7L497400-66 contact lens-associated papillary conjunctivitis
(CLPC).
369 Potentially, a problem confronting contact lens
wearers is MGD, especially in an aging population.
CL PROBLEMS IN DRY EYE

• Photophobia

• Decreased wearing time

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370 After-Care of the Dry Eye Contact Lens Wearer

DRY EYE & CONTACT LENS WEAR: PLTF NIBUT determination should be used
AFTER-CARE routinely in all after-care visits. As a NIBUT
• PLTF NIBUT should be part of the after-care determination depends on close observation of the
routine for every visit behaviour of the tear film, more than one
• Changes from baseline (@ delivery) indicate a determination should be made.
loss of lens hydrophilicity
• Possible causes of loss of lens hydrophilicity:
Changes from the trial fitting data probably indicate
- deposits
a loss of hydrophilicity of the lens front surface.
- scratches/surface damage
Improvements are not expected, only decreases.
Losses of wettability are attributable to deposits,
- interaction of lens with lens care products
scratches, and possibly lens care product chemistry
• Polish (RGPs) or replace (SCLs & RGPs) ?
97400-242S.PPT
interacting with material surface chemistry.
7L497400-242 These alterations can affect wearer comfort
adversely, and may induce lid changes and lid
reactions.
371 Any PLTF NIBUT decreases approaching 25% are
DRY EYE & CONTACT LENS WEAR: an indication that hydrogel lens replacement is due
AFTER-CARE (Guillon and Guillon (1993). If RGP lenses are
being worn, a surface polish, at the very least, is
• Staining (sodium fluorescein, Rose advisable. If this is not possible, lens replacement
Bengal, Lissamine Green, etc.) may be required. If the tear film stability (as
- present?
measured by BUT) does not recover rapidly
following lens removal (<10 minutes Kline and
– location(s) DeLuca [1975], <26 minutes Faber et al. [1991]) the
– extent prognosis is also not good because the tear film
problems are obviously not only contact lens-based.
– severity
97400-374S.PPT
Staining, using the agents detailed elsewhere in this
lecture, is also advisable as it will disclose valuable
7L497400-374 information about the extent and severity of
damage, if any, sustained by the ocular surfaces.
372 Scratches and deposits are also more likely to
produce an irregular PLTF that ruptures over the
DRY EYE & CONTACT LENS WEAR:
whole of the lens surface rather than in initially
AFTER-CARE: CEASE WEAR?
• Patient motivation isolated spots as occurs with a new lens.
• Comfort
• Tear film stability Ultimately, a decision to recommend cessation of
• Ocular surface condition lens wear may be required. Some of the factors
• Wearing time required (expectations) that warrant consideration are listed in the slide
• Options remaining, e.g.:
- ' lenses/replacement rate/LCPs opposite.
- ' environment
- punctal plugs
- re-wetting drops/artificial tears
- blinking exercises ?
- treatment of underlying condition(s)
- other ? 97400-375S.PPT

7L497400-375

373 Dry Eye and Contact Lens Wear: Prognosis

EXISTING DRY EYE & CL WEAR: “Is dry eye a contra-indication to contact lens wear?”
PROGNOSIS asked Farris (1987). While acknowledging that dry
• Does dry eye (DE) contra-indicate contact lens eye wearers must accept a higher level of risk, he
wear?
- the experts are divided ! supported a case-by case approach depending on
• DE may increase the risks aetiology, the response of the eyes, and the
- nrisk of infection individual to contact lens wear.
- nexfoliation
- p protein levels (pantibacterial) Mackie (1985) asserted that, as there were
• nrisk of lens fitting problems considerable dangers from wearing contact lenses
- decentration in dry eye in the presence or absence of
- excessive movement conjunctival and corneal changes, the decision to
- adherence
97400-241S.PPT
go ahead should not be taken lightly, and adequate
provision for close follow-up and after-care be
7L497400-241 made.

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 Module 7: Contact Lens-Related Ocular Complications

374 It is difficult to make a case for contact lens wear as

dry eye therapy. This is because they remain an
EXISTING DRY EYE & CL WEAR unproven treatment for dry eye and, because the
PROGNOSIS cases for which a contact lens may be beneficial
• n risk of conjunctivitis & asymptomatic (for their bandage effect) are uncommon. The latter
infiltrates (AI)
usually involve a serious underlying condition (e.g.
- compromised ocular surface
recurrent corneal erosions) making an element of
- compromised mechanism
risk acceptable in light of the seriousness of the
- p tear exchange
underlying condition.
• n risk of CLPC
- n front surface deposits If the difficulties experienced are based on the
- ptear lubricity
lenses, lens care, or a combination of these factors,
- nlens movement
the prognosis is good because these problems can
97400-372S.PPT
be solved.
7L497400-372 If the problems relate to a solvable underlying
problem or disease, the prognosis is also good, e.g.
MGD.
375
If the dry eye is due to autoimmune diseases,
EXISTING DRY EYE & CL WEAR lacrimal gland infiltration, burns, etc. the prognosis
PROGNOSIS for ongoing contact lens wear is poor.
• n risk of symptoms
- irritation
The overlap between dry eye as an eye condition,
and dry eye in a contact lens wearing context is
- photophobia
proof that it is impossible for a contact lens
- p wearing time practitioner to fit contact lenses exclusively, to the
• Patient counselling exclusion of all other aspects of eyecare.
- possible consequences
It is always desirable to end on a positive note,
- importance of compliance
instead this lecture will end with an observation.
- expectations of lens wear
97400-373S.PPT
Many contact lens practitioners excuse their own
7L497400-373
lack of ‘leading by example’, i.e. not wearing contact
lenses themselves, with a statement to the effect
that they have dry eyes, and contact lens wear is
376 too problematic for them. Based on the number of
such statements heard, contact lens practitioners
EXISTING DRY EYE & CL WEAR worldwide must have the highest incidence of dry
PROGNOSIS eye of any occupational group. This seems unlikely.
• Prognosis should be based on a case-by-case
assessment
• If problems are lens, lens care, or wear modality
– they are probably soluble
• If problems are an underlying condition, e.g.
MGD, prognosis may be good
• If the problem is autoimmune based – prognosis
is probably poor
• If BUTs are slow to recover after lens removal –
prognosis is also poor
97400-371S.PPT

7L497400-371

444 IACLE Contact Lens Course Module 7: First Edition

 Lecture 7.4: Diagnosis and Management of Dry Eye in Contact Lens Wear

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