OPHTHALMOLOGY

Cavendish
Publishing
Limited

London • Sydney
 TITLES IN THE SERIES

ACCIDENT AND EMERGENCY

CARDIOLOGY

DENTISTRY

EAR, NOSE AND THROAT

GENERAL PRACTICE

MEDIATION AND ARBITRATION

NEUROLOGY

OPHTHALMOLOGY
 OPHTHALMOLOGY

Emanuel Rosen, BSc, MD, FRCSE, FRCOphth, FRPS,

Consultant Ophthalmic Surgeon
William Rosen, BA, Solicitor

SERIES EDITOR
Dr Walter Scott, LLB (Hons),
MBBS, MRCGP, DObstRCOG

Cavendish
Publishing
Limited

London • Sydney
First published in Great Britain 1997 by Cavendish Publishing Limited, The
Glass House, Wharton Street, London WC1X 9PX.
Telephone: 0171–278 8000 Facsimile: 0171–278 8080

© Rosen, E and Rosen, W, 1997

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, electronic,
mechanical, photocopying, recording or otherwise, without the prior
permission of the publisher and copyright owner.

The right of the authors of this work has been asserted in accordance with the
Copyright, Designs and Patents Act 1988.

Any person who infringes the above in relation to this publication may be
liable to criminal prosecution and civil claims for damages.

Rosen, Emanuel S
Ophthalmology for lawyers—(Medico-legal practitioner series)
1. Ophthalmology—Law and legislation—England
I. Title
617.7’0024344

ISBN 1-85941-211-4

Printed and bound in Great Britain by

Biddles Ltd, Guildford and King’s Lynn
 We dedicate this volume to the late Lionel Rosen
(1907–77)—a much respected lawyer and author,
and always a patient and encouraging father and
grandfather.

And to June, Caroline and Edward.

 FOREWORD

Those who have shown an interest in the ‘medico-legal practitioner’s series’

may like to learn something about its origins and the history of its development.
With this objective in mind I will devote a few moments to the past and I will
then turn to the future which is, after all, even more important for us.
I first conceived the idea of such a theme in the Summer of 1994. By that
stage I had been preparing reports for lawyers on cases of alleged medical
negligence for about five years. I had also been looking at other doctors’ reports
for the same length of time and it was becoming increasingly apparent to me
that one of the lawyers’ most difficult tasks was to understand the medical
principles clearly. To be fair to the lawyers, there were some doctors who did not
always make matters very clear. This, coupled with the difficulty which many
doctors have in understanding the legal concept of negligence and related topics,
merely served to compound the problem.
It therefore occurred to me that a possible solution to the difficulty would be
to develop some material on medical topics written by doctors who had a
particular interest in the medico-legal field. The authors would require at least
four attributes. First, they would have to be specialists in their own field. Secondly,
they would need the ability to explain their subject to non-medical readers in
clear language that was easy to follow. Put another way there was no case for
writing a medical textbook for their students or colleagues. Thirdly, they would
require a fair amount of experience in medico-legal reporting, analysis of cases
and dealing with lawyers who were defending or advancing cases. This would
give them an understanding of how the lawyer’s mind works and an appreciation
of the medical areas which can cause difficulty in practice and where accidents
can happen. There would be a contrast with medical books where the emphasis
is on the diseases which most commonly present to the doctor. Fourthly, the
authors would need the ability to work in harmony with a series editor who
was anxious to achieve some degree of uniformity across the whole range of the
material.
Having identified these four points as being desirable characteristics of the
potential authors the next step was to find a publisher who would be sufficiently
interested to give the project the support it needed. This was to be no small task
and was likely to involve a very long-term commitment because, after the initial
launch, it was inevitable that much more work would be required by way of
future editions and additional titles. I was most fortunate to be dealing with
Cavendish Publishing in connection with my own book, The General Practitioner
and the Law of Negligence, and I am pleased to say that they seized this new idea
with the utmost enthusiasm. At last I thought that the ‘medico-legal practitioner
series’ would become a reality.
It then only remained to find the authors, commission the work and wait for
the results. It was at this point, however, that I began to realise that I was still
only at the very beginning of my task. Eventually, however, after numerous
discussions with various people a team materialised. When the early chapters

vii
 Foreword

of the first books began to arrive it was starting to look as though we really were
going to have something which was quite unique. When the final manuscripts
arrived my confidence increased still further. More than two years after my initial
plans the first set of books has become available and the dream has turned into
reality.
This, then, is how the project came into being but it must be emphasised
that, in a manner of speaking, we have really only just got ourselves started. For
the series to thrive it must be flexible and respond to the needs of its users. It
must adapt to medical developments and legal changes. Clinical subjects are a
primary consideration but it is my firm intention to expand the series to involve
other areas of interest. Indeed the first non-clinical title should appear almost as
soon as the initial set becomes available. On a more long term basis, I would like
the series to cover every field of expertise that is of concern to the medico-legal
practitioner.
Uniformity of approach and clarity of presentation must be hallmarks of the
individual titles but the series as a whole must be independent and objective. If
we can aspire to these criteria we should achieve a fair measure of success in
assisting our readers to give good advice to their clients.
It remains for me to express my gratitude to all the authors and to the
publishers for their cooperation. In another kind of way I will be equally grateful
to all our readers for placing their reliance on us and for sharing our
optimism.
Walter Scott
Series Editor
Slough
August 1996

viii
 PREFACE

This is not intended to be a textbook of ophthalmology but rather, as its title

implies, a guide for the layperson to the structure, function and malfunction of
the eye. Our concern has been to provide an overview of ophthalmic anatomy
and pathophysiology so that medico-legal ophthalmic problems can be
understood. Whether it is personal injury or alleged medical negligence, the
lawyer needs the feel of the problem to elaborate a case. When pathology is
considered, the emphasis is centred on those structures within the eye or those
disorders which figure most frequently in the legal context. Issues of lesser
profundity are considered more simply, or in the glossary only, to provide a
starting point for comprehension. The option remains to consult the vast
ophthalmic literature for greater detail and current practice which, in any case,
is the province of the medical expert who will be called upon for opinion. This
text is further intended to add to the understanding of medical ophthalmic reports
by providing essential background information.

Emanuel Rosen
William Rosen

ix
 ACKNOWLEDGMENT

We are indebted to Mrs Elizabeth King for her patient

transcription of much of the text and her forbearance in
translating, amongst other things, a medical
practitioner’s traditionally-difficult handwriting, an
unfortunate condition which has proved to be hereditary.

xi
 CONTENTS

Dedication v
Foreword vii
Preface ix
Acknowledgment xi
Table of figures xvii
1 INTRODUCTION 1
Medical negligence and the medical report 3
2 OVERVIEW OF THE EYE 7
3 OCULAR STRUCTURES AND THEIR FUNCTION 17
Eyelids 17
The ocular surface 18
The cornea 18
Scleral coat of the eye 20
Uvea 21
Iris 21
The pupil 21
Aqueous humour, trabecular meshwork and the ciliary body 22
The crystalline lens 23
Zonular fibres 25
Vitreous body 26
The retinal vascular circulation 27
The retinal pigment epithelium 27
Retinal pathophysiology 29
The retina 29
Choroid 31
Optic nerve head (optic disc) 32
4 HISTORY OF THE OPHTHALMIC DISORDER—SYMPTOMS 37
Clinical history 37
Ophthalmic symptomatology 38
5 CLINICAL EXAMINATION AND INVESTIGATION OF
THE EYE AND VISION 41
External examination 41
Anterior chamber 41
Gonioscopy 41
Ophthalmoscopy 42
Visual acuity 42
Clinical measure of visual acuity—is it a reliable guide
to what a patient can see? 45

xiii
 Ophthalmology

Glare visual acuity test 47

Contrast sensitivity 47
Visual field examination (spatial projection of vision) 47
Ocular alignment and motility 49
Examination of the pupil 49
Intra-ocular pressure measurement (tonometry) 50
Colour vision testing 51
Pachymetry 51
Specular microscopy 51
Ophthalmic photography 52
Ultrasonography 53
Refraction 53
Corneal topography 55
Electro-diagnosis 57
Magnetic resonance imaging (MRI) 59
Computed tomography 59
6 VISUAL DEFECTS AND BLINDNESS 61
Major causes of blindness 64
Eye assessment/examination 65
General aspects of visual development and visual defects 66
7 AGEING, OPTICS AND THE EYE 69
Introduction 69
Visual function and ageing 70
Repair and regeneration (healing processes) 70
8 OCULAR PATHOLOGICAL PROCESSES 71
Systemic approach to disease 71
Eye infections 74
Sterilisation 77
Disease classification 78
9 CATARACTS 81
Definition and overview 81
Prevention or therapy? 85
Congenital cataract 96
10 RETINAL DETACHMENT 99
Treatment in historical perspective 103
Macular detachment 103
11 MACULAR DEGENERATION 105

xiv
 Contents

12 GLAUCOMA 111
Acquired glaucomas 113
Diagnosis and screening of the glaucomas 121
Referral—the roles of optometrist, GP and ophthalmologist
in glaucoma 123
Treatment overview 124
Medical management of COAG 125
Treatment compliance 127
Lasers in the treatment of glaucoma 128
Surgical treatment of glaucoma 129
Glaucoma in recent historical perspective 131
13 DIABETIC EYE DISEASE 133
Definition 133
Diabetic cataract 140
14 RED EYES 143
Overview 143
Anatomy 143
Pathophysiology 144
Uveitis 147
Endophthalmitis 149
15 TRAUMA 153
Eye injuries 153
Specific injuries 154
16 PAEDIATRIC AND DEVELOPMENTAL PROBLEMS 165
Overview of paediatric ophthalmology 165
Ocular pathology in children 165
17 REFRACTIVE SURGERY 173
Definition 173
Refractive surgery 178
18 MISCELLANEOUS OPHTHALMIC DISORDERS OF
OCCASIONAL MEDICO-LEGAL INTEREST 193
Corneal opacification 193
Headache and the eyes 194
Sudden and unexplained loss of vision 196
Hemianopia 200
Lasers in ophthalmic practice 200

xv
 Ophthalmology

APPENDICES
Duties of health care professionals in ophthalmic practice 203
Standards of vision for various occupations and activities 211
Abbreviations and notations in common usage by ophthalmic
medical practitioners and optometrists 245

Glossary 253
Bibliography 285
Index 287

xvi
 TABLE OF FIGURES

Chapter 2
Figure 1—Diagram of the front view of the eye showing the anterior landmarks
of lids and eye.
Figure 2—Cross-section of the eye globe.
Figure 3—Cross-section of an eyelid.
Figure 4—Side view of the eye within the orbit, illustrating its relationship to
the supporting and surrounding structures, including the paranasal sinuses.
Figure 5—A view behind an eye showing its attachments visible in the eye socket.
The optic nerve is surrounded by the extra-ocular muscles and nerves within
the bony walls of the orbit.
Figure 6—Clinical photograph of the cornea, the anterior chamber containing
the aqueous humour and the crystalline lens by special (Scheimpflug)
photography, showing the anatomical relationships and the nuclear zones
within the crystalline lens.
Figure 7—Diagram of the structures in the angle of the anterior chamber.
Figure 8—Retinal diagram illustrating the relationships at the posterior pole of
the eye—especially the optic nerve head, macula, fovea, retinal arteries and
veins.
Figure 9 —The peripheral, visual field.
Figure 10—The optic nerve pathways from retina to visual (occipital) cortex,
showing the crossing over of the nasal retinal fibres from each eye to the
opposite pathway in the optic chiasma.

Chapter 3

Figure 11—Chronic, open-angle glaucoma. Aqueous humour is produced

constantly by the ciliary gland and drained in equal amounts through the
trabecular meshwork in the angle of the anterior chamber. If less aqueous
humour is produced than is drained, the pressure will rise in the closed
globe of the eye. This imposes compression of the delicate optic nerve head
structures, resulting in their slow destruction if the pressure remains elevated
for a sustained period. In acute, closed-angle glaucoma, the pressure change
is dramatic, with corresponding vision loss.
Figure 12—Diagram of the crystalline lens.
Figure 13—A fluorescein angiogram of a normal retina but with a variation in
the usual vascular pattern. Note the tortuosity of the retinal arterioles. This
picture has no pathological significance but makes the point that no two

xvii
 Ophthalmology

retinas are alike. Understanding what is normal and what is pathological

requires an understanding of variations within the norm.
Figure 14—Cross-sectional, diagrammatic representation of the retinal structure
to illustrate the relationship of the rods and cones to the underlying retinal-
pigment epithelium and choroid, and their connections to the nerve fibres (1
million) which constitute the optic nerve.
Figure 15—Clinical (ophthalmoscopic) view of the optic nerve head showing its
boundaries (the edge of the retina) and the central retinal vessels
whichtraverse its substance to supply the anterior portion of the retina.
Thecentral pit in a healthy optic nerve head or disc is known as
thephysiological pit. In glaucoma, the central pit widens and deepens; this
is known as cupping of the optic nerve head, a key clinical sign in the
diagnosis of glaucoma.
Figure 16—The optic nerve head in a Negroid eye, where the heavily-pigmented
retina and choroid clearly demarcate the boundaries of the nerve head. The
neural rim, which is pink, contrasts with the physiological optic cup through
which the central retinal vessels emerge to branch onto the retina.
Figure 17—Histological (microscopic) cross-section of an optic nerve, showing
the bundled nerve fibres and the central retinal artery and vein passing
through the nerve.
Figure 18—The optic nerve head in a myopic (large) eye. In contrast to figure 19,
the fundus is lightly pigmented, a feature emphasised by the retinal stretching
which occurs in myopia. The retinal-pigment epithelium and retinal
tissues fall far short of the nerve head, giving a whitish halo around the disc.
Because of the transparency of the tissues, choroidal blood vessels in a very
different pattern to those of the retinal circulation can be seen in the
background.
Figure 19—Hypertensive papilloedema, with congested retinal veins, swollen
nerve head due to capillary congestion and small haemorrhages on the
surface.

Chapter 5
Figure 20—The Snellen visual acuity chart.
Figure 21—The Logmar visual acuity chart.
Figure 22—Bi-temporal hemianopia (demonstrated on a visual field chart) caused
by compression of the central fibres of the optic chiasma due to a pituitary
tumour.
Figure 23—An example of an incomplete homonymous hemianopia
(demonstrated on a Goldmann visual field chart); in fact, a ie loss of the

xviii
 Table of figures

lower left field of vision in each eye caused by a defect in the right optic
pathways from a stroke or cerebro-vascular accident for example.
Figure 24—Fluorescein angiography of the fundus of the eye. Figure 24 shows
the arterial phase. As the fluorescein dye appears in the retinal arteries, the
photograph shows them as white threads on a mottled background. The
mottling is due to a combination of fluorescein dye in the choroidal circulation
of the eye and the overlying, retinal-pigment epithelium, which is most
densely pigmented at the macula.
Figure 25—shows the venous phase. Within a second the dye has permeated the
retinal capillaries and is draining out of the eye through the retinal veins.
Consequently, all the retinal vessels (arteries, capillaries and veins) appear
white against the mottled background of choroidal fluorescence and
pigmentation.
Figure 26—Corneal topography. Shown is a black and white representation of a
colour-coded map of corneal shape and refractive power. It is an essential
precursor to refractive surgery and an invaluable tool for monitoring post-
operative progress and communication.

Chapter 9
Figure 27—A cataract is a clouding of the crystalline lens.
Figure 28—A cataract after extraction is replaced by an intra-ocular lens implant,
here seen encased in the crystalline-lens, capsular bag which is left in situ at
surgery to sequester the implant from other ocular tissues.
Figure 29—Cystoid macular oedema (CMO), a complication of low-grade,
postoperative inflammation following cataract surgery. The retinal capillaries
in the central retina develop a temporary incontinence in response to anterior-
segment inflammation and the fluid-leakage pools in the retina to inflate
microcystic spaces, which are unequivocally identified clinically by
fluorescein angiography. The dye stains the fluid in the microcysts which
appears as a mottled, white fluorescence.

Chapter 10
Figure 30—A fluorescein angiogram of a detached retina lower aspect. The in-
focus, out-of-focus aspect of the retinal blood vessels indicate that the retina
is elevated by sub-retinal fluid. In the lower part of the picture four retinal
holes are demonstrated by the absence of any blood vessels. It is through
these holes that fluid percolates from the vitreous humour underneath the
retina to cause the physical detachment. The initiating event is the formation
of holes in the retina, usually secondary to retinal degeneration which is
more common in myopic (large) eyes.

xix
 Ophthalmology

Chapter 11
Figure 31—An example of a fluorescein angiogram of the retina. This case
illustrates a detachment of the retinal-pigment epithelium, giving a blister-
like elevation of the macula. The fluid in the detachment stains with
fluorescein to identify its precise location. Retinal-pigment, epithelial
detachment is one component of macular degeneration syndromes.
Figure 32—A fluorescein angiogram of a right eye with early, age-related
degeneration, characterised by atrophy of pigment epithelium with pigment
migration and pigment clustering, seen contrasted against the background
fluorescence of the choroid. The inference from an appearance like this
is that the rods and cones which are the light-sensitive elements of the
retina will be decaying, and vision reserves and acuity of the eye will be
limited.
Figure 33—The fellow left eye of the same patient in figure 32 with a disciform
(disc-like) scar at the macula which has end-stage, age-related degeneration,
ie no residual central vision. The eye still maintains peripheral vision which
is usually not compromised by the age-related degeneration affecting the
central retina.

Chapter 12
Table 1—The five groups of drugs used in the medical management of glaucoma.

Chapter 13

Figure 34—Red-free photograph of proliferative diabetic retinopathy showing

a cluster of new vessels (neo-vascularisation) emanating from the retina and
causing a sub-hyaloid haemorrhage (between retina and the posterior hyaloid
membrane bounding the vitreous humour). The haemorrhage into a ‘free
space’ shows a flat level where the red blood cells have settled out of the
serum under the influence of gravity.
Figure 35—Fluorescein angiogram of the area seen in figure 34 after focal
destruction of the new vessels (neo-vascularisation) by argon-laser therapy.
Neo-vascularisation occurs because of damage by the diabetic process to
existing retinal blood vessels. Note the area adjacent the laser-treated area
where closure of retinal capillaries and distortion of arteries and veins is
apparent. These areas were obliterated by further laser therapy to stabilise
the retinopathy.

xx
 Table of figures

Chapter 16
Figure 36—Pseudostrabismus, the appearance in this case of a convergent squint
when observing the white of the eyes. But note the corneal reflections which
are equal and central, indicating that the squint is an illusion, or
pseudostrabismus caused by the fold of skin obscuring the white of the eye
at its inner aspect (epicanthus).

Chapter 17

Figure 37—Optical ray diagram to indicate the focussing of parallel rays of light
onto the retina (clockwise from above): in an emmetropic eye; in front of the
retina in a myopic eye; and behind the retina in a hyperopic eye.
Figure 38—Diagram showing the principle of astigmatism within the cornea.
Regular astigmatism shows two principle meridia measured by keratometry
or corneal topography: one steep and one flat meridian. Diagrammatically
this gives the cornea the shape of a rugby ball, seen here lying on its side. Its
effect is to magnify the image in the vertical plane and reduce its size in the
horizontal plane. By equalising the radii of curvature of the principal meridia,
the cornea appears spherical when the image magnification is equalised to
give the observer normally-proportioned images.
Figure 39—Refractive surgery landmarks on the cornea. Note that the geometric
centre of the cornea does not correspond with the visual axis; the optical
zone of the cornea is the important zone whose clarity is to be preserved in
cataract surgery whilst influencing a change of shape (refraction).
Figure 40—Diagram illustrating the principle of radial keratotomy. Micro-
incisions into the cornea at a depth of 90% are placed around the central
optical zone to effect flattening of that zone and correct myopic, refractive
errors. Peripheral, corneal incisions cause a microscopic gap in the incisedarea
of the cornea due to the effect of intra-ocular pressure. Accordingly,the
corresponding effect on the central cornea is for it to flatten, ie its radius of
curvature being reduced for the correction of myopia.
Figure 41—Computer-derived plan for the incisions in radial keratotomy (usually
four or eight equally-spaced incisions). Note the clear, central, optical zone,
ie the eye is not looking through the operated area; of PRK.
Figure 42—Diagram to illustrate the principle of arcuate keratotomy. Arcuate
micro-incisions are placed into the cornea at a depth of 60% and a diameter
of 7mm, well away from the optical zone but on the steep meridian of an
astigmatic cornea to effect reduction of the astigmatic error. Arcuate incisions
are titrated according to the refractive defect. The incisions typically leave a
central clear zone of 7mm.

xxi
 Ophthalmology

Figure 43—Operation plan for combined radial and arcuate keratotomy to

neutralise a refractive error of myopic astigmatism.
Figure 44—The pre-operative, corneal topography map shows the ‘bow tie’
pattern of the astigmatism. The post-operative map shows a spherical, corneal
shape, ie no astigmatism. The difference map shows the surgical effect
achieved by a combination of arcuate and radial incisions into the cornea
(AK and RK).
Figure 45—Photorefractive keratectomy (PRK) is effected by ablating the optical
zone of the cornea. Any opacification or irregularity will result in degradation
of vision.
Figure 46—Lasik: laser-assisted intrastromal photorefractive keratectomy
(keratomileusis). A 160µ flap is raised in the cornea. Excimer-laser ablation
of the bed is performed before the hinged flap is replaced. Vision is restored
within an hour or two and stabilises rapidly. This technique is superseding
corneal-surface, excimer-laser keratectomy because it avoids the variable-
surface healing properties of the cornea which may blight the outcome
of PRK. The cross-sectional diagram shows the internal ablation under a
160µ 8mm corneal flap which is cut surgically by using an automated
microkeratome. The ‘flap’ adheres back onto the cornea without the
aid of sutures; within a few hours it may be difficult to detect the surgical
site.
Figure 47—Corneal topography—a method of mapping corneal shape, curvature
and refractive power according to the mathematical algorithms used to
convert the data obtained by video capture of a reflected image of a series of
illuminated rings (Placido’s disc) from the target cornea. Each of the 360° of
each ring is measured for radius of curvature and the whole data is integrated
to yield a ‘computerised map’ of the cornea. In this example, a cornea before
and after Lasik application is shown, together with a difference map to
illustrate the surgical effect. Normally there is numeric data shown adjacent
the map, which utilises a colour-coding system for radius of curvature to
enable easier interpretation. Note the symmetrical flattening of the central
cornea.
Figure 48—Corneal refractive surgery by the intrastromal corneal-ring segments
(ICRS), which effects a flattening of the optical zone of the cornea. The
intrastromal corneal ring (ICR™) consists of two 150° segments of a cone
which are implanted at two-thirds depth in the cornea around an 8mm clear
opticalzone. The ring is the only adjustable and reversible refractive
procedure for the correction of myopia. It underwent final clinical trials in
1996.
Figure 49—The ICR™ in profile within the cornea to illustrate how the thickness
of the ring elevates that portion of the peripheral cornea, causing an arc-
shortening effect to flatten its centre (hammock effect).

xxii
 Table of figures

Table 2—Refractive surgical procedures.

Table 3—Problems which can be caused by PRK.

Chapter 18

An inferotemporal-branch, retinal-vein occlusion in a patient with hypertensive

retinopathy, ie raised systemic blood pressure.
Figure 50—a black-and-white reproduction of a red-free photograph, shows
bleeding in the lower temporal quadrant of the retina congested by its
interrupted venous drainage.
Figure 51—a fluorescein angiogram, demonstrating blood-vessel perfusion or
failure, with the incontinence of congested vessels to the injected dye
fluorescein appearing white.
Figure 52—Papilloedema and a secondary cancer of the breast which has lodged
in the choroid of this eye (white area). This patient has papilloedema (swelling
of the optic nerve head) as a consequence of an intracranial, space-occupying
lesion, another metastasis from the breast carcinoma. This is a terminal
situation.

xxiii
 CHAPTER ONE

INTRODUCTION

Ophthalmology is that portion of the medical spectrum concerned with the eye
and related structures in health and disease. It combines both medical and
surgical skills. In the UK its structure within the National Health Service (NHS)
is the same as other specialities, with the backbone of the system being the
consultant ophthalmologist of which there are currently about 650. They are
supported in clinical practice by a variety of medical assistants and paramedical
personnel.
All consultant ophthalmologists are appointed competitively, having
acquired the necessary training and certification (which is currently in a state of
flux, with European certification not quite in accord with UK requirements).
Training of ophthalmologists (ophthalmic surgeons) is undertaken in approved
hospital departments. Consultant ophthalmologists are now required to
undertake approved, continuing medical education (CME) supervised by the
Senate of Royal Colleges. From 1996 this has become a new requirement for
continuing in practice.
Ophthalmology, like many medical and surgical specialties, has advanced
rapidly in its capabilities during the past generation, taking advantage of
technological evolution. Many conditions considered untreatable only a few years
ago are now either preventable or curable. Practice of ophthalmology is therefore
in a constant state of transition as the era of the general ophthalmologist gives
way to the higher-quality services provided by subspecialists. Defined areas of
sub-specialisation within ophthalmic practice include vitreo-retinal surgery,
retinal medicine, ocular motility and neuro-ophthalmology, paediatric
ophthalmology, glaucoma, oculo-plastic and orbital disease and, perhaps more
controversially, the practice of cataract and refractive surgery.
Concentration of effort and the higher-volume exposure to special areas of
practice brings greater depth of experience and insight into medical and surgical
problems. Accordingly, hospital ophthalmology is being increasingly organised
to incorporate a primary care system that directs the presenting problem into
the specialist area for management. However, this approach to ophthalmic
practice is in a state of transition, with the change being resisted by some while
being welcomed by others.
In a medico-legal context this background information should be of value,
enabling each issue to be placed in recent historical context. The major question
to be answered is—what constitutes a reasonable body of medical opinion? Is it

1
 Ophthalmology

the management provided by a general ophthalmologist or the higher standard

achieved by the sub-specialist, between which there may be significant
differences? Did the standard of treatment fall below the standard of a reasonably
competent practitioner in the relevant field at the relevant time?
It is a defence to an allegation of professional negligence to show that a
reasonable body of reputable medical opinion in that field would have carried
out the same investigations and or treatment as were carried out by those against
whom the allegations are being made.
The purpose of this text is to provide an insight into the structure and function
of the components of the eye, to consider how the components may malfunction
naturally and review the effects of trauma and disease.
Trauma may occur accidentally or may be self-inflicted or surgically induced.
Most patients have a simplistic view that something they have done or had done
to them has caused the defect from which they now suffer. They seek to relate an
incident in the recent past to the ocular or visual problem which now afflicts
them. Sometimes they are correct, but in other cases it is the natural history of
the disease which is the triggering factor.
Exacerbation of pre-existing disease or acceleration of its onset may be caused
by inter-current trauma. In medical malpractice and personal injury cases it is
the medical specialist who will discuss cause and effect. When two experts fail
to agree, the legal process arbitrates on the difference of opinion. What the lawyers
require is an overview of the issues involved, and to achieve that end they need
insights into the increasingly specialised world that medicine in general, and
ophthalmology in particular, presents today. Thus, this text will review the eye
by structure, but then consider the ocular syndromes embracing more than one
ocular component, so that the readers can integrate their knowledge of component
parts and their collective malfunction.
Ophthalmology, more than any other branch of medical practice, utilises
terms and shorthand phrases that are specific and probably unintelligible to the
uninitiated. Throughout this volume, reference should be made to the glossary
for a concise insight into a technical term. The terminology, abbreviations and
notations are explained in the appendices.
The text concentrates on those aspects of ophthalmic practice which most
frequently figure in legal practice. For encyclopaedic information, ophthalmic
textbooks and the massive on-line ophthalmic literature are available. This book
is designed for easy reading and to provide a working knowledge of the eye and
the misfortunes, both natural and acquired, that may torment the eye and vision.
Inevitably this book requires order and planning. There will be areas of overlap
because few pathological processes in the eye are not interrelated. A working
knowledge of the natural history of living tissues and organs is an invaluable
aid to the reader prior to embarking on this volume, but is not an essential
requirement, as explanatory sections are intended to reinforce existing knowledge
or provide ample explanation for the initiate.

2
 Introduction

Finally, the lawyer may find the visual standards for occupations a useful
source of reference. Clients seeking compensation for loss of employment through
degrees of visual disability may have their opportunities or limitations considered
in a wide variety of professions and occupations with specific visual standards.

MEDICAL NEGLIGENCE AND THE MEDICAL REPORT

The purpose of a report from an ophthalmologist in medical negligence

proceedings is to appraise the lawyer of the medical issues and areas where, on
the stated facts and the accounts in the medical records, there appears to have
been a departure from acceptable practice at the time of the treatment. A report
should assist lawyers to understand the essential medical issues as they appear
to the expert, and give such guidance and instruction as may be thought
necessary for those issues to be dealt with in an informal conference.
The layout of an ophthalmic report should helpfully include:

(a) a title page to show

(i) the name of the plaintiff and date of birth,
(ii) the substance of the report, eg medical report on the treatment of ‘X’ at
‘Y’ hospital on or about (date),
(iii) name and qualifications of the expert reporting,
(iv) the date and purpose of the report, eg condition, prognosis, liability or
causation,
(v) for whom the report has been prepared, and
(vi) a detailed list of all medical records, reports, statements and materials
upon which the opinion is based;
(b) a chronological account of the facts—from the source materials—with dates
and reference to page numbers (if applicable);
(c) identification of the important events in the history of the case, giving an
account, where appropriate, of the relevant medical principles (in lay terms)
involved in the plaintiff’s management (plus references and/or quotations);
and
(d) opinions on the standard and acceptability of all aspects of the plaintiff s
care and, if appropriate, discussion on any other areas where standards have
not been achieved.

The legal attitude to medical negligence claims is based on the judgment in

Bolam v Friern Hospital Management Committee [(1957) 1 WLR 582 et seq].

In the ordinary case which does not involve any special skill, (negligence) in law
means a failure to do some act which a reasonable man in the circumstances would
do, or the doing of some act which a reasonable man in the circumstances would

3
 Ophthalmology

not do; and if the failure or the doing of that act results in injury, then there is a
cause of action…in the ordinary case it is generally said that you judge (negligence)
by the action of the man in the street…but where you get a situation which involves
some special skill or competence, then the test as to whether there has been
negligence or not is not the test as to the man on the top of the Clapham omnibus,
because he has not got that special skill. A man need not possess the highest
expert skill; it is well established law that it is sufficient if he exercises the ordinary
skill of an ordinary competent man exercising that particular art.

In the realm of diagnosis and treatment there is ample scope for genuine
difference of opinion, and one person clearly is not negligent merely because his
conclusion differs from that of other professionals, nor because he has displayed
less skill or knowledge than others would have shown. The true test for
establishing negligence in diagnosis or treatment on the part of the doctor is
whether that person had been proved to be guilty of such failures of which no
doctor of ordinary skill would be guilty of when ‘acting with ordinary care’.
Negligence is purely a legal concept, so it is lawyers who decide whether
comments and criticisms on the question of competence in the medical report
are sufficient to amount to a formal claim in negligence.
In respect of liability, the issue is therefore whether the standard of care was
that which should have been provided by a responsible body of medical
practitioners. If the treatment was that which no responsible body of medical
practitioners should have provided, it is likely to be a breach of the standard of
care. It is a defence to show that there is a responsible body of medical practitioners
which would have carried out the treatment on the patient in the manner in
which it was carried out, even if that responsible body is in a minority. This
takes into account real and genuinely held differences in treatment which are
accepted equally by the medical profession. Therefore the requirement is:

(a) to identify precisely what was wrong with the patient, and its cause prior to
the medical treatment administered;
(b) to identify and itemise clearly the treatment administered to the patient; and
(c) to state, in relation to such treatment, whether or not the medical personnel
treating the patient
(i) administered a treatment which they should not have administered
(and, if yes, what was that treatment, and what are the alleged reasons
why they should not have administered it),
(ii) failed to administer treatment which they should have administered
(and, if yes, what was that treatment, and what are the alleged reasons
why they should not have administered it), and
(iii) failed adequately to diagnose (and, if yes, what is it that has not been
adequately diagnosed, and what are the alleged reasons why it should
have been diagnosed). Furthermore, if relevant, was there a delay in

4
 Introduction

diagnosis and, if yes, for how long, and why should this diagnosis
have been made earlier?

In respect of causation, in order for the patient to succeed in a claim it is

necessary to prove that, as a result of the defect in treatment, he has suffered
loss. It is only necessary to show that, on the balance of probabilities, the loss has
arisen as a result of the negligence.
On the balance of probabilities means ‘more likely than not’ (more than a
50% chance). It is important when considering causation to assess precisely what
damage flowed from the negligence as opposed to any underlying condition.
In relation to any failure, one must look at what injury or damage was
sustained as a result, and determine:

(a) the pain, suffering and loss of amenity flowing from that failure; and
(b) the pain, suffering and loss of amenity the patient would have endured had
the medical management not fallen below the standard of care.

With respect to health authorities, it is possible for them to be negligent above

and beyond any vicarious liability they may have in respect of their employees;
eg a doctor may be put in a position in which he is insufficiently experienced to
meet the demands of the job, but his competence is sufficient to defend
personally a negligence claim. A patient may still seek redress against the
employer for allocating an inexperienced doctor to a post from which the
patient would be entitled to expect more competent treatment.

5
 CHAPTER TWO

OVERVIEW OF THE EYE

Figure 1 (above). Diagram of the front view of the eye showing the anterior landmarks
of lids and eye.

Figure 2 (below). Cross-section of the eye globe.

The human eye is a complex organ. It is housed and protected in all aspects by
the bony eye socket, except for its frontal aspects (Figure 3, page 8) where the
eyelids and eyelashes serve to prevent the ocular surface from drying out and
inhibit access to foreign material. The lacrimal or tear gland located under the

7
 Ophthalmology

Figure 3. Cross-section of an eyelid.

upper, outer portion of the eye socket produces one component of tears which
continuously bathe the eyes with moisture and nutrients. Other components are
produced by the meibomian glands located in the substance of both upper and
lower eyelids. They secrete an oily component of the tears, while mucous cells in
the conjunctival surface of the eye globe formulate the mucous component.
Excess tears either evaporate or drain through two small ducts on the inside
corner of the upper and lower eyelids near to the nose—the lacrimal punctae.
With each blink the tears wash away debris and potentially harmful bacteria
into the nose. The production of tears, although a continuum, is varied by reflexes
which produce a response when the eye is stimulated by bright light, by variation
in temperature (hot or cold), by debris bombarding the eye (dusty atmosphere)
or by emotion. Thus, when people cry the nose runs as the excess of tears pours
into it through the lacrimal drainage system.
The eye is covered by a mucous membrane, a soft, glistening membrane
called the conjunctiva which covers the inner surface of the eyelids and the surface
of the ocular globe that terminates at the edge of the cornea, the clear window of
the eye. This continuum of surface material, collectively known as the ocular

8
 Overview of the Eye

Figure 4. Side view of the eye within the orbit, illustrating its relationship to the
supporting and surrounding structures, including the paranasal sinuses.

surface, is the barrier between our environment and the eye itself. It is this tissue
which becomes red when the eye is inflamed, as well as the tissue beneath it,
leading to red-eye problems (see Chapter 14). The outer coating of the eyeball
itself under this membrane is a tough tissue called the sclera. Between the sclera
and the conjunctiva exist the connective tissue layers of episclera and Tenon’s
membrane.
Attached to each eyeball are six eye muscles (Figures 4 and 5), four of which
are the superior, inferior, lateral and medial rectus muscles which allow the

Figure 5. A view behind an eye showing its attachments visible in the eye socket. The
optic nerve is surrounded by the extra-ocular muscles and nerves within the bony
walls of the orbit.

9
 Ophthalmology

eye to move in horizontal and vertical directions. The remaining two oblique
muscles, superior and inferior, allow the eye to rotate in its socket. All these
muscles act in concert as well as with the corresponding muscles in the fellow
eye. Each muscle on an eye has an antagonist muscle, ie a muscle which
opposes its action. The two eyes together produce binocular vision, which
gives us three-dimensional or stereoscopic vision, a facility resulting from
physical separation of the two eyes and their slightly different angle of view.
In the brain these two views are fused to give us the impression of three
dimensions or depth perception.
The movements of the eyes are controlled by central areas of the brain which
co-ordinate their activities, served by the cranial nerves (III, IV and VI—
occulomotor, trochlear and abducens) which innervate them from the brain stem.
Abnormalities in the ability of the eye muscles to maintain ocular alignment
results in the condition of strabismus or squint and the symptom of double vision
or diplopia.
The clear covering or window at the front of the eye is known as the cornea,
which is one component of the eye’s twin-lens focussing system. It is the most
powerful component of this system, accounting for two-thirds of its focussing
power. As light rays enter the tear film and then the cornea from the less-dense
atmosphere of the air, they are refracted and focussed onto the retina. The cornea
also serves the important function of filtering out the light and near-visible
elements of the electromagnetic spectrum wavelengths which are potentially
harmful to the delicate retinal tissues at the back of the eye. These include both
infrared and ultraviolet portions of the electro-magnetic spectrum.
As the cornea plays such an important role in the focussing of light,
abnormalities or irregularities in the shape of the cornea will affect clarity of vision,
producing ‘refractive errors’. The full cornea is generally spherical in shape but
specifically is known as a toroidal asphere, ie it is shaped like the side of a barrel
or the convex side of a teaspoon with the handle towards the nose, and it is steeper
on the nasal side and flatter on the outer or temporal side. This design is nature’s
method of minimising the physical phenomenon of spherical aberration. Light
rays impinging upon the periphery of a spherical lens are refracted more than
the central rays, to produce different focussing effects. The eye as an optical system
requires precise focussing, hence the aspherical design of the cornea. A variation
in the refractive process is the phenomenon of astigmatism, a condition in which
the cornea produces more than one principal focus.
Refractive errors are corrected by sphero-cylindrical combinations of lenses,
spectacles or contact lenses, which add to or reduce the refractive power of the
cornea according to its variation in shape and its relation to the overall size of
the eye globe. A further refinement in the optical process is the Styles-Crawford
effect, wherein light impinging upon the centre of the cornea is weighted by the
brain more than the peripheral rays of light, a phenomenon that also serves to
minimise optical aberrations.

10
 Overview of the Eye

Figure 6. Clinical photograph of the cornea, the anterior chamber containing the aqueous
humour, and the crystalline lens by special (Scheimpflug) photography, showing the
anatomical relationships and the nuclear zones within the crystalline lens.

Light passing through the cornea travels next through the watery fluid in
the front of the eye, the aqueous humour (Figure 6), one of whose functions is
also to absorb that portion of ultraviolet and infrared light which has managed
to pass through the cornea. The aqueous humour is contained within the anterior
and posterior chambers of the anterior part of the eye (Figure 7, page 12). The
light is modulated by the pupil, the central aperture in the coloured part of the
eye, the iris diaphragm. The iris regulates the amount of light entering the eye
through the pupil assuming large dimensions in the dark and becoming smaller
when it is exposed to increased light intensity. The iris diaphragm itself contains
a common body pigment called melanin. The lower the pigment content the
more blue the iris appears; the higher the pigment content the more brown it
appears.
After the light passes through the pupil it meets the crystalline lens, the
second element in the eye’s twin-lens system. This lens fine tunes the image,
providing approximately one third of the focussing power of the eye. Where the
crystalline lens becomes cloudy or contains opacities or significant variations in
its consistency, the process of cataract formation occurs which will variously

11
 Ophthalmology

Figure 7. Diagram of the

structures in the angle of
the anterior chamber.

12
 Overview of the Eye

Figrue 8. Retinal diagram

illustrating the relationships
at the posterior pole of
the eye—especially the
optic nerve head,
macula, fovea,
retinal arteries
and veins.

interfere with vision. The crystalline lens is also designed to maximise the clarity
of the image ultimately received by the retina. It too is shaped in an aspheric
fashion, though the anterior surface is flatter than the posterior surface, with the
periphery of the lens curved less than the centre of the lens.
The vitreous gel which is clear in adult life fills the cavity between the retina
and the crystalline lens. In the embryological development of the eye this
compartment contains a vascular system which provides the building blocks of
nutrients for the developing eye, but as the eye matures in the embryo so the
vascular system, having fulfilled its function, regresses and in so doing secretes
the clear gel which fills that void between the crystalline lens and the retina. The
gel is bounded by an extremely thin layer, the hyaloid membrane, on both its
anterior aspect (the anterior hyaloid membrane) and its posterior aspect (the
posterior hyaloid membrane) which abuts against the retina. Any imperfection
in the clarity of the vitreous, especially in the major axis between the pupil and
the central retina will lead to an individual perceiving floaters or mobile fly-like
spots in the field of vision. These imperfections, consisting of fibres and cellular
material or blood, in pathological conditions will cause a shadow to be cast upon
the retina which is perceived as a floater as it moves around with eye movements.
The retina (Figure 8) is the light-sensitive layer that lines the posterior two-
thirds of the inner, eye globe. From a functional point of view it is divided into

13
 Ophthalmology

Figure 9 (above). The peripheral, visual field.

Figure 10 (below). The optic nerve pathways from retina to visual (occipital) cortex,
showing the crossing over of the nasal retinal fibres from each eye to the opposite
pathway in the optic chiasma.

14
 Overview of the Eye

the central area known as the macula, which subserves the property of sharp
vision, and the peripheral retina, which provides the visual field or projection of
sight into space. All healthy eyes with a normal visual field (Figure 9) have a
small area towards the nose known as the ‘blind spot’, which is the space
representing the part of the retina occupied by the optic nerve, the bundle of
neural tissue carrying the impulses from the photoreceptors scattered throughout
the retina back towards the visual part of the brain.
The focussing system of the eye provides an inverted image onto the retina
which is transmitted by the nerve chain, through the optic nerve and the visual
pathways in the brain, to the occipital cortex (Figure 10) where the interpretation
of vision resides. Here the image is re-inverted so that the objects we see in a
familiar sense have an upright orientation.

15
 CHAPTER THREE

OCULAR STRUCTURES AND THEIR FUNCTION

EYELIDS

The eye globe is housed in a bony socket, the orbit, which has a bony posterior
wall, superior, medial and lateral walls, but with its anterior aspect protected by
the upper and lower eyelids. The function of the eyelids first and foremost is to
protect the eye from noxious physical stimuli including light, heat, cold and
debris. The eyelids fulfil these functions by a series of reflex responses initiated
by stimulation of nerve endings in the ocular surface and by light sensitivity
mediated through the retina (Figure 3, page 8).
Structurally, each eyelid is composed of skin on the surface, a transitional
zone on the margin, and the mucous membrane of the conjunctiva on its posterior
surface. Between the two there is a layer of muscle underneath which is the
tarsal plate, a rigid connective tissue that gives each eyelid its firm substance.
The tarsal plate is shaped like a crescent, deepest centrally and thinnest
peripherally, and is curved to accommodate the shape of the anterior part of the
eye globe. The tarsal plate contains a row of meibomian glands whose function
is to secrete the oily fraction of the tear film to enhance eye lubrication.
There are two essential muscular components. The first is the circular
sphincter muscle, the orbicularis oris, which is the muscle that allows the eyes to
be screwed up tight. The second is the levator palpebrae superiori muscle that
retracts the upper lids in order to open the eyes. There are subsidiary muscles—
Müller—which have a different type of muscle composition to that of the
orbicularis and the levator. Issuing from the lid margin are the eyelashes whose
roots lie deep in the lid into the thickness of the tarsal plate. The function of the
lashes is to screen particulate matter from reaching the eye whilst still allowing
the eye to serve its visual function.
The gap between the eyelids is known as the palpebral aperture (see Figure
1, page 7). In its normal dimension the palpebral aperture is sufficiently wide for
the whole of the cornea to be exposed, ie the whole of the iris tissue. The coloured
iris diaphragm is revealed but there are considerable variations within the normal
range. However, when the upper eyelid droops, a condition known as ptosis,
and is patently different from that of the fellow eye, it may be deemed to be
pathological. Ptosis may be a congenital or an acquired condition (see page 276).
The eyelids change with age. The skin of the eyelids tends to become thinner
and may become excessive, creating redundant folds of skin on both upper and
lower lids. The muscles of the eyelids may become weaker causing sagging of

17
 Ophthalmology

the lower lid (ectropion) with inevitable spillage of tears, or, as it affects the
upper lid, causing age-related ptosis. Conversely, the fibres of the orbicularis
muscle in the lower lid may undergo spasmodic contraction to cause in-turning
of the lower eyelid (entropion), which produces irritation and watering of the
eye on an intermittent but persistent basis.
There are a number of congenital anomalies of the eyelids worthy of note,
including extra rows of eyelashes (distichiasis) and a narrow palpebral aperture
(phimosis of the eyelids).
The function of the eyelid is best appreciated when it fails to close through
disease or trauma, exposing part or whole of the eye. The eye globe will not
survive severe exposure drying. Ulceration, infection and a whole catalogue of
disasters will ensue if exposure lasts for more than a few minutes.

THE OCULAR SURFACE

Behind the eyelids there is a continuum of mucous membrane extending from

the margin through recesses known as the fornices as the conjunctiva turns to
line the surface of the globe terminating at the limbus, the junction of the
scleral coat of the eye and the cornea. The ocular surface is a mucous
membrane lubricated by tears, which have several components. The main
component is watery issuing from the lacrimal gland located in the upper
outer aspect of the orbit. The second is the oily component, the secretion of the
meibomian glands which appears as small droplets often seen on the margin
of the eyelid where the meibomian glands open. Third is the mucous
component, formed in goblet cells which are scattered throughout the
conjunctiva and its sub-tarsal and bulbar portions, ie on the back of the eyelids
and the conjunctiva lining the globe. The conjunctiva is lax and plentiful,
allowing unimpeded movements of the eye globe in all directions of gaze. It is
a mucous membrane containing blood vessels and a supporting, sub-
conjunctival, connective-tissue structure.
The tear film which protects the eye and is also the major refracting surface
of the eye additionally contains lysozyme, a natural antibiotic substance. This
film also lubricates the eye surface, and provides a medium for oxygen transfer
for metabolism of the tissues and protection against environmental pollutants.
The ocular surface is completed by the epithelial layer which covers the cornea
and which is contiguous with the conjunctival epithelium.

THE CORNEA

The cornea is the ‘front lens’ of the eye forming a twin-lens system with the
crystalline lens. It is contiguous with the white, tough, scleral wall of the eye,
its clarity providing the transmission window for the images which are

18
 Ocular Structures and their Function

ultimately focussed onto the retina. The cornea has a shape which can best be
likened to the underside of a teaspoon. If a teaspoon is held in front of a face so
that the handle is towards the nose, the back of the spoon will simulate fairly
accurately the shape of the cornea, which is steeper centrally, flatter
peripherally, steeper on the nasal side and flatter on the temporal side.
Optically the shape of the cornea is known as a toroidal asphere (see corneal
topography, page 55). It is so shaped to limit the spherical aberration which
would otherwise occur if the cornea had a spherical contour, in which
circumstance peripheral rays of light would be bent or refracted more
powerfully than the central rays of light, causing a defocussing effect which is
known as spherical aberration.
Structurally the cornea is composed of bundles of collagen tissue which
mainly lie in parallel, but the layers of which are interwoven. The cornea is about
0.5mm thick at the centre, and is thicker towards the periphery, being thicker on
its nasal than temporal aspect. On the anterior surface lies the corneal epithelium,
a multi-layered epithelial barrier to the outside world which is maintained by
the surface tear film. The basement membrane of the epithelium lies in fairly
loose apposition with the corneal stroma, but is held in place by the relative
suction force that follows the normal, slightly dehydrated status of the cornea.
When this fails in disease then the corneal epithelium becomes wrinkled or
blistered.
There are relatively few living cells in the corneal stroma, as the collagen
bundles are known collectively. The living cells are called keratosites and they
facilitate the minimal metabolic requirements of the stromal tissue. On its
inner surface the cornea has a single layer of cells—the corneal endothelium.
This is irreplaceable and, when damaged, is only capable of minimal repair.
When these cells become damaged, the adjacent, healthy cells enlarge in size
to cover their function. Each cornea has a specific number of cells,
approximately 3,500/mm2, but the population declines throughout life and
especially in later life. The population can be further reduced by disease,
trauma or surgical intervention.
Just anterior to the endothelium is a layer called Descemet’s membrane,
which is a condensation of the corneal-stromal connective tissue on its innermost
aspect. While one function of the endothelial layer is to maintain corneal
metabolism, transferring metabolites from the aqueous humour on its posterior
aspect to the corneal tissue, its most important function is to act as a pump,
removing excess fluid from the cornea to maintain its state of relative dehydration
and therefore its optical clarity. The cornea in people aged 70 and over often
shows slight yellowing in colouration due to photochemical changes which have
taken place throughout the course of life. One of the most important functions of
the cornea is to act as a barrier filter to the passage of short-wavelength light in
general, and ultraviolet light in particular, which, if transmitted, would be
damaging to the crystalline lens and to the retina. With the yellowing of age, the

19
 Ophthalmology

barrier-filter effect increases. Another age change commonly seen is an arcus

senilis, a white ring which is sometimes incomplete and occasionally forms a
thick band of whitish material in the peripheral corneal stroma. It used to be
considered that this represented deposition of fatty material in the cornea
indicating a tendency for high blood-fat levels, but this relationship has never
been confirmed.
The cornea can be subject to degeneration and disease and is clearly
vulnerable to trauma because of its exposed position. Its protection lies in the
eyelids and the tear film with its anti-bacterial content and its washing effect.
There are natural degenerations which can cause dramatic thinning of the
peripheral or central cornea, causing profound changes in corneal shape. The
most common of these is keratoconus, a cone-shaped deformation of the cornea
which can lead to spontaneous perforation but which causes severe distortion of
the image projected into the eye.
The cornea is well endowed with nerves and is exquisitely tender to surface
damage. It receives its metabolic requirements not only from the aqueous
humour but also through the tear film, and finally from the limbal blood
supply, ie the junctional area between cornea and sclera which boasts a
profound vascular plexus. However, the cornea itself is necessarily avascular,
which allows it to function as an optical element in the eye. Owing to its
avascular nature it can be readily replaced by corneal tissue from a fellow
human eye without the major rejection problems that face transplantation of
vascular organs or tissue.
The cornea, being the main refracting service of the eye, is also amenable to
shape alteration (see refractive surgery, Chapter 14, page 143), an aspect of
ophthalmic surgery of increasing importance.

SCLERAL COAT OF THE EYE

The wall of the eye is composed of thick, white, collagenous material, the sclera,
which, on its outer surface, is covered with a looser network of connective
tissue, the episclera. Anteriorly its covering is completed with the conjunctiva,
but posteriorly it is surrounded by the contents of the orbit, blood vessels,
nerves, fat and connective tissue. The sclera, which is composed of soft,
collagenous material in the newborn’s eye, gradually becomes more rigid with
the passage of time and, by old age, is a fairly rigid enclosure. It is fenestrated
and perforated by the blood vessels and nerves that enter the globe all over its
surface, but mainly on its posterior aspect. Where the optic nerve emerges there
is approximately a 1.5mm exit foramen straddled by connective tissue bands
known as the lamina cribrosa, through which the bundles composing the optic
nerve emerge to travel back into the brain.
The sclera and episclera are relatively inert in disease terms but can be subject
to inflammatory disorders which affect collagen tissue (see episcleritis and

20
 Ocular Structures and their Function

scleritis, pages 262 and 279). The scleral coat can be repaired when perforated
and can be replaced by transplanted tissue. In highly myopic eyes in which the
globe is much larger than the norm, a myopic eye may be 30mm or more in
diameter compared with 22–23mm for a normally-sighted eye, and the sclera
may be stretched and extremely thin. In contrast, in hyperopic or small eyes of
20mm or less it may be relatively thick. In a normal eye, like the cornea it is
approximately 0.5mm thick.

UVEA

The vascular coat of the eye is known as the uveal tissue or uvea. It comprises
several components, comprising (from front to back) the iris diaphragm, the
ciliary body and the choroid layer which lies behind the retina. Its vascular
content supplies the essential nutrients for eye metabolism, but it also houses
the eye’s immune system designed to protect against infection. Therefore it is
the source of inflammatory responses within the eye.
Inflammation is a necessary response to infection or the presence of foreign
material within the eye, but as the eye is a closed and delicate system designed
for optical purposes, inflammation may have devastating effects on its function
(see Chapter 14).

IRIS

The iris diaphragm is the most visible portion of the uveal tract. It comprises a
circular muscle (sphincter) and a radial muscle (dilator) as well as a pigment
layer which provides the ‘colour’ of the eye. Heavily-pigmented irides appear
brown whilst lightly-coloured irides are blue, with combinations of
pigmentation providing intermediate colouring. The pigment is called
melanin which is produced by cells called melanocytes, much the same system
which produces the suntan pigmentation of the skin. Eyes lacking pigment
(albinotic) have almost transparent irides with a pink glow through the pupil
(Figure 7, page 12).

THE PUPIL

The central aperture in the iris diaphragm is known as the pupil. To an observer
the pupil appears black because internal pigmentation in the eye, specifically in
the choroid and retinal layers, absorb light which is therefore not reflected, to
give the pink or red glow that otherwise would apply. If the intensity of light
shone into an eye is sufficiently powerful, the pigment layer will be unable to

21
 Ophthalmology

quench all the light, with resultant outward reflection of that quantum not
absorbed—hence the pink pupil in an albino eye or the ‘red eye’ of the direct
flash photograph.
The function of the pupil is to control the amount of light entering the eye,
by dilation in darker environments and constriction in bright light conditions.
The pupil is controlled by the light reflex, with a feedback system operating
through retinal light exposure. Other reflexes, eg the near reflex, cause the pupil
to constrict when the eyes converge to observe near objects. A smaller pupil
reduces the optical aberrations that naturally occur and thereby sharpen the
image, a necessary corollary of the better discrimination required when viewing
near objects, eg when reading. There are many clinical tests for pupil function
which are capable of yielding valuable information regarding the viability of
the visual process as well as signs of specific disorders.

AQUEOUS HUMOUR, TRABECULAR MESHWORK AND THE

CILIARY BODY

The eye as an optical organ requires nutrition to be delivered by transparent

media rather than blood. The ciliary gland positioned circumferentially

Figure 11. Chronic, open-angle glaucoma. Aqueous humour is produced constantly by

the ciliary gland and drained in equal amounts through the trabecular meshwork in
the angle of the anterior chamber. If less aqueous humour is produced than is drained,
the pressure will rise in the closed globe of the eye. This imposes compression of the
delicate optic nerve head structures, resulting in their slow destruction if the pressure
remains elevated for a sustained period. In acute, closed-angle glaucoma, the pressure
change is dramatic, with corresponding vision loss.

22
 Ocular Structures and their Function

behind the iris diaphragm secretes the watery aqueous humour. The fluid
circulates through the pupil to fill the anterior chamber of the eye before
leaving the eye through the trabecular meshwork in the angle between the
corneal periphery and the root of the iris diaphragm. Aqueous humour is an
isotonic solution with an ionic and glucose content that supplies the
nutritional requirements of the corneal endothelium, as well as absorbing the
waste products of metabolism.
Secretion of aqueous humour is a continuous process that has to be
balanced by drainage of an amount equivalent to that which is secreted. If an
imbalance occurs because the drainage system is not efficient, then the eye,
being a closed compartment, will suffer an increase in internal pressure.
Persistent elevation of intra-ocular pressure has a destructive effect on the
delicate nerves in the region of the head of the optic nerve, causing pressure
decay of its substance. This, in its varied forms, is the syndrome of glaucoma
(see Figure 11 and Chapter 12).

THE CRYSTALLINE LENS

The structure and functions of the human, crystalline lens is both interesting
and instructive in providing an appreciation of the process of cataract
formation. Cataract surgery accounts for 60–70% of all ophthalmic surgical
procedures, a fact which is of relevance in the field of ophthalmic litigation.
Embryological development of the crystalline lens begins late in the first
month of gestation. After about three weeks, at the 4mm stage of the whole
embryo, ectodermal cells derived from the outer layer of the embryonic tissue
covering the optic outgrowth from the primitive brain (the optic vesicle),
differentiate to form a slight thickening known as a lens placode or plate. This
occurs after contact and interaction of the anterior wall of the neuro-
ectodermal optic vesicle with the epithelial lining of the embryo.
Approximately 23–25 days after gestation the cells of the plate arch posteriorly
and invaginate into the developing optic cup to form the lens pit. This process
continues until a hollow lens vesicle forms. The primary vesicle is surrounded
by a capsule. During lens development this basement membrane is
continuously laid down by deposition of material from the adjacent epithelial
cells until the definitive lens has formed. Soon after the formation of the lens
vesicle the front and rear walls differentiate into dissimilar structures. While
cells in the anterior (front) of the vesicle remain as a single layer of cuboidal
epithelial cells, those at the posterior (back) terminally differentiate to form
fibres. As this process occurs and the cells elongate towards the epithelial
layer, the hollow nature of the vesicle is lost, and the nuclei of these primary
fibres migrate towards the middle of the vesicle (Figure 12, page 24). The
formation of this solid, embryonic, fibrous nucleus becomes completed
towards the end of the second month of gestation. Throughout life, cells

23
 Ophthalmology

Figure 12. Diagram of

the crystalline lens.

differentiate from the equatorial epithileum to form the lens fibres, whose
older brethren are continually compressed towards the centre of the lens
(Figure 6, page 11) forming successive layers as it grows, rather like an onion.
Unlike an onion, however, the lens size is largely constrained as the innermost
fibres lose fluid content and, importantly from a functional point of view,
produce a lens core of increasing refractive index. Light rays are consequently
refracted more effectively producing a myopic shift in the refractive power of
the eye—a frequent, early aspect of cataract formation (Chapter 9, page 81).
Initially, the lens fibres extend from the anterior to the posterior poles so that
the lens remains spherical. As growth proceeds, this pole to pole growth is no
longer maintained, sutures develop and the lens becomes a flattened, biconvex
sphere. Sutures are fanned where the secondary fibre-cell ends overlap, either at
the anterior or the posterior pole; no sutures are found in the primary cell mass.
From the onset of secondary fibre cell formation until birth, two Y-shaped sutures
are present. The anterior Y is erect, whereas the posterior Y is inverted. Each
growth shell of secondary fibres has both an anterior and a posterior suture
composed of three branches which are positioned essentially equidistant from
one another. Since identical sutures are laid down in each shell, continuous suture
planes are formed. After birth, growth is more asymmetric so complicated
branching patterns are observed.
The adult human lens is an asymmetrical oblate spheroid which does not
possess nerves, blood vessels or connective tissue. The lens grows throughout
life, the rate of growth being linear from the ages of 10–90. The weight of the lens
increases from 65mg at birth to 130mg at one year of age, and then increases

24
 Ocular Structures and their Function

very slowly until the age of 90 when it reaches approximately 250mg. The adult
lens is about 10mm in diameter, and has both an anterior and a posterior surface
which meet laterally at a rounded border known as the equator. The anterior
surface is in contact with the aqueous humour and the posterior surface with
the vitreous humour. The central thickness of the adult lens is 3–5mm. The radius
of curvature of the anterior surface is 9mm and the posterior surface 5.5mm (see
Figure 6, page 11).
Histologically, the lens consists of three major components—lens capsule,
lens epithelium and lens substance. The lens capsule is a structureless elastic
membrane which completely encloses the lens. Its thickness depends upon
age and the area being measured. At its thickest region it is the thickest
basement membrane in the body. The capsule is thinnest at the equator and the
anterior and posterior poles—4pm (picometre—10–12m) at the posterior pole.
The thickest regions are the concentric areas anterior and posterior to the
equator (up to 23pm). In contrast to other basement membranes, the capsule is
continuously produced throughout post-natal life. Its mass increases 5–8 fold
(see Chapter 9, page 93).

ZONULAR FIBRES

The crystalline lens is held in place by the zonular fibres (Figure 7, page 12), an
annular ligament composed of hundreds of fibres with a radial inclination, with
each fibre attached to the lens capsule running from the lens to the ciliary body
(a circular organ composed of glandular tissue which secretes the aqueous
humour, and a muscular portion which controls lens accommodation). The
anterior sheet of fibres terminates 2.5mm anterior to the equator in a circular
zone. The posterior sheet terminates 1 mm posterior to the equator in a similar
zone. The fibres attached to the anterior capsule are stronger, whereas the
posterior fibres are finer and more numerous.
Accepted theory suggests that contraction of the ciliary muscle to reduce its
diameter reduces the tension within the radially-arranged fibres of the zonular
ligament. The fibres (hundreds) are inserted into the crystalline lens capsule,
which is an elastic structure in youth but becomes less pliable with ageing. As
the zonular-fibre tension relaxes so the crystalline lens contracts, ie becomes more
spherical and therefore more powerful as a focussing lens. The effect is to aid the
focussing of near objects. Conversely, if the ciliary muscle relaxes, the increased
force applied to the zonular fibres ‘stretches’ the capsule and contents of the
crystalline lens to reduce its refractive power, as is required for distant-object
viewing. There is a feedback system from the visual cortex of the brain to the
nerves innervating the ciliary muscle to invoke the necessary muscle contraction
or relaxation according to the requirements for accommodation, ie the variability
of the focussing system to bring near objects into focus. Loss of accommodation
with age is known as presbyopia (see Chapter 17, page 173).

25
 Ophthalmology

VITREOUS BODY

The bulk of the posterior segment of the eye is hollow and is occupied by the
vitreous humour (Figure 2, page 7), a gel-like structure in young eyes which
degenerates with age to become a heterogeneous solution of aqueous humour
and collapsed gel fibres. It is bounded by a molecular membrane—the hyaloid
membrane—which is clinically differentiated into an anterior and posterior
portion. Both membranes figure in clinical ophthalmology, the posterior

Figure 13. A fluorescein angiogram of a normal retina but with a variation in the usual
vascular pattern. Note the tortuosity of the retinal arterioles. This picture has no
pathological significance but makes the point that no two retinas are alike.
Understanding what is normal and what is pathological requires an understanding of
variations within the norm.

26
 Ocular Structures and their Function

membrane in relation to retinal disease and surgery as it lies contiguous with

the anterior layer of the retina but separate from it. The anterior hyaloid
membrane may be perforated in complicated cataract surgery to influence the
occurrence of later complications affecting the retina. Macular oedema and
retinal detachment are the most frequent and visually-disabling consequences
of disruption of the anterior hyaloid membrane.
The vitreous humour represents the transparent remnant of an
embryological vascular stem that provides the source of materials for eye
development. In foetal development the structure changes as the eye is
formed, and the blood vessels regress as the gel forms to allow the eye to
function later as an optical organ.

THE RETINAL VASCULAR CIRCULATION

Unlike blood circulation, in many parts of the body the retinal circulation is an
end-artery system that has no parallel supply. In other words, if there is an
obstruction to the flow of blood through a retinal artery then the retina is
doomed, as its exceptionally high metabolic needs are lost when oxygen supply
is denied for more than a few seconds. The retinal, vascular circulation is
ultimately a derivative of the carotid artery circulation and is particularly
susceptible to vascular disease (see Chapter 13, Figure 13).

THE RETINAL PIGMENT EPITHELIUM

The retinal-pigment epithelium is the outermost layer of the retina (Figure 14,
page 28). It is non-neural tissue consisting of a single layer of cells which act as
an underlay separating the retina from its source of metabolites, the choroidal
vascular system. The retinal-pigment cells are extremely active and provide a
waterproof barrier between the capillaries of the choroid and the outer retina,
which is remote from the inner retina in terms of vascular supply and delivery
of materials. The retinal-pigment epithelium is an active transport system
transmitting oxygen and glucose and other metabolites from the choroidal,
sponge-like, capillary plexus to the outer retina and the photoreceptors in
particular. Each retinal-pigment epithelial cell has fine hairs or cilia on is retinal
side into which the photoreceptors nestle. These cells play a key role in the
processes of repair and regeneration which is a continuum in the life cycle of
every tissue in the body. The outer segments or photoreceptors have a limited
existence, and those whose active life is finished are absorbed and digested by
the pigment epithelial cells.
Electron microscopy of the pigment epithelial cells in the ageing retina show
particles of rod and cone outer receptors as they are degraded. The whole layer
of cells also provides an anti-reflective coating for the retina through the medium

27
 Ophthalmology

of their melanin pigment. In later life, as the cells become engorged with the life-
time debris of degenerating material from the outer retina, pigment migrates,
disperses and clusters to give a characteristic patchy pigmented appearance
underneath the retina when viewed by the ophthalmoscope. Beneath the retinal-
pigment epithelium is a layer known as Bruch’s membrane, consisting of
collagenous tissue including an elastic tissue component. The digested debris of
retinal-pigment epithelial activity is passed out of the cell into the region of
Bruch’s membrane, where accumulated debris is seen as white dots or colloid
bodies, also known as drusen (taken from the Czech word druse, meaning a rock
or white crystal).

Figure 14.
Cross-sectional,
diagrammatic
representation of
the retinal
structure to
illustrate the
relationship of the
rods and cones to
the underlying
retinal-pigment
epithelium and
choroid, and their
connections to the
nerve fibres (1
million) which
constitute the
optic nerve.

28
 Ocular Structures and their Function

The retinal pigment epithelium is bound firmly to the underlying Bruch’s

membrane, but in contrast the retinal photoreceptor layer of rods and cones is
in loose apposition with the pigment epithelial cells. The outer segments of the
photoreceptors interdigitate between the hairs (cilia) on the retinal surface of
the pigment cell layer. Thus, there exists a natural, potential space between the
pigment epithelial cells and the outer retina. This is the important plane
of cleavage in the pathological condition of detachment of the retina
(Chapter 10).

RETINAL PATHOPHYSIOLOGY

The retina is subject to congenital and acquired disorders, the latter having
varied origins. For example, there may be traumatic, vascular, inflammatory or
physical separation of the layers within the retina, or degenerative (age-related)
conditions which represent the major types of pathology which can disturb
retinal function.
In terms of pathological anatomy the retina can be divided into peripheral
retina, central retina including macula, and inner and outer retina together with
its pigment layer. There are specific entities which affect the macular retina, which
in turn have a profound effect on visual performance (and colour vision), as this
is the seat of finely discriminating visual acuity, whereas defects of the outer
retina have an effect on visual field, ie the projection of vision into space.

THE RETINA

The retina is the light-sensitive lining at the back of the eye—the film in the eye’s
camera. The light-sensitive elements in the retina are of two principal types,
rods and cones. Rod receptors generate a monochrome image (shades of grey),
whilst cones, be they sensitive to red, blue or green light, generate colour vision.
The photoreceptors are aligned so they actually face away from the light and are
in intimate contact with the retinal-pigment epithelium, a mono-layer of cells
supporting the retina and dividing it from the vascular coat of the choroid
(Figure 14, page 28).
The rods and cones contain the visual pigments which are bleached by light.
A degree of bleaching of the pigment within the cell alters its electrical potential
and causes, in effect, a discharge of a signal through a network of connecting
nerve fibres all the way to the occipital cortex, that portion of the brain serving
visual function. The retinal cones are mainly aggregated in the centre of the retina
(the macular area) which serves the function of sharp vision and colour vision,
as compared to the rods which serve the general field of vision and especially
cope with dusk and night vision where colour is not relevant because of the lack
of light.

29
 Ophthalmology

The rods and cones are supported by special cells within the retina and
connect through a chain of neural elements or nerve cells. There are
approximately 110 million light-sensitive receptors feeding about 1 million nerve
fibres (Figure 17, page 35) which lie on the surface of the retina and coalesce at
the optic nerve, which they collectively form. The retina receives its metabolic
requirements from two sources. The vascular choroid layer lying outside the
retina feeds the outer layers, while the retinal vascular circulation lying more or
less on the surface of the retina supplies the inner layers.
The implication of this arrangement is that, in order for light to reach the
light-sensitive cells (photoreceptors), it has to travel through the substance of
the retina, through blood vessels and nerve cells, before it can achieve its effect.
As a consequence of this there is a degree a of diffusion of light, which means
that the peripheral retina is not capable of sharply-formed vision. It generates
the field of vision but without absolute clarity.
This point is demonstrated when you fix your eye on a specific object. You
will see it clearly, but whilst concentrating on that object you will nevertheless
also be aware of a field of vision which will not be sharp, like the object at the
centre of your attention.
The sharp vision and the colour vision that we have is a function of the
central retina and its special anatomical arrangement. In the macular area of the
retina, photoreceptor cones are arranged in a radial, fan-like fashion with their
supporting nerve fibres splayed to one side so that light does not have to traverse
the substance of the retina to reach the light-sensitive cells. Thus, in this particular
area the light is not scattered. Furthermore, the macula is constructed of densely-
packed photoreceptor cones whose relationship with their supporting nerve fibres
is on a one-to-one basis, allowing perception of fine detail. This arrangement
contrasts with the peripheral retina where 100 or more photoreceptor cells may
feed into one nerve fibre. Therefore, the macula, both structurally and functionally,
is designed to give a sharp image. The centre of the macula is known as the
fovea, which clinically demonstrates a small, depressed, pit-like area in its centre;
therein the above architecture is at its most refined.
The functional aspects of the retina are to provide vision, which is divisible
into central vision served by the macula and fovea and peripheral vision served
by the retina in general.
The inner surface of the retina is in intimate contact with the posterior
boundary of the vitreous humour and is defined as the posterior hyaloid
membrane. Between the two is a potential space into which blood may flow
from retinal disease. Blood may occupy any part of the retinal substance and the
character of the haemorrhage—be it round, splinter-like, pooled or lake-like—
indicates at what depth in the retina the haemorrhage exists. The field of vision
extends about 120° at the horizontal plane and about half that in the vertical
plane, giving a vertically-flattened, oval field of vision. The field of vision of
each eye overlaps to some extent to give a broader field of vision of about 160°.

30
 Ocular Structures and their Function

The ability to visualise objects from different viewpoints due to the separation
of the eyes on the face, allows the brain to interpolate the data in the form of
three-dimensional images or stereoscopic vision.
Any fault in the retina, optic nerve or visual pathways gives rise to blank
areas in the field of vision known as scotomata. If the defect is in one eye or its
optic nerve, the blank area or scotoma will appear in the field of vision of that
eye alone. If the defect lies within or behind the optic chiasma—the point where
the optic nerves unite behind the eyes—the defect will affect the vision of both
eyes because of the fibre arrangement therein. Thus, the pattern of visual loss
provides clues as to the anatomical location of the defect. Once the anatomical
location is appreciated, the pathological cause can be considered.
The retina itself is subject to disorders which may be congenital, inborn or
acquired. The acquired defects may be due to trauma, inflammation, infection,
vascular faults and other pathological events. The retina may be affected by local
problems and disorders or be remotely affected as a consequence of generalised
disorders, eg those which affect blood and the blood vessels. Retinal response to
disease and disorders is limited because of its innate structure. It may suffer
from haemorrhage or bleeding; obstruction to its blood supply; fluid
accumulation within its substance; infection; inflammation; and invasion by
tumours arising in adjacent structures.
The retina has a particular response to a reduction in blood and oxygen
supply which is a condition which can also affect other parts of the eye. When
the retina is deprived of its oxygen requirement, chemical changes take place
that stimulate the formation of extra blood vessels (referred to as either new
blood vessels or neovascularisation). These grow on the surface of, or out from,
the retina. Unfortunately they do not achieve any functional purpose, but do
provide a great disadvantage to the eye as they are fragile and bleed easily, causing
visual obscuration as blood is opaque (see Chapter 13).

CHOROID

The choroid is a vascular layer which lies between the outer retinal layer—the
pigment epithelium—and the outer wall of the eye—the sclera. It comprises
feeding arterioles, a spongy capillary layer and large draining veins, the four
major ones being known as vortex veins because of their appearance. Cells
containing the pigment melanin permeate the choroid to give the inner aspect of
the eye a dark appearance. This will vary according to the person’s intrinsic
pigmentation. Thus, Negroid eyes are heavily pigmented while albino eyes
contain no pigment.
The purpose of pigment is to absorb light and avoid internal reflections from
light entering the eye. This improves the visual process, which understandably
is diminished in albino eyes, which are excessively light sensitive (photophobic).
The choroid is the posterior aspect of the uveal layer within the eye.

31
 Ophthalmology

OPTIC NERVE HEAD (OPTIC DISC)

Each retina contains approximately 110 million light receptors. Their collective
impulses are funnelled into 1 million nerve fibres which traverse the retinal
surface to coalesce in the region of the optic nerve. From here they travel
backwards into the brain, initially to meet the fibres from the corresponding
eye, to form the optic chiasma, an X-shaped nerve junction which lies in the
skull on top of the bony box that contains the pituitary gland. The anterior
portion of the optic nerve is visible ophthalmoscopically in normal eyes
(Figures 15–18, pages 33–35). It has a general shape and form with many
natural variations.
In pathological situations the optic nerve head changes its appearance with
characteristic signs. Because of its anatomy, the optic nerve head may not only
reveal evidence of ocular pathology, but also, most importantly, intracranial
pathological events. It is often referred to as the visible window on the brain.
Swelling of the nerve head is known as papilloedema, whereas death of optic
nerve tissue leaves the nerve head white in appearance, called optic atrophy
(Figure 19, page 34).

32
 Ocular Structures and their Function

Figure 15 (left). Clinical (ophthalmoscopic) view of the optic nerve head showing its
boundaries (the edge of the retina) and the central retinal vessels whichtraverse its
substance to supply the anterior portion of the retina. Thecentral pit in a healthy optic
nerve head or disc is known as thephysiological pit. In glaucoma, the central pit widens
and deepens; this is known as cupping of the optic nerve head, a key clinical sign in
the diagnosis of glaucoma.

Figure 16 (below). The optic nerve head in a Negroid eye, where the heavily pigmented
retina and choroid clearly demarcate the boundaries of the nerve head. The neural rim,
which is pink, contrasts with the physiological optic cup through which the central
retinal vessels emerge to branch onto the retina.

33
Ophthalmology

34
 Ocular Structures and their Function

Figure 17 (above left). Histological (microscopic) cross-section of an optic nerve, showing

the bundled nerve fibres and the central retinal artery and vein passing through the
nerve.

Figure 18 (above). The optic nerve head in a myopic (large) eye. In contrastto Figure 19
(left), the fundus is lightly pigmented, a feature emphasised by the retinal stretching
which occurs in myopia. The retinal-pigment epithelium and retinal tissues fall far
short of the nerve head, giving a whitish halo around the disc. Because of the
transparency of the tissues, choroidal blood vessels in a very different pattern to those
of the retinal circulation can be seen in the background.

Figure 19 (left). Hypertensive papilloedema, with congested retinal veins, swollen nerve
head due to capillary congestion and small haemorrhages on the surface.

35
 CHAPTER FOUR

HISTORY OF THE OPHTHALMIC

DISORDER SYMPTOMS

CLINICAL HISTORY

History taking should precede any eye or patient examination. By listening to a

patient’s history it is often possible to make a diagnosis prior to examination.
History taking provides vital clues to diagnosis. The following are the key
elements to the taking of an ophthalmic/medical history.

Presenting complaints
(a) What are the symptoms?
(b) How long have the symptoms been present?
(c) Is the problem getting worse, better or is it static?

Previous ocular history

(a) Do you wear, or have you ever worn, glasses or contact lenses?
(b) Have you ever had eye surgery?
(c) Have you had any significant eye problem in the past?
(d) Are you taking any prescribed ocular medication or over-the-counter
preparations?

Present and past medical history

(a) What medications are you currently taking?
(b) From what medical disorders are you suffering, or have you suffered in the
past?
(c) Has there been any previous surgical treatment?

Social history
(a) Alcohol intake?
(b) Other drugs?
(c) Smoking habits?

37
 Ophthalmology

Family history
(a) Is there any family history of significant eye disease or disorder?
(b) Is there any general medical problem that affects more than one member of
the family?

Allergies
Do you have any known allergies to medications, environmental elements,
food, etc?

OPHTHALMIC SYMPTOMATOLOGY

Of what do patients complain? What is the history of that complaint?

There are only six broad categories of ocular complaints:

(a) vision affected in one or both eyes;

(b) one or both eyes feel different;
(c) one or both eyes look unusual;
(d) discharge from one or both eyes;
(e) a history of trauma; and
(f) headaches associated with visual activity.

Listening to the history of a patient’s ocular/visual complaints and their

responses to sequential, direct questions more often than not will allow a
diagnosis to be formulated. Accurate history taking has always been the
fundamental aspect of diagnosis, of the course to be followed by logical
examination of vision, the ocular structures, related areas and other relevant,
body systems. A comprehensive ophthalmic history provides answers to the
following questions where relevant.

Is vision affected in one or both eyes?

Visual symptoms visual loss
transient
unilateral
bilateral
partial loss
central vision
peripheral vision
upper half
lower half
nasal half

38
 History of the Ophthalmic Disorder—Symptoms

temporal half
quadrant loss
night blindness
visual disturbance without area loss
distortion
Visual phenomena flashing lights
floaters
hallucinations
Light sensitivity (photophobia)
Double vision (diplopia) binocular
monocular

Do one or both eyes feel different?

Discomfort
Feel dry
Itchy
Burning
Gritty
Foreign body sensation
Ocular pain
Tired

Do one or both eyes look unusual?

Red eyes without visual disturbance
unilateral
bilateral
Squint
Drooping eyelid (ptosis)
Bulging eye (proptosis)
Bulging eyes (exophthalmos)
Is there a discharge from either eye?
Watery discharge watering eyes (epiphora)
Sticky mucous
pus
With visual disturbance blurred vision
severe visual disturbance
with pain
without pain

39
 Ophthalmology

History of trauma?
Recent
Direct
Perforating minor
major
Non-perforating mild
with pain
without pain
without visual disturbance
with visual disturbance
severe
visual loss
indirect
adjacent
remote

Headache and the eyes

See Chapter 18.

40
 CHAPTER FIVE

CLINICAL EXAMINATION AND

INVESTIGATION OF THE EYE AND VISION

EXTERNAL EXAMINATION

The purpose is to provide an assessment of the eye and its supporting tissues,
including the eyelids, the soft tissues around the eye, the lacrimal (tear)
apparatus and the visible portions of the external globe and the cornea. The
position of the eye in the orbital socket gives evidence as to whether the eye is
unduly prominent—proptosis or exophthalmos. Redness of the eyelids,
particularly the margins, may indicate that a patient suffers from blepharitis.
The quantity of tear production may be further assessed by applying a
Schirmer’s test, wherein the tear soaking of a strip of filter paper gives a
measure of tear production.

ANTERIOR CHAMBER

The anterior chamber is the dome-shaped space between the back of the cornea
and the front of the iris. In patients with small eyes the chamber tends to be
shallow (one of the risk factors for acute, closed-angle glaucoma). The anterior
chamber and the cornea are examined with the biomicroscope or slit-lamp
microscope, which provides a stereoscopic, magnified, illuminated view of the
cornea and anterior chamber, iris and pupil and crystalline lens. In other words,
the anterior segment of the eye.

GONIOSCOPY

Because of the curvature of the cornea and its high index of refraction, it is
impossible to examine the angle of the anterior chamber without optical
assistance. The angle of the anterior chamber contains the trabecular meshwork
drain. It is an area that may have visible pathology and, in order to visualise this
area through its 360° entirety, an instrument called a gonioscope is utilised. This
consists of a contact lens incorporating an angled mirror or mirrors which
enable the observer to direct the light of the biomicroscope into the angle of the
anterior chamber and visualise it.

41
 Ophthalmology

OPHTHALMOSCOPY

Ophthalmoscopy is the method of examining the posterior segment of the eye,

ie the vitreous compartment and the retina, including the optic nerve and
macula. There are two principal types of ophthalmoscopy: direct and indirect.
The former is carried out with a hand-held instrument which contains a
bright, light source which illuminates the posterior segment of the eye, and the
observer is able to visualise the retina through the magnification viewing
system. The direct ophthalmoscope usually incorporates a variety of focusing
lenses to compensate for a wide range of refractive errors which exist in the
eyes of the population.
In contrast to direct ophthalmoscopy, indirect ophthalmoscopy has a number
of differences and advantages. It provides a wider field of view and it overcomes
opacities in the optical media of the eye rather better than can be achieved with
direct ophthalmoscopy. The image, however, is inverted and reversed, so
considerable training is required to become proficient in its usage. In general it
also requires dilatation of the pupil, a condition of the eye which facilitates all
forms of ophthalmoscopy.
The indirect ophthalmoscope takes many forms. One is an optical system
worn on a headband with a viewing lens held in the operator’s hand between
the observer’s eyes and the patient’s eye under examination. The optical system
may also be mounted on a spectacle frame to provide a more convenient system.
Finally, high-powered lenses can be used in conjunction with the slit-lamp
biomicroscope to provide a more magnified and variable field of view of the
posterior segment.
Indirect ophthalmoscopy provides a stereoscopic view of the fundus, whereas
direct ophthalmoscopy involves the use of just one eye of the observer and
therefore does not provide the three-dimensional view that the indirect
ophthalmoscope does. The indirect ophthalmoscope principle can also be
incorporated into a photographic apparatus, the fundus camera, which enables
the observer to record the image of the retina and optic nerve in varying degrees
of angle of view and magnification in order to provide a permanent record. The
fundus camera is also the instrument which enables the test of fluorescein
angiography to be performed (see below).

VISUAL ACUITY

Form vision—the ability of an eye to discriminate fine visual detail.

Distance acuity test

This procedure measures distance visual acuity by the reading of a chart at a
standard distance. The chart is known as the Snellen chart (Figure 20), which

42
 Clinical Examination and Investigation of the Eye and Vision

consists of Snellen opto-types or specially-

formed letters of the alphabet arranged in
rows of decreasing letter size. The size of the
letters are standardised so the letters in each
row should be clearly legible at a designated
distance to a person with normal vision. The
chart is normally placed at a distance of 6m.
For illiterate patients or children a variation
on the theme is the use of the letter E in
various arrangements, which the patient can
mimic by being given a letter E to hold in the
appropriate direction to conform with the
one on the chart. Alternatively, pictures of
decreasing size can be used with children,
eg well-known objects such as a cat, dog, car,
etc.
The distance of 6m is used because it
approximates to optical infinity, ie light rays
from this distance and beyond are considered
to be parallel, so that an emmetropic or
normal-sighted eye need not accommodate
to focus the image onto the retina. At the end
of each line of characters is a numeric
notation, 6, 9, 12, 18, 24, etc. These values are
used as measures of visual acuity. When a Figure 20. The Snellen
visual acuity is 6/18 for example, the 18 visual acuity chart.
corresponds to the distance at which letters
can be read by a person with ‘normal’ visual
acuity; ie, if the smallest letters an eye can read correctly are on the 6/18 line, a
patient is able to read at 6m what a normal eye can read at 18m and visual acuity
is therefore recorded as 6/18. If the patient can read the smaller characters (in
the 6/6 line) at 6m, the patient’s visual acuity is equivalent to that of a normal
eye. Many people are able to read even smaller letters at 6m, in which case their
acuity might be recorded at 6/5 or even 6/4.
There are 10 Snellen letters, each element of which subtends an angle of one
minute of arc, making the entire letter five minutes in angular height. There
should be a minimum of five letters on a line, and the line should increase or
decrease in size by 0.1 log units (25%) between lines. The letters should be greater
than 85% contrast (black letters on a white background) with a background
illumination of 85Cd/m2 (the international standard).

43
 Ophthalmology

Pinhole acuity test

If an uncorrected visual acuity is less than 6/9 for example, in order to
discover whether this is attributable to a refractive error without refracting the
patient, the pinhole acuity test may be performed. In this test the patient views
the Snellen chart through a pinhole occluder, a hand-held device which
completely covers one eye and allows the other to view the chart through a
tiny, central opening. A pinhole only admits central rays of light which do not
require refraction by the cornea, allowing an eye to resolve fine detail on the
chart without optical correction. Thus, if use of the pinhole improves a
patient’s poor, uncorrected acuity to 6/6 or even 6/9 or 6/12, the chances are
the patient has a significant refractive error. If poor, uncorrected acuity is not
improved with a pinhole, the visual problem may be due to a cause other than
a refractive error, eg problems with the optical media (transmission of light) or
the retina (visual perception).

Near acuity test

While the Snellen acuity test measures the patient’s ability to see fine detail at
a distance, ie it is a distance visual acuity test, in order to test near visual acuity
a test is performed as the patient reads a suitable chart. As with the Snellen
chart, numeric notations are printed next to each line or are near the test card
as a measure of near visual acuity. Various units of measurement are used,
some of which are distant equivalent. One example is the Jaeger notation,
which assigns each line on the card to a single arbitrary numeric value
corresponding to a Snellen value; eg Jaeger 2 (J2) is equivalent to 6/9 Snellen
distance acuity.

Other acuity tests

Patients with poor vision may not be able to see the largest letter on the Snellen
chart (6/60). Under these circumstances a patient may move closer to the chart
until the point is reached where she can read the largest letter, in which case the
acuity would be recorded as 1/60, 2/60, etc. Notations used for even lower
levels of acuity are counting fingers at an appropriate distance (eg CFat 1m).
Below that level, hand movements (HM) is the notation used to describe
movement of a hand in front of the eyes. Thereafter, the lowest level of
perception is noted as ‘just perception of light’ (PL), and this can be sub-
specified by checking in which direction the light can be perceived, either
straight ahead, above, below or to either side, which may give some indication
of the pathological process at work or the viability or otherwise of the retina.
For the illiterate patient, the E-test can be used when a patient is given a
large letter E and is asked to hold it in the direction corresponding to the E of
different size on a chart which is printed according to the Snellen standards.

44
 Clinical Examination and Investigation of the Eye and Vision

For children there are a variety of tests including picture tests where common
objects such as a dog, cat, cow, horse, bicycle or car are represented in a Snellen
layout in decreasing size, and the child is asked to identify the object, giving a
fair indication of the acuity of the eye under test.

Visual acuity—international system equivalents

CLINICAL MEASUREMENT OF VISUAL ACUITY—IS IT A RELIABLE

GUIDE TO WHAT A PATIENT CAN SEE?

Visual acuity is a numerical value attached to the discrimination of spatial detail

that can be discerned by an eye. Traditionally, two types of acuity are recorded
as an essential part of a clinical eye examination, distance acuity and near acuity.
The former value is expressed as a ratio of the size of letters displayed at a fixed
distance. As noted previously, in the UK 6/6=letters subtending an angle of one
minute of arc at the fovea in the centre of the retina at a distance of 6m;
6/60=10% of that acuity. In the US 20ft is the fixed distance of the test chart and
the same acuity would be 20/20; 20/200 being the equivalent of 6/60. On the
continent of Europe a metric system is used—6/6=1.0, 6/60=0.1, the ratios
remaining the same (see table for visual acuity denomination conversion). Near
vision assessment utilises reading test types of dimensions measured by print
size 8 point, 10 point, etc (n5, n8, n12, etc), or the Jaeger test type (J1, 2, 3, etc).

45
 Ophthalmology

Distance visual acuity as measured in the consulting room is performed in

an artificial situation—dim lighting and brightly lit test chart with excellent
contrast. In real life, environmental circumstances including lighting, shade,
mist, fog, low sun, oncoming headlights, all provide a different type of test for
visual function. For example, if there are opacities in the optical media of the
eye, eg a cataract, then different lighting situations may provide very variable
visual acuities. Similarly, the status of the pupil will have an effect on acuity,
especially if an eye has undergone a refractive surgical procedure which may
cause symptoms such as glare and blur due to spherical aberration. Loss of
contrast of the image is also a potential consequence of some refractive
procedures such as photo-refractive keratectomy. Therefore, consulting room
assessment of visual performance will provide a reference which, under
similar test conditions, will provide information on the stability of visual
performance or otherwise, but clinical decisions should be based on other
evidential information gathered by listening to the patient’s responses to
direct questioning on lifestyle and needs.

Figure 21. The Logmar visual acuity chart.

46
 Clinical Examination and Investigation of the Eye and Vision

The Snellen acuity chart, which historically has been used as the assessor of
visual acuity function, is itself flawed because it is sensitive to proximity or visual
crowding, ie failure of adequate spacing between letters and rows. Variation in
the number of letters on each line presents the subject with a task of increasing
difficulty, rather than providing an equivalent task at all acuity levels. While
clinical decisions may be based in part on Snellen acuities, the Logmar acuity
chart may provide a more reliable guide to acuity (Figure 21).

GLARE VISUAL ACUITY TEST

Away from the consulting room, our environment provides varied lighting
conditions. If there are opacities in the optical media of the eye, principally the
cornea and lens, then light scatter from the opacities within the eye has the effect
of reducing visual capabilities. Contrast is lost and with it resolution of detail.
Thus, patients with cataracts may perform well in the dimmer light of the
consulting room than they would in an outdoor, brighter-light situation.
In determining the indications for surgical intervention, a patient’s
description of his visual problems must be accorded significance. Objective
assessment of the reported disability may, in part, be confirmed by the glare
acuity test. In this test a light of varying brightness is placed in front of the test
eye, utilising an opaque, white, plastic hemisphere with a central aperture. The
eye can see the test chart through the aperture and the visual acuity is recorded
at different brightnesses in order to stimulate natural environmental conditions.
The brighter the light, the greater the glare and, in media-opacity-affected eyes,
the acuity diminishes and is accordingly measured.

CONTRAST SENSITIVITY

The loss of contrast of an image means loss of image quality and therefore visual
performance. Tests are devised to provide a quantitative measure of the eye’s
response to images of reducing contrast. Such information is invaluable in the
assessment of natural, visual disabilities, eg corneal scars and cataracts, as well
as iatrogenic effects, eg excimer-laser, photorefractive keratectomy or other
corneal, refractive, surgical procedures.

VISUAL FIELD EXAMINATION (SPATIAL PROJECTION

OF VISION)

A visual field examination measures the projection of retinal light-sensitivity

into space. In effect, it measures the peripheral aspects of vision in contrast to
the central vision which provides definition in the imaging of the eye. Defects of

47
 Ophthalmology

Figure 22 (above). Bi-temporal hemianopia (demonstrated on a visual field chart) caused

by compression of the central fibres of the optic chiasma due to a pituitary tumour.

Figure 23 (below). An example of an incomplete homonymous hemianopia

(demonstrated on a Goldmann visual field chart); in fact, a quadrantinopia, ie loss of
the lower left field of vision in each eye caused by a defect in the right optic pathways
from a stroke or cerebro-vascular accident for example.

peripheral vision may often be subtle and pass unnoticed by a patient. Such loss
may be due to disease or defects in the retina or optic nerve or in the visual
pathway to the brain (Figures 22 and 23).
An understanding of peripheral visual field defects can give very positive
clues as to the location of the pathology in the brain. Confrontation visual-field
testing is a method of gross evaluation of a patient’s peripheral vision, wherein

48
 Clinical Examination and Investigation of the Eye and Vision

the boundaries of the patient’s field of vision and that of the examiner are
compared by a face-to-face confrontation process.
A second test can be applied to the central vision by the Amsler grid test,
which determines the presence and location of defects in the central visual field.
In this test, a grid of thin, black, evenly-spaced horizontal and vertical lines with
a central dot on a square of white paper is viewed one eye at a time. Whilst the
patient stares at the central dot she may be aware of deficiencies or distortions in
the regular lines of the grid pattern around the dot. The location of the defect
should correspond to a definable lesion in the central retina.

OCULAR ALIGNMENT AND MOTILITY

Correct alignment of the eyes and the normal functions of the extra-ocular
muscles are a requirement for normal visual function. In those patients whose
eyes are misaligned, or whose extra-ocular muscles are unable to move the eyes
in a co-ordinated manner, the brain will not be able to fuse the images from the
two eyes. Failure to achieve fusion of the images in eyes which developed
normally will cause the symptom of double vision (diplopia). If this condition
(failure of image fusion) exists from birth or infancy (due to strabismus) with or
without failure of visual acuity development (amblyopia), a resultant loss of
stereoscopic vision will occur. Most patients who have a sudden onset of ocular
misalignment seek help for the consequential symptom of diplopia. Evaluation
of ocular alignment and ocular motility is an important component of a full, eye
examination.
There are three parts to an examination for these functions:

(a) eye movements (motility);

(b) ocular alignment; and
(c) ability to fuse an image.

Testing usually commences with a gross assessment of ocular motility followed

by more precise testing if the initial test indicates the presence of an alignment
or motility problem. The ophthalmic sub-speciality of orthoptics is expressly
concerned with in-depth evaluation of ocular alignment and motility.

EXAMINATION OF THE PUPIL

Examination of the pupil is capable of revealing a variety of ophthalmic

abnormalities including damage to the nerves that supply the iris muscles, the
optic nerve, retina, visual pathways and the brain. Pupil reactions are tested prior
to examination of the retina, a process involving dilatation of a pupil which nullifies
the pupil reactions by paralysis of the sphincter muscle responsible for pupillary
contraction. There are four major tests applied to the pupil:

49
 Ophthalmology

(a) assessment of the size of the pupil in dimmed illumination (particularly

important in refractive surgery);
(b) the briskness of the pupil constriction when a bright light is directed into
the eyes;
(c) pupil reaction to observation of a near target under conditions of dim
illumination; and
(d) a swinging light test (provides useful information on the viability of the
retina and optic nerve).

When a pupil responds to light it is called the direct pupillary reaction. At the
same time, the pupil in the fellow eye should constrict; this is known as the
consensual pupillary reaction. This should occur even if the non-stimulated eye
is blind and is unable itself to react to light. However, failure of the pupil in the
non-stimulated eye to react consensually would indicate abnormal function of
the iris sphincter muscle or the nerve pathways to and from the brain. In an eye
with normal function of the iris sphincter muscle, failure of the pupil to constrict
in response to direct light stimulation suggests that the optic nerve or retina is
not functioning normally.

INTRA-OCULAR PRESSURE MEASUREMENT

(TONOMETRY)

The intra-ocular pressure (in the closed system of the eye) is maintained by a
balance between the production of aqueous humour and its drainage out of
the eye through the trabecular meshwork. Disturbance or malfunction of any
of the structures involved will cause variation in intra-ocular pressure.
Malfunction usually involves a fault in the drainage of fluid out of the eye
with a consequential rise in intra-ocular pressure. Such conditions can
permanently damage the optic nerve and lead to serious visual defects (see
Chapter 12 on glaucoma).
Raised intra-ocular pressure (IOP) may be asymptomatic. Measuring IOP
with a tonometer is therefore a critical part of a comprehensive eye examination.
The most frequently-used method is applanation tonometry. The Goldmann
applanation tonometer is utilised either on the clinical eye microscope, the slit-
lamp microscope or a hand-held version—the Perkins tonometer. The applanation
tonometer measures the force required to flatten a small area of a central cornea.
The precise area to be flattened is predetermined and varies with the instrument
used. More force is required to flatten the circle on the cornea when the intra-
ocular pressure is high than when it is low. Alternative devices are the electronic
tonometer, the tono-pen which also works by applanation, and the
pneumotonometer which provides a continuous IOP trace of minor variations
in intra-ocular pressure coinciding with the heartbeat.

50
 Clinical Examination and Investigation of the Eye and Vision

COLOUR VISION TESTING

The impaired ability to perceive colour is generally an inherited condition

affecting males rather than females. Pathological conditions of the optic nerve
or retina may also cause defects in colour vision. The majority of patients with a
colour defect of red see it less brightly or more brown than is perceived by a
normal individual. A defect in colour vision is not generally visually disabling,
but it is a barrier to the pursuit of certain careers.
Evaluation of colour vision is most often performed with pseudo-
isochromatic colour plates (Ishihara plates). Each eye is tested separately; the
patient is instructed to look at a book of plates consisting of patterns of coloured
and grey dots. A patient with normal colour vision can easily detect numbers or
figures composed within the multi-coloured dots. Patients with colour vision
defects have difficulty, or are unable to distinguish the numbers and figures.
There are various combinations of colours used in the plates to categorise the
specific colour vision defect.
The 15-Hue Farnsworth-Munsell-D-15 test provides a more precise
determination of colour vision defects. In this test, 15 pastel-coloured chips with
similar brightness but subtly different hues have to be arranged by the patient in
a related, coloured sequence. The sequence is obvious to patients with normal
colour vision, but patients with colour defects make characteristic errors in
arranging the chips.

PACHYMETRY

Pachymetry is the measurement of the thickness of the cornea, which is

normally 0.5–0.6mm thick at the centre and 0.75–0.95mm at its periphery. The
measurement of corneal thickness is very important in the practice of refractive
surgery, and especially those aspects which apply to corneal thinning or
incision. In addition, several diseases called corneal dystrophies cause swelling
or thinning of the cornea. The measurement device known as the pachymeter
(also spelt pachometer) is an ultrasonic device which uses reflected sound
waves to measure corneal thickness. An optical device also exists which fits
onto the slit-lamp biomicroscope.

SPECULAR MICROSCOPY

Endothelial cell microscopy is a technique used for assessing the quantity and
status of the cells of the corneal endothelium. The single layer of cells lining the
posterior aspects of the cornea is vital for the integrity and optical clarity of the
cornea. The number of the cells in the endothelium provides an important
indicator of the health of the cornea; the shape and form of the cells provides

51
 Ophthalmology

similar information. The cells are irreplaceable and therefore photographic

recording of the status of the corneal endothelium provides a method of
assessing the quality of operative intervention in the eye, particularly in cataract
and refractive surgery.
The corneal cells can be observed on the slit-lamp biomicroscope with very
high magnification to give a clinical impression of the status of the endothelium,
but the cells are too small to get accurate information and a record is required.
There are a number of endothelial-cell cameras available, the earlier models of
which used a contact lens to applanate the cornea and bring the cells into focus.
More modern devices are non-contact, comfortable for the patient and provide
an automated method of recording this information.

OPHTHALMIC PHOTOGRAPHY

Ophthalmic photography is used to document ophthalmic conditions for

diagnosis, documentation and communication. There are three major types of
ophthalmic photograph:

(a) external eye photography;

(b) slit-lamp biomicroscope photography; and
(c) fundus photography, including colour and fundus fluorescein angiography.

External photography
External photography requires a macro-lens-equipped, 35mm, still camera with
electronic flash.

Slit-lamp microscope photography

The slit-lamp biomicroscope exists in photographic versions, some of which are
automated, allowing excellent photography of all aspects of the anterior
segment of the eye.

Ocular fundus photography and fundus fluorescence

photography/angiography
This procedure utilises a fundus camera, which is an indirect ophthalmoscope
adapted to record the images on film (or via a CCD to provide electronic
imaging). If the camera is equipped with two filters, a blue filter over the flash
lamp (excitation filter) and a yellow filter (barrier filter) in front of the film, the
camera is equipped to undertake fluorescein photography or angiography
(FFA) (Figures 24 and 25, pages 54 and 55).

52
 Clinical Examination and Investigation of the Eye and Vision

This is a technique where a yellow-dye fluorescein is injected into a patient’s

vein. As it circulates through the blood vessels in the retina and choroid at the
back of the eye, the blue-light rapid-sequence flashes excite the dye to fluoresce,
The fluorescence of light which is emitted at a different wavelength to the dye
itself passes through the barrier filter to be recorded on film. The barrier filter
excludes the transmission of the reflected light, which is blue in colour. The
resultant images give a brilliant, detailed picture of the retinal arteries, veins
and capillaries and demonstrates many pathological features in the fundus, some
of which are clinically invisible. Fundus fluorescein photography has been a
valuable clinical tool over the past 20 years.

ULTRASONOGRAPHY

A-scan—a form of ultrasonographic tracing of the echoes from the eye using
ultrasonic signals. A-scan is a time amplitude, one-dimensional display where
echoes occur as vertical deflections from a base-line on the screen of an
ultrasound instrument.
B-scan—a form of ultrasound scanning of the eye to provide a two-dimensional
display where echoes occur as dots on the screen of an ultrasound instrument.
It provides a brightness-intensity-modulated display.

These techniques use the reflection or echo of high-frequency sound waves from
various structures in the eye to give information which may not be visible in an
eye with opaque media for example, or it provides information regarding eye
measurements, in particular the length of the eyeball, the thickness of the lens
and the depth of the anterior chamber. For measurement purposes A-scan mode
ultrasound is used. This utilises sound waves travelling in a straight line to
reveal the position of, and distance between, structures within the eye and orbit.
It is of particular importance in the calculation of a replacement lens in the
operation of cataract extraction and lens implantation.
B-scan ultrasonography delivers radiating sound waves to provide a two-
dimensional reconstruction of the eye and orbital tissue.

REFRACTION

The measurement of refractive errors in an eye is called the refraction test. It is

performed in the main by the optometric profession. The test takes two forms:
objective and subjective.

53
 Ophthalmology

Figures 24 (above). Fluorescein angiography of the fundus of the eye. Figure 24 (above
left) shows the arterial phase. As the fluorescein dye appears in the retinal arteries,
the photograph shows them as white threads on a mottled background. The mottling
is due to a combination of fluoresceindye in the choroidal circulation of the eye and
the overlying, retinal-pigment epithelium, which is most densely pigmented at the
macula.

Figure 25 (above right) shows the venous phase. Within a second the dye has permeated
the retinal capillaries and is draining out of the eye through theretinal veins.
Consequently, all the retinal vessels (arteries, capillaries and veins) appear white against
the mottled background of choroidal fluorescence and pigmentation

(a) The objective test consists of shining a light into an eye through correcting
lenses until a lens combination is discovered that causes a neutral reflection
of the light from the retina. This technique is known as retinoscopy and is
an acquired skill. In recent years a variety of electronic devices have been
utilised to automate this procedure, the instruments being known as
autorefractors.

54
 Clinical Examination and Investigation of the Eye and Vision

(b) Once the refractive error is discovered by the objective method, the efficacy
of the lenses needed to correct the focussing error of the eye are tested by
placing them in a trial frame or phoropter (a housing containing the entire
range of correcting lenses mounted on wheels, so that they can be sequentially
rotated in front of the test eye—a more convenient method of testing favoured
by some optometrists) in front of the test eye. The patient’s responses are
sought in relation to minor variations around the basic error until subjective
satisfaction is achieved, whereupon the spectacle formula may be prescribed.

CORNEAL TOPOGRAPHY

Also known as videokeratoscopy and corneal mapping (Figure 26, page 56), this
is a technique which provides data with regard to the refractive power of the
corneal surface (tear film/air interface), corneal shape and corneal irregularity.
It is a technique performed by video recording of the reflection of a concentric

55
 Ophthalmology

series of black and white rings from the corneal surface, which acts as a convex
mirror. The interface between the black and white rings is measured by
computer programs which receive data from each of 360 points, ie at each
degree in each circle which bounds each ring. With 18 or more rings the
computer has thousands of reference points which can be checked against a
standard surface in order to provide a mathematical representation of corneal
shape, refractive power and surface regularity.
The resultant data is conveniently expressed in hard copy form as colour-
coded maps with ‘hotter’ colours (red, orange and yellow) representing
corneal refractive powers steeper than an average cornea, and ‘cold’ colours
(greens and blues) lesser powers or flatter regions of the cornea. Such maps—
and there are many variations on the theme—are invaluable in the
management of refractive surgical procedures. Conversely, to proceed to
surgery without their use may constitute an inadequate standard of care.
Furthermore, the maps provide an excellent means for documentation
(record), communication and education.

Figure 26. Corneal topography. Shown here is a black and white representation of a
colour-coded map of corneal shape and refractive power. It is an essential precursor to
refractive surgery and an invaluable tool for monitoring post-operative progress and
communication

56
 Clinical Examination and Investigation of the Eye and Vision

ELECTRO-DIAGNOSIS

Recording electrical signals from ocular structures is known as electro-

diagnostic testing. There are three main forms: the electroretinogram (ERG); the
electro-oculogram (EOG); and the visually-evoked potential (VEP).
Electro-diagnosis provides an objective evaluation of ocular function. It does
not tell the observer what an eye can see, but it will demonstrate through normal
recordings that the tissues and the organ are functioning properly. Conversely,
abnormal responses will confirm that trauma or disease have compromised ocular
function. It is an important investigation in the medicolegal sense, for claims of
visual disability in the face of normal ocular anatomy on clinical examination
may be confirmed or denied objectively.

Electro-retinography
The normal retina creates electrical changes when exposed to light. The
measurement of the changes in the electrical potential in the retina under the
influence of light is known as electro-retinography, and the output is known as
an electroretinogram (ERG). The ERG indicates the difference in electrical
potential between an electrode in a corneal contact lens and a electrode on the
forehead. The ERG is a wave-form response with multiple elements which
result from several superimposed events. There are four principal waves:

A-wave—the initial negative response after a latent period following the light—
it originates in the photoreceptor cell layer (rods and cones);
B-wave—the quality of deflection emanating from electrical changes in the
bipolar cell layer, ie the layer of the neural or the nerve layer of the retina
connecting the light-sensitive elements, rods and cones to the retinal nerve
fibres;
C-wave—a slight, positive deflection in the wave; and
D-wave—the effect of removing the light, producing a positive potential.

The value of electro-retinography is in the evaluation of retinal function in eyes

where the optical media are obscured, or where there is no clinical evidence to
support the patient’s contention that the eye cannot see. Recent developments in
the technique of electro-retinography allow discreet areas of the retina such as
the macula to be targeted to elucidate further their function.

Electro-oculography (EOG)
A difference in electrical potential occurs between the cornea and the posterior
part of the eye which is known as the corneo-retinal or resting potential.
Although it is difficult to measure the actual resting potential, the problem is
resolved by placing electrodes on the skin on either side of the eye at the medial

57
 Ophthalmology

and lateral canthi. The patient then makes horizontal eye movements of a
constant size to induce a change in the resting potential, which is picked up by
the electrodes and revealed as the electro-oculogram. The changes in potential
relate to the resting potential if the eye movements are constant.
The EOG is affected by the state of light or dark adaptation of the eye. With
light adaptation there is a progressive rise in amplitude of the waves, whereas
with dark adaptation there is a fall. Thus, the ratio between the maximum
amplitude achieved in light adaptation (the light peak) and the minimum of
amplitude achieved in dark adaptation (dark trough) is determined to evaluate
the response. Normal patients have EOG ratios of 1–60 or greater. It is believed
that the EOG largely reflects the metabolic activity of the retinal-pigment
epithelium, and thus the technique can be used to provide an evaluation of some
aspects of the condition of the retina. The technique can also be used to monitor
eye movements such as in nystagmus, lazy eye conditions (amblyopia) and with
abnormal fixation of objects by the retina (eccentric fixation).
The EOG as a test of retinal function compliments the ERG, and together
they provide some information about a portion of the ocular apparatus. While
pathological processes in the eye that cause alteration in one response also cause
similar responses in the other technique, there are some exceptions. For example,
in juvenile macular disease, Best’s disease or vitelliform macular dystrophy, the
EOG ratio is abnormal not only at an early stage in those affected by the disorder,
but also in those who carry the gene for the disorder. In these patients the ERG is
normal. In retinitis pigmentosa in its later stages the EOG and the ERG tend to
parallel each other, but there are variations in some of the specific forms of the
disease.

Visual evoked response (VER) or visual evoked potential

(VEP)
When a flash of light reaches the retina it causes the emission of a volley of
nerve impulses which are transmitted along the neural visual pathways to the
posterior aspect of the brain where the visual cortex resides in the occipital
region. The response of the brain to the light stimulus can be recognised by
placing electrodes over that portion of the brain and using computer programs
to eliminate other brain activity on the display. The technique is of great value
in providing objective evidence of the function of the optic pathways. By
stimulating each eye separately, nerve lesions can be recognised by the
absence of a response on one side or the other, thus identifying the affected
nerve. Similarly, partial lesions of the optic nerve will result in delay of
conduction and a reduction in the amplitude of the response. It is therefore an
important tool in the objective investigation of the visual system in
nonresponsive patients such as infants and malingerers.

58
 Clinical Examination and Investigation of the Eye and Vision

MAGNETIC RESONANCE IMAGING (MRI)

Proton magnetic resonance imaging with the utilisation of surface coils

produces high-level resolution of body tissues. It is a modern, non-invasive
technique that provides rapid insight into brain and orbital problems in relation
to ophthalmic and neuro-ophthalmic disorders. As MRI does not utilise X-rays
or ionising radiation it is not harmful to biological tissues or systems. Tumours,
fat, blood, nerve tissue and bone are examples of body materials which have a
characteristic MRI appearance. The scans may also be enhanced by coupling the
technique with contrast media.

COMPUTED TOMOGRAPHY

CT scanning uses thin, X-ray beams to obtain tissue density values, from which
cross-sectional images of the body are derived. It is a technique particularly of
use in the evaluation of the brain, orbit and eye. It is a safe and rapid, non-
invasive technique which has revolutionised improvements in neuro-
ophthalmic diagnosis. Techniques have progressed to the point where high
resolution and contrast facilitates detailed examination of the intracranial and
orbital structures, and also to some extent within the eye. Certainly the optic
nerve eye muscles and optic canal can yield computer-derived reconstruction,
which is an x-ray technique and a primary procedure for diagnosing orbital
disorders.

59
 CHAPTER SIX

VISUAL DEFECTS AND BLINDNESS

Visual defects may result from faults in the transmission of light through the optical
system of the eye from the cornea to the retina, or from failure of the retina or
visual pathways (nerve system). In broad terms, visual defects arising from
conditions which affect the path of light from cornea to retina can be regarded as
treatable, whereas defects affecting the nerve tissue of the retina or optic pathway
are rarely affected by medical or surgical intervention. While the optical system
of the eye can be repaired or replaced, the neural tissue and its supporting layers
(the retina, its choroidal vascular supply, the optic nerve and the visual pathways
of the brain) are irreplaceable and, for the most part, irreparable.
The definition of blindness varies from country to country throughout the
world. While the World Health Organisation describes 65 different definitions
of blindness, in the UK a patient may be certified blind if her visual performance
is so poor that she is unable to perform work for which sight is required. Generally
speaking, this means a visual acuity of 6/60 or less, ie 10% or less of best visual
acuity (6/6 or better). The definition would also include those eyes disabled by
gross loss of visual field. In the UK there is a second category of visual disability
known as partial sight. Patients are registered on form BD8.

BD8 (1990) parts 1–4

Record of examination—to certify a person as blind or partially sighted
Whether to certify a person as blind or partially sighted requires the of use your
own judgment.
Parts 1–4 are for consultant ophthalmologists to record the results of their
examination.
Part 5 is for consultant ophthalmologists to record the causes and conditions that
affect the person’s vision. This part is for statistical purposes only.
Please fill this form in with a typewriter if possible. If you cannot arrange for the
form to be typed, use a black, ball-point pen. Please write clearly and make sure
that your writing goes through to every copy. You do not need to use carbon.
Please make sure that both sections are filled in.
Blindness
Definition
The National Assistance Act 1948 says that a person can be certified as blind if
they are:
‘so blind that they cannot do any work for which eyesight is essential’.

61
 Ophthalmology

The test is whether a person cannot do any work for which eyesight is essential
and not just their normal job or one particular job. Only the condition of the
person’s eyesight should be taken into account. Any other physical or mental
condition should be ignored. The main condition to consider is what the person’s
visual acuity is. But the conditions set out below should also be considered.
Visual acuity is the best direct vision that can be obtained, with appropriate
spectacle correction if necessary, with each eye separately, or with both eyes
together if a person has both. Visual acuity is tested according to Snellen’s type.
Who should be certified blind
People can be classified into three groups:
1 People who are below 3/60 Snellen
Certify as blind—most people who have visual acuity below 3/60 Snellen.
Do not certify as blind—people who have visual acuity of 1/18 Snellen unless
they also have considerable restriction of the visual field.
In many cases it is better to test the person’s vision at 1m. 1/18 Snellen
indicates a slightly better acuity than 3/60 Snellen. But it may be better to
specify 1/18 Snellen because the standard test types provide a line of letters
which a person who has full acuity should read at 18m.
2 People who are 3/60 but below 6/60 Snellen
Certify as blind—people in this group who have a very contracted field of
vision.
Do not certify as blind—people who have had a visual defect for a long time
and who do not have a very contracted field of vision, eg people who have
congenital nystagmus, albinism, myopia and other such conditions.
3 People who are 6/60 Snellen or above.
Certify as blind—people in this group who have a very contracted field of
vision especially if the contraction is in the lower part of the field.
Do not certify as blind—people who are suffering from homonymous or
bitemporal hemianopia who still have central visual acuity of 6/18 Snellen or
better.
Other points to consider
These points are also important because it is more likely that you will certify a
person as blind in these circumstances
How recently the person’s eyesight has failed—A person whose eyesight has failed
recently may find it more difficult to adapt than a person with the same visual
acuity whose eyesight failed a long time ago. This applies particularly to people
in groups 2 and 3 above.
How old the person was when their eyesight failed—An old person whose eyesight
has failed recently may find it more difficult to adapt than a younger person with
the same defect.

62
 Visual Defects and Blindness

Partial sight
Definition
There is no legal definition of partial sight. The guidelines are that a person can be
certified as partially sighted if they are:
‘substantially and permanently handicapped by defective vision caused by
congenital defect or illness or injury’.
People who are certified as partially sighted are entitled to the same help from
their local social services as people who are certified as blind. But they may not be
able to get certain social security benefits and tax concessions that only people
who are certified as blind can get.
Who should be certified partially sighted.
As a general guide, certify as partially sighted people who have visual acuity of:
• 3/60 Snellen to 6/60 Snellen with full field;
• up to 6/24 Snellen with moderate contract of the field, opacities in media or
aphakia; or
• 6/18 Snellen or even better if there is a gross field defect, eg hemianopia,
or if there is marked contact of the visual field, eg in retinitis pigmentosa or
glaucoma.
Other points to consider
Infants and young children—who have congenital ocular abnormalities leading to
visual defects should be certified as partially sighted, unless they are obviously
blind.
Children aged four and over—should be certified as blind or partially sighted
according to the binocular corrected vision.

(For comparison it is interesting to note that in the US, legal blindness is

represented by a corrected visual acuity of 20/200 or worse (6/60 UK
equivalent) in the better eye or less than 20° of visual field remaining in the
better-seeing eye (a normal visual field extends at least 120° in the horizontal
meridian and 65% in the vertical meridian).)
In the UK the visual performance required to drive a motor vehicle is
measured by the number plate test (see Appendix 2, p 227), which represents a
visual acuity of at least 6/10 and a visual field of not less than 120° in the
horizontal and 20° above and below fixation—in the vertical meridian with no
significant islands of visual loss in the general visual field.
The visual requirements for driving a heavy goods vehicle are much more
stringent, as are certain occupational requirements such as police service, fire
service, the armed services, civil aviation, etc (see Appendix 2, page 211).

63
 Ophthalmology

MAJOR CAUSES OF BLINDNESS

The four major causes of blindness in the UK in order of frequency are:

(a) macular degeneration (see Chapter 11);

(b) cataract (see Chapter 9);
(c) glaucoma (see Chapter 12); and
(d) diabetic retinopathy (see Chapter 13).

Of course, blindness may be caused by many other diseases, but these occur
much less commonly. The four major causes of blindness listed above are
associated in part with advancing age. The average age of patients with
macular degeneration is about 70 years, for glaucoma 72 years, cataracts 69
years and for diabetic retinopathy 61 years. There are racial and geographic
variations in these figures, eg cataract is more prevalent in sub-tropical
climates and Caucasians. Glaucoma is more prevalent in patients of African
origin and is more severe in its type. Diabetic retinopathy is particularly severe
in some American Indian tribes. Macular degeneration is inevitable in all eyes
if patients live long enough.
In general the human body consists of vital organs—heart, brain, kidneys
and liver—and non-vital organs—eyes, ears, joints, etc. As with all bodily tissues
there is a constant process of cellular turnover, but in the ultimate failure of the
processes of repair and regeneration (ageing) there is in a sense a race between
which systems fail first. If a vital organ fails, by definition the person dies. If the
vital organs continue to function, the non-vital organs inevitably decay.
Some repair is possible, eg to the optical system of the eye. Cataracts are
extremely treatable because they are part of the optical system of the eye.
However neurological tissue such as retinal tissue cannot be replaced, and it is
an unfortunate fact that if a person lives long enough, his central retina
(macula) will degenerate to cause a gradual or occasional dramatic loss of
visual performance. When the problem occurs it is a consequence both of the
genetic strength of tissues and the effects of the environment to which they are
exposed.
In addition to eye diseases seen with increasing frequency as people age,
the need for eye glasses is almost universal. Approximately 40% of Western
populations aged 5–20 years require the use of eye glass correction. Past the age
of 40–50 years there is almost of doubling in the need for eye glasses, and by 65
almost 100% of the population require eye glasses to see clearly. As eyes age the
crystalline lens in particular changes its form and consistency, compromising
the eye’s ability to focus near objects, hence the requirement for reading glasses
to correct the condition of presbyopia.
The increased incidence of eye disease as ageing occurs, and the ability of
the eye to reflect inner diseases of the body, suggests that regular eye examination
is prudent. Comprehensive medical eye examinations to check for early signs of

64
 Visual Defects and Blindness

eye disease and to provide corrective lenses are advised: for pre-school children;
for all family members if there is a family history of eye disease; if there are any
visual problems; and for everyone from 40 years onwards. Optometrists provide
primary eye care in the UK, and there are approximately 7,000 optometrists
compared to only 650 ophthalmologists.
It is the statutory duty of optometrists to request further advice should they
discover that the vision of an eye is sub-standard for reasons that were not
previously known, or if they detect any pathological signs in the eye (see Chapter
18). It is not necessary for them to make a diagnosis, simply to be aware that
there may be a problem. Optometrists then complete form GOS 18, which
indicates the visual performance of the eye with and without corrective lenses,
the previous, best-corrected visual acuity (if known) and observations and reasons
for referral to the patient’s family doctor.
The family doctor may then deal with the problem if she has ophthalmic
expertise; if not she will refer the patient on for expert ophthalmic opinion, as
there is a statutory duty to add medical information that may be of help to the
examining ophthalmologist. This will include a history of general disorders, past
ocular history if known and medication if appropriate.
How frequently should eye examinations be undertaken? In the UK it has
become traditional for patients over the age of 40 to receive an appointment to
see an optometrist every two years for routine testing. This is a sensible approach
to screening the population’s eyes with a view to early detection of disease. Early
diagnosis and treatment may solve many problems, whereas delay can cause
irreparable harm. Individuals also bear responsibility to report visual or ocular
symptoms at the earliest opportunity to serve their own best interests.
Delay in reporting symptoms by the patient, failure to refer by the
optometrist, delay in referral by GPs, and delayed hospital appointments for
ophthalmic review are all major items in the litigation process with regard to
ocular and visual defects.

EYE ASSESSMENT/EXAMINATION

A comprehensive eye examination has two parts, the first of which is used to
gain historical information with regard to previous history of eye disorders and
general medical considerations. This includes the history of recent and current
medication. A family history which might reveal familial tendency for certain
disorders and a social history are also relevant, as certain pursuits such as
smoking may have an impact on vision (see Chapter 3).
The second component is the physical examination of the eyes (see Chapter
4), which commences with an assessment of visual performance. The first point
to assess is uncorrected visual acuity before vision is assessed with any refractive
correction, ie the patient’s own glasses, or a re-test or refraction to ascertain best
corrected visual acuity. Other aspects of visual assessment include visual field

65
 Ophthalmology

estimation. This can be done crudely by confrontation testing, in which a patient

covers one eye while the remaining eye stares into space at a fixed point (usually
the observer’s own contra-lateral eye) and a small, white object is moved from
the periphery and blind areas to the point where the patient becomes aware of
its presence. In this way a rapid assessment of visual field can be obtained which
will reveal gross faults in the field.

GENERAL ASPECTS OF VISUAL DEVELOPMENT AND

VISUAL DEFECTS

Presbyopia
Many people believe, incorrectly, that poor vision is a natural part of the ageing
process. This misconception is fostered by the common observation that reading
glasses or bifocals are more likely to be required by those over 40 years of age.
Whilst millions of ordinary people may require eye glasses to see clearly, those
who are near-sighted or myopic require glasses for distance tasks but not for
close work such as reading. Far-sighted or hyperopic individuals, however, find
that eye glasses are required both for distance and near vision, a process that
progresses usually over the age of 40 but sometimes later. This process is the
result of thickening and stiffening or hardening of the crystalline lens which
steadily grows in size due to the continuous production of lens fibres within its
substance. In youth the crystalline lens is able to change its dimensions so that it
bends light more effectively, a condition necessary to bring into focus near
objects. As it loses this ability so supplementary glasses or reading glasses or a
bifocal element in distance glasses are required to provide that additional
focussing power. This loss of accommodation is known as presbyopia and is one
aspect of far-sightedness or hyperopia.

Does the wearing of glasses make eyes dependent upon them?

The wearing of glasses is simply the use of an appliance to focus an image when
eyes are no longer capable of doing it on their own. Not wearing glasses does
not make the eyes worse, it simply makes the vision blurred and may lead to
symptoms of eye strain such as fatigue when reading, or headaches. Many
people consider the wearing of eye glasses a handicap, an overt admission of
the ageing process, or have self-image problems that make them resist their
sensible use. People with astigmatism, ie eyes with more than one principal
focus in the eye, go through most of their life without glasses but suddenly find,
as a facet of ageing or not uncommonly after trauma, that they can no longer
achieve satisfactory vision without the aid of glasses to correct the astigmatism.

66
 Visual Defects and Blindness

It is quite a common complaint of patients in their third, fourth and fifth decades
after minor personal injuries, which seem, often in a indefinable way, to disturb
the psyco-optical processes that have previously allowed a person to manage
happily enough without glasses. This phenomenon is more common around the
onset of presbyopia than it would be in younger people.

Does the wearing of contact lenses slow down the deterioration in

vision?

Contact lenses are a reasonable alternative for many people to having to wear
eye glasses. They may effect minor transient changes in the shape and focussing
power of the eye when they are withdrawn. There are a number of
complications of contact lens wear, but in general they serve a valuable function
for hundreds of thousands of people.

If a person needs to change the eye glass prescription regularly, does

it mean the eyes are deteriorating?

In childhood, the wearing of eye glasses may require fairly frequent change
of spectacle prescription. This is associated with the phenomenon of eye
growth-as the size and shape of an eye changes with growth, so the prescription
for lens power will also change. This process usually stabilises on attainment of
adolescence and early adulthood. If multiple changes continue, the most likely
abnormal situation such as pathological or progressive myopia may be
occurring, or the patient may be developing a cataract, or it may be an early sign
of the onset of diabetes.
On the other hand, not all eyes, especially in early adulthood, accept the full
and necessary refractive correction, for, with the juvenile flexibility of the
crystalline lens, the eye may unwittingly provide part of its own adjustment for
abnormalities of shape and size of the eye globe. Thus, there may be a natural
reason for regular change of eye glasses over a period of 1–2 years. If an
optometrist under-corrects by design or for any other reason, the change of
spectacle prescription may be more frequent than is really necessary.

What is an amblyopic or lazy eye?

Amblyopia is the inability of an otherwise physically-normal eye to achieve a

normal visual acuity. It may be relative amblyopia, eg visual acuity no better
than 6/9 or 6/12, or significant amblyopia when the vision may be less than
6/60. The more common cause are eyes not working together, as in congenital

67
 Ophthalmology

stabismus when the vision of the squinting eye fails to develop as it is

suppressed within the brain to avoid the sensation of double vision.
Alternatively, if there is a discrepancy between the focussing power of the two
eyes in an individual, the eye with the greater focussing disability, usually
hyperopic or astigmatic, will fail to develop to its full potential.
It is important to realise that the process of vision is something that is learned
by each individual and initiated at birth. Though an eye may be physically normal
at birth, it has to transmit a focussed image to the brain to allow the neural
network between the eye and brain to mature. The process of maturation occupies
the early years of life and, if it is interrupted by either of the processes mentioned
above or any diseased process that will obscure the visual pathway between the
cornea and the retina, visual development will be arrested. During those
formative years, if vision is developing normally but the visual pathway is
obscured by disease or any disorder such as injury that might affect the focus of
the eye or the transmission of light, the continuing process of visual development
may be arrested or even reversed.
If there is interference between the type of image from either eye because it
is not aligned with the fellow image, as in the squinting eye, or because it has a
different focus, then visual development suppression will occur, a condition
known as amblyopia. If amblyopia, either strabismic or due to an equal focus
(anisometropic amblyopia), can be identified in early childhood, it can be treated
by correcting the focus of the eye and patching the fellow eye for varying periods
to concentrate on visual development to the lazy or amblyopic eye. By the age of
seven or sometimes earlier the vision is fixed, and if failure to diagnose amblyopia
has occurred at that stage then no treatment, medical, orthoptic or surgical, will
influence the quality of vision in the affected eye. Deprivation amblyopia, the
failure of an image to be formed on the retina due to obscuration of the light
path through the eyes, can only be overcome by early diagnosis of the cause,
which, however, is not always amenable to therapy (see congenital cataract,
Chapter 8).

When should a child’s eyes be examined?

A child is never too young for an eye examination. If there is a family history of
eye disease or refractive disorder, an eye examination by an ophthalmologist
should certainly be performed before a child starts school and periodically
thereafter, depending on the results of the examination. If there is an indication
that there may be a problem, eg the presence of a strabismus, then a very early
examination may follow. If there is simply an abnormality of focus between the
two eyes, this is often not detected because the child cannot communicate the
problem to parents or health care professionals. Latterly, sophisticated objective
methods of assessing the focus of a child’s eye can be undertaken, especially by
photographic methods, which suggest that a screening process for the very
young could be effective.

68
 CHAPTER SEVEN

AGEING, OPTICS AND THE EYE

INTRODUCTION

Optometrists advise the general public to have an eye test every two years. They
send reminders to former patients, but is this necessary? What is the purpose of
the service? Do eyes, their focus and their vision change with such regularity?
What diseases may be lurking to be uncovered by regular testing?
Eyes do change with age. At birth, eyes are approximately 80% of their final
adult size and eyes which will become normal sighted (ie focussed) are hyperopic
in infancy as their smaller size dictates. From the mid-teens, eyes are relatively
stable in size and focus until the fifth decade of life, when presbyopia (the need
for reading glasses) arrives consequent upon physical changes in the crystalline
lens, causing it to lose its powers of accommodation. In childhood the range of
accommodation will be 10 dioptres or more; a person of 50 years may only have
1–2 dioptres of accommodative function.
As accommodation declines with age so stronger reading glasses are required
in order to keep near objects, eg reading matter, at within arms length distance.
In dioptric power terms, reading glasses start at 1 dioptre and increase by 0.5
dioptre increments to a maximum usefulness of 3.5 dioptres. Higher
magnification in a spectacle correction is counterproductive because of the
magnification effects and the closeness of objects in focus with a restricted field
of view. Such magnification may aid the visually disabled but is not relevant for
the normal-sighted person. Thus, all a normal-sighted person has to do is to try
glasses of different powers to find which is suitable.
From an optometric point of view, therefore, the times of change are
childhood through adolescence and the over 40 age group. As a person ages the
eye undergoes gradual, physical decline, with the crystalline lens and the retina
showing most effects. The fluid drainage system in the eye may become less
efficient causing the intra-ocular pressure to rise and create the syndrome of
glaucoma.
Optometrists in the UK are in the first line of duty in relation to ocular and
visual problems. They are the most accessible and are effectively the means of
screening the public’s eyes. It is their duty to refer abnormalities to medical
practitioners (see Chapter 4). Some ocular disorders are silent in onset and
irreversible in effect. Therefore, an optometric test coupled with an eye
examination is of real value, and has the potential to unearth significant disorders
and avoid visual problems.

69
 Ophthalmology

VISUAL FUNCTION AND AGEING

Vision is a product of the image formed by the optical system of the eye,
focussed on the retina and transmitted to the occipital cortex of the brain where
it is perceived. With advancing age, especially past mid-life, changes in the
optical system of the eye make focussing on near objects increasingly difficult.
With loss of corneal and lens transparency the image deteriorates. If cataract
formation occurs, as it does in everyone to a degree, the image quality suffers.
Retinal ageing (see Chapter 10) makes for loss of acuity, even in the healthy-but-
ageing retina. The 6/4 acuity of youth becomes 6/9 as normal in an 80 year old.
Of course there are many exceptions; rate of ageing is genetically determined
with some environmental influences.
The import of these physiological changes that occur with age is the
establishment of visual norms for particular ages against which claims of visual
deficit can be measured. Visual field does not vary with age in healthy eyes, but
colour vision may deteriorate to a degree conforming with age changes in the
macula.

REPAIR AND REGENERATION (HEALING PROCESSES)

The tissues we possess at one stage of our lives are replaced by similar tissues
throughout life. Molecules are replaced by fresh ones and so, throughout life, a
continuous process of tissue repair and regeneration occurs. The material in our
old bodies is quite different from that in our young forms as worn parts are
replaced. However, the ageing process infers that our capacity to replace and
repair tissues falters and tissue degeneration follows with loss of function as a
consequence.
The eye provides a special example of these processes, especially in the
macula—that complex, ultra-sensitive tissue that provides the mechanism
whereby we achieve our sharpest vision. The light-sensitive units in the macular
retina are constantly being repaired and replaced, and their supporting cellular
system, the retinal pigment epithelium, demonstrably becomes overloaded with
a lifetime’s accumulation of processed debris, eventually compromising its
performance. Damaged tissues, either traumatised or diseased, have variable
powers of recovery or repair.
For example, the endothelial cell layer lining the posterior aspect of the cornea
cannot be replaced. If cells are lost the remaining cells assume their function
until the depletion is too great for the surviving cells to maintain the cornea
whose metabolic functions they serve. Tissues separated from their support
systems may have very limited survival times or capacities to recover. This aspect
of repair and regeneration is frequently of medico-legal importance in relation
to delayed diagnosis or treatment, with compromised visual function.

70
 CHAPTER EIGHT

OCULAR PATHOLOGICAL PROCESSES

SYSTEMATIC APPROACH TO DISEASE

Textbooks of ophthalmology provide a classified account of all ocular disorders.

For detailed understanding of the whole range of ophthalmic medicine and
surgery, such texts, reference works and current literature need to be consulted.
For the non-medical person, an understanding of the classification of disease
may be helpful and is therefore considered in this chapter. Succeeding chapters
will consider some of the more common areas of ophthalmology where
personal injury and litigation complaints lie.
A systematic approach to consideration of disease is as follows.

Anatomy
The structure of the tissue or tissues of the eye and related formations to enable
the reader to have a better understanding of malfunction and its management.
The anatomy of the eye is generally considered in Chapter 3. Therefore, to avoid
repetition, cross-referencing will be supplied.

Pathophysiology
Tissue and organ malfunction is explained in the context of the particular.
Physiology is the study of how biological cells, tissues and organs function.
Pathology is the study of malfunction generally in altered tissues (pathological
anatomy). Pathophysiology is how tissues and organs fail to function normally.
The reasons are considered herein, for this book is not directly concerned with
normal physiology.

Symptoms
Patients complain of a variety of ocular and visual symptoms. These are
classified as presenting complaints, the history thereof, duration, degree,
localisation, improvement, deterioration, etc. More often than not, the history of
a problem will suggest a narrow differential diagnosis to be specified after
clinical examination and investigation.

71
 Ophthalmology

Clinical signs
Examination of a patient’s eyes reveals normality or abnormalities known as
clinical signs. Training, experience, powers of observation based on specialised
examination procedures, all contribute to the successful recognition of variation
from the usual and categorisation as pathological.

Investigations

Investigations, ie laboratory, radiological and special tests, are less used in

ophthalmic diagnosis than in other areas of medicine because, not only is the
eye the organ of vision, but most of its tissues are visible to the trained observer
to whom most pathological entities, of which there are thousands, are once and
seen never forgotten.

Natural history

All disease and degenerative processes run a natural, if variable, course if

untreated. Clinicians must be aware of the expectation of allowing a condition
to run its course, whilst weighing up the risk versus benefit prospects of medical
or surgical intervention. Failure of therapy may be balanced against the natural
history and thereby lay the clinician open to criticism. The natural history of
ophthalmic conditions is an important consideration in the matter of prognosis
once the present condition has been established. Some conditions run a self-
limiting course whilst others fluctuate in the general direction of deterioration.
Remission and variable periods of stability characterise some syndromes. It is
therefore of considerable importance that the natural history of conditions is
understood, particularly in the context of treatment. Would the condition have
improved anyway? Did treatment adversely affect outcome when compared to
natural evolution of the disease?

Referral

Clinicians should not assume responsibility for management of conditions they

are not competent to treat, especially if recognised expertise is available.
Optometrists should refer any pathological condition in an eye, or an
unexplained deterioration of vision, to general medical practitioners who may
refer the patient for expert ophthalmic opinion. When to refer is often a simple
decision. Failure to refer with consequential problems for the patient is one form
of error of omission.

72
 Ocular Pathological Processes

Treatment
Medical—by drugs applied to the ocular surface (topical) systemically (by
mouth or injection, sub-conjunctivally by injection, inside the eye by
injection).
Surgical—by incision, or by laser or other physical devices.
These terms are self-evident. The decision to treat or not to treat depends on the
natural history of the condition and the evidence for efficacy for particular
treatments. Has the correct treatment been applied? Was there undue and
unnecessary delay in implementing treatment? These questions figure
prominently in litigation for medical malpractice, therefore it will be
appropriate to indicate some guidelines for intervention and time-scales.

Outcome expectations
What are the risks? What are the potential benefits of treatment? In some areas
statistical information may be persuasive, though individuals have to weigh
their own prospects in the light of the confidence they have in the physician or
surgeon to match the statistical overview, and further to handle complications if
and when they arise. Does the patient proceed? Does she accept that the natural
history of the disorder may give her an acceptable outcome? Does she seek
corroboration of advice received from a third party?

Complications

Complications in any procedure may arise as a consequence of anaesthesia in its

various forms, occurring during the operative stage (per-operation) and/or in
the early, late or later post-operative period. An uneventful or technically-
successful operative procedure will limit the prospect of post-operative
complications at any stage; conversely, a complicated operation will enhance
the prospect of complications and undoubtedly delay, if not finally
compromise, full recovery. The skills required to manage complications are as
complex as the procedure itself. Clinical judgment as well as technical
knowledge is needed. It is the responsibility of a surgeon to manage the patient
post-operation as well as perform the surgery.

Prognosis—at stages

What is the outlook or prognosis for the function of an eye at various stages of
its presentation to the ophthalmologist? Clearly, late presentation will prejudice
the prospects for stabilising the condition let alone reversing its effects.

73
 Ophthalmology

Informed consent
Patients in the UK are required to sign a consent form for surgery or any
invasive procedure. Most hospitals utilise a general form which merely states
what the procedure is and confirms that its nature has been explained to the
patient by the medical signatory. Fully-informed consent is not a requirement
for invasive procedures in the UK, whereas in the US fully-informed consent is
the medical practitioner’s defence against malpractice accusations. The
questions surrounding this complex issue are considered in more detail in
Chapter 3.

Treatment in historical perspective

There is a consistent and considerable delay in the legal process in cases of
alleged medical negligence. At the time the incident occurred, was the standard
of practice employed consistent with that which would be approved by a
responsible body of medical opinion? In the interim period, the rapid progress
enjoyed by all medical specialties, and ophthalmology in particular, may have
changed management criteria significantly, but the case has to be considered in
the light of the historical perspective.

Management errors
Omission
Failure to act responsibly in the face of obvious visual loss or deterioration, or to
examine eyes correctly and miss important pathology, thereby denying a
patient timely treatment, are the important errors of omission that do occur in
the management of ophthalmic problems. Failure to carry out appropriate
investigations leading to delays in treatment is another example of an error of
omission.

Commission
This type of error occurs as a result of performing inappropriate invasive
procedures or the misapplication of correct therapy, eg laser burns to the
macular retina in the treatment of diabetic retinopathy.

EYE INFECTIONS

Micro-organisms exist freely in the environment on land, in soil, in food, on

plants and in animals. Some exist as parasites which may have a symbiotic
relationship with a host, ie the parasite feeds on the host but in return provides

74
 Ocular Pathological Processes

essential elements. Micro-organisms may exist in a harmless relationship

with a host and with a neutral existence, and are known as commensal
organisms.
There are five types of micro-organism of relevance in eye infections: bacteria,
chlamydia, viruses, fungi and protozoa.

Bacteria
Bacteria are widely dispersed in nature. They are single-cell organisms that
reproduce simply by division into two. Some are round-bodied, some rod-like
and some corkscrew-shaped (spirochaetes).
One method of classification of bacteria rather than shape is their reaction to
laboratory dyes, the best known of which is the gram stain. Organisms identify
either as gram-positive or gram-negative, a feature which is of clinical significance
as gram-negative bacteria are less harmful than gram-positive.
The resistance of bacteria to destruction is very variable. Some have a
precarious existence and are easily destroyed by sunlight and air, while others
are resistant and can survive for hours or days, even in the absence of air
(anaerobic bacteria). Some bacteria produce a resistant form as microcysts, which
can survive some months or years before reactivating the process of replication,
and hence problems for the host tissue.
There are thousands of bacterial types which share a common feature when
infecting tissue, namely the production of pus. Some produce enzymes that
destroy tissue, the range of effects being from mild nuisance (blepharitis) to fatal
eye infections (endophthalmitis) (see Chapter 14), In general they are counteracted
by the human immune system, with white blood cells being the chief defensive
agent. Antibiotic therapy may be general or specific; resistant mutations seem to
occur quite readily, requiring the pharmacological industry to try and keep at
least one step ahead.

Chlamydia
These are intracellular bacterial organisms of the bacterial type. Like bacteria
they reproduce by division into two and are sensitive to antibiotic therapy. In
other respects, however, they have more in common with viruses in that they
require living tissue to reproduce. The three known species of chlamydia are
Chlamydia trachomatous, Chlamydia pneumoniae and Chlamydia psittacosis. The
first two are frequent ocular pathogens causing ocular infections. When
Chlamydia trachomatous reproduces in an infected cell, it produces a distinctive
micro-colony of the organisms, called an inclusion body. Infection due to
Chlamydia trachomatous is a major, sexually-transmitted disease and is also
responsible for many ocular infections, including neo-natal conjunctivitis,
inclusion conjunctivitis, lymphogranuloma venereum (LGV) and trachoma, a

75
 Ophthalmology

form of scar-producing conjunctivitis with a chronic time-scale. Trachoma is a

major cause of preventable blindness, particularly in the Middle East,
southeast Asia and north Africa.

Viruses

Viruses are among the smallest, known micro-organisms and require an

electron microscope producing a magnification of at least 100,000 to be
identified. Viruses only multiply within a living cell. Once within the cell the
virus diverts the cell’s metabolic activities to produce thousands of clones,
destroying the whole cell in the process. Viruses are not responsive to antibiotics
in general but some systemic and topical anti-viral drugs can effect a degree of
control, but must be used for limited periods because of their toxicity. The major
viruses from the point of view of the eye are the herpes virus family, including
herpes simplex virus type one (HSV-1) and type two (HSV-2), cytomegalovirus
(CMV), varicella-zoster virus (VZV) and the Epstein-Bar virus (EBV). These
cause blepharitis, blepharo-conjunctivitis, keratitis, uveitis and retinitis. HSV-1
is the cause of cold sores on the lips and is responsible for lesions on the cornea
and eyelids. HSV-2 is more commonly infective in the genital region and is
transmitted by sexual contact. Newborn children exposed to the virus through
an infected birth canal are at serious risk of ocular infection.
CMV retinitis is an ocular infection commonly seen in patients infected with
the Aids virus. It is often the first indication of a patient who has been positive
for human immunodeficiency virus (HIV) and has made the transition to Aids.
HIV infection weakens the host immune system, allowing opportunist, infected
agents, including bacterial viruses and chlamydia, to become active.

Fungi

Fungi are multi-cellular micro-organisms that differ from bacteria in being more
complex in structure. They are able to reproduce themselves both by sexual and
asexual means. There are two groups of fungi—yeasts and moulds. Yeasts
produce creamy or pasty colonies whereas moulds produce woolly, fluffy or
powdery growths. Mild, fungal infections may follow treatment of an eye with
antibiotics or topical cortico-steroids, but when ocular tissue is weakened by
trauma then a fungal infection may be added to a primary bacterial infection. A
common fungal eye infection is the yeast Candida albicans. There are anti-fungal
medications available to treat fungal infections.

76
 Ocular Pathological Processes

Protozoa

Protozoa are large, single-cell micro-organisms found in fresh water, salt water,
soil, plants, insects and animals including humans. Ocular protozone infections
include some important eye-infective agents. For example, acanthamoeba, a
species living in soil and fresh water, hot tubs and swimming pools and home-
made, contact lens salt solutions, can cause irreparable damage to the cornea by
acanthamoeba keratitis. In contrast the retina can be infected by Toxoplasma
gondii protozoa which infects humans through the eating of under-cooked meat
containing cysts of the protozoa. Cysts can also exists in cat and dog faeces and
poor hygiene can result in infection, particularly in children.
Another form of choroido-retinitis, infection of choroid and retina often
involving the macula with destructive effects on central vision, is the worm
parasite Toxocara canis which is excreted by dogs and also found in the soil. The
eating of contaminated or unwashed vegetables may allow the parasite entry
into the host, which burrows through the intestinal wall, enters the blood stream
and lodges in the choroid, causing the choroid or retinopathy.

STERILISATION

Sterilisation is the process whereby all micro-organisms that may infect

instruments and materials used in surgery are destroyed. Disinfection is the
process used to sterilise the operation area, a particular problem in relation to
the eye because of the difficulty in isolating the eyelids, and eyelashes in
particular, from the operation site. Disinfection of the eye during the surgical
process is effected by an antiseptic called povidone-iodine in a 50% aqueous
solution. This can be used to irrigate the conjunctival sac where generally-
harmless bacteria may exist, to become opportunistic infecting agents
particularly after prolonged or traumatic surgery.
The instruments used in modern eye surgery are complex and miniaturised,
and some use plastic tubing. All these elements add to the risk of the harbouring
of bacteria, particularly in biological residues that can contaminate the
instruments, especially if they are not properly cleansed in the post-operative
period. Accordingly, they have to be exposed to a severe sterilisation process
carried out in an autoclave. Autoclaves operate under high pressure with a high
temperature of at least 270°F. As an autoclave cools down there is a vacuum
effect which sucks out material from tubing.
An alternative sterilising method which is not generally available, but does
exist in special centres, is the use of ethylene oxide gas which can effectively
sterilise instruments and materials without damaging the articles themselves.
This is particularly relevant when sterilising plastic rubber and other substances
that would otherwise be destroyed by heat or chemical agents. Ethylene oxide

77
 Ophthalmology

gas sterilisation is slow and expensive and the gas itself is toxic, which is why
the facilities are limited.

Gamma-radiation

Very-short-wave, electromagnetic radiation can be used to sterilise articles that

otherwise would require gas sterilisation because of their susceptibility of
damage by heat. This method is used in the industrial process of sterilising
intra-ocular lenses for example.

DISEASE CLASSIFICATION

Disease classification for the eye based on pathological processes has the
following form (which is not exhaustive).

Congenital disorders

(a) Inherited – dominant transmission

recessive transmission
sex-linked transmission
carriers
(b) Acquired in utero
(c) Acquired at the time of birth – infection
trauma

Acquired disorders
(a) Degenerative (eg macular degeneration)
(b) Infective (eg conjunctivitis)
(c) Inflammatory (eg uveitis)
(d) Metabolic (eg diabetic eye disease)
(e) Tumours (eg malignant melanoma)
(f) Trauma – physical
chemical
radiation

Special ocular classification of retinal disorders

(a) Retinopathies (eg diabetic retinopathy)

(b) Central (eg macular degeneration)

78
 Ocular Pathological Processes

(c) Peripheral (eg retinitis pigmentosa)

(d) Vascular (eg central, retinal-vein thrombosis)
(e) Sub-retinal (eg sub-retinal neovascularisation)

Eye disorders involving different ocular tissues

For example, glaucoma of various types (see Chapters 9–16).

79
 CHAPTER NINE

CATARACTS

DEFINITION AND OVERVIEW

A cataract is an opacity in the lens which impairs vision (Figure 27). It is the
major cause of blindness worldwide. Cataract surgery has been in existence for
more than 5,000 years, though in an extremely crude manner until very recent
times. It is less than 20 years since extracapsular cataract extraction (ECCE)
treatment was developed with the insertion of a posterior-chamber, intra-ocular
lens, which is now the treatment of choice, at least in the highly-industrialised
countries of the world. This approach preserves the intact, posterior capsule of
the crystalline lens, whose opacification forms the cataract (the Greek word
kaetorakt means waterfall, the Latin word means portcullis or obstruction) vastly
reducing the potential for post-operative complications. Posterior capsule
opacification (PCO) develops in up to 50% of eyes between two months and five
years after the initial ECCE surgery, the major cause of which is the
proliferation, migration and metaplasia (change in character of lens, epithelial
cells left behind) after the initial surgery which largely removes the lens
contents, but not all the cellular material.
Cell proliferation causes opacification on the capsule to form a secondary
cataract, causing a decrease in visual acuity. Restoration of vision is readily
achieved by removing the central portion of the posterior lens capsule by
neodymium:yttrium-aluminium-garnet (Nd:YAG) laser ablation.

Figure 27. A cataract is a

clouding of the crystalline lens.

81
 Ophthalmology

Cataracts and their management are of interest in the area of litigation because
of the potential for many varieties of trauma to initiate the cataractous process.
This is of relevance in personal injury cases and because of the complications
that can ensue, both during the operation for removal of a cataract and post-
operatively when issues of medical negligence can arise.
Taken in its widest context, cataract is the major cause of blindness
worldwide. It is the primary cause of blindness in 116 countries covered by the
blindness data bank (Hyman L, ‘Epidemiology of Eye Disease in the Elderly’
(1987) Eye 1, pp 330–41) and (Harding J, Cataract Biochemistry Epidemiology and
Pharmacology (1991) Chapman and Hall, London). The medical and economic
significance of cataract is increasing due to its prevalence in the ageing
population. Age-related cataract constitutes the main surgical work load of
ophthalmic services and the bulk of ophthalmic surgical waiting lists in the
UK and elsewhere.
In sheer numerical terms there are 42 million blind people worldwide,
about 40% of whom it is estimated are blind due to the presence of cataract. Of
these, some 30 million live in developing countries but 4 million in developed
countries. The problem in developing countries is partly gross lack of
ophthalmic services, but also a higher incidence of advanced cataract, an
earlier age of onset and adverse environmental conditions. Wherever cataracts
exist in the world the need for surgery based on modern standards far
outstrips the resources available. The difference between the need and the
demand for surgery in developed countries is changing as the population
becomes more educated about the rapidity of rehabilitation with modern
surgical methods, making the age-old adage of waiting for cataracts to ripen
before they are removed completely obsolete.

Anatomy
The crystalline lens is about 10mm in diameter and 3–5mm thick, dependant
upon age. It is sited immediately behind the pupil of the iris diaphragm where it
is suspended through the 360° of its equator from the annular ciliary muscle by
the strands of the zonule which are attached to the capsular coat of the lens.
Within the lens capsule the lens substance consists of fibres which are generated
continuously throughout life, the older fibres being compressed towards the
centre of the lens by successive generations of new fibres. Opacification of the
lens in part or whole causes impairment of its function, which then becomes
known as a cataractous lens or cataract.

Pathophysiology
Precipitation of proteins within the constituent lens fibres results in defective
light transmission. Why do proteins precipitate? The answers are complex,

82
 Cataracts

involving ageing, chemical changes, phototoxicity effects, endocrine influences

and physical insults.

Cataract causes and risk factors

There are many risk factors in the initiation and development of cataract which
include personal—ie individual susceptibility based on genetic factors—
nutritional, medical and environmental factors. Opacification of the lens results
from the cumulative effect of various insults to the lens contents.
Personal factors that are associated with the increased incidence of cataract
in a population include levels of education, occupation, race and geographic
location. Nutritional studies have shown that cataract is often associated with
marked changes in the ionic balance of the lens. The association of cataract with
other medical problems and medication shows that increasing age, diabetes,
glaucoma, cardiovascular disease, smoking, excess alcohol intake, gastrointestinal
problems, the use of diuretics and other drugs, as well as trauma, are all cataract
risk factors. Finally, environmental, contributory causes include the ultraviolet
component of sunlight, exposure to which will increase the chance of cataract
development.

Symptoms
The symptoms of a cataract are:

(a) progressive blurring of vision;

(b) worse vision in bright light;
(c) difficulty with near/reading vision;
(d) desaturation of colour vision; and
(e) glare.

Clinical signs—cataract types (morphology)

Morphological classification is based on the location of the opacity within the
lens. This is at the front, the back, the middle or the periphery of the lens,
affecting the capsule of the lens or the subcapsular zones. Nuclear cataracts are
found in the centre of the lens, ie the nucleus. Its early stages are characterised
by an increase in the compressed, central fibres of the lens comprising the
nucleus, with a change in colour from clear to yellow to brown, and
consequential change in refraction of the lens and diffuse scattering of light. The
yellowing or browning of a cataract is an exaggeration of the normal ageing
process. Specifically, nuclear cataracts occur as a result of protein within the lens
fibres becoming denatured, which increases hydration and deposition of a uro-
chrome pigment responsible for the colour change.

83
 Ophthalmology

Opacities in the periphery of the lens are known as cortical cataracts, are
usually wedge-shaped, and progress slowly. Unlike centrally-located opacities
they impair vision to a much lower degree, especially if not associated with
central lenticular problems. In cortical cataracts the lens cells become large and
round and are known as balloon cells. The lens fibres in the cortex become fused
into discreet masses, and round droplets or globules occupy the spaces within
the clefts which form between the groups of fibres. If this cataractous process is
allowed to continue long enough the whole of the cortex of the lens becomes a
milky, liquid mass. Under those circumstances the nucleus, lacking its peripheral
support, may move from its natural, central position under the influence of
gravity and the surrounding milky fluid, a special situation known as a
Morgagnian cataract.
When the opacities within the lens are underneath the lens capsule, which
occurs much more commonly at the back of the lens than the front, the opacities
are known as posterior sub-capsular cataracts. Their central location, and the
importance of the rear of the crystalline lens in the focussing of images on the
retina, means that even small posterior sub-capsular opacities can be visually
disabling, especially when the pupil contracts to limit the passage of light through
more peripheral parts of the lens. In other words, as this is on the optic axis of
the eye, a small opacity may cause a disproportionate decrease in visual
performance. Posterior sub-capsular cataracts occur because the germinal cells
of the lens, those cells in the equator of the lens which develop into lens fibres,
migrate towards the posterior pole of the crystalline lens. When these cells swell
as a result of absorbing proteinaceous fluid derived from liquefied cortical fibres,
they become known as bladder or Wedl cells.
Anterior capsular cataracts are caused by a fibrous change in the anterior-
lens, epithelial cells, so called fibrous metaplasia. This cataract is most often the
result of irritation or disruption of the anterior lens as occurs in trauma or
inflammation in the eye (uveitis). In modern cataract surgery where some
anterior-lens capsule remains after surgery, unless the epithelial cells are removed
from its underside they will undergo fibrous metaplasia with consequential
opacification.
It is rare for cataracts to be simple. Mixed cataracts involving combinations
of all the above categories are common, though cortical cataracts often remain
relatively simple.
The Italian-American Cataract Study Group in 1994 showed that the three
year accumulative incidence for people aged 65–74 years, which was the largest
age group, was 18% and 6% for cortical, nuclear and posterior sub-capsular
cataracts respectively. Progression was much higher in the incidence for each
type of opacity. Although some general risk factors have been commented on
above, different types of cataract have different risk factors.

84
 Cataracts

PREVENTION OR THERAPY?

There are potentially three ways in which the problem of blindness due to
cataract may be approached. The first is the surgical removal of cataract; the
second is the reduction of the incidence by eliminating the risk factors; and
finally there is the possibility of development of anti-cataract drugs.

Cataract surgery
Modern cataract surgery is dramatically successful. However, health-care
providers face the twin problems of an ever-increasing, elderly population and
surgical innovation, with a dramatic improvement in benefit/risk ratio
providing much broader indications for surgical intervention. In developed
countries cataract surgery today is no longer concerned with the relief of
blindness, but with the reduction of visual disability even in its less dramatic
stages.
Modern, cataract, surgical techniques (ie very small incision into the eye to
perform the surgery and the introduction of a foldable lens implant through

Figure 28. A cataract after extraction is replaced by an intra-ocular lens implant, here
seen encased in the crystalline-lens, capsular bag which is left in situ at surgery to
sequester the implant from other ocular tissues.

85
 Ophthalmology

that small incision, Figure 28) have a very high success rate indeed—of the
order of more than 98% in healthy eyes, ie no coincident morbidity. Thus,
when an eye is visually disabled because a person is unable to read small print
or road signs, or is intolerant to bright light and glare, surgical intervention
may be indicated. In developed countries it is increasingly rare for cataracts to
be allowed to progress to the point where they cause blindness. There are
sophisticated tests for assaying the degree of cataract, the rate of progression
and its visual effects, but in essence the indication for surgery is the patient’s
own subjective response to visual difficulties. A further indication for surgical
intervention in the modern context is the coincident occurrence of significant,
refractive errors. When a cataract is removed the focus or refractive power of
the eye may be adjusted, both by changing the power of the lens implant and
by reshaping of the cornea. Thus, the combined existence of developing
cataract and a significant refractive error may provide an extra incentive for
the patient to undergo surgical correction.

Elimination of risk f actors

The reduction of the incidence of cataract by the elimination of risk factors and/
or the use of anti-cataract formation agents is an illusive goal. Certainly, care
should be taken from a personal point of view, and in the general health from a
physician’s management point of view of medication, but the emergence of
specific anti-cataract drugs or preparations has never been established to any
convincing degree.

Special investigations
The following are performed by ultrasonography.

(a) B-scan—when a cataract is completely opaque, used to ascertain the state of

the posterior segment of the eye.
(b) A-scan—used to determine the axial length of the eyeball, an essential
component of the computation of the replacement, intra-ocular lens dioptric
power.
(c) Keratometry—an essential component of the computation of the
replacement, intra-ocular-lens, dioptric power.
(d) IOL power calculation.
(e) Specular microscopy—to determine the density and morphological character
of the corneal endothelial cells and confirm the safety of proposed cataract
surgery in relation to the cornea; also to provide a baseline for the post-
operative status of the endothelial layer, a quality control for the cataract,
surgical technique.
(f) Corneal topography—used to assess corneal shape, and is an essential
requisite for the refractive aspect of cataract surgery and the management of

86
 Cataracts

astigmatism, as well as a quality control for surgical technique and the

estimation of surgically-induced, refractive change.

Natural history

Cataracts cause progressive visual deterioration. The rate of change is extremely

variable. Traumatic cataracts may completely opacify within hours of trauma.
Age-related cataracts may take years to progress. However, as cataract surgery
has changed so dramatically over the past five years, the indications for surgical
intervention have changed. Early surgery for apparent, relatively-mild, visual
defects more often than not provide a dramatic improvement in visual
performance well beyond a patient’s expectation.

Referral
In the light of the above remarks, a patient with early manifestation of cataract
should be referred for a surgical opinion to an ophthalmologist with a special
interest in cataract and refractive surgery.

Treatment
Though cataract surgery dates back at least 5,000 years, spectacle correction for
post-surgical eyes have only been available since the 14th century. The necessity
for this is the loss of approximately one third of the focussing power, which has
to be replaced. When it is done in the form of a thick, spectacle lens the
consequent distortion of vision is considerable. The provision of cataract
spectacles in elderly patients may be contributory to the shortening of life, not
least because of the disabling effects of the distortion causing patients to trip or
fall downstairs and fracture limbs.
In the modern era, since the pioneering work of Harold Ridley of St Thomas’
Hospital in London in 1949, replacement of the focussing power of the crystalline
lens when it becomes cataractous and is removed, and the use of a replacement
lens has become the treatment of choice. Indeed to remove a cataract without
replacing its focussing power with an intra-ocular lens is only performing half
the required task. Though contact lenses can provide some sort of solution in
older patients, the ability to handle contact lenses diminishes. A contact lens on
the front of the eye changes the magnification factor in the eye and makes the
patient intolerant from a condition known as anisokonia (difference in
magnification of the image of the two eyes). Cataract surgery not only improves
visual acuity to the degree that the eye allows, according to the health and
integrity of its other components, but also allows the focus of the eye to be changed
and should therefore provide an improvement.

87
 Ophthalmology

Types of cataract surgery

There are two main types of cataract surgery. The first is known as intracapsular
cataract surgery (ICCE), and involves total removal of the crystalline lens. This
was the surgical treatment of choice in the modern era up to the mid-1970s, but
the removal of the whole lens limits the potential support and location for a
replacement lens. Under those circumstances the replacement lens either had to
be clipped in the pupil (iris-supported lens) or braced across the anterior
chamber of the eye, where it had significant potential for causing corneal
destruction and uveal tissue irritation (iritis).
ICCE with lens implantation was successful in general but had a significant
complication rate, some of which had blinding consequences including loss of
the cornea, corneal decompensation, and uveitis glaucoma hyphaema (UGH)
syndrome where inflammation, bleeding of the eye and raised intra-ocular
pressure could lead to rapid destruction of the visual systems.
From the mid-1970s extracapsular cataract extraction became the accepted
norm. In this procedure the lens is opened by tearing a window in the anterior
lens capsule to gain surgical access to the cataractous contents of the
crystalline lens. These were then removed and the replacement lens placed
inside the lens capsular bag. This had the considerable advantage of
sequestering or separating the lens implant from other eye tissues whilst
retaining a barrier between the front of the eye and the back (the anterior
segment of the eye and the posterior segment), limiting the transfer of post-
surgical chemical agents that are released into the anterior segment from the
susceptible posterior segment, the retina and macula, and in particular
reacting adversely to the presence of inflammatory agents and thus degrading
the visual effects of cataract surgery.
It goes without saying that cataract surgery, the removal of a lens from an
eye which in general is only 23mm in diameter, is a microsurgical procedure.
Since the early 1960s cataract surgery has essentially been performed as a
microsurgical procedure, but in the intervening years the technology, not only
of microscopes but of surgical instruments and bio-materials, has changed out
of all recognition, making the operation of today very different from that of 30
years ago. Because of poor technique in extracapsular surgery, all the
cataractous material may not be removed, and if that occurs the residual
material would lead to irritation and inflammation of the eye, and
occasionally a severe immune response to lens proteins which a patient’s
immune system would unfortunately recognise as foreign material. The
thickening that would occur as a response of lens remnants would obstruct the
pupil or cause the formation of a secondary cataract, wherein the residual
lens capsule gradually becomes opaque, requiring its later removal or
disruption.
During the early 1970s an American surgeon, Charles Kelman, developed a
technique of using ultrasound, which had been developed for dental surgery, as

88
 Cataracts

a means of fragmenting hard cataractous material which has to be removed

during an extracapsular, cataract, surgical technique. For the past 20 years that
technique has been ultimately refined so that, today, virtually any cataract can
be removed by that method, and thereby utilise a very tiny incision, maintaining
a closed eye condition during surgery with bountiful effects in the post-operative
recovery of the eye. The parallel development in the past 10 years of lens-implant
materials that allow the implant (which has to measure at least 5–6mm in diameter
from an optical point of view) can now be inserted through incisions as small as
2.5mm.
Changes in technique are not easy to acquire by the individual surgeon and
require determination, dedication and retraining, but all to good effect. The past
30 years has seen a change in attitude in medicine in general and ophthalmology
in particular, where continuing medical education is essential so that modern
methods can be delivered in patient care.

Intracapsular cataract extraction

This procedure involves removal of the whole cataractous lens. The lens is first
loosened using an enzyme, alpha-chymotrypsin, which dissolves the zonular,
suspensory ligament enabling the lens to be removed without traction on
other intra-ocular structures. Lens implantation is limited to the placement of
an anterior-chamber lens, which superseded the previous, pupil-supported
lens which was the traditional attempt at locating and fixing an intra-ocular
lens.
Intracapsular cataract extraction is linked with some specific complications
because of the removal of the barrier between the face of the vitreous humour
and the aqueous humour, allowing transmission of inflammatory agents from
the surgically-traumatised anterior segment to the central retina and optic nerve
in particular. Further, the removal of the barrier allows anterior displacement of
the vitreous body, which may lead to a much higher incidence of vitreo-retinal
complications such as retinal breaks and retinal detachment.

Extracapsular cataract extraction (ECCE)

The basis of an ECCE is to preserve an intact, posterior, lens capsule, thus

separating the anterior and posterior segments of the eye. In order to gain access
to the cataractous contents of the lens, an opening is made in the anterior lens
capsule. In former years this used to be a rough tear similar to the opening of a
tin can, but in the past five years techniques have improved so that a continuous
circular tear (capsulorhexis) is now the method of choice, because this preserves
the integral strength of the lens capsule into which the replacement lens can be
incorporated.

89
 Ophthalmology

In ECCE a large incision is still required into the eye (7–12mm) because the
hard nucleus of the lens is removed, either by expressing it through pressure on
the posterior part of the eye or by placing an instrument underneath it and
scooping it out of the eye. The residual lens material, the cortex of the lens which
is soft, is then removed with an irrigating, aspirating instrument, a cannular,
allowing the remnant capsular bag to be clear and polished. The new lens is
implanted into this capsular bag. When a large incision is made into the eye,
either for ICCE or ECCE, the aqueous humour naturally drains out of the eye
and the anterior segment tends to collapse. This makes surgery difficult because
of the lack of space and makes many tissues vulnerable to surgical trauma, in
particular the corneal endothelium and the iris diaphragm.
Since 1980 a way round this problem has been achieved by the introduction
of a visco-elastic material, of which the original was called Healon. This is a
pure solution of sodium hyaluronate, a naturally occurring substance in many
sites of the body, particularly in the umbilical cord and as a lubricating material
in joints. In nature it occurs in concentration in the comb of a cockerel, from
which the material is extracted, purified and concentrated to allow its use in
ophthalmic surgery. It has virtually no side effects provided the material is
removed at the end of surgery. Failure to remove it may cause transient rise in
intra-ocular pressure.
The complications of extracapsular surgery arise because of surgical trauma
inflicted on the cornea, iris diaphragm or lens capsule. If the lens capsule is not
secure the intra-ocular lens implant may migrate and cause chronic inflammatory
changes in the eye. Capsular tears (ie in the posterior lens capsule during surgery)
will also create a significant increase in the incidence of post-operative
complications through anterior movement of the vitreous body and the
transmission of inflammatory agents from the anterior segment of the eyes to the
posterior segment. Particular complications include retinal detachment, cystoid
macular oedema (fluid engorgement of the macula retina), corneal decompensation,
plus the general but low risk of post-operative infection (endophthalmitis).

Phacoemulsification
This technique represents an improvement over ECCE as the surgery can be
performed through a very small incision. The incision may be performed in the
sclera, the corneal scleral junction or the cornea. It has several advantages over
ECCE:

(a) it avoids alteration of corneal shape, which would induce astigmatism as a

result of surgical trauma;
(b) it allows surgery to be carried out in a closed-eye environment, reducing
surgical trauma and post-operative inflammation;
(c) it allows surgery without the use of sutures, so that rehabilitation is much
quicker and no post-operative suture irritation is encountered; and

90
 Cataracts

(d) vision is restored within minutes of completion of the surgery and tends to
be stable thereafter, thus dramatically altering the need for post-operative
supervision leading to the virtually immediate resumption of normal
activities by the patient. Owing to the dramatic improvement in outcomes
and marked reduction in complications, bilateral, simultaneous cataract
surgery is more relevant because it avoids the imbalance that occur when
different refractive errors exists in a pair of eyes because only one has
undergone surgery.

In the presence of bilateral cataracts, bilateral, simultaneous, phacoemulsi-

fication extraction of the lens and replacement with a lens implant is the best
way of affording rapid rehabilitation of the patient, not just the eye.
The surgical technique is sophisticated and prone to serious complications
if technical problems occur. The process may be likened to a skier descending a
black run. If he is confident of his technique he will be exhilarated and safe. If he
is uncertain about his technique, severe difficulties with disastrous consequences
may follow. So it is with small-incision, cataract surgery. As long as complications
are avoided the outcome is exhilarating for surgeon and patient. If complications
occur they can be disastrous. The complications include traumatisation of the
cornea, the iris diaphragm, the lens capsule, loss of the lens nucleus into the
vitreous humour, loss of part of the vitreous gel with all the attendant
consequences of post-operative inflammation or infection, corneal clouding or
retinal detachment.

Intra-ocular lens implants (IOLs)

IOLs are manufactured from hard materials such as clinical quality Perspex
(polymethylmethacrylate or PMMA) or soft materials which are compounds of
silicone and methacrylate (Figure 28, page 85). Soft, lens materials are gaining
popularity over the historic material of PMMA, as the requirement to implant
the IOL through the micro-incision of current cataract surgery has to be met. Soft
materials are flexible, foldable or rollable, allowing their insertion through
incisions of 3mm or less.
There are special indications for the use of specific lens designs as well as
materials, just as there are contra-indications to some IOLs. One example is the
avoidance of using silicone IOL when there is a prospect of the patient having to
undergo surgery for retinal detachment, when silicone IOL is sometimes utilised
as a medium to push the detached retina back into place. Silicone oil does not
react well with the hydrophobic surface of a silicone IOL, causing a smearing
and droplet effect which ruins the optical characteristic of the IOL, requiring its
removal and replacement with a PMMA IOL.

91
 Ophthalmology

Outcome expectations
With modern methods poor results should be rare. However, even in the
absence of surgical problems, some eyes develop retinal problems that may or
may not permanently affect vision. These complications are generally a result of
low-grade inflammation as a consequence of the surgery, but most of these
problems do respond to treatment. A satisfactory, planned, refractive outcome
of the surgery is to be expected today.

Complications
Complications of cataract surgery during the surgical process occur because of
faulty technique or intrinsic pathological features within the eye. Before surgery
has commenced, anaesthesia administration carries its own complication rate.
Whilst it is beyond the scope of this book to discuss complications of general
anaesthesia, injected local anaesthesia has significant potential complications,
including:
(a) retrobulbar haemorrhage—caused by blood vessel penetration by the needle
which is inserted (blind!) into the eye socket or orbit; techniques in use include
retrobulbar injection aiming for the extra-ocular muscle cone, or peribulbar
injection wherein the needle tip is placed in the outer orbit from where
anaesthetic solution diffusion effects the desired anaesthesia and akinesia
(paralysis of eye movement);
(b) perforation of the eye globe—which occurs because the injection needle is
misdirected; the larger the eye globe (myopia) the higher the risk. Perforation
of the globe will lead to intra-ocular haemorrhage and, possibly, subsequent
retinal detachment;
(c) injection of anaesthetic solution into the cerebrospinal fluid—causes
respiratory distress, loss of consciousness or paralysis; though rare, such
incidents are reported in the literature, eg needle penetration of the meningeal
coat of the optic nerve in a retrobulbar injection; and
(d) injection of anaesthetic solution into an extra-ocular muscle—with
intramuscular distension and/or haemorrhage, causing muscle paralysis
which may be transient or permanent with consequential diplopia.
Surgical trauma may cause post-operative problems for an eye. Per-operative
problems include:
(a) trauma to the corneal endothelium resulting in death of irreplaceable corneal-
endothelial cells which will result in early or late clouding of the cornea as it
becomes oedematous (waterlogged), with failure of the water-transport
function of the endothelial cells;
(b) trauma to the iris diaphragm, which will enhance post-operative
inflammation (uveitis) with its potentially-destructive effects on visual
function;

92
 Cataracts

(c) trauma to the suspensory ligament of the cataract (lens) with consequential
prolapse of vitreous gel into the anterior segment of the eye, limitation of
support for an intra-ocular lens in the posterior chamber of the eye and
increased risk of subsequent retinal detachment;
(d) perforation of the posterior lens capsule with consequential prolapse of
vitreous gel into the anterior segment of the eye, limitation of support for an
intra-ocular lens in the posterior chamber of the eye and increased risk of
subsequent retinal detachment; and
(e) loss of the lens nucleus or fragments into the vitreous gel with probability of
severe, post-operative inflammation and increased risk of subsequent retinal
detachment. A second operation is required to remove all cataractous material
by a vitrectomy if the debris is not removed at the initial, surgical event.

Early post-operation, the major problems encountered after seemingly

uncomplicated surgery (more likely after complicated surgery) are
inflammation (uveitis) and infection. The major problem, which is very rare but
potentially devastating, is intra-ocular infection or endophthalmitis

Endophthalmitis
Endopthalmitis following intra-ocular surgery, particularly cataract surgery,
has a prevalence of approximately 0.1%, ie one per thousand surgical cases. It is
generally regarded that the source of infection in most cases is bacteria lingering
on the patient’s own eyelids and eyelashes. It is very difficult to isolate the eye in
a surgical field though every attempt is made to do so. Nevertheless the flora
that naturally exist on eyelids and eyelashes may contaminate the wound and
enter the eye. In cataract surgery it is possible for bacteria to adhere
electrostatically to the intra-ocular lens if it brushes the eyelashes on its route
into the eye, emphasising the importance of isolation of the lids and lashes from
the operating site, sterilisation of the area as far as possible and a proper aseptic
technique.
The commonest pathogens which may be carried into the eye under these
circumstances are Staphylococcus aureus, coagulase-negative staphylococci such
as Staphylococcus epidermidis and Propionibacterium acnes. Staphylococcus aureus in
particular causes a devastating infection within days of surgery which usually
results in loss of vision and even the eye. Other bacteria which can cause even
more serious effects include the streptococci of the beta-haemolytic variety as
well as Streptococcus pyogenes. The coagulase-negative staphylococci, ie of low
virulence, and Propionibacterium acnes cause a lowgrade infection with
considerable morbidity as far as the patient is concerned. Because
endophthalmitis is fortunately a rare event, exact data on its prevalence is not
available. It is currently the subject of a long-term, multi-centre study in both the
US and Europe. In the meantime, the infection has to be prevented as far as
possible and treated if it occurs (see also Chapter 13).

93
 Ophthalmology

Prevention
Various stratagems are adopted with the best of intentions but, as noted above,
hard data is not available. The regimes include:

(a) application of antiseptic (povidone iodine) to the conjunctiva, cornea, eyelids

and surrounding skin immediately before surgery; this has been shown by
laboratory studies to reduce the population of bacteria, if not eliminate it
altogether;
(b) careful draping of the eyelid to isolate the eye as far as possible from the
eyelids and eyelashes;
(c) pre-operative, broad-spectrum topical (ie eye-drop therapy) prior to surgery;
(d) adding antibiotics to the irrigation fluids used during cataract surgery (it
has been demonstrated that this does kill bacteria which may contaminate
the intra-ocular fluids during the surgical procedure);
(e) injection of a foldable-lens implant through the nozzle of a cartridge, which
serves to isolate completely the lens implant from the ocular surface and
prevent adsorption of potentially-harmful bacteria onto its surface, where
they can be carried into the eye;
(f) immediate, post-operation injection of a sub-conjunctival solution of
highdose antibiotic (Cefuroxime—the cephalosporin is a bactericide against
staphylococci and Propionibacterium acnes as well as streptococci); gentamicin
is more toxic and not as effective against streptococci.
(g) topical antibiotic drops after surgery and wound closure used up to eight
weeks post-surgery by some surgeons (probably not effective, except for
preventing localised wound abscess or stitch abscess in the first 48 hours).
Such eye drops do not penetrate into the eye and therefore cannot reach
bacteria which may be adsorbed onto the intra-ocular lens through poor,
surgical technique.

A parallel situation in the field of orthopaedic surgery occurred during the

implantation of metal and plastic hip joints two decades ago. The infection rate
was quite severe at 15% but was reduced to 1% by the use of:

(a) sterile, ultra-clean air delivered in a down draft operating theatre; and
(b) short courses of high-dose, intravenous, antibiotic prophylaxis with
bactericidal drugs commencing at the time of surgery; or
(c) combinations of both.

As noted above, the infection rate is extremely low in cataract surgery which
accounts for the bulk of intra-operative procedures in the field of ophthalmic
surgery. Nevertheless, the eye is so vulnerable that any infection has to be
prevented if at all possible.
In the absence of hard evidence, good clinical practice dictates that, in cataract
surgery, all patients should receive topical iodine as a prophylaxis immediately

94
 Cataracts

before surgery and topical anti-biotic drops for 48 hours post-operation. A further
procedure might include the inclusion of a bactericidal antibiotic, eg a
cephalosporin, added to the anterior chamber irrigation during the surgical
procedure.

Cystoid maculopathy
Post-operative inflammation or uveitis may cause changes at the macula,
especially in patients with pre-operative uveitis or who are diabetic. Although
this may be a transient phenomenon if it lingers, it may induce cystic
degeneration of the macula with serious visual consequences (Figure 29).

Figure 29. Cystoid macular oedema (CMO), a complication of low-grade, post-operative

inflammation following cataract surgery. The retinal capillaries in the central retina
develop a temporary incontinence in response to anterior-segment inflammation and
the fluid-leakage pools in the retina to inflate microcystic spaces, which are
unequivocally identified clinically by fluorescein angiography. The dye stains the fluid
in the microcysts which appears as a mottled, white fluorescence.

95
 Ophthalmology

Later post-operative complications of cataract surgery

Corneal problems—decompensation, ie failure of the corneal, endothelial-cell
function as a fluid pump, resulting in oedema of the cornea and blistering of
the corneal epithelium (bulbous keratopathy). Corneal replacement may be
necessary.
Glaucoma—aphakic glaucoma was a not uncommon problem in former times
when surgical trauma was excessive compared with modern techniques.
Surgical and inflammatory debris compromises drainage of aqueous humour
on a transient or permanent basis. Medical or surgical management may be
required.
Macular oedema—with persistence causes cystic degeneration of the macula
with serious impairment of central (sharp) vision.
Retinal detachment—occurs more frequently after complicated cataract surgery
when loss of vitreous humour may disturb retinal integrity, with hole
formation and detachment following. It may also occur due to coincidental,
age-related shrinkage of the vitreous humour, perhaps enhanced by the
altered internal fluid dynamics. Any abnormal, vitreo-retinal adhesions may
cause retinal traction and tearing as the vitreous gel collapses, a more common
event in post-cataract surgical eyes than in an unoperated, matched
population. Symptoms of retinal detachment may allow prophylaxis, but if
a detachment occurs it will require surgical treatment (see Chapter 10).

Informed consent
It is most helpful to provide patients with a written description of the procedure
they are about to undergo in order to allay their inevitable anxiety and to
engender confidence in the procedure and the surgeon.

CONGENITAL CATARACT

Causes—inherited
(a) About 30% of congenital cataracts are of the inherited variety, most with
variable expression. That is to say that asymptomatic family members may
still show signs of lenticular abnormality. Where parental consanguinity
occurs, autosomal recessive and ex-linked recessive patterns can also
occur.
(b) Associated with other ocular disorders including persistent hyperplasic
primary vitreous (the persistence of a developmental stage of the vitreous
gel as it changes from a vascular, building core for the eye to a clear gel
during life). Microphthalmos (small eye), anophthalmos (absence of the iris),

96
 Cataracts

retinoblastoma (malignant tumour of the retina), retinopathy of prematurity,

retinal detachment and inflammatory disorders (uveitis).
3 Intra-uterine-infected problems, of which the best known is German measles
or rubella, which results from direct invasion of the embryonic lens by the
virus. A cataract may also result from maternal herpes zoster, herpes simplex,
cytomegalovirus, polio, influenza, hepatitis, toxoplasmosis and syphilitic
infections.
4 Metabolic causes: galactosaemia is due to deficiency of an enzyme that allows
metabolism of the sugar galactose; galactokinase deficiency is another
enzymatic deficiency related to sugar metabolism; hypocalcaemia is due to
hypoparathyroidism or pseudo-hypoparathyroidism, a deficiency of the
parathyroid glands.

Finally, there is a variety of infantile syndromes with multiple problems, and

generally of an inherited nature, which include cataract as one of their features.

Management when a unilateral cataract occurs

Even if early and appropriate surgery is performed, the visual outlook is very
poor because of a competitive failure of the eye-brain developmental processes.
The brain receives satisfactory images from the unaffected eye and, in spite of
management which includes periodic occlusion of the better eye to stimulate
functional development of the operated, formerly-cataractous eye, the outcome
is generally poor.
On the other hand, where bilateral, dense cataracts occur in a neonate, early
surgery is essential if the visual processes are going to be stimulated to develop.
With modern, surgical technology the cataract surgery in infants has dramatically
improved, and from very early ages should incorporate lens implantation to
ensure proper focus in the eyes. Former management included carefully-
supervised, contact lens wear in infancy to promote a satisfactory, visual image
and thus the stimulus to visual development.

97
 CHAPTER TEN

RETINAL DETACHMENT

Definition
The retina, the light-sensitive, multilayered structure in the posterior segment of
the eye, has an inner and an outer layer. The junction between the two lies
between the neurosensory layer (rods and cones) and its supporting, retinal-
pigment epithelium or layer. The relationship between these structures is one of
adjacent tissue without any firm binding. Thus a potential space exists between
them which, if occupied by fluid, blood or other substances, will cause the
anterior layer to peel away from its pigment layer. Such an occurrence is known
as retinal detachment. It happens for two reasons:

(a) due to a hole in the inner retina causing fluid to detach the retina
(rhegmatogenous detachment, Figure 30, page 100); and
(b) due to the presence of solid material, eg tumour tissue, fluid from
inflammatory causes or blood (non-rhegmatogenous detachment).

Presenting symptoms
Retinal detachment causes loss of vision, which takes the form of a shadow or
curtain spreading across the field of vision. The size of the visual loss varies
according to the degree of detachment. The area of lost vision is inverted in
relationship to the detaching retina, thus an inferior retinal detachment will present
as a curtain descending from the top of the field of vision, whereas a superior
retinal detachment will present as a curtain rising from the bottom of the field of
vision. The initial symptoms may be missed by a patient; these include a sudden
flash of light and a cloud of floating spots, often called ‘black rain’ if they are profuse.
The spots are caused by a cascade of blood cells emanating from a torn blood vessel
in relation to a retinal tear. If the retinal detachment involves the macula or central
retina then the visual loss will be extreme. As inferior retinal detachments tend to
progress slowly, symptoms may be disregarded by the patient until the central
vision is affected as the macula detaches.
The symptoms of a flash of light and a shower of black spots may precede
visual-field defects by days, weeks or months. They are due to a retinal tear
occurring generally as a response to a vitreo-retinal adhesion causing the retina
to tear at a site of previous retinal degeneration. The retina only detaches when
fluid seeps through the tear into the potential space between the neuro-sensory
layer of the retina and the underlying pigment epithelium layer to cause a peeling
effect.

99
 Ophthalmology

Figure 30. A fluorescein angiogram of a detached retina lower aspect. The in-focus,
out-of-focus aspect of the retinal blood vessels indicate that the retina is elevated by
sub-retinal fluid. In the lower part of the picture four retinal holes are demonstrated
by the absence of any blood vessels. It is through these holes that fluid percolates from
the vitreous humour underneath the retina to cause the physical detachment. The
initiating event is the formation of holes in the retina, usually secondary to retinal
degeneration which is more common in myopic (large) eyes.

Clinical signs
Clinical signs include loss of visual field, loss of visual acuity and loss of the red-
reflex when the reflection from the retina is observed with an ophthalmoscope
through the pupil. A detached retina, when viewed ophthalmoscopically, is
darker in colour than the normal retina due to the fluid separating the retina
from the underlying tissues. A superior detachment may appear as a balloon
half obscuring the fundus of the eye. A retinal detachment associated with a
superior, giant-retinal tear may reveal the retina having peeled back on itself, so

100
 Retinal Detachment

that the ophthalmoscopic view shows the bare choroid and sclera above and the
folded retina below.

Investigations
The only worthwhile investigation is careful ophthalmoscopic observation of
the retina to ascertain where the break or breaks exist; the principle of surgical
treatment is to close the retinal breaks, and in order to do so they have to be
identified. Some retinal detachments occur as a result of a small break or hole in
the retina, others as a result of multiple breaks. The principal investigation is to
examine the retina thoroughly to ascertain the location of break or breaks so that
surgical treatment can be planned. In the event of a haemorrhagic consequence
of a retinal tear and a retinal detachment, if the vitreous compartment is
obscured for any other reason, if the crystalline lens is cataractous or if the
cornea is not transparent, then the diagnosis and morphology of retinal
detachment can be ascertained by B-scan ultrasound.

Natural history
As noted above, the natural history or progression of the pathology will depend
on the location of the retinal tear, its size and form and the consequential
morphology of the retinal detachment. The slowest progressive retinal
detachments are those due to an inferior retinal break, but an inferior retinal
detachment may be a consequence of a superior retinal break where fluid seeps
through the tear and, under the influence of gravity, travels inferiorly to peel the
retina slowly from below.

Optometrist and GP ophthalmologist’s roles—when to refer

If the optometrist’s advice is sought initially by the patient, which is usually the
case, then even if the diagnosis is not apparent but a change in visual status is
documented, the patient should be referred immediately. If the optometrist
suspects the presence of a retinal detachment, he should indicate to the GP that
the matter requires the urgent opinion of an ophthalmologist. The GP’s role is to
arrange the earliest possible appointment if a retinal detachment is suspected,
as early diagnosis and treatment may be vital factors in the restoration or
preservation of visual function.

Treatment options
The only treatment option for retinal detachment or retinal holes or tears is
surgical. Retinal holes or tears may be secured before a detachment has
occurred if they are diagnosed. They are closed by the application of any process

101
 Ophthalmology

that will induce inflammation and resultant scarring between the retina and
underlying choroidal tissue. The modality applied in such circumstances is
primarily argon-laser therapy to the edges of the tear; cryotherapy is equally
potent but not as convenient to apply. If the retina is detached, a full surgical
procedure is required wherein the area of the retinal tear or tears is identified,
the area being treated from the external eye aspect through the scleral wall by
application of cryotherapy to induce an inflammatory response. That area of
sclera and overlying choroid is then buckled in towards the area of the retinal
hole or tears to allow adhesion to take place.
If this process is capable of being effected without drainage of the sub-
retinal fluid, then it avoids the potential complications of bleeding, both under
and through the retina. The situation is dependent upon the compressibility of
the eye by the external application of silicone rubber materials which create
the bulge in the wall of the eye that brings the ‘sticky’ choroidal tissue into
contact with the area of the tear. The process may be done in reverse by putting
pressure on the retina to push it back towards the area treated by cryotherapy
using a gas bubble of air or expanding gas (CF6) and by suitable posturing of
the patient so that the gas bubble lifts the retina back into apposition with the
surgically-inflamed area. Once the retinal hole is sealed, the gas is absorbed
after the retina becomes re-attached. The major urgency in the surgical
treatment of retinal detachment is the status of the macula, as it should be re-
attached as soon as possible in order to try and restore continuing visual
function. The longer the macula is detached, the less the chance of restoration
of central vision.

Risks v benefits of treatment

The risks of treatment for retinal detachment are related to poor surgical
technique. The benefit of treatment is restoration of vision, which otherwise
would be lost without treatment.

Outcome expectations

Modern retinal detachment surgery in the presence of single or simple breaks of

the retina should anticipate a 70–80% chance of success in securing
repositioning of the retina with one surgical repair, and over 90% within two
surgical repairs. The visual outcome will depend on the duration of the
detachment and the macula in particular. If a retinal detachment is not treated
promptly, the untreatable condition of proliferative vitreo-retinopathy may
occur due to migration of cells through the retinal breaks to cause a proliferative
fibrotic reaction and a vitreous gel which permanently fixes the retina in an
untreatable form. This blinding complication will occur in almost all

102
 Retinal Detachment

long-standing, retinal detachments, but can also occur rapidly within days or
weeks, especially in younger patients.

TREATMENT IN HISTORICAL PERSPECTIVE

The successful management of retinal detachment has improved dramatically

in the past 10–20 years, coinciding with the emergence of ophthalmic sub-
specialists in the field of vitreo-retinal surgery. Even during this period, general
ophthalmologists would, and indeed still do, undertake retinal detachment
surgery, but their volume of surgery is limited because of the relative
infrequency of the condition. Conversely, the volume of surgery managed by a
vitreo-retinal specialist is much higher with higher degrees of technical
expertise and experience. All regions of the UK have vitreo-retinal specialists,
and it is very much in the patient’s interest to be referred to such sub-specialists
for their treatment, though the chain of referral may include optometrist, GP,
general ophthalmologist and vitreo-retinal specialist.

Complications

Major complications of retinal detachment are loss of vision consequent upon

either failure to diagnose, failure to treat or unsuccessful treatment. Loss of
vision in the end is due to loss of macular function, though peripheral vision
may be retained if the retina is re-attached or total loss of vision may result if
there is failure to re-attach the retina.

Management errors

Errors which can result in retinal detachment are delay in referral, diagnostic
failure, and failure to find retinal breaks (at least 10% of retinal detachments do
not reveal a break on full clinical evaluation prior to surgical intervention). The
percentage is reduced by further investigation during the surgical process when
small holes or breaks may be highlighted much more easily than preoperatively.
In the final analysis, if no hole or break is discovered then a general surgical
procedure to take account of invisible breaks can be performed.

MACULAR DETACHMENT

Recovery of visual acuity after a retinal detachment involving the macula was
investigated by Thomas C Burton MD (Transactions of the American
Ophthalmological Society (1982) vol 90), who reported that:

103
 Ophthalmology

‘Intuitively, perhaps more than by any other method, ophthalmologists have

thought that prompt surgery for a retinal detachment would provide optimal
visual recovery. It has been long observed, and more recently confirmed, that
visual results are best when the macula has not become involved in the detachment
process. Unfortunately, in most large retinal detachment series, the macula is
involved about 75% of the time, a figure which has changed little over a period of
many years. Pre-detachment or early detachment symptoms obviously are not
alerting patients adequately, or often their physicians, to the urgent need for
thorough retinal evaluations.’

He concludes as a result of his own studies involving nearly 1,000 cases of

retinal detachment that nearly 90% of cases with pre-operative acuities of 6/6 to
6/18 maintain the same level of vision post-operatively. Over 80% of cases with
macular sparing achieve 6/18 acuity or better, compared with 20% of cases with
macular involvement. Only 2% of patients with macular detachment of known
duration regain 6/6 acuity.

‘After macular involvement occurs, duration of macular detachment becomes the

most important factor in determining the final visual acuity’.
‘… The macula does not fail to recover function after a specific time limit. However,
there is no duration beyond which visual acuity is lost precipitously; instead visual
recovery behaves as a function of a biological system, declining rapidly during
the initial stages of the detachment and more slowly as the detachment becomes
chronic. The relationship between visual acuity and duration of macular
detachment is analogous to the decay curve of a radio—active material.’

He concludes:

‘Every reasonable effort should be made to minimise duration of macular

involvement. There is no excuse for unnecessary delay of detachment surgery,
whether for the convenience of the patient, surgeon, anaesthetist or operating
room schedule. Since visual decline is a continuous process, there are no definite
intervals when surgery is more or less advisable. Emergency status probably
should be assigned to patients with macular symptoms of recent onset.’

In Dr Burton’s study no patient regained 6/6 vision with a macular detachment

exceeding five days, a time when an average of 6/18 acuity is anticipated.
Patients with macular detachments of longer duration should still be regarded
with urgency. After five days, approximately one line of vision would be lost for
each additional seven days up to 27 days. Beyond four weeks, one line of vision
would be lost for each additional 10–11 days of macular detachment, at least
until approximately 70 days when 6/60 would be the average visual recovery.

104
 CHAPTER ELEVEN

MACULAR DEGENERATION

Definition
The functional failure of the central retinal area (macula) due to age-related or
inherited conditions that cause premature failure of the tissue with resultant,
clinically-visible scarring and consequential poor, central-visual acuity.

Pathophysiology
During the course of life the retina is a very active tissue, necessarily achieving
a high metabolic rate. The light receptors, the rods and cones, are constantly
undergoing repair and regeneration and the waste products of their activity
are dealt with by the underlying retinal-pigment epithelium and its
supporting structures in the choroid layer. As part of the ageing process, the
continuum of this activity causes accumulation of waste products that reduce
the efficiency of the scavenging processes required to support and maintain
vital cells. Ultimately these effects may lead to a degeneration that results in
reduction of vision.
The phenomenon of age-related (formerly and inappropriately called
senile), macular degeneration is an inevitable consequence of the ageing
process, depending on one’s inheritance and, to a lesser extent, environmental
conditions. The macula is the most susceptible part of the retina in
degenerative terms and, if a person lives long enough, the macula will
degenerate and the quality of vision will be disturbed. The macula may
simply atrophy or decline in its cell population with loss of function.
Alternatively, the natural healing processes may come into play with
production of new vessel membranes which seem to develop in response to
the degenerative processes and reduction of oxygen supply that follows. The
presence of a sub-retinal, sub-macular, neovascular membrane may
precipitate dramatic loss of vision and consequential scarring with permanent
loss of central vision (Figures 31–33, pages 106–07).

Treatment
Macular degeneration in general is not amenable to treatment. The retina is not
capable of replacement and has only a limited capacity to repair itself. When a
sub-retinal, neovascular response occurs this can precipitate dramatic loss of
vision, but depending on the pathological anatomy that situation may, to some

105
 Ophthalmology

Figure 31 (above). An example of a fluorescein angiogram of the retina. This case

illustrates a detachment of the retinal-pigment epithelium, giving a blister-like elevation
of the macula. The fluid in the detachment stains with fluorescein to identify its precise
location. Retinal-pigment, epithelial detachment is one component of macular
degeneration syndromes.
Figure 32 (above right). A fluorescein angiogram of a right eye with early, age-related
degeneration, characterised by atrophy of pigment epithelium with pigment migration
and pigment clustering, seen here contrasted against the background fluorescence of
the choroid. The inference from anappearance like this is that the rods and cones which
are the light-sensitive elements of the retina will be decaying, and vision reserves and
acuity of the eye will be limited.
Figure 33 (below right). The fellow left eye of the same patient in Figure 32 with a
disciform (disc-like) scar at the macula which has end-stage, age-related degeneration,
ie no residual central vision. The eye still maintains peripheral vision which is usually
not compromised by the age-related degeneration af fecting the central retina.

106
Macular Degeneration

107
 Ophthalmology

extent, be recoverable. The neovascular membrane is, in essence, the precursor

of a scarring process which is destructive to the delicate retinal tissue. If the sub-
retinal, neovascular membrane is away from the fovea which serves to provide
our sharpest visual function, it may be destroyed by laser application, thus
protecting the fovea from the scarring processes. If the sub-retinal, neovascular
membrane is beneath the fovea, it is beyond therapy. Sub-retinal, neovascular
membranes may be multi-focal as well as sub-foveal, and new ones may arise
after old ones have been eliminated. Thus, the prospect for protecting an eye
suffering from this progressive degeneration and prolonging its useful function
is extremely limited.
In order to identify whether a degenerating macula is treatable or not the
eye needs to undergo evaluation by fundus fluorescence angiography, a technique
designed (see page 52) to identify vascular and other tissues in the retina. The
resultant angiogram provides information on the potential treatability of the
lesions and a guide for laser therapy.
When one eye is affected by this degenerative process the patient is often
unaware until, by chance, the unaffected eye is occluded, revealing the poor
vision in the affected eye. As a consequence, when such patients present, that
eye is invariably beyond treatment. The patient then has to be counselled so that
the warning signs are reported if the same degenerative processes affects the
surviving eye.
With regard to second eyes, the onset of symptoms is immediately noticeable
because it is only that one eye that is providing sharp vision for the patient. The
warning sign of an impending downturn in the fortunes of the central retina is
distortion of vision. Should the clinical signs suggest that sub-retinal repair
processes are taking place as described above, then fluorescence angiography
should be performed with consideration given to laser treatment.
In general, the outcome of laser ablation of sub-retinal, reactive, neovascular
tissue is not very satisfactory. For every 100 eyes that so present, only 10 may
provide the potential for treatment and, of those treated, only half would show
some long-term benefit. Because laser treatment in a sensitive area may produce
its own deficit, it may be a question of being cruel to be kind in destroying a little
living tissue to provide a longer term survival of other tissue, which would
otherwise be implicated and destroyed in the natural healing or scarring
processes. This is a particular area where informed consent is important. The
patient must appreciate that the treatment itself can be destructive or may not be
effective. It is important to realise that the treatment is not going to be the
instrument of visual destruction if properly applied.

108
 Macular Degeneration

Vulnerable populations
Age-related macular degeneration (ARMD) is a problem mainly affecting
patients over 60 years, but is much more common over 70 years. The older the
patient, the greater the chance of it occurring. However, there are inherited,
degenerative diseases of the macula that can affect young people in their 20s,
30s and 40s. Those problems are usually bilateral, fairly symmetrical in onset,
appearance and effect, and there is often a family history of similar problems.
Such syndromes include Best’s disease and Stargardt’s disease.

Functional loss of vision

The functional effect of macular degeneration is to leave a patient in a state of
visual disability. Because patients have intact, peripheral vision, they can
remain mobile and independent but would have difficulty seeing details such
as print, recognising people or driving vehicles, etc.
To some extent the problem can be ameliorated by the use of visual aids, but
these have severe, practical limitations. The best visual aid is a magnifying glass
placed onto print. Visual aids with any significant magnification, when placed
on the eye, will reduce the visual field. Thus, someone might be able to see letters
but not a whole word with a high telescopic magnifier placed on the eye. There
is, in fact, a wide range of visual aids available. If the patient has sufficient
motivation and determination, the disability created by macular disorders can
be offset to a degree.

109
 CHAPTER TWELVE

GLAUCOMA

Definition
Glaucoma is a term used as a general reference for many syndromes which have
in common the loss of nerve fibre tissue at the optic nerve head (ONH). The
visual effects are progressive loss of visual field and acuity leading to eventual
blindness in untreated cases. The concept is that raised pressure within the eye
(intra-ocular pressure—IOP) damages the nerve fibres either by direct action or
indirectly by compromising their blood supply, as raised IOP limits perfusion of
blood in the sensitive region of the ONH.
The problem originates in the anterior segment of the eye where aqueous
humour is produced to be subsequently drained away. It is the imbalance between
production and drainage that causes the IOP to elevate in the closed system
within the wall of the eye (Figure 11, page 22). However, the effects of raised IOP
are realised in the posterior segment of the eye at the ONH. The exception to this
general rule within the glaucoma syndromes is that cluster of conditions
characterised as normal or low-tension glaucomas, wherein the ONH seems
sensitive to other (unidentified) factors, resulting in its decay. The clinical
syndrome is the same as other glaucomas, namely that progressive visual field
loss and acuity may lead to blindness.
(See Chapter 3 for the anatomy of glaucoma.)

Pathophysiology
There are many glaucoma syndromes. The condition may arise as a congenital
or inborn problem or be acquired later in life. The acquired varieties may be
either acute in onset with a dramatic threat to vision in the affected eye (acute
closed-angle glaucoma) or of insidious onset but chronic in nature (chronic
open-angle glaucoma) or secondary to other intra-ocular disorders (secondary
glaucoma).
All the glaucoma syndromes have a common, final, fatal, visual effect—loss
of nerve tissue in the retina as a specific result of damage effected at the optic
nerve head at the point where retinal nerve fibres leave the eye through the optic
nerve to the brain. With the exception of one variant known as low-tension
glaucoma, all the other types present with varying degrees of raised intra-ocular
pressure. This is a consequence of the relative failure of the drainage mechanism
for aqueous humour located in the anterior segment of the eye.

111
 Ophthalmology

Aqueous humour, the physiological fluid that bathes the internal aspects of
the front portion of the eye, is continually produced by the ciliary gland which
is annular in form, lying immediately behind the crystalline lens. The lens is
suspended by the zonular fibres to the muscular part of the ciliary body, the
glandular portion being known as the ciliary processes. The aqueous humour
so produced enters the narrow chamber formed by the crystalline lens
posteriorly and the posterior aspect of the iris diaphragm. Thereafter it
circulates through the pupil into the anterior chamber of the eye and drains
out through the angle of the anterior chamber formed by the root of the iris
diaphragm and the posterior periphery of the cornea. Within the angle is a
drain known as the trabecular meshwork, through which the aqueous fluid
percolates to rejoin the systemic blood circulation from which it was originally
generated.
As the eye is a closed system, if there is disparity between the production of
aqueous humour and its drainage, then more fluid is pumped into the eye than
can be drained. It follows, therefore, that the pressure in the eye increases. In
acute glaucoma it increases rapidly, whereas in chronic and secondary glaucomas
it usually increases slowly. Sustained, raised, intra-ocular pressure has a
damaging effect on the ONH. There are many theories as to why this damage
occurs, but the fact is that the ONH is extremely susceptible to raised pressure
and the damage that follows is irreversible.
The mean intra-ocular pressure in a normal population is 15mm of mercury
(Hg). It is accepted that two standard deviations above the norm, ie about
21mmHg, is the upper limit of normality. Beyond that, pressure must be
considered as a risk factor in the causation of glaucoma. However, raised
pressure alone is not sufficient to cause glaucoma; there must be a
predisposition within the eye to suffer the damage to the nerves. Some eyes
suffer from a condition known as ocular hypertension where the normal
pressure for that eye is above 21 but usually below 30mmHg. Other risk
factors for chronic glaucoma include a family history of glaucoma in near
relatives, diabetes and myopia.

Basic science of glaucoma

Despite modern scientific advances in molecular biology, immunology and cell
physiology, the genetic defects responsible for chronic glaucoma remain
obscure. It is certainly realised that glaucoma is not simply ‘hypertension’ of the
eye, but rather a multi-factorial disease resulting in a characteristic optic
neuropathy (damage to the optic nerve), making it likely that eventually a
number of genetic defects will be found that work together in the ultimate
expression of the disease known as glaucoma.
The trabecular meshwork is of course intimately involved in the regulation
of aqueous humour outflow and therefore intra-ocular pressure, but the normal

112
 Glaucoma

functioning of the trabecular meshwork in the drainage angle of the anterior

chamber is not yet completely understood. The homeostatic mechanisms in the
eye, ie those that balance inflow and outflow of aqueous humour, fail in some
forms of glaucoma. However, the fact that many patients with raised intra-ocular
pressure never get glaucomatous nerve damage suggests that some form of
increased susceptibility to pressure damage is also required for glaucoma to
occur. This increased susceptibility may take the form of abnormal optic nerve
blood flow or as yet unrecognised factors.

Congenital glaucoma
In this form of glaucoma, which is diagnosed in infancy, the sclero-corneal wall
of the eye is still soft and malleable so that, if there is a disparity between
production and drainage of aqueous humour which results in raised pressure,
the eye globe becomes distended and permanently enlarged. Hence the term
buphthalmos or ‘ox-eye’. Damage to the optic nerve follows a persistent
pressure elevation, in spite of the globe enlargement, with consequential visual
defects. The affected eyes inevitably become myopic or short-sighted because of
the expanded size of the globe.

ACQUIRED GLAUCOMAS

Chronic (or primary), open-angle glaucoma (COAG)

This is the commonest type of glaucoma and is said to affect about 2% of the UK
population. Its onset usually occurs in patients over 40 years of age but that is
only a rough guide to the population who may be affected. Its cause is the slow
obstruction of the trabecular meshwork due to clogging of the fine drainage
pores by material produced in susceptible eyes. The onset is insidious and
painless and the presenting sign may be the loss of vision occurring at an
advanced stage. Both eyes are usually affected but the nerve damage may be
asymmetric; thus, when the diagnosis is made one eye may be damaged or
severely damaged, the other eye less so.

Symptoms
The condition is usually asymptomatic until its later stages at which point
decreased peripheral and or central vision may be noted. It is the insidious
nature of COAG that encourages screening programmes to detect
asymptomatic sufferers. There are risk factors which may expose an individual
to a higher probability of contracting the disorder, such as a family history of
glaucoma, coincident diabetes or hypertension, myopia, age and race, it being
more common in Negro populations.

113
 Ophthalmology

Clinical signs
(a) A large or increasing cup:disc ratio, often with asymmetry between eyes.
(b) Visual field defects, commonly nasal, paracentral or extending with arcuate
distribution from the blind spot.
(c) Elevated intra-ocular pressure (the upper limit of normal is recognised at
about 21mmHg), ie two standard deviations above the mean in a normal
population. Intra-ocular pressure fluctuates in a diurnal pattern, generally
being higher in the morning and lower in the evening. This pattern is
exaggerated in glaucomatous eyes.
(d) The drainage angle of the anterior chamber between the root of the iris and
the periphery of the cornea is usually visible through 360° on microscopic
examination.
(e) The optic nerve head may be surrounded by a halo due to loss of retinal
tissue. The optic cup may be elongated more vertically than horizontally.
The retinal nerve fibre lawyer may be seen to be thinned. Differential
diagnosis includes:
(i) low-tension glaucoma;
(ii) chronic-angle, closure glaucoma, a condition in which there are
adhesions between the peripheral iris and the periphery of the cornea
limiting access of the aqueous humour to the drainage system of the
anterior segment of the eye;
(iii) secondary, open-angle glaucoma due to inflammatory debris, pigment
drugs, trauma, external eye conditions, eg Sturge-Weber syndrome,
carotid-cavernous fistular intra-ocular tumours; and
(iv) other causes of optic atrophy, ischaemia, retinal vascular disease,
chiasmal tumours and drug-related, optic neuropathy.

Clinical management
(a) History
(i) previous ocular history;
(ii) family history of glaucoma;
(iii) history of trauma;
(iv) history of local or systemic drug use in particular steroids;
(v) history of diabetes, hypertension, asthma or congestive heart disease.
(b) Examination
(i) intra-ocular pressure;
(ii) gonioscopic evaluation of the anterior chamber angle;
(iii) assessment of the optic nerve head and surrounding retinal nerve
fibre layer, including photographs for serial study.
(c) Visual field examination—automated or Goldmann field.

114
 Glaucoma

Treatment
The goal of treatment is to prevent visual-field loss by further degradation of the
ONH, the main stratagem being to lower intra-ocular pressure. The primary
treatment is by medication in the form of eye drops or topical medication with
which a patient can comply, ie a maximum of twice daily or a 12-hourly
application. Drug therapy is based on improving the drainage of fluid out of the
angle of the anterior chamber of the eye or reducing inflow of aqueous humour
by drug effects on the ciliary gland epithelium. Newer drugs have achieved
alternative methods of lowering intra-ocular pressure by improving uvea-
scleral outflow of fluid from the eye, ie through the wall of the eye.
If medical methods fail to control the disorder, as demonstrated by
persistently raised intra-ocular pressure and progressive visual-field loss, then
surgical intervention is indicated. The principle of surgical intervention is to
create a fistula or valve in the wall of the eye to allow a balance to be achieved
between the inflow of aqueous humour and its drainage. The operation that is
usually performed is known as a trabeculectomy. In eyes in which the surgery
has not succeeded the first time or in eyes which have a higher risk of surgical
failure, enhancement of the trabeculectomy by local use of anti-inflammatory
agents and anti-metabolise agents, to prevent closure of the fistula by fibrosis,
may be indicated.
It is essential that patients with glaucoma are regularly monitored to ensure
that the condition is properly controlled.

Topical medication (eye drops)

(a) Beta-blocking agents (drugs which act on the beta-adrenergic fibres of the
autonomic nervous system of the body which influence production and
drainage of aqueous humour); eg twice daily applications of 0.25–0.5%
Timolol, 0.3% Metipranolol or 1% Carteolol often effectively lower intra-
ocular pressure but cannot be given to patients with breathing problems
such as asthma, cardiac arrhythmias or congestive heart failure. Betaxolol
twice daily may be used cautiously in patients with emphysema or heart
disease.
(b) Miotics (drugs which act on the parasympathetic component of the
autonomic nervous system and have effects on drainage of aqueous humour);
eg Pilocarpine (formerly the treatment of choice) is not a comfortable solution,
especially in older patients where the miosis (small pupil), may have
significant ocular effects; particularly in the presence of early cataract and
where accommodative spasm may be painful. To be effective the drug also
has to be used at least four times per day.
(c) Adrenaline compounds (which act on the adrenergic component of the
autonomic nervous system, influencing both production and drainage of
aqueous humour); eg 1.0% Propine or Epinephrine, which enhances the effect

115
 Ophthalmology

of other drugs that are rarely used as a primary treatment, not unusually
causes redness and irritation of the eyes.
(d) Prostaglandin eye drops; eg Latanoprost (Xalatan Pharmacia & Upjohn).
This is now the commercially available preparation, a new approach to
glaucoma therapy inducing outflow of fluid from the eye through the uveal
tract and the sclera. This is a promising new approach to medication.
(e) Systemic medication—eg oral carbonic and anhydrase inhibitors,
acetazolamide (Diamox) in sustained-release form 250mg once or twice daily.
Diamox and similar agents are mild diurectics and are extremely useful for
short-term usage. However, longer-term usage may cause potassium
deficiency, and monitoring of blood electrolytes is required.

Alternative treatments (laser therapy)

Argon-laser trabeculoplasty can be used as an adjunct to medical treatment
when surgical intervention is not possible. It is easy to apply but will only result
in modest lowering of the intra-ocular pressure and may not be of lasting
duration.

Normal-tension and low-tension glaucomas

Definition
A large or enlarging cup to disc ratio often with asymmetry between the two
eyes, with paracentral, nasal or extending arcuate visual field defects. These
conditions manifest all the symptoms and signs of chronic open-angle
glaucoma despite ‘normal’ or even lower intra-ocular pressures. These patients
may also have low systemic blood pressure suggesting, that blood perfusion of
the posterior segment of the eye is compromised by the low perfusion pressure,
ie the difference between intra-arterial blood pressure entering the eye and the
intra-ocular pressure.
The differential diagnosis includes:

(a) primary, chronic open-angle glaucoma;

(b) sub-acute closed-angle glaucoma where a patient has intermittent attacks of
raised intra-ocular pressure with or without mild blurring of vision;
(c) previous drug therapy, eg steroids;
(d) previous ischaemic episodes;
(e) ischaemic optic neuropathy;
(f) compressive optic nerve disease by tumour or aneurysm; and
(g) congenital nerve defects, eg myopic disc, coloboma of the ONH, pit of the
ONH and optic nerve colloid bodies or drusen.

116
 Glaucoma

Treatment
The post-diagnosis management and treatment is identical to that of chronic
open-angle glaucoma or primary, open-angle glaucoma, with the emphasis on
reducing the intra-ocular pressure to the lowest possible level.

Secondary glaucomas
(a) Any condition that produces inflammation within the eye will produce
inflammatory debris which can obstruct the outflow of aqueous humour
from the eye. Anterior uveitis, posterior uveitis, pan-uveitis and kerato-uveitis
are examples of inflammatory disorders.
(b) Steroid response glaucoma—ophthalmic inflammatory disorders require
treatment, usually by steroidal anti-inflammatory agents which themselves
may cause raised intra-ocular pressure and the damage that follows
thereafter.
Symptoms—usually has insidious onset and, unless detected by a clinician,
the first awareness a patient may have is with visual loss.
Significant signs—increased intra-ocular pressure, usually within a
few weeks of starting. Steroid-containing eye drops, eyelid skin creams
or injections around the eye to treat inflammatory disorders may cause
a rise in intra-ocular pressure; this may be immediate or delayed. It is
typical of the condition that the intra-ocular pressure will revert to normal
levels after discontinuing the drug.
Treatment—discontinuing steroid therapy, reduction of dosage or
concentration of steroid therapy, alternative use of non-steroidal, anti-
inflammatory agents such as 0.1% Diclofenac, or glaucoma therapy as
for chronic or primary, open-angle glaucoma.

(c) Other secondary glaucomas

(i) Pigmentary glaucoma—a condition consequent upon the dispersion
of pigments from the uveal tract into the drainage system of the eye,
usually associated with mid-peripheral, spoke-like iris
transillumination defects from where pigment has dispersed. Dense
pigmentation of the trabecular meshwork is seen on gonioscopic
examination of the anterior chamber of the eye through 360° and a
glaucomatous atrophy (cupping) of the optic nerve head with
consequential visual-field loss.
(ii) Pseudo-exfoliative glaucoma—usually asymptomatic. Clinical signs are
the presence of white, flaky material on the pupillary margin, the
anterior crystalline lens capsule, where the exfoliating material may
have rolled up edges around a central clear zone with peripheral
capsular cloudiness.

117
 Ophthalmology

(iii) Phacolytic glaucoma—leakage of lens material from a cataract

through an intact lens capsule leads to trabecular meshwork outflow
obstruction.
(iv) Lens-particle glaucoma—lens material (usually cataractous) liberated
by trauma or surgery which obstructs the outflow channels.

The management of all the sub-types of chronic glaucoma and secondary

glaucomas is the same as for chronic or primary glaucoma, namely control of
intra-ocular pressure through use of appropriate medications, or reversion to
surgical control of aqueous fluid outflow in the event of failure of compliance or
effect of medical treatment.
Any mechanism that will affect the free drainage of fluid through the
trabecular meshwork will cause a disparity between aqueous humour production
and drainage and therefore lead to a rise in intra-ocular pressure. These
mechanisms additionally include:
(a) glaucoma secondary to intra-ocular haemorrhage where the capsules of red
blood cells may accumulate and block the drainage of aqueous humour
(ghost cell glaucoma);
(b) post-traumatic glaucoma, wherein post-traumatic, inflammatory debris
compromises the trabecular meshwork’s function;
(c) aphakic glaucoma wherein the drainage mechanism is compromised by the
cataract surgical process, a not uncommon complication in former times
when intracapsular cataract surgery was crude by today’s standards. In the
absence of the crystalline lens, vitreous humour gained access to the anterior
chamber and caused obstruction to aqueous humour outflow by physical
obstruction of part or all of the drainage angle. However, it is a less common
occurrence with modern, small-incision cataract surgery.
(d) post-operative glaucoma—in the immediate aftermath of intra-ocular
surgery, particularly anterior segment surgery such as cataract, glaucoma
and corneal transplantation, intra-ocular pressure tends to rise a few hours
post-operation but naturally may return to normal within a further few hours.
If surgery has been unusually traumatic or if visco-elastic agents have been
used but not removed, temporary obstruction to the outflow of aqueous
humour will occur and produce a dramatic if short-lived rise in IOP. Its
transient nature requires treatment if it causes symptoms or is persistent
beyond a few hours, or the eye will be vulnerable to short-term pressure
elevation because of its pre-operative status.
(e) uveitis glaucoma hyphaema syndrome (UGH syndrome)—a more insidious
form of post-operative glaucoma which classically occurs because of uveal
irritation as a result of malposition of an intra-ocular lens implant placed in an
eye after removal of a cataract. In modern cataract surgery, where the lens is
sequestered inside the lens capsular bag, it would be a rare phenomenon for
this to occur, but in recent years with non-bag placement of the intra-ocular
lens it could provide a not uncommon, serious source of ocular destruction.

118
 Glaucoma

Neo-vascular glaucoma
This is a form of glaucoma that occurs as a result of aberrant growth of vascular
tissue in the region of the drainage of aqueous humour, ie on the surface of the
iris diaphragm and invading and thereby obstructing the drainage angle
between the root of the iris and the corneal periphery. Neovascular glaucoma
may occur as a consequence of ischaemic (poor blood supply) problems in the
eye such as diabetic retinopathy, central retinal vein occlusion, central retinal
artery occlusion, and ocular ischaemic syndrome associated with carotid
occlusive disease, and other retinal, vascular disorders such as branch retinal
vein occlusion, radiation retinopathy and chronic detachment of the retina.

Symptoms
These are usually associated with pain, redness of the eye, photophobia and
decrease of vision. It may be a complication that occurs in a blind eye as a result
of retinal ischaemia.

Clinical signs
Stage 1—abnormal, engorged, new blood vessels along the pupillary margin,
the peripheral iris and the trabecular meshwork, but with normal intra-ocular
pressure.
Stage 2—stage 1 plus increased intra-ocular pressure.
Stage 3—partial or complete angle-closure glaucoma caused by a fibro-vascular
membrane covering the trabecular meshwork. Often associated with
inflammatory signs in the aqueous humour, hyphaema or bleeding into the
anterior chamber. Eversion of the pupillary margin allowing visualisation
of the iris pigment (ectropion uvea). Optic nerve atrophic cupping and visual
field loss.
Stage 4—a painful blind eye often requiring enucleation as the only means of
pain relief.

Management
This comprises early reduction of intra-ocular pressure by use of pressure-reducing
agents administered topically or systemically coupled with anti-inflammatory
agents such as steroids. The problem is essentially due to stasis of aqueous humour
in the eye, which can be ameliorated by creating a surgical drainage fistula, ie
trabeculectomy. This can often produce dramatic resolution of the neovascular
tissue produced as the eye’s response to the formation of vaso-proliferative
substances, the common ocular response to ischaemic conditions.

119
 Ophthalmology

Acute (angle closure) glaucoma

This form of glaucoma invokes a different mechanism to the more slowly-
progressive glaucomas as its name implies. It usually affects smaller eyes
(hyperopic eyes) and occurs due to a crowding phenomenon within the eye,
wherein the peripheral iris is forced against the peripheral cornea to deny
aqueous humour access to the trabecular meshwork drains. The blockage of the
passage of aqueous humour through the pupil is the initiating mechanism, for
even a relative block at that site will cause an accumulation of aqueous humour
behind the flexible iris diaphragm, pushing it forward to create a vicious cycle
of events resulting in an acute rise of pressure in the eye. Symptoms include
pain, redness of the eye and rapid loss of vision. The cause of pupil block may be
related to an increase in size of the crystalline lens, which is a natural
phenomenon (see crystalline lens, page 23). This circumstance classically occurs
in small (hyperopic) eyes, for when the pupil dilates naturally in dim-light
conditions (or iatrogenically by the instillation of mydriatic, or pupil-dilating,
eye drops), then the crowding of the iris into the angle of the anterior chamber
can initiate the above cycle of events

Symptoms
Pain, blurred vision, coloured haloes around lights, frontal headaches, nausea
and vomiting. The symptoms may occur in isolation or in combined form.
Vomiting may cause the unwary physician to suspect an abdominal rather than
an eye problem.

Clinical signs
Closed drainage angle (observed using the gonioscopy contact lens) with acute
elevation of intra-ocular pressure often 40 or 50mmHg or higher. Severe corneal
oedema, redness of the eye, and the pupil may be semi-dilated and
unresponsive to light or other stimuli.

Management
This will depend on severity and duration of the attack. Systemic agents such as
acetazolamide (Diamox) will reduce intra-ocular pressure, and medication
including topical beta-blockers (Timolol 0.5%) and topical steroids every 15
minutes will reduce inflammation; osmotic agents such as mannitol 1-2g/kg
should be given intravenously over 45 minutes. Once the eye’s pressure is
under control, the immediate need is to recreate a flow of fluid from behind the
iris through the pupil to gain access to the angle of the anterior chamber. This is
achieved by creating an additional opening in the peripheral iris by an
iridectomy or iridotomy carried out by surgical or laser methods. Where it is

120
 Glaucoma

seen that the problem is due to enlargement of the crystalline lens in a small eye,
removal of the lens and replacement with a lens implant is the procedure of
choice.

Chronic closed-angle glaucoma

If there is intermittent but recurrent inflammation in an eye to cause adhesions
between the peripheral iris and the peripheral cornea, there may be a proximal
physical block to the access of aqueous humour into the trabecular meshwork—
so called chronic closed-angle glaucoma. In effect, it behaves clinically as
chronic open-angle glaucoma, the distinction being based on gonioscopic
examination.

Malignant glaucoma
If the aqueous humour was to leak behind the crystalline lens rather than
circulate naturally into the anterior chamber of the eye, it would cause the lens-
iris diaphragm to be pushed forwards. Under these rare but drastic conditions
there is a dramatic loss of vision accompanied by unremitting pain in and
around the eye. This is a rare form of acute glaucoma.

DIAGNOSIS AND SCREENING OF THE GLAUCOMAS

Presenting symptoms will depend on the type of glaucoma; as outlined above,

congenital glaucoma should be detected during routine screening of infants’
eyes, as the infant will not complain. Often, detection is relatively late when the
eyes are observed to be larger than expected. The condition may be confused
with a harmless anatomical variation of megalocornea, in which the cornea is
much larger than usual but functions quite normally, as does the aqueous
humour production and drainage system within the eye.
Chronic glaucoma (open-angle glaucoma) is so called because the aqueous
humour has access at all times to the drainage angle in the anterior chamber, but
the trabecular meshwork is not as freely permeable as is necessary to balance
aqueous humour production and drainage. As noted above, this is an insidious
condition which may only be detected when the patient complains of visual
loss. Because the nerve damage is irreversible, all that can be done at this stage is
to contain the situation and prevent further visual loss.
Screening programmes for chronic open-angle glaucoma within a population
have been demanded at various times by the Glaucoma Society and other
responsible, ophthalmic organisations. In practice, routine eye tests by
optometrists are used to screen the public when reduction in visual acuity, visual-
field defects and pathological changes (cupping) of the ONH are the presenting
symptoms and signs.

121
 Ophthalmology

Secondary glaucomas may present in a similar fashion to chronic open-angle

glaucoma, and if a patient is being treated for other medical conditions in the
eye in which glaucoma is recognised as a potential complication, it should be a
matter of routine clinical management to make the necessary checks to rule out
raised intra-ocular pressure and other signs. This includes patients who are using
steroid eye drops or having systemic steroid administration for medical
conditions.
Acute angle closure glaucoma may initially present as a sub-acute form when
the presenting complaint is transient blurring of vision. If such symptoms are
reported, then the size of the eye, the dimensions of the anterior chamber and
examination of the angle of the anterior chamber by gonioscopy may lead the
ophthalmologist to suspect that the patient is having self-limiting attacks of acute
closed-angle glaucoma and take the necessary steps to prevent a full-blown,
acute attack. On the other hand, if an acute attack does occur and the patient
presents with dramatic loss of vision, severe pain and redness of the eye, and
haziness of the cornea in response to acute rise in intra-ocular pressure, emergency
treatment is required.

The spectrum of clinical signs in the glaucomas

(a) Raised intra-ocular pressure (IOP), except in normal-tension or lowtension
glaucoma.
(b) Atrophy and cupping of the optic nerve head.
(c) Visual-field loss.
(d) Visible loss of retinal nerve fibres.
(e) Corneal oedema (in eyes with high pressures).
(f) Visible changes in the anatomy of the angle of the anterior chamber
(dependent on the type of glaucoma).
(g) Reduced visual acuity (dependent on glaucoma type and stage).
(h) Dilated, fixed pupil (acute closed-angle glaucoma).
(i) Red eye (acute closed-angle glaucoma).

Investigations for suspected glaucoma

(a) Visual acuity check.
(b) Measurement of IOP, either by contact or non-contact tonometry (page 51).
(c) Clinical observation of the status of the optic nerve head. The ONH consists
of a neural rim of pink tissue in a healthy optic nerve (Figure 15, page 32)
and a central depression known as the physiological pit through which
the central retinal artery appears into, and the central retinal vein disappears
from, the eye. The margin of the ONH is usually clearly defined by the
adjacent retinal-pigment epithelium. The ONH is also known as the optic
disc because of its disc-shaped appearance. In glaucoma the neural tissue

122
 Glaucoma

becomes paler and depressed in relation to the level of the retina, as intra-
ocular pressure seems to force the tissue back down the stalk of the optic
nerve to give rise to the description ‘cupping of the optic nerve head’.
Enlargement of the physiological or normal optic cup occurs, which usually
occupies less than 0.3 of the diameter of the optic disc, both vertically and
horizontally. The vertical diameter is usually longer than the horizontal
diameter. The ratio between the diameter of the central cup and the overall
diameter of the nerve head or optic disc is used as a descriptive ratio to
indicate the clinical impression of the status of the ONH. Thus, a cup to disc
ratio (C/D) of 0.5, 0.6, 0.7, etc, would indicate advanced or advancing degrees
of glaucomatous damage. There are various stereoscopic, photographic and
scanning devices which can document the status of the ONH, providing a
factual ratio rather than an estimate. Such images taken in sequential fashion
document stability or degradation of the tissue at the nerve head, but these
instruments are not in common usage. Ophthalmologists generally rely on
their ophthalmoscopic examination of the nerve head and the above notation.
(d) Gonioscopy—The use of a contact lens containing a mirror allowing the
observer to evaluate the status of the drainage angle of the anterior chamber
of the eye through a bio-microscope. This examination provides more
accurate diagnostic information, allowing glaucoma sub-types (eg
pigmentary glaucoma and chronic closed angle glaucoma) to be accurately
documented.
(e) Visual field estimation—Early signs of glaucomatous visual defect would
be an increase in the size of the blind spot followed by radiating arches of
visual loss (upper and lower arcuate scotomata), and then by coalescence of
these arches of visual loss and the general narrowing of the visual field as
the visual loss spreads out to the retinal periphery. As glaucoma progresses,
so the visual field of view narrows, and in end-stage glaucoma there would
remain a tunnel field of vision, prior to loss of all light perception

REFERRAL—THE ROLES OF OPTOMETRIST, GP AND

OPHTHALMOLOGIST IN GLAUCOMA

Optometrists are usually the first to suspect the presence of glaucoma in

patients, because they are the first source of professional ophthalmic
examination and advice sought by members of the public. Once that suspicion
arises it is the duty of the optometrist to refer the matter for further medical
evaluation. The chain of referral is through the family doctor or GP and then to
a specialist ophthalmologist. Referral should always take place if there is a
suspicion of glaucoma, particularly if that suspicion is supported by other
known risk factors such as family history, or other conditions which have

123
 Ophthalmology

known associations with an increased risk of glaucoma, such as diabetes,

myopia, extreme hyperopia, etc.

TREATMENT OVERVIEW

Congenital glaucoma
The treatment of congenital glaucoma is primarily by surgical intervention. Its
purpose is to provide the plane of cleavage between the peripheral iris and the
cornea which is missing in these eyes due to the failure of that cleavage to occur
during development of the eye. A needle is placed between the iris and cornea
internally and physical separation of the layers is achieved. The operation is
known as goniotomy. It may require one or more interventions to achieve the
appropriate balance between aqueous humour production and drainage which
would stabilise the position.

Acute angle closure glaucoma

Initial treatment is on an emergency basis using medical rather than surgical
means to lower the intra-ocular pressure as quickly as possible. Treatment
includes instillation of eye drops or topical therapy for the purposes of reducing
aqueous humour production, and breaking pupillary block and the cycle of
events that leads to the condition. Systemic administration of drugs such as
acetazolamide or Diamox has the effect of further reducing aqueous humour
production, and anti-inflammatory agents are valuable to combat the inevitable
inflammation associated with an acute rise in intra-ocular pressure.
Once the pressure of the eye has stabilised, or if that situation fails to
materialise rapidly (within hours), then surgical intervention is necessary. The
simplest procedure that can be carried out is the provision of an alternative
aperture other than the pupil, to allow aqueous humour access to the anterior
chamber of the eye and thereby relieve the pressure from behind the iris
diaphragm. This aperture through the iris diaphragm may be created with a
neodinium:yttrium-aluminum-garnet (Nd:YAG) laser. This can be fired through
the cornea without opening the eye to allow aqueous humour to percolate into
the anterior chamber and bypass the blockage at the pupil. An alternative and
more certain method of achieving the same objective is to remove a small segment
or triangle of peripheral iris secondary to an incision through the cornea, a surgical
procedure known as a peripheral iridectomy (see also surgical treatment of
glaucoma, below).

124
 Glaucoma

MEDICAL MANAGEMENT OF COAG

COAG is a syndrome characterised by an increase in intra-ocular pressure. This

is due to an imbalance between the inflow of aqueous humour produced in the
ciliary gland of the eye and the outflow through the trabecular meshwork. Thus,
if drugs can inhibit the production of aqueous humour or improve its outflow
from the eye, balance may be restored and the pressure effects controlled. There
are five groups of drugs used in medical management of glaucoma (Table 1,
page 126).

Sympathomimetic agents

These agents (adrenergic agonists—simulating an adrenaline-like response

with alpha and beta-types of adrenergic reaction) act primarily through the
lowering of intra-ocular pressure by facilitating the drainage of aqueous
humour through uveal and scleral channels.

Prostaglandins

These are a new class of drugs delivered as eye drops, and have a similar action
which may also enhance the effects of other drugs used in glaucoma
management.

Beta-adrenergic blocking agents

These may be used alone or in conjunction with other agents. They act by
reducing the production of aqueous humour in the ciliary gland and have the
advantage that they do not affect the pupil or its accommodation. They do have
systemic side effects in some patients, eg bronchospasm, cardiac failure or blood
lipid elevation, hence the profusion of options, as some are selective in their
actions and may be tolerated without general effects.

Cholinesterase inhibitors
These enhance the effects of endogenous acetylcholine by inactivation of the
enzyme cholinesterase, hence they are also known as anticholinesterase drugs.
This type of drug has numerous disadvantages, and though they were the
mainstay of glaucoma management in earlier years, the small pupil (miosis)
and paralysis of accommodation (no focus for near vision) plus their required
frequency of administration (compliance problems) make their continued use
generally unacceptable except in very difficult cases.

125
126
Ophthalmology

Table 1. The five groups of drugs used in the medical management of glaucoma.
 Glaucoma

Hyperosmotic agents
These, including orally-administered glycerol and intravenously-administered
mannitol, act in emergency situations to reduce acutely-raised, intra-ocular
pressure—usually acute closed-angle glaucoma. They act by deturgessing the
eye by osmotic attraction of fluid into the hyperosmotic blood stream, which
attracts fluid to dilute its higher concentration.

TREATMENT COMPLIANCE

The fundamental problem with the medical treatment of glaucoma remains

that of patient compliance. Patients are often resistant to treating an essentially
symptomless disease with medications that may be inconvenient and produce
both ocular and systemic side effects. Ophthalmologists are often not able to
detect the degree of compliance with treatment of their patients. In recent
years, therefore, pharmaceutical developments have focussed on enhancing
patient compliance by simplifying dosages whilst reducing the side effects.
Topical beta-blockers were introduced in the 1970s and rapidly became
the medication of choice for the treatment of glaucoma because of their
efficacy and generally excellent safety profile. Newer forms of the drugs have
been introduced in recent years because side effects were more common than
originally thought. The key to prevention of side effects from these beta-
blocking agents is both patient selection and education. Patients should be
instructed in methods to avoid systemic absorption of medications such as
closing the eye after instillation and pressing on the lacrimal sac to prevent
drug absorption through the nasal mucous membrane. Limitation of drop
instillation (one drop is sufficient) must also be counselled. Side effects include
reactive airway disease (difficulty with breathing) and abnormal cardiac
rhythms (arrhythmias).
More recently, a new class of medication, the alpha-adrenergic agonist
(Apraclonidine), has been introduced. This lowers intra-ocular pressure by
decreasing aqueous humour production, although the mechanism is obscure.
However, a major side effect of this drug is an allergic response, and up to one
third of patients develop that reaction.
Topical carbonic anhydrase inhibitor is another new agent recently
introduced. Systemic carbonic anhydrase inhibitors such as acetazolamide
(Diamox) lower intra-ocular pressure by suppressing aqueous humour
production, again through a mechanism that remains poorly understood. Taken
orally, these medications are extremely effective in lowering intra-ocular pressure,
but have a number of side effects that result in 50% of patients having to
discontinue their use. Formulation of the same drug in a topical form avoids the
systemic effects of oral administration.

127
 Ophthalmology

Finally, prostaglandins, some of which have been shown to have significant

pressure-lowering effects, are about to be introduced, although the mechanism
relies on improving outflow of aqueous humour through the uveal and scleral
tissue, quite a different mechanism to the other drugs.

LASERS IN THE TREATMENT OF GLAUCOMA

Laser trabeculoplasty is a useful tool for the management of chronic open-angle

glaucoma, being safe and moderately effective. The technique involves
application of pulses of argon-laser energy directly to the trabecular meshwork
in the angle of the anterior chamber, using a contact lens gonioscope whose
mirror allows the beam to be directed at will into the angle of the anterior
chamber. All 360° of the angle are visualised in turn and the laser treatment
applied. Laser trabeculoplasty is more effective in some secondary glaucomas
such as pigmentary and pseudo-exfoliative glaucoma, and less effective in
uveitic, post-traumatic and aphakic glaucoma. It is more effective in Caucasian
patients eyes than in Negroid patients.
Cyclo-ablation destruction of part of the ciliary gland is usually reserved
for eyes considered to be poor surgical candidates, and is usually performed
under retrobulbar anaesthesia. Laser cyclo-photocoagulation is quite
successful in selected cases and appears to be a more controlled cyclo-
destructive procedure than cyclo-cryotherapy (freezing technique). Since laser
cyclo-destruction is a relatively new procedure, long-term data for incidence
of phthisis bulbi and sympathetic ophthalmia remain to be collected. Laser
cyclo-destructive technology is quite expensive and probably out of the reach
of most ophthalmologists, but new instrumentation is rapidly reducing the
price.
Lasers are also being used to perform filtering surgery. Both the holmium
laser and the Nd: YAG laser, whose energy is delivered through a fibre-optic
probe, have been used to create full-thickness valve formations through the scleral
wall of the eye. Although these procedures can be performed with a minimum
of conjunctival manipulation and subsequent inflammation, they are essentially
unguarded sclerostomies (drainage valves or perforations of the scleral wall of
the eye). Most problems associated with full thickness procedures, eg soft eyes
(hypotony), superchoroidal haemorrhage (ie haemorrhage between the choroid
and the scleral wall), cataract, etc, have been described following laser
sclerostomy. Since a surgical peripheral iridectomy is not being performed, some
of these procedures fail because of internal occlusion of the opening in the sclera
(sclerostomy) by the iris. Some clinics have performed laser sclerostomy and,
although claiming good success rates in highly selected patients, how the
treatment will fit with the overall surgical management of glaucoma remains to
be seen but is worthy of note.

128
 Glaucoma

SURGICAL TREATMENT OF GLAUCOMA

When aqueous drainage is obstructed on a permanent basis, either by chronic

closure of the angle of the anterior chamber or chronic obstruction of the
trabecular meshwork, the drainage has to be effected by the fashioning of a
drainage valve in the wall of the eye in the region of the trabecular meshwork;
the operation is known as a trabecultomy. It has a success rate in excess of 80% in
most eyes, but some eyes, particularly those of African patients, produce an
abnormal healing response and close off the drainage valve. The operation may
be enhanced by the application of cytotoxic agents at the time of surgery which
inhibit the healing process and thereby facilitate maintenance of drainage of
aqueous humour out of the eye.

Anti-metabolites
As science began to understand the cell biology of wound healing in the early
1970s, it became increasingly apparent that properly-performed, filtering
surgery, ie formation of a valve in the wall of the eye to allow aqueous humour
to drain out of obstructed trabecular systems, may fail because of an exuberant
healing response that causes conjunctival scarring and closure of the filtration
valve. With this insight into the causes of surgical failure anti-metabolite drugs
were introduced to control the healing response in eyes undergoing filtration
surgery.
Injected sub-conjunctivally, 5-fluorouracil (5-FU) has been shown to be an
effective anti-metabolite in this application. Therefore, eyes considered to be at
high risk of failure of filtering surgery, including those that have undergone
previous eye surgery or in which the fellow eye has undergone filtering
surgery and failed because of an exuberant scar and response, are candidates
for application of this treatment. However, the question of whether anti-
metabolites should be used in all patients undergoing filtering surgery
remains controversial.
Mitomycin-C is a more potent anti-metabolite than 5-FU and has come into
increasing use in filtration surgery because it can be applied intra-operatively,
avoiding the necessity for post-operative, sub-conjunctival injections. Those
filtering valves created with support of mitomycin-C appear to result in a lower
intra-ocular pressure, but the effects of the drug are impossible to titrate in the
post-operative period and persistent wound leaks and profound hypotony (soft
eyes) have been described as complications of its use. However, mitomycin-C
has proven extremely useful in the management of glaucoma in children where
post-operative injections are not possible.
There remains the longer-term concern of the use of any anti-metabolite with
regard to the risk of devastating ocular infection from a breakdown of the filtration
site and admission of pathogens into the eye. Thus, the filtration valves that

129
 Ophthalmology

develop after use of anti-metabolites are thinner and lack the cellular support of
the regular filtration valves, and they undoubtedly present a more tenuous barrier
to the entry of pathogenic organisms.

Very complicated glaucomas—tube/shunt procedures

In those cases where the trabeculectomy operation fails persistently, for it can be
repeated at different locations around the anterior scleral area, then a
mechanical valve may have to be inserted.
Such procedures, using Maltino implants and derivatives, have gained
increasing acceptance in the management of very complicated glaucomas,
especially those which have failed to respond to conventional filtering valve
surgery. In all complicated eyes, a small-calibre, silicone tube is introduced
into the anterior chamber. The tube drains to an external reservoir system that
maintains an area of filtration often quite far-posterior on the wall of the globe.
Filtration occurs through the surface of the capsule that develops over the
reservoir. Success rates have been reported to be as high as 80%, but they are
not without high complication rates in all series which have been reported.
However, they are being performed in very-high-risk eyes in which other
forms of glaucoma surgery have a poor prognosis, and thus the risk/benefit
ratio is in favour of surgery. The conditions which may benefit from such
intervention include neovascular glaucoma, epithelial in-growth glaucoma
and cases in which conventional filtering valve surgery or the use of anti-
metabolites has failed, congenital and juvenile glaucomas in which numerous
conventional procedures have failed, and situations where, for whatever
reason, the conjunctiva and epi-scleral tissues are so severely scarred it is
unlikely that the surgeon can successfully create a filtration site using
conventional techniques.
Other methods used to treat intractable conditions include the inhibition of
the production of aqueous humour by freezing the ciliary gland (cyclo-
cryotherapy), or laser application to the gland through the wall of the eye or
delivered through an endoscope (see page 128).

Combined surgical procedures

With the advent of small-incision, cataract surgery utilising the
phacoemulsification principle, the possibility has arisen of combining
glaucoma and cataract surgery. This enables an optimal glaucoma procedure
and optimal cataract procedure with lens implantation to be accomplished at
the same time. As a consequence, the ease with which trabeculectomy (the
glaucoma valve-filtration procedure) and its combination with small-incision,
phacoemulsification cataract extraction, has lowered the threshold at which

130
 Glaucoma

combined surgery is performed, and it is reasonable to perform the combined

procedure even when the glaucomatous condition is well controlled medically.
Patients who have been on sustained treatment for glaucoma utilising the
older medication of meiotics, such as Pilocarpine (treatments which make the
pupil small and, as a consequence, may make cataract surgery difficult because
of failure of the pupil to dilate) gives rise to management problems during cataract
surgery. The problem is overcome by mechanical means by physically opening
the pupil or using traction devices allowing access to the cataractous crystalline
lens.

GLAUCOMA IN RECENT HISTORICAL PERSPECTIVE

It is now realised that early and aggressive intervention is of value in this group
of blinding eye disorders. Early detection of glaucoma has advanced
significantly because computer technology and electronic imaging are being
used to detect, follow and manage the condition. These advanced detection
techniques, combined with the clinician’s increasing ability to lower intra-
ocular pressure profoundly without adverse side effects, has improved the
outlook for patients suffering from glaucoma.

131
 CHAPTER THIRTEEN

DIABETIC EYE DISEASE

DEFINITION

Diabetes is a systemic disorder characterised by abnormal sugar metabolism.

One of the most significant complications of the disorder is diabetic retinopathy,
though diabetes may also cause or accelerate the onset of cataract and have
effects on nerve tissue in the eye (diabetic ocular neuropathy).

Anatomy

Diabetes mellitus is a condition with many ocular manifestations. The best

known affect the retina although many parts of the eye can be affected,
including the iris (diabetic neuropathy), the lens (cataract), and the optic nerve
(optic neuropathy).

Types of diabetes mellitus

Diabetes mellitus is a chronic condition characterised by chronic, raised blood
sugar (hyperglycaemia) and is classified into two principal forms: insulin-
dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes
mellitus (NIDDM). The former is also known as type-1 diabetes and primarily
affects younger people, whereas the latter (type-2) typically has a later onset.
Type-2 diabetes may present initially with visual symptoms or retinal signs.

Prevalence
This varies dramatically between races and populations. In the UK type-1
diabetes has an overall prevalence of about 0.25% with a peak onset at the ages
of 11–13 years. Type-2 diabetes is much more common than type-1 and is a
condition suffered by at least half a million people in the UK. Its prevalence
varies from 1% in a Caucasian population to 5% in an Asian community.

Pathophysiology
Diabetic retinopathy is the most serious ocular complication of diabetes and is a
very common cause of blindness and visual disability in younger people. As an
approximation, 1,000 new, blind registrations occur each year in the UK. The

133
 Ophthalmology

probability of a diabetic patient going blind is 10–20 times greater than that of a
non-diabetic person.
Diabetic retinopathy is a problem of small blood vessels. The primary
problem is believed to occur in the capillaries of the retina where specific cells
known as pericytes undergo degeneration; this is associated with a thickening
of the basement membrane of the capillary and distortions of their contours
with a ballooning effect known as a microaneurysm. This variation in the structure
of retinal capillaries is also associated with changes in the blood flowing through
them. These patients demonstrate an abnormal form of haemoglobin and the
flow characteristics (rheology) are also changed. The consequence of all these
effects is that blood vessels become occluded. When retinal arterioles become
occluded, the supply of blood to the dependent retina is denied (ischaemia).
Retinal capillaries also become abnormally permeable allowing fluid to leak into
the retina.
Unlike other body tissues, the retina does not have a lymphatic system and
fluid escaping into its substance tends to linger and cause structural damage.
The lipid or fatty content of blood leaks into the retina to become crystallised
into the form of hard retinal exudates which have a glistening, yellowish
appearance. The lipid material accumulates in scavenger cells or macrophages
which remain clustered in the retina to give one of the characteristic features of
a diabetic retinopathy. The presence of excess fluid in the retina is known as
retinal oedema and is a particular problem when the central retina or macula is
affected.

Intra-retinal micro-angiopathy (IRMA)

The complex of retinal-microaneurysm-occluded vessels within the retinal
circulation is known as intra-retinal micro-angiopathy and is a prominent
feature of background diabetic retinopathy with associated bleeding from
fragile capillaries, the haemorrhage attaining different forms according to the
entrapment of blood at different levels in and on the retina. For example, if it is
superficial amongst the retinal nerve fibres, the haemorrhages have a streaky or
splinter-like appearance. If it is deeper in the retina amongst the cell bodies of
retinal nerves, then it has a rounded or dot-like appearance. If it is beneath the
retina it has a lake-like appearance, as it also appears superficial to the retina
and behind the vitreous gel and its posterior hyaloid membrane.

Classification of diabetic retinopathy

Background retinopathy
The characteristics of background retinopathy include dilatation of the retinal
veins, micro-aneurysms, hard retinal exudates and retinal oedema, and
haemorrhages of the dot and blot form as they are intra-retinal.

134
 Diabetic Eye Disease

Diabetic maculopathy
A major constituent of a background retinopathy is that which affects the
macula because of its potential deleterious effects upon the patient’s vision. Any
abnormalities that occur close to the fovea, at the centre of the macula, are sight
threatening.

Pre-proliferative retinopathy

The progressive nature of diabetic retinopathy allows a second stage to be

identified—pre-proliferative retinopathy—an intermediate stage between
background retinopathy and a very serious proliferative retinopathy (see
below). In pre-proliferative retinopathy there are increasing signs of loss of
retinal blood supply (retinal ischaemia) together with examples of localised
death of retinal tissue, known as retinal infarcts or descriptively as cotton wool
spots. There is excessive dilatation and irregular sausage-like dilatations of the
retinal veins and an increase in the presence of the intra-retinal micro vascular
abnormalities (IRMA) described above.

Proliferative retinopathy
A proliferative or neovascular response indicates the development of new
retinal and pre-retinal vessels, the retina’s response to loss of blood supply
(ischaemia) and subsequent reduction in oxygen supply (hypoxia). If the new
blood vessels arise from the optic nerve head they are known as new vessels
from the disc (NVD). Those that arise elsewhere in the retina are known as new
vessels from elsewhere (NVE). (See Figure 34, page 136, and Figure 35, page
137.)
It is agreed that the primary stimulus for the neo-vascular response in diabetic
retinopathy is depletion of oxygen supplies to the retina (retinal hypoxia). NVD
consists of fine, spindly blood vessels on the surface and edge of the optic nerve
head which grow progressively outward, pushing the vitreous gel forward or
entering into its substance to form fan-like clusters of retinal vessels often seen
following the path of the major, normal, retinal vessels, namely nasal, temporal,
superior and inferior.
NVE is usually associated with large retinal veins and generally arise from
areas of the retina where the perfusion of blood is extremely poor.

End-stage retinopathy
This includes the blinding complications such as traction retinal detachment,
neovascular glaucoma and uveitis which often cause blind eyes to become
painful.

135
 Ophthalmology

Figure 34. Red-free photograph of proliferative diabetic retinopathy showing a cluster

of new vessels (neo-vascularisation) emanating from the retina and causing a sub-
hyaloid haemorrhage (between retina and the posterior hyaloid membrane bounding
the vitreous humour). The haemorrhage into a ‘free space’ shows a flat level where the
red blood cells have settled out of the serum under the influence of gravity.

In vivo observation of microscopic aspects of diabetic retinopathy

The living pathophysiology of diabetic retinopathy in all its forms is
demonstrated in vivo, ie in the living patient by the technique of fundus
fluorescence angiography (see Chapter 5). This technique allows the
retinopathy to be fully documented and to be monitored in terms of its natural
history and its response to therapy.
Proliferative diabetic retinopathy is a progressive disease in which the new
retinal vessels attract supporting fibrous tissue in their wake. Fibrous tissue by

136
 Diabetic Eye Disease

Figure 35. Fluorescein angiogram of the area seen in Figure 34 after focal destruction of
the new vessels (neo-vascularisation) by argon-laser therapy. Neo-vascularisation occurs
because of damage by the diabetic process to existing retinal blood vessels. Note the
area adjacent the laser-treated area where closure of retinal capillaries and distortion
of arteries and veins is apparent. These areas were obliterated by further laser therapy
to stabilise the retinopathy.

its nature is contractile and because of its adhesion on the retina, the ultimate
consequence of proliferative diabetic retinopathy is traction on the retina, with
traction retinal detachment, bleeding from the new blood vessels into the
vitreous gel and consequential blindness.

Natural history
Diabetic retinopathy may selectively affect different parts of the retina, eg the
macula, in which case vision is seriously compromised, or the peripheral retina,
where the macula is unaffected leaving visual performance normal or near
normal. Some retinopathies are characterised by the presence of oedema in the
retina and the macula, others by prominent bleeding and/or by a more
aggressive response to ischaemia with retinal infarction and new vessel

137
 Ophthalmology

formation. The pattern of the retinopathy should be denoted in the patient’s

records so that its course can be more effectively monitored.
Untreated diabetic retinopathy follows a variety of patterns. These include
distribution patterns, ie peripheral retinal involvement and/or central (macula)
retinal involvement; and progressive patterns leading to preproliferative
retinopathy and thence to proliferative retinopathy with consequential intra-
vitreal bleeding, fibrosis and retinal traction with detachment. In rare cases an
advanced retinopathy undergoes a spontaneous regression, presumably due to
the withdrawal of retinopathy-initiating factors (unknown) or chemical/
hormonal/enzymatic changes (unknown).
From the visual perspective, patients with advanced retinopathy may have
excellent central vision until the final progressive stages of the disease, whilst
others with minimal retinopathy affecting the macula may have serious visual
loss.

Risk factors in the development of diabetic retinopathy

(a) Duration of the disease. In type-1 diabetes it is unusual to find retinopathy

when the disease has been present for less than 10 years. Thereafter, about
50% of this group of patients will develop retinopathy, 10% of whom will go
on to develop proliferative retinopathy if untreated.
(b) In type-2 diabetes approximately 30% of patients will have signs of
retinopathy when the systemic condition is first diagnosed.
(c) Other risk factors include: poor control of the systemic condition of diabetes;
raised blood pressure (hypertension), with pregnancy possibly accelerating
progression of retinopathy; and patients with raised fat levels in the blood
(hyperlipidaemia).

Systemic consequences of diabetes mellitus

Diabetes mellitus is a disease of small vessels, the other vital organ being
affected by the condition is the kidney. Patients with significant diabetic
retinopathy invariably have evidence of diabetic nephropathy, some of whom
ultimately require dialysis or kidney transplant for survival.

Referral
Diabetic retinopathy may be completely asymptomatic, especially in its early
stages, although this may also be the case when it is in an advanced stage. Its
detection is simple, and when diagnosed in its early stages effective treatment is
available. If an optometrist or a general medical practitioner were to see signs of
retinopathy of any sort, especially those associated with diabetes, the patient

138
 Diabetic Eye Disease

should be referred for ophthalmic specialist opinion. If a general

ophthalmologist is managing cases of diabetic retinopathy with progressive
characteristics or advanced, diseased features, they should make a tertiary
referral to a vitreo-retinal specialist. Diabetic patients being managed in a
diabetic clinic by general physicians should have a working relationship with a
local ophthalmologist, so that all cases of retinopathy can receive expert
attention.

Screening
Community screening of diabetic patients is still controversial. There are special
cameras available for photographing and therefore documenting the fundus of
the eye that are effective without the use of pupil-dilating drops. They can
therefore be used by unskilled personnel, but any group trained in
ophthalmoscopy is capable of producing an effective screening service.

Treatment
Laser photocoagulation
A prospective, multi-centre, clinical trial, the diabetic retinopathy study (DRS),
showed that extensive coagulation by light (photocoagulation) of the retina,
using a light coagulator initially but latterly lasers, is effective in arresting the
progress of a retinopathy. When the technique is applied to all quadrants of the
peripheral retina the treatment is called pan-retinal photocoagulation (PRP). If
the treatment is applied selectively to localised areas of pathology, it is
described as focal photocoagulation. In advanced or progressive disease pan-
retinal photocoagulation is invariably indicated and should be applied until the
pathological processes are arrested. This means the conversion of large areas of
the retina into scar tissue. Surprisingly, peripheral vision may remain largely
intact but inevitably it will be compromised with heavier degrees of treatment.
Another study, the early-treatment diabetic retinopathy study (ETDRS),
demonstrated that laser photocoagulation can usefully be applied to eyes with
clinically-significant, macular oedema.
It goes without saying that beyond the eye, control of the diabetes, the blood
pressure and the condition of the blood are vital factors in patient management.

Surgical treatment
In advanced cases of proliferative retinopathy, when the vitreous compartment
is obscured by fresh or old blood, surgical clearance of the vitreous
compartment (vitrectomy) may be indicated. This problem is often associated

139
 Ophthalmology

with retinal tractional problems, in which case retinal detachment surgery will
need to be applied by the vitreo-retinal specialist.

Outcome expectations
The earlier the disease is diagnosed and the earlier treatment applied, the better
the expectation for maintenance of a patient’s vision. However, the pattern of
retinopathy, ie whether the macula is affected or not, will have a profound effect
on the visual outcome. Early expert advice is of paramount consideration in the
management of patients with diabetic eye disease. There is no excuse for
watching a retinopathy deteriorate or allowing it to get out of control.

Management errors

Omission
One of the earliest decisions an ophthalmologist has to make is how frequently
the eye should be monitored. It is better to observe them more frequently
initially to assess the progress or stability of the retinopathy, so that
consultations can be further spaced apart in appropriate cases.

Commission

Misapplication of laser treatment, particularly the fovea, will result in a

dramatic and sudden loss of visual function. It is not an unknown phenomenon.

DIABETIC CATARACT

True diabetic cataracts are rare and are characterised by sudden development
with dramatic loss of vision. Cataract formation in diabetic patients may occur
earlier when compared to a matched population, but their management today is
exactly the same. Namely, cataracts should be removed by the least-surgically-
traumatic process, ie small incision cataract extraction, with incorporation of a
replacement lens implant. The refractive aspects of cataract surgery should be
attended to (see Chapter 9) with special consideration being given to the needs
of the diabetic patient. For example, a patient who needs to manage insulin
injections might preferentially require the focus of the operated eye to be for
near vision, whilst wearing glasses for distance vision. This is the opposite effect
generally required, ie good uncorrected distance vision and the provision of
glasses for near vision.

140
 Diabetic Eye Disease

Another consideration is the need for clear access to the posterior segment
of the eye—the retina and vitreous humour. This aspect of cataract management
is important for the treatment, by laser or surgery, of advanced or progressive
retinopathy. Accordingly, every surgical effort should be made to ensure that
the lens implant and its supporting crystalline lens capsule are as clear as possible
to enable easy visualisation of peripheral as well as central retina.

141
 CHAPTER FOURTEEN

RED EYES

OVERVIEW

Eyes normally appear ‘white’, ie the white scleral wall of the eye is visible
through the transparent conjunctival covering. The conjunctiva and the
intermediate layer between it and the scleral wall—the episclera—does contain
intrinsic blood vessels, normally almost invisible. Furthermore, the wall of the
eye surrounding the clear cornea contains blood vessels that supply the front
portion of the eye. In any situation where the eye becomes subject to
inflammatory disorders, blood vessels dilate and may haemorrhage. Against
the normal white background of the sclera, dilated blood vessels give an eye a
pink or red appearance graded according to severity of the inflammation.
Red eyes indicate a pathological problem, the nature and severity of which
is initially categorised by other symptoms, principally the effect on vision. This
occurs if the optical system is compromised by the inflammation, ie cornea
involvement, the ocular fluids (aqueous and vitreous humours) and the
crystalline lens, or if the inflammation affects the central retina (visual acuity) or
peripheral retina (visual field). Visual problems indicate a more serious diagnosis
in a red eye situation. Whilst it is the role of an ophthalmology textbook to discuss
all the potential causes of red eye in detail, the purpose here is to provide an
outline of the possibilities to guide the reader into placing a particular client
problem into a general context.

ANATOMY

The conjunctiva and its supporting tissues—the episclera and underlying

scleral coat of the eye—may all variously be tissues involved in the clinical sign
of red eye (see Chapter 9). Also, there may be a reaction of the conjunctiva in
particular and the blood vessels coursing through it, to inflammatory disorders
of the cornea and uveal tissue (iris and ciliary body). The ocular surface
comprises the tissue lining the anterior surface of the eye globe and the
posterior aspect of the eyelids. Where the conjunctiva meets the cornea, the area
known as the limbus, exist stem or germinal cells which rapidly replace the
corneal epithelium if it is damaged. The corneal epithelium provides the
interface with an eye’s external environment, albeit through the all-important

143
 Ophthalmology

tear film. If the epithelium is damaged by disease or chemical injury, it changes

character to provide an opaque, surface membrane by keratinisation (skin-like)
changes, precluding clear transmission of light with consequential blindness.

PATHOPHYSIOLOGY

Blepharitis
This is inflammation of the eyelids, especially the marginal tissues. It can be
caused by: infection (staphylococcus); infection and cyst formation in the
meibomian glands within the eyelids (chalazion or internal stye or hordoleum);
infection in the root of the eyelashes (stye or external hordoleum); or fluid
retention with swelling of eyelid tissues (lid oedema).

Conjunctivitis

The term conjunctivitis means inflammation of the conjunctival membrane

which lines the wall of the eye and the posterior aspect of the eyelids. It may be
due to a variety of causes. The conjunctiva may be infected by organisms of
bacterial, viral or parasitic origin causing inflammation, pain, redness of the eye
and a discharge. Bacterial conjunctivitis is characterised by a purulent or pus
forming discharge, whereas viral conjunctivitis is characterised by a watery
discharge. A viral conjunctivitis may be complicated by secondary infection
from bacteria to give a more confused picture.
The conjunctiva is also susceptible to allergic phenomena as it is exposed to
the environment. Its response is for the tissue to swell and become jelly-like, a
condition known as chemosis; symptoms include redness of the eyes, watering
and a foreign-body sensation. If the allergen can be identified, the condition can
be prevented. Such a response is often associated with atopic patients, ie patients
who suffer from hay fever and eczema. The condition may also affect the cornea,
causing keratoconjunctivitis.
Vernal conjunctivitis (Spring catarrh) is a malady principally affecting
younger people who are subject to allergic manifestations in the eyes and
elsewhere, such as hay fever and eczema. It is a seasonal complaint, hence its
name, where the pollen in the atmosphere initiates a severe allergic reaction to
the conjunctiva and cornea causing, in serious cases, heavy follicles or giant
collections of follicles known as papules on the under side of the eyelids,
principally the upper lid. This in turn causes serious irritation of the cornea and
blinking with a resultant ulceration, vascularisation and scarring. It requires very
careful management including the use of steroidal and non-steroidal anti-
inflammatory agents and topical antibiotic therapy. In extreme cases, removal of
the affected person from exposure to the allergen is necessary.

144
 Red Eyes

The conjunctiva can be traumatised by chemicals, a very common personal

injury problem, physical agents such as heat, and radiation including UV light.
Such agents are also likely to involve the cornea, hence keratoconjunctivitis is
more common than pure conjunctivitis.

Keratitis (corneal inflammation)

Inflammation of the cornea is known as keratitis and, like its conjunctival
counterpart, may be subject to infection by bacteria, viruses and parasites. Of
these the parasitic acanthamoeba is of special interest.
As with the conjunctival trauma, be it chemical, physical or radiation, the
cornea can be traumatised and inflamed with significant effects on its visual
performance of a temporary or permanent nature. Apart from atopic disease,
mentioned above, acne rosacea is another skin condition capable of causing
chronic ocular problems which may result in patient complaints about
mismanagement.

Some particular forms of keratitis

Acanthamoeba keratitis
This is a parasitic, corneal infection associated predominately with soft contact
lens wear, wherein the superficial layers and the deeper layers of the cornea are
involved in the infective process.
Acanthamoeba is a free-living protozoon found in soil and water. The amoeba
may lie dormant as a cyst or become active as a trophozoite. The cyst is resistant
to chemical, thermal and pH changes and is difficult to eradicate. It is also resistant
to various contact lens solutions including thiomersal edetate and potassium
sorbate. The parasite appears to invade the stroma of the cornea through an
epithelial defect caused by over wear of a contact lens. The parasite destroys the
active cells in the cornea (keratosites) causing inflammation and death or necrosis
of corneal/stromal tissue. The amoeba is mobile and may deposit cysts
throughout the cornea.

Symptoms—Keratitis produces pain, light sensitivity (photophobia), swelling

of the eyelids, swelling of the conjunctivae (chemosis), redness of the eye,
watering of the eyes (epiphora) and blurring of vision. The pain is often
severe and disproportionate to the clinical signs.
Investigations—Acanthamoeba is isolated and cultured from corneal scrapes,
thus debridement of the surface of the cornea is recommended for both
diagnostic and therapeutic purposes. If the disease becomes long standing
or chronic, the organisms may only be found in the deeper stroma, requiring
actual removal or biopsy of deep corneal tissue.

145
 Ophthalmology

Natural history—The condition will cause blindness due to opacification of

the cornea; secondary infection is common because of the epithelial
defects.
Referral—Any contact lens wearer who has any of the above symptoms should
be referred for expert ophthalmic opinion promptly by the optometrist or
the general medical practitioner.
Treatment—Propamidine and dibromopropamidine isethionate (brolene)
combined with neomycin is active against the trophozoite or active form of
the amoeba. Hourly drops are given, initially reduced during the first week
to prevent toxic reaction in the corneal epithelium. The eye is rested by use
of 1% atropine eye drops. A number of other drugs are under investigation
for their effect. Once the infection has been controlled, careful steroid therapy
may aid the healing process. Surgical treatment is indicated when scarring
cannot be resolved and reduces visual acuity, or if the cornea threatens to
perforate or does perforate.
Prevention—Contact lenses should never be rinsed in tap water. They should be
soaked in 3% hydrogen peroxide for at least 3h. Acanthamoeba cysts are
resistant to contact lens disinfecting solutions in general.
Outcome expectations—If the condition is treated medically in its early stages it
can be resolved completely. If the corneal scarring is severe, a penetrating
keratoplasty or corneal grafting should produce a good visual result.
Treatment in historical perspective—The condition has been recognised since
the early 1980s but most of the pertinent literature dates from 1990.
Management errors—failure to diagnose; failure to refer; and failure to institute
the correct treatment regime

Rosacea keratitis
Acne rosacea is a facial skin disorder which may spread to the cornea with a
tendency to cause bilateral keratitis. It progresses through intermittent attacks
involving serious pain and disability which, unless responding to treatment,
brings the patient nearer to visual incapacity. Intervals between episodes may
last several years.
Initially, rosacea keratitis causes a marginal vascular infiltration, an extension
of the conjunctival inflammation caused by an initial spread from skin to
conjunctiva (rosacea conjunctivitis). Blood vessels feeding the peripheral cornea
(the perilimbal plexus) become dilated and advance superficially into the
peripheral cornea. The sharply delimited, infiltrated area may extend all round
the peripheral cornea but is more usual in the lower quadrant. This characteristic
picture almost invariably presents in all types of rosacea keratitis to yield a
valuable, diagnostic feature.
Other associations include punctate damage to the corneal epithelium
(punctate epithelial keratopathy—PEK), sub-epithelial infiltrates causing the

146
 Red Eyes

epithelium eventually to become eroded, uneven and stippled and form ulcers
in the margin or central region of the cornea. The chalky-white ulcers are
resistant to treatment and vascularise. Healing is often followed by
breakdown, with each attack causing the infiltration to migrate towards the
centre with a resulting serious impairment of vision or deep ulceration
causing eventual perforation.
The treatment of ocular rosacea is useless unless combined with treatment
of the associated lesions of the face. The most important part of the treatment is
general, not local, and no matter what topical measures to the eye are adopted,
relapses will continue to occur and the vision will progressively deteriorate unless
the tendency to rosacea is kept in check. It is expected that the condition will not
be curable but may fade away with advancing age; treatment and supervision
must be long term.
Local ocular treatment is mainly palliative, the mainstay being steroid therapy
(topical prednisolone drops or ointment) being most effective. Secondary infection
should be resisted by use of topical antibiotics.
Corneal replacement (corneal graft—keratoplasty) is required, especially in
progressive cases resistant to medical treatment. Relapses are less prone to occur
after keratoplasty which is best performed at a reasonably early stage of the
disease before perforation is likely.

Combined disorders
These include keratoconjunctivitis, blepharoconjunctivitis and blepharo-
keratoconjunctivitis, ie inflammation of the ocular surface, of which the most
renowned is trachoma.

Trachoma

Trachoma a major source of blindness, especially in Asian and African

countries. It is caused by an infection with the chlamydia organism which is
categorised as somewhere between a virus and a bacterium. It causes
inflammation of the tear ductules causing dryness of the eye and consequential
changes to the ocular surface with characteristic down-growth of blood vessels
onto the cornea and associated scarring, permanent irritation of the eyes and
dryness.

UVEITIS

The types of uveitis found include anterior (iritis); post-operative; sympathetic

ophthalmitis (see Chapter 15); posterior (choroiditis); and pan-uveitis (anterior
and posterior).

147
 Ophthalmology

Inflammation of the uveal tissue—anterior uveitis (iritis or iridocyclitis),

depending on the tissue involved, posterior choroiditis (choroiditis) or affecting
all uveal tissue (pan-uveitis)—is a complex subject. In the majority of cases the
aetiology cannot be identified, but on the other hand there are many conditions
where the cause is known; a sinister one of these is the condition of sympathetic
ophthalmitis (see Chapter 15).
Like other causes of inflammation in the eye, uveitis may be associated with
infections associated with other bodily inflammatory conditions such as arthritis.
The condition of juvenile arthritis is a particularly serious ocular complication
including damage to the cornea, band degeneration of the cornea, uveitis and
cataract formation. As the uveal tissue contains a lot of pigment it is generally
held that an autoimmune phenomenon may occur wherein the body becomes
sensitised to the pigment normally shielded from the immune system by
unknown events, except in the case of trauma where pigment may be released
into the blood stream. This is believed to be the origin of sympathetic ophthalmitis,
the virulent form of pan-uveitis.
Inflammation of the uveal tissue may occur secondary to other conditions
in the eye, such as tumour formation, retinal detachment, leaking cataracts and
a response to a variety of traumatic events, of which radiation is the most
insidious. Operative interventions in the eye, principally the anterior segment,
will initiate a degree of uveal inflammation as the eye’s natural response to injury.
The more traumatic the surgery, the greater the uveal inflammatory reaction,
the more significant the delay in rehabilitation and more uncertain the visual
outcome. Post-operative uveitis provides some indication of the skilful
application of the surgical process or lack thereof. Surgical intervention in the
face of pre-existing uveitis requires careful suppression of the inflammatory
response, for the surgery can only exacerbate the pre-existing condition leading
to chronic morbidity and poor outcome.
Untreated inflammation of the uveal tract will rapidly lead to blindness, but
early diagnosis and treatment will often control the condition. Patients have
early warning signs of the onset of inflammation because of the visual
disturbance that accompanies it either from the inflammation itself or
secondary effects such as fluid leaking in the central retinal (macula), a
condition of cystoid maculopathy. Treatment regimes include use of steroidal
anti-inflammatory agents, non-steroidal anti-inflammatory agents and
immunosuppressive drugs in advanced cases. It is important to note that
control of inflammation in the eye must be achieved before intra-ocular
surgery is undertaken, for any surgical event within the eye will in itself cause
a degree of inflammation which is a natural part of the healing processes.
However, the eye being a very delicate organ it cannot easily resist the effects
of serious inflammation without long-term, visual consequences.

148
 Red Eyes

ENDOPHTHALMITIS

The eye is a closed system in which infection can be devastating. Dependent

upon the virulence of the infectious agent, an eye can be ruined within hours
and its contents converted into a bag of pus. Infection within the eye is known as
endophthalmitis. It may be compartmentalised initially but spreads to involve
anterior and posterior segments of the globe. If the infection spreads through
the wall of the eye to infect the contents of the orbital socket, the situation is
referred to as panophthalmitis. Infection within the orbit, but not entering the
eye globe, is called orbital cellulitis.

Aetiology
It can occur:
(a) as a complication of intra-ocular surgery;
(b) as a consequence of extra-ocular surgery with accidental perforation of the
globe eg by a suture needle;
(c) as a complication of orbital cellulitis; and
(d) by endogenous spread of infection, ie from an infected area elsewhere within
the body or from septicaemia—infection within the blood stream.

Infectious agents
The agents can be bacterial (including low grade bacteria such as Staphylococcus
epidermidis and Proprionobacterium acnes, and virulent bacteria such as
pneumococci, streptococci and Staphylococcus aureus); and fungal.

Prevention of surgically induced endophthalmitis

Although rare, with an approximate prevalence of 1 per 1,000 surgical cases
(0.1%), no exact data is available for all eye surgery, so each institution must
look to its own record. In contemplation of prophylaxis, a foreknowledge of the
major source of infection—the commensal bacteria on the patient’s own eyelids,
eyelashes and conjunctival surface and fornices—encourages every attempt to
isolate the eye in the surgical field. By careful draping, the natural bacterial flora
on lids, lashes and in conjunctival fornices may still not be prevented from
entering and thereby remaining in the eye. The adsorption of bacteria onto the
surface of an intra-ocular lens, by its brushing against an unsuspected
contaminated surface, emphasises the importance of implant isolation from the
ocular surface and surrounding drape. In spite of sterilisation of the operative
area as far as is possible and a sound aseptic technique, it is difficult to avoid
some surface contact when utilising forceps to implant intra-ocular lens
implants.

149
 Ophthalmology

The commonest pathogens that may be carried into the eye under these
circumstances are Staphylococcus aureus, coagulase-negative Staphylococcus
epidermidis, Propionobacterium acnes, non-spore-forming, gram-positive
corynebacterium species amongst others (Doyle A, Beigi B, Early A, Blake A,
Eustace P and Hone R, ‘Adherence of bacteria to intra-ocular lenses: a prospective
study’, Br J Ophthalmol (1995) 79(4) pp 347–49; Ariyasu RG, Kumar S, LaBrie LD,
Wagner DG and Smith RE, ‘Micro-organisms cultured from the anterior chamber
of ruptured globes at the time of repair’, Am J Ophthalmol (1995) 119(2) pp
181–88). Staphylococcus aureus in particular causes a devastating infection within
days of surgery, usually resulting in loss of vision and even the eye. Other bacteria
which can cause even more serious effects include the streptococci of the beta-
haemolytic variety and Streptococcus pyogenes, whilst fungal infection, though
rare, may also be catastrophic. While low-virulence, coagulase-negative
staphylococci and Propionobacterium acnes cause low-grade infections, as far as
the patient is concerned they cause considerable unexpected morbidity.
Most ophthalmic surgeons adopt preventative regimes which include:

(a) povidone iodine application to the conjunctival fornices, cornea, eyelids and
surrounding skin immediately before surgery, which will reduce or at best
eliminate bacterial populations;
(b) careful draping of the eyelid to isolate the eye as far as possible from the
eyelids and eyelashes;
(c) pre-operative, broad-spectrum, topical, antibiotic applications prior to
surgery;
(d) addition of antibiotics to the irrigation fluids to nullify contaminating
bacteria;
(e) immediate, post-operative injection of a sub-conjunctival solution of high
dose antibiotic;
(f) in cataract and lens implant surgery, the isolation of the intra-ocular lens
during transfer from package to lens capsular bag to prevent bacterial
adsorption onto its surface.

The latter condition has not received the attention it deserves, for the only
reliable method of isolating implants is to ‘inject’ them through the nozzle of a
cartridge, the loading of which is remote from the eye, thus abolishing any
possibility of contamination from the operating field. Implants handled by
forceps for insertion are readily, if inadvertently, exposed to adulteration and
the possibility of intra-ocular inoculation with pathogenic flora.
Although the aetiology of endophthalmitis is multifactorial in cataract
surgery in particular (65% of all eye surgery by volume) utilising the advantages
of the smallest possible incision for cataract extraction and lens implantation by
implant ‘injection’, one potential source of intra-ocular contamination may be
eliminated whilst preserving the concept of minimally-invasive surgery and
trauma (Corbett MC, Hingorani N, Boulton JE and Schilling JS, ‘Difficulty of

150
 Red Eyes

surgery most significantly related to post-operative inflammation’, Euro Jl

Ophthalmol (1995) 1 pp 40–47).
Hard data on the prevalence of endophthalmitis can only be acquired by the
utilisation of stable, operative techniques performed over several years in a
number of centres, so that sufficient facts can be gathered of a rare event but one
of such consequence that it has to be prevented. Long-term, multi-centre studies
are now being organised in both the US and Europe. Meanwhile, case reports of
unusual circumstance and outcomes provide useful contributions to our legacy
of experience.

Management
(a) Diagnostic
(i) Swabs from eye externally to culture for microscopic examination,
bacterial growth and antibiotic sensitivities.
(ii) Aqueous humour (anterior chamber) tap to culture for microscopic
examination, bacterial growth and antibiotic sensitivities.
(iii) Samples from vitreous humour to culture for microscopic examination,
bacterial growth and antibiotic sensitivities.
(b) Therapeutic
(i) Medical—hospitalisation, intensive topical antibiotic drop therapy,
systemic antibiotic therapy, analgesic medication, sedative medication.
(ii) Surgical—vitrectomy and anterior chamber clearance of infected and
destroyed ocular tissues, injection of antibiotic and antifungal drug
cocktail.

151
 CHAPTER FIFTEEN

TRAUMA

EYE INJURIES

The eye globe, being a soft tissue structure, is vulnerable to devastating damage
by chemical and physical trauma. The latter may take the form of blunt or
perforating injury. However, eye protection is significant in that each globe is
protected on five aspects by the walls of the bony eye socket or orbit, and on its
frontal aspect to a much lesser extent by the substance of the eyelids which
contain the semi-rigid tarsal plate. The action of blinking means that the front of
the eye only has intermittent protection consistent with its function to provide
vision. Serious trauma to the eye socket may well compromise the survival of
the eye globe and its delicate nerve support.
Treatment of eye injuries is a staged process occurring initially on-site, and
is often crude in nature. Once access has been gained to a medical or ophthalmic
unit, careful diagnosis and primary treatment or repair of the damage follows.
As the effects of the primary repair are assessable over the next days or weeks, a
secondary repair of damaged structures may restore some or all of the visual
function.
The optical and neurological structures of the eye are easily damaged and
the processes of repair may leave scars which permanently compromise visual
function. Such visual loss is inevitably accompanied by easily-defined clinical
signs on ocular examination. It is not so unusual, however, for a disparity to
exist between a patient’s symptoms and detectable clinical signs. Accordingly,
objective methods of assessment of the visual process are required to distinguish
fact from fiction.

Sympathetic ophthalmitis
The phenomenon of sympathetic ophthalmitis should be highlighted in any
discussion of ocular trauma as it can lead to rapid blindness. While sympathetic
ophthalmia was not unusual a generation ago, it is a rarer phenomenon today
because the processes which cause it to occur are now better understood.
Sympathetic ophthalmitis is an inflammatory condition characterised by severe,
anterior and posterior uveitis. It occurs as an autoimmune process consequent
upon exposure of the pigmented uveal tissue in an eye to the body’s immune
system due to trauma. The system becomes sensitised to ocular tissue which
anatomically is separated from exposure. A perforating injury of the globe involving
prolapse of uveal tissue (iris, ciliary body and choroid) is the initiating event.

153
 Ophthalmology

The process of sensitisation takes about 10 days. Therefore if the injured eye
is removed before the end of that period the condition will be prevented. In
the case of serious eye injuries where survival of any sight is questionable, the
prospects for initiating sympathetic ophthalmitis is a major factor in the
decision as to whether or not the eye is allowed to remain in situ or be
enucleated. Suppression of inflammation by use of cortico-steroids and non-
steroidal anti-inflammatory agents in eyes which have suffered uveal prolapse
may also be factors in the reduction of the risk of developing sympathetic
ophthalmitis. If the process does occur, it may not be immediate. Latent
periods of up to 40 years have been recorded, making compensation
settlements more problematical.

SPECIFIC INJURIES

Corneal abrasion
A corneal abrasion causes symptoms of pain, foreign body sensation, light
sensitivity (photophobia) and watering of the eye (epiphoria).

Diagnosis
Microscopic examination reveals epithelium defect, particularly demonstrated
by the dye fluorescein. The eyes are invariably red with swelling of the
conjunctiva (chemosis).

Treatment
Antibiotic drops or ointment are used. The occasional use of steroid drops or
non-steroidal anti-inflammatory agents, eg Voltarol, enhances healing and
ameliorates discomfort.

Exposure injuries
The front surface of the eye is normally protected by the tear film and the
eyelids. If these systems fail through exposure of the eye resulting from trauma
(or head injuries, oculo-plastic surgery, brain surgery, etc), the eye, in particular
the cornea, deteriorates within minutes. Initially the cornea and exposed ocular
surface dries. Then the surface cells become incompetent, thus exposing the
underlying tissues which lack the cellular characteristics which effect
replacement and repair. Infection is admitted, and ulceration with corneal
melting and intra-ocular inflammation and/or infection rapidly destroys the
eye. Therefore it is imperative for eyes to be protected by lid closure if the
patient is unable to achieve this through any other mechanism.

154
 Trauma

There are supporting therapeutic requirements including antibiotic usage

and lubricant solutions. Where tissue loss occurs, either through trauma or
iatrogenic causes, the loss has to be made good by tissue transposition or
transplantation. Corneal-bandage contact lenses are another therapeutic modality
but, as in all problems of exposure of an eye, ophthalmic supervision is called
for, bearing in mind that vulnerable patients are often managed in non-ophthalmic
units, eg intensive care, plastic and neurosurgical units.

Traumatic hyphaema (haemorrhage into the aqueous humour)

Definition
This is when blood in the anterior chamber varies from a few red blood cells,
which will blur vision, to a total blood clot in the anterior chamber.

Symptoms
Blurring or loss of vision dependent upon degree of haemorrhage. Pain if
associated with a corneal abrasion or secondary pressure rise (glaucoma).

Diagnosis
This is based upon clinical examination of the eye utilising the slit-lamp bio-
microscope.

Laboratory evaluation
This includes a complete blood count, clotting studies, platelet count and liver
function test to eliminate the possibility of an associated bleeding disorder.

Treatment
(a) Hospital admission—young children and elderly patients should be
hospitalised. All patients should be examined daily for five days to anticipate
the possibility of re-bleeds.
(b) Bed rest—young children especially, with elevation of the head.
(c) Sedation as required.
(d) Avoidance of straining including constipation.
(e) Reduced ocular activity by minimisation of visual tasks.
(f) Cycloplegia recommended (paralysis of iris and ciliary muscles), use of 1%
atropine two or three times daily.
(g) Topical steroids—prednisolone eye drops three to four times daily if a
fibrinous reaction or other evidence of inflammation occurs in the anterior
chamber.

155
 Ophthalmology

(h) Avoidance of Aspirin—use of non-Aspirin-containing compounds for relief

of pain.
(i) Anti-glaucoma treatment—topical beta-blocking eye drops, eg Timolol.
Possible addition of acetazolamide (Diamox) twice daily. In severe cases,
use of intravenous mannitol l-2g/kg, delivered over 45 minutes, once every
24h.
(j) Surgical intervention to evacuate profound bleeding or blood clot in anterior
chamber. Indications include persistent, raised intra-ocular pressure:
(i) if not resolved within 24–48h;
(ii) at the first sign of corneal blood staining regardless of the grade of
hyphaema and if associated with raised intra-ocular pressure;
(iii) in the persistent presence of a blood clot in the anterior chamber, even
in the absence of corneal blood staining.

Traumatic-loss pupil constriction and dilatation (traumatic

mydriasis)

Definition
The pupil reactions fail as a consequence of trauma. In these circumstances the
pupil becomes dilated and fixed.

Diagnosis
There is a history of trauma and a failure of pupil responses to reflex
stimulation, eg light, and to drugs, eg miotics, to effect pupillary constriction
such as pilocarpine.

Symptoms
Blurring of vision occurs due to spherical and chromatic aberration or
associated trauma to other ocular structures, eg the cornea, lens or retina.

Treatment
The condition is not responsive to medical therapy. Surgical reduction of the
pupil is possible and desirable if the traumatised pupil is excessively large
(>6mm).

Commotio retinae

Definition
Bruising of the retina as a result of blunt trauma.

156
 Trauma

Symptoms
This depends on the location of the defect. If it is central then there will be a
significant drop in visual acuity. If it is peripheral the condition may be
asymptomatic but would correspond to a visual field defect.

Clinical signs
A confluent area of whitening of the retina in its acute phase gives way to a
mottled appearance of the retina due to pigment migration and clumping the
retinal-pigment epithelial layer, associated with destruction of neuro-sensory
elements—rods and cones—the cause of visual defect.

Treatment
There is no specific therapy. The condition will heal spontaneously, but
invariably with a corresponding visual defect.

Choroidal rupture
Definition
This is a rupture of the sub-retinal vascular layer, the choroid being associated
with trauma.

Symptoms
Variable loss of central vision (absolute or relative, central or paracentral
scotoma) occurs.

Clinical signs
A yellow or white, crescent-shaped, sub-retinal streak is seen, which is generally
concentric with the optic nerve head; single or multiple lesions may be manifest.
In the acute phase the rupture may be obscured by sub-retinal accumulation of
blood, but when this clears a characteristic crescent-shaped scar with central
whitening, peripheral pigmentation is obvious. It is usually associated with
visual defect, particularly if the rupture occurs between the optic nerve head
and the macula.

Treatment
There is no specific treatment; associated haemorrhage will absorb spontaneously.
If a complicating, sub-retinal, neo-vascular membrane develops and threatens
residual central vision, its ablation by laser therapy may be indicated.

157
 Ophthalmology

Blow-out fracture of the orbital wall

Definition
Fracture of the floor or medial wall of the orbit occurs as a result of blunt trauma
to the globe or orbital rim.

Pathophysiology
Pressure on the globe and orbital contents as a result of a blow to the eye and
orbital rim can result in permanent depression of the eye backwards into the
socket (enophthalmos), prominence of the eye (proptosis) and restriction of
extra-ocular muscle movement (consequential diplopia).

Symptoms
Pain, double vision, loss of skin sensation below the orbit, altered appearance of
the eye in relation to its socket and the fellow eye, and bruising.

Clinical signs
Peri-orbital bruising (haematoma), enophthalmos, restricted ocular
movements, surgical emphysema (air in the tissues around the eye and orbit).

Investigations
X-ray examination of the sinuses will show opacification of the fluid level in the
maxillary sinus or a tear drop sign in the presence of a fracture of the floor.
Computed tomography will lineate the fracture and identify its prolapse of
orbital contents. Ocular motility can be documented using ocular-deviation
prism measurements, serial Hess charts and binocular field of single vision.

Referral
When this condition is suspected it should be referred to a department of
ophthalmology, and therein to an orbital specialist.

Treatment
Medical treatment is invoked initially, allowing the swelling and bruising
(haemorrhage) to settle and local nerve damage to recover, with continued
assessment of eye movement and the status of double vision (diplopia). Surgical
treatment may be indicated with an enophthalmos of more than 3mm,
persistent double vision at one to two weeks after injury, especially double

158
 Trauma

vision in the primary position (looking straight ahead) and pain on attempted
up-gaze, and evidence of muscle entrapment usually affecting the inferior
rectus muscle but possibly the medial rectus in case of a medial wall blow-out.
The timing of surgery is generally agreed to be 10–14 days after the injury,
allowing post-traumatic assessment and, at the same time, resolution of traumatic
haemorrhage and oedema. Surgical management involves exposure of the
fractured wall of the orbit, usually the floor, lifting of the trapped orbital contents
back into the socket and replacement of a prosthesis over the fracture site to
prevent further complications.

Outcome expectations
Surgery is no guarantee of abolition of double vision or of diplopia. Further
intervention may be required to free adhesions or make muscle adjustments to
combat the double vision.

Complications
Infection of the prosthesis or extrusion of the prosthesis.

Management errors (omission)

Failure to diagnose; failure to refer; failure to carry out appropriate radiological
investigations; and failure to intervene surgically in the presence of positive
indications.

Eye globe lacerations

Definition
A laceration of the corneal tissue from a sharp instrument or glass, creating a
linear incision, or irregular lacerations from blunter trauma. Lacerations may
extend into the sclera (corneo-scleral laceration), and may be associated with
prolapse of the intra-ocular contents (uveal tissue, lens, vitreous and retina). The
worst-case scenario is associated with an intra-ocular foreign body (IOFB) or a
totally-ruptured globe.

Management
Primary repair will ensure that the intra-ocular contents are protected while
medication will prevent or combat infection. Dependent on circumstances,
secondary repair may be necessary weeks or months later to resurrect the visual
and optical function of the eye. Eyes with no visual prospects should be removed
within 10 days of injury to abort the possibility of sympathetic ophthalmitis.

159
 Ophthalmology

Chemical injuries

Overview
Of all chemical injuries to the eye, those resulting from exposure to alkaline
material are potentially the most serious. This is because alkaline substances
penetrate the eye rapidly as well as damaging the ocular surface. Thus, the
clarity of the cornea is at risk and the structures within the anterior segment of
the eye will be exposed to violent inflammation. A further problem with
alkaline substances is that there is continuous damage even after the initial
injury has been promptly treated.
The management of alkali injuries begins with the prompt and profuse
washing of the eye, usually with water. The use of acidic solutions such as salt
solutions is more ideal, but generally does not apply for obvious reasons. The
primary injury then needs to be assessed in an accident and emergency situation,
with careful documentation because of the claims that inevitably result from
such damage. Thus, at the time of the injury, the chemicals involved and the
immediate action taken should be noted. Of all the noxious substances (generally
cleaning agents used in industry), sodium hydroxide and ammonia compounds
have very rapid corneal penetration. While solid alkali materials such as lime
(calcium hydroxide) are less penetrative than liquid alkaline materials, granules
of the contaminating compound may linger in the fornices of the conjunctiva
and compound the problem.

Definition
Damage caused by alkaline substances with access to the eye, in industrial or
domestic environments.

Pathophysiology
Alkaline substances penetrate the eye rapidly as well as severely, damaging the
ocular surface, the cornea, its supporting endothelial layer and the intra-ocular
structures. In particular, alkaline substances destroy the epithelial layer on the
surface of the eye, something which is easily demonstrated by fluorescein-
staining of those areas. Particularly vulnerable are the limbal stem cells, those
cells from which the new epithelial layer will be derived. Failure will follow if
the damage is severe.
Behind the epithelial layer, the corneal opacification and inflammatory
activity in the anterior chamber will occur. The peri-orbita, that area surrounding
the eye, may also be affected, with the potential for later complications such as
lid shrinkage and irregularity as a consequence of scarring. After the initial insult,
the repair processes may go on to damage other structures within the eye even if
only superficial injuries occurred initially.

160
 Trauma

Symptoms
Severe pain, blurring of vision, loss of vision, redness of the eye.

Clinical signs
Corneal and conjunctival epithelial loss, corneal opacification, aqueous-
humour-inflammatory signs, cataract.

Natural history
If untreated the condition not only leads to painful blindness but also exposure
problems, as the rear surface of the eyelids adhere to the globe preventing the
ocular protection of normal eyelids. Keratinisation or skin-like changes can
occur in the ocular surface. The adhesions between the eyelid and globe are
known are symblepharon.

Referral
Wherever the accident takes place, immediate washing of the eye is essential
with a dilute salt solution (mildly acidic to neutralise the alkaline effect) and
emergency transfer to an ophthalmic accident and emergency department.

Treatment
(See above for first aid treatment.) On arrival in the accident and emergency
department, a detailed assessment and the history of the circumstance of the
injury should be noted, including the timing, the chemicals involved and the
first aid given.
Of the alkaline substances, ammonia and sodium hydroxide (caustic soda)
give rapid corneal penetration, while lime (calcium hydroxide) gives less-rapid
corneal penetration, but particulate matter which may lodge in the fornices of
the conjunctiva may give persistent damage due to its continuing presence.

Documentation
It is necessary to note the extent of epithelial loss at both the cornea and
conjunctiva, as well as the all-important, limbal, stem-cell tissue. The amount of
extra-ocular damage, ie to the skin and peri-orbital region, should also be noted.

Classification
Classification of chemical injuries relates both to the clinical findings and the
prognosis.

161
 Ophthalmology

Grade 1—no limbal ischaemia, damage limited to corneal epithelium; prognosis

is good.
Grade 2—limbal non-perfusion less than one-third, produces corneal haze but
iris details visible; prognosis is good.
Grade 3—non-perfusion of one-third to one-half of the limbus with total corneal
epithelial loss and corneal opacification obscuring details of the iris
diaphragm; prognosis inevitable, corneal scarring may reduce visual acuity
to less than 6/60.
Grade 4—non-perfusion of over one half of the limbal tissue and an opaque
cornea; prognosis is very poor and corneal perforation is possible.

Treatment

The following treatment pattern should be used, with speed being essential:

(a) immediate irrigation with water or salt solution;

(b) continued irrigation in a general casualty or in ophthalmic emergency
department, followed by taking a detailed history and an examination;
(c) double eversion of the lids to ensure that all particulate matter is removed
from the conjunctival fornices (children will require a general anaesthetic to
ensure a satisfactory examination and emergency treatment).
(d) admission to hospital for all severe alkali injuries. Medical treatment includes:
topical cortico-steroids on an hourly basis; topical broad-spectrum antibiotic
therapy, eg chloramphenicol, to prevent secondary infection; topical
cycloplegic, eg atropine, to reduce pain and ocular discomfort due to
contraction of ciliary muscles; topical ascorbic acid, eg 10% sodium ascorbate
drops every hour, to reduce the incidence of sterile ulceration of corneal
perforation, as it acts as a free-radical scavenger and replaces natural ascorbic
acid in corneal cells (keratosites) and aqueous humour which is reduced
after chemical injury; oral vitamin-C ascorbic acid 1g four times daily to
supplement the topical ascorbate; topical citric acid, eg 10% sodium citrate
eye drops every hour, as sodium citrate chelates calcium, inhibits
inflammatory cell motility and depresses the activity of the coliagen-
destructive enzyme collaganase.

Later management

Surgical treatment includes utilising healthy tissue: eg healthy conjunctiva

rotated to replace damaged conjunctiva; conjunctival flap to protect the
damaged cornea; or a limbal cell transplant from the fellow eye to replace the
epithelial germinal cells which provide the normal covering to the cornea and
conjunctiva.

162
 Trauma

Outcome expectations
Grade 1 injury—corneal epithelial damage only, no limbal ischaemia; prognosis
very good.
Grade 2 injury—corneal epithelial damage plus minimal corneal haze, allowing
details of the anterior segment (iris) to be visualised, and less than one third
limbal ischaemia; prognosis still good.
Grade 3 injury—total corneal epithelial loss plus severe corneal haze obscuring
intra-ocular details, plus between one-third and one-half of limbal ischaemia;
prognosis is for severe corneal scarring with the probability of visual acuity
being less than 10%.
Grade 4 injury—all the above, but more than one half of the limbus affected,
ie stem cells; the prognosis is poor and corneal melting or perforation is
possible.

Complications

Long-term corneal damage results from a combination of limbal-cell

dysfunction (the germinal cells for the surface covering of the cornea—the
epithelial layer) and ocular-surface-wetting problems. The latter is a
consequence of diffuse damage to the conjunctiva as well as the lacrimal gland
ducts (the components of tears together with the oily secretion of the meibomian
glands). Scarring in the conjunctiva may result in poor lid-globe apposition.
Corneal-epithelial defects, if persistent, will be associated with corneal-stromal
melting or thinning, with consequential risks of secondary bacterial infection.

Management errors

Omission—failure to provide emergency and satisfactory irrigation; failure to

remove all particulate foreign material; failure to document history and
examination on arrival; and failure to institute the correct drug regime.

163
 CHAPTER SIXTEEN

PAEDIATRIC AND DEVELOPMENTAL

PROBLEMS

OVERVIEW OF PAEDIATRIC OPHTHALMOLOGY

Paediatric, ophthalmic, medico-legal situations are more problematic than

adult problems because there are three people seeking solutions to alleged
failures of management, namely the patient and two parents. Therefore at every
stage of the management of paediatric ophthalmic problems, careful
counselling of parents on the situation and its management is called for, to avoid
the potential, later accusation of failure to communicate.
Paediatric, ophthalmic problems arise either because of an inherited condition
(congenital) or acquired problems. The congenital problems are either due to
genetic defects, where a positive family history of the trait can be traced, or to
intra-uterine problems during the nine months of foetal development. Some of
these problems are unaccountable but others are due to identifiable risks such as
maternal rubella (German measles), toxoplasmosis or the effects of maternal drug
ingestion, of which thalidomide is the best known. Problems can occur during
the birth period when a child’s eyes can become infected with the mother’s
venereal infection such as chlamydia, herpes or gonorrhoea. Infectious diseases
of infancy such as measles or chickenpox can have ocular manifestations, and
trauma plays a significant role in the morbidity of children’s eyes.
Apart from the aetiological classification of children’s disorders, ie congenital,
acquired, inflammatory, traumatic or neoplastic, an alternative classification is
concerned with visual function, both referring to the individual eye and to the
joint function of the two eyes, ie binocular vision.

OCULAR PATHOLOGY IN CHILDREN

Children’s eyes are subject to the same disease processes as adult eyes, ie
susceptibility to infection, inflammation, trauma, glaucoma (see Chapter 12 on
congenital glaucoma), cataract, retinal detachment, inherited retinal
degenerations. They suffer from binocular problems not only in intrinsic or
inherited forms of strabismus but acquired or paralytic strabismus. Children’s
eyes will manifest the symptoms and signs of systemic disease including intra-
cerebral pathology and vascular haematological pathology. There are some
syndromes, eg juvenile rheumatoid arthritis, that have specific ocular
associations such as inflammation (uveitis), corneal degeneration (band
keratopathy) and cataract.

165
 Ophthalmology

Amblyopia (lazy eye)

When infants are born, their eyes and the eye-to-brain neurological connections
have to undergo a process of development. The development is dependent
upon the projection of a sharp image from each eye to the brain. During the
developmental period of the important first few months and years of life, the
neuronal connections that subserve the high quality images that normal eyes
perceive are developed. Thus, if conditions arise wherein the image is either
defocussed or obscured, visual development will fail because of the lack of
stimulus of the neuronal connections between the eye and the occipital visual
cortex of the brain. An image is projected from each eye and, if one eye is
projecting a sharp image and the other a blurred image, the brain happily
accepts the sharp image while neglecting to develop, through failure of an
adequate focussing system, the visual potential of the fellow eye. Thus the term
‘lazy’ or amblyopic eye is born.
There are three main reasons why this situation arises. The first is one of
binocular confusion, wherein the child’s eyes are not aligned, ie has a squint
from birth, and it is not possible because of failure of retinal correspondence to
fuse the images transmitted from each eye. In such a state of confusion the brain
suppresses the image of the squinting eye—hence, if uncorrected, the condition
of strabismic amblyopia, ie failure of vision to develop because of the failure of
the image to correspond with that of the straight eye.
An alternative cause of amblyopia is poor focussing of the image of one or
both eyes due to failure to appreciate that the child has a significant refractive
error. When one eye has a normal focus but the other eye an abnormal one, be it
myopic, hyperopic and/or astigmatic, there is a consequential failure of visual
development due to the above reasons. This condition is categorised as
anisometropic amblyopia. It is not unusual for this condition to be diagnosed
past the age of child development. Once again the child cannot volunteer the
fact that one eye sees well and the other does not, and in the absence of a squint
it requires screening to detect the abnormality. Pre-school checks, ie at four years,
may be too late, though potentially it is possible to correct amblyopia by treatment
up to the age of seven. The earlier it is detected the better. Latterly, photographic,
refractive methods have been developed for ascertaining the refractive power of
children’s eyes and it may be that screening of this nature will reduce the problem.
The third cause is amblyopia of arrest, wherein there is a physical obscuration
of the focussing of light upon the retina due to ocular disease. Thus, any
pathological process that will cause damage to the optical system of the eye,
including the cornea, aqueous humour, crystalline lens or vitreous humour, will
cause obscuration or a defect in the image quality in an infant, with resultant
failure of visual development.
The importance of amblyopia is often discovered in later life and is not an
uncommon aspect of personal injury or litigation cases. There seems to be a not-
uncommon situation when people with one good eye and one amblyopic eye

166
 Paediatric and Developmental Problems

succumb to disease or trauma, and it is the healthy eye that is affected. Under
these circumstances, in later life it is accepted as a general rule that the vision of
the ‘lazy’ amblyopic eye will not improve beyond that level to which it developed.
There seems to be no doubt that an amblyopic eye may appear to deteriorate
from the time of diagnosis in childhood to mid-life or later. If it is then called
upon to act because of loss of a fellow eye, it may seem to improve, but the
accepted reasoning is that it will not improve beyond its original, best
performance, even if that has deteriorated mildly with disuse.

Strabismus

Strabismus or squint is an abnormal condition of ocular alignment and motility.

Eyes may be deviated inward (convergent or esotropic), outward (divergent or
exotropic) or misaligned in the vertical axis (hypertropic) if one eye is higher
than the fellow eye (or hypotropic if the lower eye is cited). Misalignment may
also occur in a torsional sense. The effect of uncontrolled misalignment is
double vision or diplopia if a patient has developed binocular vision, wherein
the images from each eye fuse in the brain’s visual cortex. Misalignment results
in an inability to fuse disparate images, with resultant diplopia. Strabismus may
be a congenital condition, in which case binocular vision (BV) and stereopsis
(for which BV is necessary) fail to develop. In such cases diplopia does not
follow. However, if a strabismus is acquired, either because of intrinsic faults in
ocular alignment (phoria or latent strabismus) or extra-ocular muscle weakness
or paralysis, diplopia will follow.
Strabismus may therefore be classified as paralytic or non-paralytic. In
children, the onset of a paralytic strabismus is a condition that requires urgent
evaluation, as it may be due to pathology affecting intracranial nerves that
would require neurosurgical intervention. Non-paralytic strabismus requires
evaluation and treatment, especially in relation to problems with visual
development. If an infant’s eye deviates, the phenomenon of vision
suppression will occur in order to avoid otherwise inevitable diplopia. When
suppression occurs at a stage in an infant’s development when visual
development is being cemented, long-term visual deficiency or amblyopia
may occur. It is such children who, on diagnosis, are treated by patching or
occlusion of the non-squinting eye in order to promote use of vision and its
development. Once this is demonstrated, treatment of the strabismus can
proceed, usually by surgical adjustment of extra-ocular muscles.
The principles of surgical treatment are to weaken muscles which appear to
be overacting whilst strengthening those that are ineffective. Extra-ocular muscles
work in antagonistic pairs. One contracts whilst its opponent relaxes. In the fellow
eye the movements and muscle actions are co-ordinated so that the eyes move
in the same direction to maintain binocularity and single vision. Thus muscles

167
 Ophthalmology

Figure 36. Pseudostrabismus, the appearance in this case of a convergent squint when
observing the white of the eyes. But note the corneal reflections which are equal and
central, indicating that the squint is an illusion, or pseudostrabismus caused by the
fold of skin obscuring the white of the eye at its inner aspect (epicanthus).

may be described as ipsilateral (same eye) agonists and antagonists, eg the medial
and lateral rectus muscles working in concert with the contralateral (fellow eye),
medial and lateral rectus muscles in a synergistic action controlled by a nerve
centre in the brain which effects muscular action by transmission through the
third and sixth cranial nerves.
Evaluation of ocular motility disorders is undertaken by orthoptists who
are specially-trained, paramedical personnel with expertise in paediatric and
adult strabismic disorders. They participate in diagnosis and treatment whilst
working in concert with ophthalmic specialists.
Surgical intervention takes the form of removing part of a muscle to shorten
it and strengthen its action, or moving the muscle insertion back on the wall of
the eye to make its leveraged traction less effective. Because intra-ocular blood
supply is carried to some extent through the extra-ocular muscles, it is unwise to
remove and reattach more than two muscles at any one time in order to avoid
ocular ischaemia (reduced blood supply). There are many variations on this
theme, including moving muscle insertion locations and utilising adjustable
sutures so that exact alignment can be effected after the anaesthetic has worn
off. An alternative to surgery in selected cases is to use the neuromuscular
botulinum toxin, which causes temporary paralysis of muscles which require a
weakening procedure. If effective, the injections, which are given under the
control of electrodes temporarily placed in the muscle, can be repeated (see
glossary for botulinum toxin).
One danger of extra-ocular muscle surgery is the possibility of perforation
of the eye wall or sclera during the passage of suture needles during the
reattachment of muscles. If this does occurs, then intra-ocular examination and
prophylactic therapy is required to avoid bleeding and infection.

168
 Paediatric and Developmental Problems

Pseudostrabismus
It is not unusual for parents or health care workers to diagnose a convergent
squint in infants when none is present. The situation arises because, in some
children, the folds of skin at the inner aspect of the eyelids known as
epicanthus covers part of the white of the eye to give an appearance of a
convergent squint. When the reflections from light in front of the eyes is
observed from the cornea, and the reflections are seen to be parallel, the
function of the eyes in terms of alignment is assured and the diagnosis is
pseudostrabismus (Figure 36).

Congenital glaucoma (buphthalmos)

See Chapter 12.

Leucocoria (white pupil)

Retinoblastoma is a malignant tumour arising from retinal tissue, which is

peculiar in that it affects only infants and young children. It is usually inherited
as a result of a dominant genetic problem, but it also occurs sporadically and is
seen to be due to genetic mutation, ie alteration of genetic pattern in the
individual. Retinoblastoma causes loss of sight and, if untreated, will advance
by direct spread through the optic nerve to the brain with fatal consequences, so
early diagnosis and treatment is important, not only to preserve sight but to
preserve life.
Presenting symptoms in children that cannot communicate about the state
of their eyesight do not really exist, so it is the abnormal signs that have to be
detected. These include: the development of a strabismus or squint due to the
visual failure of the affected eye; the presence of a white pupil due to growth
of the tumour and its appearance in the pupil; and signs of inflammation in
the eye, a secondary phenomenon to the tumour which would include redness
of the eye, cloudiness of the anterior chamber and irregularity of the pupil.
The diagnosis in discreet tumours is based on clinical observation and is not
difficult, but where presentation is late it is difficult to distinguish between
tumour and a non-malignant, inflammatory condition such as parasitic
infestation of the retina and sub-retinal tissues from the worm toxocara,
transmitted from puppies.
Early diagnosis is imperative. Suspected cases must be referred
immediately.

169
 Ophthalmology

Retinopathy of prematurity (ROP)

Definition
Retinopathy of prematurity (also known as retrolental fibroplasia) is a condition
that affects premature babies, whose survival is dependent upon being exposed
to high oxygen saturation in the incubator in which they are nursed from birth.
The retinal development at that stage in the neonate is incomplete, and when
the baby is removed from the incubator into normal, atmospheric oxygen the
retina suffers a relative deprivation of oxygen and responds by undergoing a
dramatic proliferation of blood vessels, particularly at the periphery of the
developing retina. The condition has different grades of severity but, at its
worst, causes traction detachment of the retina and blindness.

Screening
Screening is therefore recommended for all babies at risk of severe retinopathy
of prematurity (ROP), particularly those of birth weight less than l,500g or less
than 31 weeks gestational age. The aim of screening is to identify severe ROP,
ie stage 3 which may require treatment, or to identify the potential to reach
that degree of severity. Accordingly, the first examination should be at six to
seven weeks post-natal age, with subsequent examinations until retinal blood
vessel development has progressed to the stage where the severe ROP has
passed. It is recommended that the examination should be undertaken every
two weeks.
It is important that parents are advised about the risk to their infant, and
they should be appraised of the risks of ROP developing, the need for immediate
or later treatment and of the potential visual consequences.

The general problem

As survival rates for pre-term babies have increased during the past generation,
particularly for babies of birth weight less than l,000g, but also up to l,500g, the
number of infants with ROP has risen. It has been demonstrated by a US-based
trial that cryotherapy (freezing of the diseased areas of the retina) can improve
the outcome of advanced ROP (stage 3) making early identification invaluable.
The recognised stages of ROP are as follows.

Stage 1—demarcation line, comprising a thin white line lying within the plane
of the retina which separates the avascular from the vascular retinal regions.
Stage 2—formation of a ridge, wherein the line of stage 1 has increased in volume
to extend out of the plane of the retina. In this stage, isolated vascular tuffs
may be seen posterior to the ridge.

170
 Paediatric and Developmental Problems

Stage 3—the ridge progresses to extra-retinal, fibro-vascular proliferation which

may be continuous with the posterior edge of the ridge or disconnected
from it, or proliferating forward into the vitreous humour.
Stage 4—sub-total retinal detachment, either sparing the macula or involving
the macula.
Stage 5—total retinal detachment. For the purposes of description the retina is
divided into zones. Zone 1 extends from the optic nerve head to the centre of
the macula (foveal distance) with a radius of 30°. Zone 2 extends from the
periphery of the nasal retina in a circle around the anatomical equator. Zone
3 is temporal, inferior and superior to zone 2, but does not include the nasal
retina.

In summary, all babies with birth weights under l,500g or who have been born
nine weeks or more premature, should have their eyes examined routinely at
least once to assess the risk of ROP. The main cause of ROP is prematurity,
therefore the more premature the birth the greater the risk. The amount of
oxygen treatment and the baby’s general condition may also influence the
development of ROP and its severity. Some premature babies who have no
serious illness may nevertheless develop ROP, whilst others who have had
difficult survivals do not develop the condition.
ROP affects developing blood vessels of the retina. Mild degrees of ROP are
very common and, in these babies, recovery is complete without treatment. The
purpose of screening is to discover those babies who develop severe ROP so that
they can receive effective treatment. Examination should be conducted a few
weeks after birth and certainly before the baby is discharged. Further
examinations may be necessary. In general, ROP is common in premature babies,
but it is mild, resolves without treatment and therefore does not affect vision.
Those babies who do require treatment generally develop normal vision. The
treatment of severe forms of ROP is by cryo or laser therapy to the retina with
the same end result.

171
 CHAPTER SEVENTEEN

REFRACTIVE SURGERY

DEFINITION

Surgical adjustment of the refractive power of an eye to effect a planned,

permanent change.

The need for refractive surgery

Refractive surgery is a mysterious concept for most lay people, who equate it to
laser treatment for short-sighted eyes. Delivered by lasers and controlled by
computers, the treatment is believed, by the patient, to be infallible, wide
ranging in its capabilities and painless. In fact, photorefractive keratectomy,
alias laser treatment for myopia, is an extremely fallible and limited process
accompanied by severe pain and ocular discomfort for many hours after
treatment. However, the wider concept of refractive surgery embraces many
techniques applicable to most refractive errors with well-understood risks and
benefits, despite the infancy of some methods.
Refractive surgery has become the latest sub-speciality to develop within
the general practice of ophthalmology. The scope for its expansion is dramatic,
as 10% of the population is short-sighted (myopic) and 20% farsighted
(hyperopic), while everyone becomes presbyopic, ie needs reading glasses, at 40
years plus [Spertudo R, Siegel D et al, ‘Prevalence of myopia in the United States’
(1983) Arch Ophthalmol 101, 405–07]. Add to this the huge number of cataract
operations (150,000 per annum in the UK, with a need for 300,000) and recognising
the refractive aspects of cataract surgery, there is an undeniable need for
ophthalmic refractive (and cataract) surgical specialists. In practice, most of the
demand for refractive surgery will be catered for in the private health care sector.
In general the NHS resources will not be available for such non-sight threatening
procedures. As private health insurance would not cover refractive disorders it
becomes patient-funded surgery. Nevertheless, the lure of visual freedom from
glasses and contact lenses ensures that demand for treatment will accelerate as
techniques become more sophisticated and predictable.

Normal vision
The ability of an eye to focus near and far objects without the aid of corrective
lenses is described as normal vision (Figure 37, page 174). People under the age

173
 Ophthalmology

Figure 37. Optical ray diagram to

indicate the focussing of parallel
rays of light onto the retina
(clockwise from above): in an
emmetropic eye; in front of the
retina in a myopic eye; and behind
the retina in a hyperopic eye.

of 40 have the ability to accommodate, ie to shift the focus from near to far
objects in an automatic sense. Usually, over the age of 40 (but with some
individual variation), the ability of the eye to see near objects becomes
compromised as the crystalline lens becomes thicker and less elastic. This
condition is known as presbyopia. In normal vision, otherwise known as
emmetropia, the image is focused onto the fovea, the most sensitive part of the
central retina, able to discriminate fine detail. If the lens inside the eye becomes
opacified, the condition is known as a cataract, which causes blurring and
darkening of vision and fading of colours. It is a matter of degree, the more
opaque the lens the more these phenomena become apparent.

Refractive errors

Refractive errors are classified as myopia (short-sightedness), hyperopia (long-

sightedness) and astigmatism (Figure 37). Myopia, hyperopia and astigmatism
are known as ametropia, a mis-match between the optical system of the eye and
the length of the eyeball. It is a disorder which is usually developmental, but can
be acquired as a result of disease or injury. Normally-focussing eyes
(emmetropia) have a distance of approximately 23mm from the front surface of
the cornea to the retina. Their optical system (cornea and lens) focusses parallel
rays of light (objects at 6m or more) onto the central retina and specifically the
macula, whose most sensitive area is the fovea.

174
 Refractive Surgery

Myopia

In myopia, as a general rule the eyeball is too long for the focussing system of
the eye. Myopic eyes may extend up to 30–35mm in length; alternatively, the
focusing system at the front of the eye, principally the cornea, bends rays of light
excessively, causing the focussed image to fall short of the retina. A nearsighted
or myopic eye has a far point of clear vision which is very close to the eye,
depending on the degree of myopia. One dioptre (1D) of myopia would give an
eye a far point of 1m, while 10D would give a far point of just 10cm—in other
words, beyond 10cm all the image is blurred.
Myopia or short-sightedness is sub-classified into two groups. In
physiological myopia the axial length of the eye, as well as the cornea and the
lens power, are within normal limits for the population but are mis-matched, so
the image focus is anterior to the fovea; its onset is usually during the early
years of development, progresses between five to 15 years and is usually stable
from 20 years onwards.
Pathological myopia is a more serious form; it is degenerative and progressive
and therefore a sight-threatening process. The degree of myopia is generally
accepted to be more than 6D and the axial length of the eyeball more than 26.5mm.
This is a congenital or neonatal problem. The eyeball may be enlarged but, as its
contents do not grow, they are stretched, creating the typical, myopic, fundus
appearance characterised by very thin retina and a degenerate vitreous gel. A
progressive problem may develop at 12 to 50 years.
In high-refractive errors, particularly high myopia, the edge thickness of
high-minus spectacle lenses are not only cosmetically unsatisfactory but the image
quality is reduced by minification and optical aberrations. For example, there is
a ring scotoma (blank area) emanating from the periphery of the lens and the
spectacle frame. The visual freedom that beckons with refractive surgical
procedures is very appealing to patients who are not only visually disabled with
their refractive correction, but are legally blind without it.
American psychologists Schapero and Hirsch [Schapero M and Hirsch M,
‘The relationship of refractive errors and Guilford-Martin temperament test
scores’ (1952) American Journal of Optometry 29–32] reported personality studies
on patients with ametropia, relating refractive errors and temperament. They
carried out various tests in their 1952 study. They generalised, and found that
patients who are myopic or short-sighted tended to have an inhibited disposition,
are studious and tend towards an over-controlling nature.

Hyperopia
Hyperopia, in contrast to myopia, is a condition wherein the image is focussed
behind the eye; in effect the eyeball is too short for the optical system either due
to a small eyeball, usually 21mm or less, or a cornea that is too flat and is unable

175
 Ophthalmology

Figure 38. Diagram showing the principle of astigmatism within the cornea. Regular
astigmatism shows two principle meridia measured by keratometry or corneal
topography: one steep and one flat meridian. Diagrammatically this gives the cornea
the shape of a rugby ball, seen here lying on its side. Its effect is to magnify the image
in the vertical plane and reduce its size in the horizontal plane. By equalising the radii
of curvature of the principal meridia, the cornea appears spherical when the image
magnification is equalised to give the observer normally-proportioned images.

to bend the rays of light sufficiently to focus on the fovea or centre of the
macular retina. In hyperopia or farsightedness, contrary to popular belief, all
images are blurred. Distance vision is blurred by a degree according to the
degree of hyperopia, but no part of the image is strictly clear. For a hyperope, the
near point in particular is distant. The 1D hyperope would not be able to see at
all clearly up to a near point of 1m, and a 10D hyperope would have a near point
of 10m. In their studies, Schapero and Hirsch described hyperopes, in contrast
to myopes, as happy-go-lucky, carefree and not particularly studious.

Astigmatism

Astigmatism refers to a condition of the focussing system of the eye wherein the
principle focus lies in more than one plane. In other words, there is no principle
focus (known as astigmatic); it is physiological, usually of a small degree and
has little effect on the vision. The image formed within the eye may have two
general points of focus between which the image is often reasonably sharp,
depending on the degree of astigmatism. Both images may come to a focus short
of the retina or behind it, one may be on the retina, and one may be in front and
one behind, giving rise to terms such as compound hyperopic, compound
myopic or mixed astigmatism.

176
 Refractive Surgery

A stigmatic system is point-like, meaning the principle focus approximates

to a point or lies on one plane. This is known as anastigmatic or more simply
stigmatic. The usual cause of astigmatism is to be found in the cornea, which is
not spherical as may be supposed, but is described as a toroidal asphere. Put in
simple terms, it is shaped like the side of a barrel—steeper centrally and flatter
peripherally. This is known as a prolate shape and is designed so as to minimise
spherical aberration, even when the pupil is large. If the cornea was entirely
spherical, the peripheral rays of light hitting it would be refracted more than the
central rays, giving rise to an aberration of the spherical type. The system is also
designed to minimise chromatic aberration and therefore maximise the sharpness
of the image. As noted above, in the general population most eyes have
astigmatism of a very small degree, be it long or short sight. Corneal astigmatism
is due to a different radius of curvature in two meridians at right angles to each
other (regular astigmatism), causing an image to be focussed on two different
planes. Schematically this is illustrated in Figure 38.

Presbyopia
The human, crystalline lens matures throughout life, gaining 100% in weight
over a 90 year life span. It doubles in thickness and inevitably becomes
cataractous. The continuous generation of lens fibres by the equatorial,
germinal epithelium causes increasing compression of the older fibres towards
the centre of the lens. This creates the lens nucleus, divisible into aged stages,
ie embryonic, infantile and adult, each with a definable presence identified by
a zone of optical discontinuity with an oblique, bright-light beam utilised in
ophthalmic microscopes. In the fifth decade of life the accumulated changes in
lens anatomy reaches a critical level in relation to near focusing and causes a
loss of elasticity—the arms become too short! The loss of accommodation is
known as presbyopia. Myopic eyes without their correction can of course
bring close objects into focus at a distance dependent upon the level of
correction. Lay persons often confuse presbyopia with shortsightedness, when
in fact it is a variant of hyperopia.

Ametropia
The incidence of ametropia in a general population was studied by Stromberg
and reported in Acta Ophthalmologica in 1936. His studies showed that, in a
Western population, 80% had a refraction of 0–0.75D; 15% were hyperopic with
a refraction of 1–3D; and 10–11% were myopic with a refraction of-0.25 to-4.0D.
The very high myopes, above 4D, comprise 3–4% of the population. The same
incidence applies to the high hyperopes of more than 4D.
Is ametropia an affliction, a disease or even a cosmetic problem? To make an
analogy with hearing, deafness would never be described as a cosmetic problem;

177
 Ophthalmology

it is a problem that can be helped by a hearing aid. Ametropia is a visual disability;

without a visual aid the eye is disadvantaged by the creation of a blurred image,
it is certainly not a cosmetic problem but is a disorder that can be corrected by an
optical system, such as spectacles or contact lenses, or by surgery.

REFRACTIVE SURGERY

The goal of refractive surgery is to correct any refractive error by surgical

adjustment. Refractive surgery requires specialist knowledge from both a
diagnostic and treatment point of view, and is therefore clearly definable as a
sub-speciality within ophthalmology.
It is worth reiterating that the main refracting surface of the eye is the cornea,
which gives the eye approximately 44–45D of light-bending or refracting power.
In fact, it is not the cornea but the tear-film interface at which the rays of light are
refracted. Within the eye the lens is the secondary focussing system and, in an
unaccommodated form, contributes approximately 21D of focussing power. This
increases with accommodation so that near objects may be brought to focus on
the retina. The failure of this process with advancing years is known as
presbyopia.
From a surgical point of view the cornea is accessible for surgical processes
to alter the shape; altering the shape of the cornea produces a different focussing
performance. The other option is surgery. Modern micro-incision surgery of the
eye and lens offers the opportunity to change the focussing power of the eye
through implantation of a lens of appropriate power. It is an established, safe,
predictable and fast procedure.

New directions in medicine

Change is not always universally acceptable. New developments need the

confidence of its practitioners that the techniques are safe, predictable and
stable.
In a brief glimpse of the history of invention and change it is appropriate to
quote Jonathan Swift who noted that ‘there is none so blind as those who will
not see’. For example, in the 13th century Mr Cross, the vicar of Chew Magna in
Somerset, recorded ‘that the newly-invented optick glasses are immoral as they
pervert the natural sight, and make things appear in an unnatural and false
light’. In fact, spectacles were invented around 1275 AD and were made of glass
from Venice. Roger Bacon, a Franciscan monk and philosopher at Oxford who
lived between 1214 and 1294, in his reference work on science noted ‘there was
difficulty of the aged seeing near objects’. He thought this was due to wrinkling
of the cornea, with the changes being similar to ageing skin. The remedy was a
spherical, glass crystal for magnification.

178
 Refractive Surgery

Another example of resistance to change is the modern history of lens

implantation. In 1949 Harold Ridley of St Thomas’ Hospital in London
invented the intra-ocular lens, the replacement for the cataract, and performed
the first operation. He was helped at that time by Ernest Ford of the optical
company Rayners, who fashioned a lens not dissimilar in size and shape to the
crystalline lens in the eye. Ridley was ostracised and vilified by his
contemporaries who thought he was performing dangerous and unwarranted
experiments on his patients, yet his invention changed the future of
ophthalmic surgery and countless recipients have been revitalised by his
foresight. In the past 20 years he has happily received world-wide acclaim for
his invention.

Evolution in surgery

When an idea is formulated by a pioneer, the feasibility of its application is

investigated by that person, by scientists, by applications in animal studies,
applications in cadaver eyes and in blind eye studies. As the rationale evolves,
so the process can enter clinical trials which are in three phases, wherein small
numbers of clinical patients are fully informed and carefully studied to
demonstrate the clinical effectiveness and safety of the process. If phase one is
successful, the study is enlarged to phase two and finally rapidly expanded to
phase three, so that as much data can be gathered to confirm the original
findings.
As refractive surgery is primarily involved with new techniques, often based
upon new technology, it will immediately become apparent that ophthalmologists
who specialise in refractive surgery today are part of an evolving sub-speciality
which is not always subject to the above developmental constraints. In some
countries, eg the US, rigid regulation limits application of new procedures;
elsewhere applications are generally at the surgeon’s discretion. Once the process
has accumulated sufficient data and experience it may then pass into more general
clinical use, dependent on demand.
At this stage only a few clinical users tend to embark on early application of
the techniques—these can be described as the aggressive end of the surgical
spectrum. As they succeed and spread the method by teaching, so the technique
passes to the main body of ophthalmic surgeons who are instinctively more
cautious, and finally to the very conservative ophthalmologists, who adopt the
process much later. In general usage there is a massive accumulation of data
allowing refinements to be made to the technique.
Lens implantation for cataract surgery is just such a technique; from its
pioneering days in 1949 it developed slowly, being resisted by the majority of
ophthalmologists, but eventually adopted by all of them.

179
 Ophthalmology

Informed consent
Once a technique has passed into clinical use, the patient needs to be informed
about the risks and benefits of the process, and its effectiveness, safety and
stability. They should also be informed about the time-scale of the process
because some techniques involve months or even years of healing before the
effects can be achieved. Surgeons must always be aware of the patient’s
psychology, his motivation for surgery and the aspects of his character that may
make acceptance of problems, minor or major, a bar to embarking on the
surgery (see Chapter 18).

Scope of refractive surgery

Refractive surgery today is capable of intervention in gross myopia as well as
gross hyperopia. It has a range of, say,–37D of myopia to +16D of hyperopia;
from small degrees of astigmatism to gross degrees of astigmatism up to 12D
and with eyeballs of short axial lengths less than 20mm, to long eyes of more
than 26mm and up to extremes such as 35mm.

Refractive surgical options

The optional sites for refractive surgical intervention are the twin-lens systems,
ie cornea and lens. Surgical techniques may be applied to either or both
dependent upon the refractive problem. The currently-available techniques
include those which are well established (a significant track record) or are
developmental (short track record) or investigational (feasibility studies/early
clinical trials).
The cornea may be reshaped by:

(a) surface ablation;

(b) surface/stromal incision; or
(c) lamellar interventions.

The refractive surgery landmarks on the cornea are illustrated in Figure 39.
The options for the lens are:

(a) cataract and lens implant surgery;

(b) clear-lens extraction and lens implantation; or
(c) a supplementary intra-ocular lens, including
(i) an anterior chamber implant for high myopia, or
(ii) an internal (implantable) contact lens for myopia and hyperopia.

Established techniques for the cornea include the incisional methods of radial
keratotomy (Figures 40 and 41, page 182) and/or astigmatic keratotomy
(arcuate or transverse keratotomy) (Figures 42–44, pages 183–184).

180
 Refractive Surgery

Figure 39. Refractive surgery landmarks on the cornea. Note that the geometric centre
of the cornea does not correspond with the visual axis; the optical zone of the cornea is
the important zone whose clarity is to be preserved in cataract surgery whilst influencing
a change of shape (refraction).

Figure 40. Diagram illustrating the

principle of radial keratotomy. Micro-
incisions into the cornea at a depth of
90% are placed around the central optical
zone to effect flattening of that zone and
correct myopic, refractive errors.
Peripheral, corneal incisions cause a
microscopic gap in the incisedarea of the
cornea due to the effect of intra-ocular
pressure. Accordingly,the corresponding
effect on the central cornea is for it to
flatten, ie its radius of curvature being
reduced for the correction of myopia.

Developmental situations where data is rapidly being gathered include surface-

ablation methods such as photorefractive keratectomy or PRK (Figure 45, page
181) performed by the excimer laser. Intrastromal methods, also developmental,
include keratomileusis (automated lamellar keratectomy or ALK) or a
combination of keratomileusis and PRK (laser-assisted intrastromal
keratomileusis—Lasik, Figure 46, page 185 and Figure 47, page 186). A method
in an advanced stage of development is the intrastromal corneal ring (ICR™,
Figures 48 and 49, page 187), the only reversible procedure and one which is
also easy to adjust. Experimental methods include an intrastromal insert for
presbyopia and intrastromal laser ablations for myopia.

181
182
Ophthalmology

Figure 41. Computer-derived plan for the incisions in radial keratotomy (usually four or eight equally-spaced incisions). Note the
clear, central, optical zone, ie the eye is not looking through the operated area; of PRK.
183
Refractive Surgery

Figure 43. Operation plan for combined radial and arcuate keratotomy to neutralise a refractive error of myopic astigmatism.
 Ophthalmology

Figure 42. Diagram to illustrate the

principle of arcuate keratotomy.
micro-incisions are placed into the
cornea at a depth of 60% and a
diameter of 7mm, well away from the
optical zone but on the steep meridian
of an astigmatic cornea to effect
reduction of the astigmatic error.
Arcuate incisions are titrated
according to the refractive defect. The
incisions typically leave a central clear
zone of 7mm.

45° twin arcs at 7mm from the optical zone

Figure 44. The pre-

operative, corneal
topography map (top left)
shows the ‘bow tie’
pattern of the
astigmatism. The
post-operative map shows
(bottom left) a spherical,
corneal shape, ie no
astigmatism. The
difference map shows the
surgical effect achieved
by a combination of
arcuate and radial
incisions into the cornea
(AK and RK).

184
 Refractive Surgery

Figure 45.
Photorefractive
keratectomy (PRK)
is effected by
ablating the optical
zone of the cornea.
Any opacification
or irregularity will
result in
degradation of
vision.

Some procedures are more applicable to lower degrees of myopia (1–5D, eg

PRK, RK and ICR); others to higher degrees of myopia, 6–10D (eg Lasik). Some
are more effective in patients older than 30 years (eg RK); others have an
extended recovery period of weeks or months (eg PRK), whilst an immediate
effect occurs with RK and ICR.
Experience, time-scales, staging, predictability, stability, safety, adjustability
and reversibility are some of the considerations in choosing an application,
whilst patient motivation, needs and attitude also govern choice (see Table 2,
page 188).

Figure 46. Lasik—laser-assisted intrastromal photorefractive keratectomy

(keratomileusis). A 160µ flap is raised in the cornea. Excimer-laser ablation of the bed
is performed before the hinged flap is replaced. Vision is restored within an hour or
two and stabilises rapidly. This technique is superseding corneal-surface, excimer-laser
keratectomy because it avoids the variable-surface healing properties of the cornea
which may blight the outcome of PRK. The cross-sectional diagram shows the internal
ablation under a 160µ 8mm corneal flap which is cut surgically by using an automated
microkeratome. The ‘flap’ adheres back onto the cornea without the aid of sutures;
within a few hours it may be difficult to detect the surgical site.

185
 Ophthalmology

Figure 47. Corneal topography—a

method of mapping corneal
shape, curvature and refractive
power according to the
mathematical algorithms used to
convert the data obtained by
video capture of a reflected image
of a series of illuminated rings
(Placido’s disc) from the target
cornea. Each of the 360° of each
ring is measured for radius of
curvature and the whole data is
integrated to yield a
‘computerised map’ of the cornea.
In this example, a cornea before
(top right) and after (bottom
right) Lasik application is shown,
together with a difference map
(top left—reduced in relative
scale) to illustrate the surgical
effect. Normally there is numeric data shown adjacent the map, which utilises
acolour-coding system for radius of curvature to enable easier interpretation. Note the
symmetrical flattening of the central cornea.

Radial keratotomy
In 1939 a Japanese ophthalmologist named Sato performed radial keratotomy.
He was aware that making incisions into the cornea would change its shape and
refractive power, but what he failed to appreciate was that incisions performed
on the back of the cornea would violate the corneal endothelium, an
irreplaceable and vital life support system for the cornea. His operation,
therefore, rapidly fell into disrepute as the operated corneas succumbed to

186
 Refractive Surgery

Figure 48. Corneal refractive

surgery by the intrastromal
corneal-ring segments (ICRS),
which effects a flattening of the
optical zone of the cornea. The
intrastromal corneal ring (ICR™)
consists of two 150° segments of
a cone which are implanted at
two-thirds depth in the cornea
around an 8mm clear
opticalzone. The ring is the only
adjustable and reversible
refractive procedure for the
correction of myopia. It
underwent final clinical trials in
1996.
Figure 49 . (below). The ICR™ in profile within the cornea to illustrate how the thickness
of the ring elevates that portion of the peripheral cornea, causing an arc-shortening
effect to flatten its centre (hammock effect).

decompensation, ie became oedematous and useless as an optical instrument.

Fyoderov in the USSR in the 1970s popularised radial keratotomy by devising
more realistic protocols for its application. In about 1978, surgeons from the US
visited Fyoderov, observed his methods and saw a huge potential for its
development in the US. At that time, at the height of the ‘cold war’, cynics
suggested that this was a secret, Soviet ploy to blind the American population,
such was the scepticism which greeted this ‘violation’ of a healthy cornea.
Radial keratotomy (Figure 41, page 182) is one form of incisional, refractive
surgery and works by weakening the mid-peripheral cornea through its deep
radial incisions performed with a fine, diamond knife. These incisions cause a
secondary flattening of the central or optical zone of the cornea, resulting in
reduction in corneal refracting power, and neutralised myopia by pushing the
image back towards (and preferably) onto the retina. The weakened mid-
peripheral cornea causes a consequential stretching and flattening of the central,
optical zone.

187
 Ophthalmology

Corneal Lenticular

Surface ablation optical zone (SAOZ) Cataract and lens implantation

Excimer-laser photorefractive Clear lens extraction and lens
keratectomy (PRK) implantation (CLE+IOL)
Excimer-laser photorefractive astigmatic Supplementary intra-ocular lenses
keratectomy (Park)
Corneal incisions Baikoff high minus IOL(–ACIOL)
Radial keratotomy (RK) Internal (implantable) contact lens (ICL)
Astigmatic keratotomy (AK)
Combined RK+AK
Lamellar corneal surgery
(Keratomileusis) or automated lamellar
keratectomy (ALK)
ALK+PRK=(Lasik)
Intrastromal procedures
Intrastromal corneal ring (ICR™)
Thermal procedures
(Hyperopic) holmium keratoplasty (LTK)

Table 2. Refractive surgical procedures.

Arcuate keratotomy for neutralising astigmatic refractive errors

Figure 38 (page 176) shows a schematic, astigmatic cornea, indicating the two
principal meridia with different radii of curvature. The objective in the process
of arcuate keratotomy is to flatten the steeper meridian, which also has the effect
of steepening the meridian at 90° (known as the coupling effect). Flattening of a
meridian is effected by a deep, arcuate incision (usually paired) well away from
the optical zone (usually at a diameter of 7mm). The longer the arcs, the greater
the effect (Figures 42–44, pages 183–84).

Photorefractive keratectomy
This technique is performed by an excimer laser utilising a UV wavelength of
193nm. A calculated dose of laser energy is delivered to the central, corneal
stroma after removal of the surface epithelium (an iatrogenic, corneal abrasion).
The laser energy disrupts the bonds between the molecules of the corneal,
stromal, collagenous tissue. An expanding-diaphragm optical system in the
laser performs a smooth ablation in the form of a concave lens, thus providing
the optical solution for the myopic eye. However, a problem exists in the degree

188
 Refractive Surgery

of unpredictability of the healing process; unexpected effects causing regression

of effect or over-correction are just two examples of this (see complications of
PRK below).

Lasik
Intrastromal, photorefractive keratectomy has the advantage of avoiding the
variable surface healing properties of the cornea which may blight the outcome
of PRK. The cross-sectional diagram in Figure 46 (page 185) shows the internal
ablation under a 160µ, 8mm corneal flap which is cut surgically using an
automated microkeratome. The ‘flap’ adheres back onto the cornea without the
aid of sutures, and within a few hours it is difficult to detect the surgical site.
Unlike PRK, the effect is almost painless, and if the laser dose is calculated
correctly the effect is attained within hours of surgery, making this procedure
preferable to the surface ablation of PRK.

Intrastromal corneal ring ICR™

The intrastromal corneal ring (ICR™, Figure 48, page 187) consists of two 150°
segments of a cone 0.25–0.45mm thick which are implanted at two-thirds depth
in the cornea around an 8mm clear, optical zone. The ring is the only adjustable
and reversible refractive procedure for the correction of myopia. It underwent
final clinical trials in 1996.
The ICR, in profile within the cornea (Figure 49, page 187), illustrates how
the thickness of the ring elevates that portion of the peripheral cornea, causing
an arc-shortening effect to flatten the central cornea.

Lens
The natural or crystalline lens may be replaced or supplemented, be it
cataractous or clear, with an implant which achieves the desired focus of the
eye. Supplementary lenses are placed in the anterior chamber of the eye for the
treatment of myopia or by placement in the posterior chamber—a contact lens
for the crystalline lens (ICL)—to treat both myopia and hyperopia. Finally, there
are combinations of lenticular and corneal methods where control of the corneal
incision can be used to adjust astigmatism. Incisions into the cornea can also be
used in conjunction with the lenticular methods described above in order to
fine-tune the result.

Cataract-refractive surgery
Cataract surgery of the modern micro-incisional type is the most widely-
practised form of refractive surgery, for not only is replacement of the clouded

189
 Ophthalmology

lens an objective, but simultaneous adjustment of the refractive power of the

eye adds an immense bonus to the procedure for the patient. A lens does not
need to be cataractous to require its removal and replacement. Clear-lens
extraction with lens implantation for the treatment of higher degrees of
ametropia (requiring thick glasses, or being blind without glasses) is not only a
feasible but also a safe procedure if practised by modern micro-incision
methods. The effect on a patient’s self-image and self-confidence have to be
seen to be believed.

Screening
It is vital that all aspects of the eye are understood before refractive surgery is
undertaken. A critical test that can be performed today is corneal mapping or
corneal topography, a computerised method of assessing the shape of the
cornea, the most significant area in terms of refraction of the eye (Figure 47, page
186). In their paper on screening for corneal topographic abnormalities before
refractive surgery (Wilson R and Klyce S, ‘Screening patients about to undergo
refractive surgery’ (1994) Ophthalmology 101, 1–147), Wilson and Klyce noted
that 33% of patients had abnormal topography, ie a variation from the normal.
These included warpage of the cornea by contact lens wear, irregular
astigmatism and a 5.7% incidence of keratoconus (see page 267) compared with
0.05% previously reported in the general population.
Before surgery is undertaken the patient needs to go through a careful
diagnostic routine, being given information about what benefits they might
achieve and what risk they might undertake.

Complications
The major complication of all refractive, surgical procedures is a failure to achieve
the desired refractive outcome. In this context complications are relative. Serious,
ie lasting, problems with loss of visual acuity or even blindness are extremely
rare but, as in any surgical procedure, serious problems such as infection can be
disastrous. If procedures are considered on a weighted basis relative to the numbers
in which they are performed, PRK, with hundreds of thousands of applications
worldwide each year, must generate most complications. Though cataract surgery
is a refractive procedure, it is not always practised in this fashion and therefore
its methodology and respective complications are outside the scope of this
discussion. Radial keratotomy is performed in volume in the US but not the UK,
where a few hundred at most would be performed annually. The newer procedures
such as Lasik are just developing.
PRK can cause manifold problems as Table 3 shows.
Retreatments may compound rather than solve the problems. In a recent
survey, only 63% of treated patients expressed satisfaction. Of the remainder,
17% were frankly dissatisfied.

190
 Refractive Surgery

Table 3. Problems which can be caused by PRK.

Occupational visual standards and refractive surgery

Where professional or military requirements for high visual standards obtain,
there are specific regulations concerning the admissibility of candidates whose
eyes have undergone refractive surgery. One example is that which applies to
Royal Navy personnel who have undergone either radial keratotomy or
photorefractive keratectomy (PRK) for myopia.
Personnel are to be informed that these procedures are not available from service
sources, and if carried out privately could have an adverse effect on their future
service career by rendering them unfit for duty. Service personnel who have had
corneal surgery carried out are to be referred to the service consultant
ophthalmologist for assessment. The highest medical category awarded will
normally be P3. In selected cases a higher category may be appropriate.
Private pilots licence and photo refractive keratectomy (PRK) and radial keratotomy (RK)
Whilst PRK and RK surgery to correct myopia are not recommended purely for
licensing or certification purposes, candidates present from time to time having
undergone these procedures. The Authority is prepared to consider licensing under
certain conditions.
(i) That an original pre-operative limited of–5 dioptres of equivalent spherical
error applies in both cases.
(ii) That subjects are referred to and assessed on their merits by a CAA
Consultant Ophthalmologist at Aviation House, Gatwick and at subsequent
intervals as recommended by the specialist.
(iii) Certification would be possible at the six-month, post-operative stage for
PRK and at 12 months for RK. An ‘as or with co-pilot’ or ‘safety pilot’ limit
would not normally be applied.
(iv) When an individual has had one eye successfully treated and the other eye
remaining untreated, fitness to fly will also need to be assessed by a CAA
Consultant Ophthalmologist.

191
 Ophthalmology

The present and the future of refractive surgery

There are sufficient techniques available today and applicable to cornea and
lens to offer a refractive, surgical solution for virtually any refractive problem.
Patients inclined to investigate these possibilities should seek advice from those
who practice a wide range of solutions, but not from clinics which only offer one
modality of treatment. Investment in expensive lasers demands a pay-back, and
the pressure to find patients for therapy by making exaggerated and therefore
insupportable claims about the efficacy of treatment must be resisted. Refractive
surgery is a real and important speciality which, by its nature, is generally
practised in the private sector. This should not preclude an academic approach
to the subject, so that knowledge, based upon accurate experience, can be
passed on for the collective good.
Successful refractive surgery engenders the most appreciative group of
patients in ophthalmic practice, substituting the ecstasy of visual freedom for
the significant anxieties they experience when contemplating and undergoing
refractive surgical procedures. That ecstasy is shared by the refractive surgeon
who requires confidence and courage to practice this speciality.

192
 CHAPTER EIGHTEEN

MISCELLANEOUS OPHTHALMIC
DISORDERS OF OCCASIONAL MEDICO-
LEGAL INTEREST

CORNEAL OPACIFICATION

This may be congenital or acquired in origin. As the cornea is the main

refracting surface of the eye, its function may be compromised by opacification
due to numerous causes.
(a) Congenital causes include:
(i) dermoid cysts of the limbus, congenital opacification of the cornea
(Pieter’s syndrome or neurocrystopathy), birth injuries to the cornea
from forceps used for delivery of the neonate); and
(ii) inherited degenerations or dystrophies—these are usually bilateral,
often symmetrical but they may be asymmetrical. The onset can be at
any age; the early adult is particularly susceptible. There is often a
demonstrable family history of the problem. In some dystrophies there
are a variety of patterns of deposits in the cornea at different levels,
some with lattice-like configuration, some granular, some occur as a
result of deposits in the corneal substance, some with degeneration of
the corneal and epithelial layer, and finally there are those, often of
later age onset, due to premature degeneration of the corneal
endothelial layer (Fuch’s endothelial dystrophy). Another dystrophy
affects corneal integrity, with thinning and abnormal shape occurring
and cone-shape dystrophy of keratoconus.
(b) Inflammation which may be mediated by infections of viral, bacterial or
fungal origin, but some causes are idiopathic.
(c) Associated with skin disorders such as acne rosacea (see above).
(d) Trauma causes corneal opacification either by blunt injury, perforating injury,
chemical injury or physical injury including radiation (see Chapter 15).
(e) Many drugs cause deposits in the cornea with varying degrees of
opacification. Such drugs include amiodarone used in the treatment of
abnormal cardiac rhythm; chlorpromazine used in the management of mental
disorders; chloroquine used in the management of rheumatoid arthritis;
indomethacin used in systemic inflammatory disease such as arthritis; and
tamoxifen used in the management of breast cancer.
(f) Crystalline corneal deposits (crystalline keratopathies) occur as a result of
systemic diseases including multiple myeloma, a cancerous condition of the
bone marrow; macroglobulinaemia, abnormality of blood proteins; and

193
 Ophthalmology

lymphoma, cancer of the lymph tissues. There are some coloured deposits
in the cornea due to deposition of copper in Wilson’s disease (Kayser-
Fleischer rings), and iron deposits, which can be normal in the form of the
Hudson-Stahli line which occurs in older eyes and deposits, may occur as
remnants of foreign bodies in the cornea.
(g) Degenerations of the cornea of which the most common is arcus senilis, a
peripheral, circumferential opacification of the cornea separated from the
limbus by a thin line of clear cornea; band degeneration of the cornea
represents a calcium deposition in the layer beneath the corneal epithelium
(Bowman’s layer). Other degenerations are nodular (Salzmann’s) and may
follow chronic inflammatory disease such as trachoma.
(h) Oedema of the cornea causes visually-disabling opacification. Causes include:
(i) Fuch’s endothelial corneal dystrophy due to an inherent failure of the
cells of the corneal endothelium to last a life span; and
(ii) failure of corneal grafts giving rise both to stromal opacification and
epithelial irregularities, including micro-cysts or bullae, which in its
more advanced forms gives rise to severe discomfort of bullous
keratopathy.
(i) Growth of tissue—a pterygium is an abnormal growth of the conjunctival
tissue onto and into the cornea. In its extreme forms it can reach the central
cornea and cause obvious visual disability. It is a condition more commonly
seen in eyes of people living in warm climates, where there clearly is an
exposure factor in its causation. Surgical removal of a pterygium before it
has optical effects is imperative.

HEADACHE AND THE EYES

When people suffer from headaches they automatically think they should get
their eyes tested. In fact, probably less than 1% of all headaches have any
relationship to the eyes, their function or malfunction. Eye-induced headaches
fall into two categories: those induced by pathology within the eye; and those
that occur as a malfunction of the co-ordination of the two eyes.
With regard to the first group, eye pain which may radiate into the region of
the eye and into the head occurs when an eye is inflamed, when the pressure
inside the eye is raised, when the surface of the eye is damaged and/or when an
eye is injured. The clinical signs, if not obvious, are easily diagnosed on
ophthalmic examination. As noted, the headaches are likely to be localised and
varying in severity according to the ocular pathology. In acute, closed-angle
glaucoma, for example, a headache can be severe (it may be non-existent but the
patient may be nauseated and vomit). In cases of injury to the ocular surface the
overwhelming symptom is one of irritation (a foreign body sensation), but severe
abrasion will give rise to radiating pain.

194
 Miscellaneous Ophthalmic Disorders of Occasional Medico-legal Interest

The second group of conditions occurs as a result of true eye strain, ie effort
of concentration to maintain alignment of two eyes where there is a defect in
their motility. Such headaches are characterised by being associated with visual
effort, particularly sustained, visual effort, eg reading. The characteristic of the
headache is a tension pain in the forehead over the eyes.
Another condition in which the eye is involved is temporal arteritis and
cranial arterial or giant-cell arteritis. This is a single condition with multiple
manifestations which include intermittent pain in the region of the eye and in
the temporal region resulting from inflammation of the arteries. The ocular
implication is that sudden loss of vision may occur due to inflammation of the
central retinal artery, therefore this sort of history in a patient over 60 years of
age warrants immediate investigation and treatment to prevent a catastrophic,
sudden loss of vision.
The migranous syndromes are common complaints that appear before the
ophthalmologist. Though the eyes are rarely implicated, there may be visual
stimuli which trigger the event. The headache is characteristically hemi-cranial,
throbbing and intense in nature. Ophthalmic migraine is a well-recognised
phenomenon which may not involve headache, but there are characteristic visual
effects such as transient loss of vision or loss of half or a quarter of the vision for
up to a few minutes. Classical migraine has visual warning signs such as zigzag
flashes in front of the eyes or other visual hallucinations or photopsia.
The syndrome of herpes zoster ophthalmicus (HZO), a virus infection
affecting the first branch, ie the ophthalmic division of the fifth cranial nerve
(the trigeminal nerve), may be associated with severe and persistent pains even
after the skin and ocular manifestations of the disorder have healed. That
condition is known as post-herpetic neuralgia and can be a very debilitating
condition requiring anti-depressant therapy as well as analgesics.
Headaches behind the eyes that occur on a periodic nature, typically in the
early hours of the morning, are characterised as the syndromes of periodic
migranous neuralgia. Patients automatically feel there is an ocular problem
because of the pain within the region of the eye, but the symptoms are
characteristic and abnormal eye signs are absent.
If a patient suffers from systemic hypertension, associated headaches are
common and systemic hypertension can cause ocular pathology. Systemic
hypertension is a condition which, if severe, can be diagnosed by simply taking
an ophthalmoscopic view of the fundus, wherein the retinal vessels may be
attenuated and irregular. Retinal haemorrhages and small retinal infarcts
(localised death of tissue) may also be present as well as swelling of the optic
nerve head (papilloedema).
Should a patient be suffering from an intracranial, space-occupying lesion
such as a tumour or a cyst, or inflammation of the coverings of the brain
(meninges), then this will be expressed in the posterior segment of the eye by
swelling of the optic nerve head. Headache is an obvious companion of such

195
 Ophthalmology

events and other signs may be a change of personality and change of habits. It is
a cluster of signs of which one has to be particularly wary in children who
complain of headaches.
Finally, the eye is the region where pain my be referred from pathology
elsewhere, particularly from the paranasal sinuses but even from teeth. In
summary it is unusual to find headaches that have any ocular contributions in
the absence of ophthalmic clinical signs.

SUDDEN AND UNEXPLAINED LOSS OF VISION

In the event of a sudden loss of vision, the important questions are:

(a) was the visual loss transient (seconds to minutes) or sustained (persistent)?
(b) were there any associated symptoms or signs such as pain, flashing lights,
watering of the eye, redness of the eye, prominence of the eye (proptosis) or 7
reduction of the motility of the eye?
(c) was the visual loss in one eye or both (unilateral or bilateral)?

Loss of vision is obviously an emergency event, a cause of dramatic anxiety for

the patient even if it is only a unilateral phenomenon. The examining doctor
needs to know the answers to the above questions.
Transient loss of vision in one eye (unilateral) usually has a vascular cause
which includes carotid artery disease. Emboli from atherosclerotic plaques on
the wall of a diseased, carotid artery may lodge in the end-arterial system of the
retina to cause transient or even permanent visual loss.
Giant-cell arteritis (temporal arteritis) may provide warning signs of
permanent blindness by causing transient loss of vision before leading to a
central, retinal, artery occlusion or an ischaemic, optic neuropathy (reduction
of blood supply to the optic nerve) which has a profound effect on the visual
process.
Cerebro-vascular disease with generalised problems may include problems
with the vascular circulation to the eye—the ocular ischaemic syndrome in which
typical signs include transient loss of vision. Problems with the retinal, venous
circulation, which is the route for drainage of blood out of the retina, cause venous
congestion. In its early phase it is characterised as incipient retinal vein occlusion,
a symptom of which is unilateral, transient loss of vision. The condition may
lead to a full occlusion of the retinal vein and blindness. Uni-ocular ophthalmic
migraine may cause partial or total loss of vision in one eye for a period of seconds
or minutes.
When transient loss of vision occurs bilaterally, the potential causes invoke
a systemic connotation such as raised intracranial pressure, where the ocular
signs include swelling of the optic nerve head (papilloedema) (Figures 50 and

196
 Miscellaneous Ophthalmic Disorders of Occasional Medico-legal Interest

51, page 198). Raised intracranial pressure may be caused by raised blood pressure
(systemic hypertension) (Figure 52, page 199), space-occupying lesions within
the cranium including tumours and cysts, and inflammatory conditions such as
meningitis. Cerebro-vascular disease, particularly of the main arteries at the back
of the skull supplying the occipital cortex (the visual cortex), namely the vertebro-
basilar arterial system, may suffer from the syndrome known as vertebro-basilar
artery insufficiency caused by atherosclerosis leading to intermittent failure of
blood supply. Cardiac arrhythmias may cause a vasomotor collapse (blood vessels
in the body dilate) with loss of consciousness, but before that happens bilateral
visual loss may occur. Classical migraine causes visual hallucinations as well as
transient bilateral visual loss such as prodromal phenomena. Transient ischaemic
attacks (TIAs), due to the scatter of micro-emboli from major arteries including
the carotid arteries, may coincidentally affect both eyes.
Sudden permanent loss of vision in one eye (unilateral sudden loss of vision)
occurs due to:
7
(a) sudden clouding of the optical system of the eye due to traumatic cataract
or sudden haemorrhage into the anterior chamber (hyphaema) or posterior
chamber (vitreous haemorrhage);
(b) vascular, retinal abnormalities (occlusion of the retinal artery or vein or severe
intraretinal haemorrhage);
(c) abnormalities in the position of the retina (retinal detachment);
(d) abnormalities in the optic nerve (ischaemic optic neuropathy due to temporal
arteritis or cranial arteritis);
(e) systemic disorders (diabetes, migraine, herpes zoster ophthalmocus); or
(f) physical causes (exposure to radiation and sudden compression of the optic
nerve in trauma).

Incomplete, sudden loss of vision may be due to:

(a) an incomplete retinal, arterial event or a haemorrhage into the more sensitive
part of the retina, the macula; or
(b) functional or hysterical blindness. In such cases there are no abnormal
physical signs, indeed on objective testing by electrodiagnosis there are no
abnormalities when the patient claims they are unable to see. There are
clinical methods of disproving the assertion by a patient that he is blind, but
in the face of constant denials it is difficult to confirm that situation, and one
conclusion is that a psychiatric disorder has to be added to the list of optical,
mechanical and neurological disorders causing visual disability or
blindness.

197
Ophthalmology

198
 Miscellaneous Ophthalmic Disorders of Occasional Medico-legal Interest

Shown is an inferotemporal-branch, retinal-vein occlusion in a patient with

hypertensive retinopathy, ie raised systemic blood pressure.
Figure 50 (above left), a black-and-white reproduction of a red-free photograph, shows
bleeding in the lower temporal quadrant of the retina congested by its interrupted
venous drainage.
Figure 51 (below left) is a fluorescein angiogram, demonstrating blood-vessel perfusion
or failure, with the incontinence of congested vessels to the injected dye fluorescein
appearing white.

Figure 52 (below). Papilloedema and a secondary cancer of the breast which has lodged
in the choroid of this eye (white area, lower left). This patient has papilloedema
(swelling of the optic nerve head) as a consequence of an intracranial, space-occupying
lesion, another metastasis from the breast carcinoma. This is a terminal situation.

199
 Ophthalmology

HEMIANOPIA

Cerebral vascular accidents (CVA) (stroke) either due to an intracerebral

haemorrhage or ischaemia from occlusion of a major blood vessel will cause a
visual disturbance if the visual pathways are affected. The most common
phenomenon is loss of half the vision from each eye, a condition known as
hemianopia which, when affecting the same side of vision, is known as
homonymous hemianopia. If it is incomplete a homonymous quadrant of vision
may be lost. If the stroke is on the right side of the brain then the temporal field
of vision of the left eye will be lost because the retinal nerve fibres from the left
eye’s nasal retina (projected into space—temporal field of vision) cross to the
right side of the brain at the optic chiasma, and the nasal field of vision from the
right eye (temporal retina) is also represented in the right hemisphere of the
brain. This is called a left homonymous hemianopia (Figure 23, page 48). A right
homonymous hemianopia results from damage to the optic pathways on the left
side of the brain. The effect of a right homonymous hemianopia is to make it
very difficult for a person to read because he has difficulty in seeing the next line
as he normally reads from left to right. A left homonymous hemianopia creates
the problem in reading of tracking from the end of a line of print to the
beginning of the next line. There are tricks that can help to adjust to these defects
but clearly it is a major blow to any person with a need to follow an occupation.
It goes without saying that severe visual defects of this nature precludes any
person from being in charge of a motor vehicle.

This list of potential causes of transient and permanent visual loss is far from
exhaustive. The purpose of this brief discussion is to indicate the scope of the
problem.

LASERS IN OPHTHALMIC PRACTICE

The use of intense or high-powered light beams to treat retinal disorders dates
back some 40 years, when Prof Gerd Myer-Schwickerath, the German inventor
of the light coagulator which utilised a xenon, high-intensity-light source, applied
the principle well known to small boys, that the sun’s light can be focussed by a
magnifying glass onto a piece of paper and cause it to heat up and ignite. By refining
this principle and directing a finely-focussed, intense beam of light onto the retina,
unwanted tissues can be destroyed. So the light coagulator was born, a huge
machine that was then found to be effective in treating diabetic retinopathy in
particular. The intense light beam was easily absorbed by the haemoglobin in the
blood vessels of the fundus of the eye and the pigment therein to cause a conversion
of light into heat energy and thereby coagulation of the target tissues. This was a
crude process but it was effective in destroying disease tissue in the peripheral
retina in order to preserve the more vital central areas.

200
 Miscellaneous Ophthalmic Disorders of Occasional Medico-legal Interest

With the development of lasers, light amplification by stimulated emission

of radiation, a coherent beam of light or energy (invisible light) could be
varied in wavelength, beam size and intensity to provide a much more refined
instrument for the treatment of eye problems. In the last decade the variety of
lasers and their applications has expanded dramatically. Light consists of
‘packets’ of energy (photons) which have two characteristics, namely wave
form and particle form. The power of a laser is a result of the energy of a
photon, which is inversely proportioned to its wavelength, the number of
photons striking the target in a unit of time, the duration of the laser pulse and
finally the laser spot size. The smaller the spot size the greater the power
invested in it and vice versa. The light from lasers is monochromatic,
colourmated and coherent.
There are four classes of lasers: those utilising gases; solid state lasers; diode
lasers; and dye lasers.

Principles of application

The lasers fall into the following types:

(a) thermal or photocoagulative, as described above;

(b) photo-disruptive, when tissue temperature is dramatically raised to create a
plasma, a state of matter which has the physical properties of a gas but the
electrical properties of a metal, with a resultant supersonic acoustic shock
wave causing mechanical stress and tissue disruption—the energy delivered
by such lasers is measured in nanoseconds (10–9 sec) or picoseconds (10–12
sec); and
(c) photo-ablative, in which the molecular bonds which bind molecules together
are disrupted, but this time without plasma formation, and thus without
release of heat, allowing precise tissue removal or etching.

Laser specifications
(a) Argon blue 488nm.
(b) Argon blue-green 514nm.
(c) Krypton 530, 568 or 647nm.
(d) Carbon dioxide 960 or 1060nm.

Solid state lasers include the Ruby laser and the Nd-YAG laser which utilises
yttrium-aluminium and garnet surrounding a core molecule of neodymium,
holmium or erbium.
The variable-centre molecule influences the wavelength of the infrared
spectrum, the neodymium-YAG being 1064nm, the holmium-YAG 2010nm and
the erbium-YAG 24900nm. In the excimer laser, an inert gas is combined with an

201
 Ophthalmology

halogen, eg argon or fluorine, to give a wavelength in the UV spectrum of 193nm,

and for krypton fluoride 222nm.
Diode lasers are scaled down versions of conventional lasers. They allow a
large, current density by concentrating a low threshold current through a narrow
channel. The lasing process is provided by a crystal of gallium-arsenic or gallium-
aluminium-arsenic. This is an efficient form of laser much easier to maintain
with wavelengths in the region of 750–1000nm. Dye lasers generate emissions
from a fluorescent, organic compound dissolved in a liquid. Their purpose is to
provide variable spectra on demand.

Some laser applications in the eye

Lasers are destructive instruments and have to be very carefully applied (see
Chapter 13). The following are some of their uses.

The cornea
The excimer laser is used for photorefractive keratectomy and phototherapeutic
keratectomy, the former being a process to alter the refraction of the eye, the
latter to remove superficial opacities from the cornea.

The iris diaphragm

The iris diaphragm may be influenced by thermal lasers, eg the argon laser, to
shrink the iris tissue and dilate small pupils, whereas the neodymium:YAG
laser may be used to disrupt adhesions between the iris and the lens capsule or
artificial lens implants after cataract surgery. The same laser is used to disrupt
the posterior lens capsule in secondary cataract formation due to opacification
of that capsule as a later complication of cataract surgery. The laser may also be
applied in the disruption of tags of vitreous gel adhering to the incision
following complicated cataract surgery, thereby relieving traction on the
vitreous gel and indirectly on the retina. Finally, it is used to perform an
iridotomy—providing an alternative channel to the pupil for aqueous humour
circulation.

Retina
The retina and sub-retinal tissues are treated with gas lasers such as argon green
or argon blue/green in the management of vascular retinopathies, particularly
diabetic retinopathy, in the treatment of other causes of retinal ischaemia (poor
blood supply) and in the treatment of sub-retinal, neovascular tissue in
degenerative, retinal disorders.

202
 APPENDIX 1

DUTIES OF HEALTH CARE PROFESSIONALS IN

OPHTHALMIC PRACTICE

SPECIALISATION IN THE EVOLUTION OF OPHTHALMIC PRACTICE,

STANDARDS OF CARE AND BODY OF MEDICAL OPINION

The practice of ophthalmology has altered dramatically in the past 20 years. It is

less than two generations since ophthalmology separated from ENT medicine
and surgery, to be practised as a special-interest subject in its own right. Since
that time the specialty has progressed beyond recognition, in the main due to
technological advances and the continuous integration of accumulated
experience. Within the general practice of ophthalmology, areas of sub-
specialisation have become well defined and are still developing. The
advantages of sub-specialisation are the higher standards of care that accrue
from concentration of experience, for the field of ophthalmic medical and
surgical practice has become too comprehensive for a generalist to practice with
complete accomplishment at all levels.
Questions therefore arise when the management of a case is disputed with
reference to the particular expertise of the practitioner, if he or she is a generalist
without sub-specialty training or comparable experience. When an area of
medical practice is undergoing transition to the higher levels embodied in the
philosophy of sub-specialisation, the question of what constitutes ‘a reasonable
body of medical opinion’ is the test applied to the standard of care provided.
Other questions that arise include whether subspecialty expertise was accessible
or necessary, and what constitutes a reasonable body of medical opinion in these
circumstances? In current litigation practice a body of sub-specialists may have
a different view from a body of generalists. As these aspects of practice are for
legal rather than medical consideration, the background to current ophthalmic
practice is one with which lawyers concerned with ophthalmic cases should be
aware.

PATTERNS OF REFERRAL IN OPHTHALMIC PRACTICE

When patients have eye problems, they almost always seek advice from an
optometrist. Optometrists in the UK number about 7,000 and are therefore
accessible and generally well informed. As noted below, if an optometrist
discovers a visual problem that cannot be rectified by provision of spectacles or
contact lenses, or if they discover ophthalmic pathology whether
comprehended or not, it is their duty to refer the patient for a medical opinion.

203
 Ophthalmology

The patient’s GP is informed by the optometrist of the problem on form GOS 19,
and it is then up to the GP either to make a diagnosis and offer treatment or refer
the patient to an ophthalmologist by letter or direct contact, with some
indication of the problem and the degree of urgency with which the referral
should be treated.
GPs generally receive little exposure to ophthalmology in their training and,
whilst there are many exceptions, it is the ophthalmologist’s role, in tandem
with the GP, to provide an appropriate standard of care for the patient. Hospital
ophthalmologists inundated with requests for appointments, and with resources
that invite prioritisation of referrals, require as much information as possible
both to direct the patient to the appropriate ophthalmic service and to arrange
the time-scale for the consultation. Some ophthalmic problems are not urgent,
whereas others involving a risk to sight should be seen quickly. (Thus, a patient
who is complaining of recent loss of vision in one eye with suspicion of a retinal
detachment should be seen urgently and not given a thrice-delayed appointment
for a strabismus clinic.)
Optometrists may sometimes bypass the GP in favour of a direct referral to
an ophthalmologist who in turn, as a matter of courtesy, will keep both the GP
and optometrist informed of the outcome. This pattern of referral is in the patient’s
interest in saving treatment time, and this should be regarded as a good standard
of care.
Ophthalmologists who discover on consultation that the patient’s problem
would be better dealt with by a colleague with specialist knowledge in that field
(an increasingly-common situation as ophthalmic sub-specialisation leaps
forward) should make a tertiary referral. Though there are cost and bureaucratic
consequences of such referrals, both in the NHS and private sector, it is clearly
in a patient’s interest to receive the most expert advice.
Self-referral of patients to an ophthalmologist is increasingly common and
not inappropriate in certain circumstances. In the new specialty of refractive
surgery (see Chapter 17) involvement of the GP may be impractical. However,
as in all medical situations, communication by correspondence is both polite
and desirable from a patient-record point of view.

OPTOMETRISTS AND THEIR PROFESSIONAL OBLIGATIONS

The General Optical Council

(Rules relating to injury or diseases of the eye)
Order of Council 1960
The General Optical Council do, in exercise of their powers under section 25(3) of
the Opticians Act 1958, hereby make the following rules:
1 These rules may be cited as the rules relating to injury or disease of the eye,
1960.

204
 Appendix 1

2 (a) In these rules, ‘the Act’ means the Opticians Act 1958, and the phrases
‘registered optician’ and ‘testing sight’ have the meaning given them by s 30
of the Act.
(b) The Interpretation Act 1889 (b) shall apply for the interpretation of these rules
as it applies for the interpretation of an Act of Parliament.
3 Where it appears to a registered optician that a person consulting him is suffering
from an injury or disease of the eye the registered optician shall, subject to rules 6
and 7 below, refer that person to a registered medical practitioner, unless he is
acting on the advice of instructions of a registered medical practitioner (other
than a medical recommendation for a sight test), in testing the sight of such a
person or in fitting and supplying such a person with an optical appliance, but in
such case the optician shall forthwith report to that practitioner any findings of
injury or disease of the eye of which the practitioner may be unaware.
4 In referring a person to a registered medical practitioner, a registered optician
shall take the following steps:
(a) he shall advise the person to consult such a practitioner, and
(b) he shall wherever practicable furnish a registered medical practitioner named
by the person with a written report on his findings indicating his grounds for
thinking the person may be suffering from injury or disease of the eye, and
where action appears urgent he shall also take such measures as are open to
him to inform a registered medical practitioner immediately.
5 If a person who appears to a registered optician to be suffering from injury or
disease of the eye is unwilling, on conscientious or other grounds, to consult a
registered medical practitioner, the optician shall record that fact and the
grounds which the person gives for his unwillingness to consult a registered
medical practitioner.
6 Nothing in these rules shall operate to prevent a registered optician from rendering
in an emergency whatever services are, having regard to the circumstances, in the
best interest of a person consulting him, or from giving treatment in accordance
with rules made under paragraph (d) of subsection (1) of s 25 of the Act.
7 These rules shall comes into operation on 1 January 1961.

Currently, NHS regulations are the same, both being covered by the Opticians
Act.
Previously, the conditions under the GOC rules were stricter than the NHS
with respect to the interpretation of how the patient’s GP was ‘informed’ about
an ocular abnormality. Now, the GOC regulations apply in either case. The only
time there are differences is when a patient who is diabetic or has glaucoma (or
a family history of it) has an NHS test, then a letter is sent to the GP regarding
the results. There is a standard NHS form for this purpose.

205
 Ophthalmology

PROFESSIONAL STANDARDS IN OPHTHALMIC MEDICAL

AND SURGICAL PRACTICE

Clinical guidelines and the law

The use of current, best evidence in making decisions about the care of
individual patients is the ophthalmologist’s responsibility. By integrating
individual, clinical expertise (proficiency and judgment acquired through
clinical experience and practice) with the best available evidence from
systematic clinical research, a patient’s problem can be managed by efficient
diagnosis and sympathetic use of individual rights and preferences in reaching
decisions about care. Any clinical guideline should be considered along with the
ophthalmologist’s clinical expertise in deciding whether and how it affects a
patient’s clinical state and preferences, and thus whether it should be strictly
applied.
But what is the legal status of clinical guidelines? It is impossible to give a
certain answer, and indeed their clinical effectiveness would not be agreed by
all practitioners. Within a health care system that has limited resources their
main role is to assist and guide in the rationing of health care. It is a concern of
all practitioners that, if they deviate from such clinical guidelines, they will be
found negligent if a patient later complains that they have suffered injury. The
question therefore arises as to whether compliance with clinical guidelines
provides protection from liability.
As discussed previously (under medical negligence and the medical report—
Chapter 1) the principles laid down by British courts in assessing the standard
of clinical care is generally held to be the standard judged as reasonable and
proper by a body of respectable doctors. What is or is not reasonable is will be
ascertained from such doctors by way of expert testimony. A court, when deciding
whether a standard is reasonable and proper, will, inter alia, look at standards of
accepted and customary care. While the courts will accept expert testimony on
protocols and guidelines, they will not accept their introduction in other
circumstances, as by merely referring to such published guidelines will give no
opportunity for a party to cross-examine on their efficacy. As such they will be
classed as hearsay evidence and thus will not enable a court to decide what is
reasonable and proper.
While clinical guidelines are of use in influencing the behaviour of individual
clinicians (as well as institutions), it should be noted that, however famous and
impressive the institution which published the guidelines, this does not mean
that what they propose is absolute nor does it guarantee that it represents
customary practice. One must also look at the scope of the guideline, how it was
developed and adopted, whether there is a binding force for its recommendation,
if there are known exceptions to its application, whether any school of medical

206
 Appendix 1

thought rejects it, adopting a different approach to treatment, and whether there
are justifiable exceptions to its application.
The relationship between clinical guidelines and medical negligence cases
remains ill defined and ever developing, but it is apparent that compliance
with clinical guidelines will not in all cases protect medical practitioners from
liability. As in many litigation matters, and especially medical negligence, this
issue has been investigated and considered to a greater degree in the US. They
have been looking at what clinical guidelines can be put in place that will be
recognised by the courts, thus ensuring that doctors who complied with such
guidelines would receive protection from liability in negligence cases.
Recently a trial scheme was set up in Maine. In that state, legally-recognised
clinical guidelines have been created under which a doctor, who can show
compliance with these guidelines, will be provided with a complete defence in
negligence claims. It remains to be seen whether a similar situation will
develop in the UK.

Informed consent
While being a US case, a common principle of informed consent was usefully
described by Cardozo J in Schloendorff v Society of New York Hospital (211NY 25,
25, 105, NE 92, 93 (1914)) who said:

‘Every human being of adult years and sound mind has a right to determine
what should be done with his or her body.’

Thus the question arises how much information is it necessary for an

ophthalmologist to disclose to a patient, and how much should an
ophthalmologist shield a patient from the anxieties that can accompany a full
explanation of diagnosis and treatment? An ophthalmologist must strike a
balance between exercising the patient’s rights with respect to medical and
surgical treatment whilst engendering the confidence and trust in management
that encompasses a joint responsibility to proceed. It is the surgeon who
shoulders the major responsibility, as a consequence of medical and specialist
training.
The exercising of professional judgment and consideration of alternative
management and risks and benefits will allow a patient to make some sort of
‘informed’ evaluation of the options. Statistical information based on
published data may be confusing. Patients may ask where they fit into the
statistics; what are the personal statistics of outcome for the surgeon offering
advice; and what guarantees are there that a particular surgeon will perform
the surgery?
A problem arises if potential material, risks and dangers are not disclosed to
a patient prior to surgery, and a complication occurs. Patients may then claim
that, had they known of such a risk, they would not have consented to the surgery.

207
 Ophthalmology

A risk is material when a reasonable person in the patient’s condition would

consider the risk or risks significant when deciding whether or not to have certain
treatment.
Problems arising from consent to perform surgical procedures can be
minimised but not completely avoided, and every contingency cannot be
completely reviewed. To minimise problems, the following steps will ensure a
thorough approach.
1 Patient education—the procedure should be described in simple language
and in a manner which allows the patient to appreciate what is being done
in order to treat the eye. Though the decision to proceed has to be the patient’s,
the surgeon should not try to pass the responsibility to the patient, but should
communicate the degree of confidence in the procedure’s outcome. The
surgeon has to assume much of the responsibility for advising treatment.
The patient cannot appreciate the intricacies of every surgical situation.
Ultimately, the patient has to have faith in the ability of the surgeon not only
to carry out the procedure, but to make that judgment such that the benefits
far outweigh the risks.
An analogous situation may be a commercial air journey. If the passengers
were to enquire of the pilot or the airline the potential risks, common sense
suggests that they would be high in number but low in expectation. The
passenger would therefore have confidence in the airline and the aeroplane’s
crew to complete a successful journey. So it is with surgery; the patient must
have confidence in the ability of the surgeon and the surgical team to carry
out a successful procedure without knowing each and every pitfall that
common sense dictates must exist.
Education of a patient with regard to consent for a surgical procedure should
include the following:
(a) a description of the purpose of surgery;
(b) a description of the surgical procedure;
(c) a description of the anaesthetic requirements;
(d) a description of commonly-experienced, visual conditions after surgery,
even if temporary;
(e) making the patient aware that even temporary, post-surgical-treatment
visual conditions may become permanent under certain circumstances;
(f) if the patient so desires, a description of the serious complications that
may follow;
(g) a description of potential pain or ocular discomfort;
(h) a description of the refractive requirements after surgery (ie provision
of glasses, contact lenses);
(i) a discussion of the potential for additional procedures (planned, staged
procedures); and

208
 Appendix 1

(j) a discussion of the alternative managements of the condition (see 2,

below).
2 Alternative stratagems for management of an ophthalmic condition should
be explained to a patient so that they can participate in the final direction of
treatment.
3 Where uncertainties exist patients should be so advised, ie the predictability
of a procedure, its stability and its safety. Statistical information on the
outcome is only of limited value when given in a general sense. Few surgeons
are in a position to give specific, statistical information about the outcome of
their own practice of certain procedures.
4 The patient should be given adequate time to decide. At the end of the
consultation a patient must have an opportunity to accept or decline the
treatment on offer. It is inappropriate to obtain a patient’s signed consent for
a procedure and then proceed at very short notice (same day) with that
treatment. The delay between consent and treatment should always be
sufficient to allow the patient to consider the matter more fully.
5 The patient should be advised of the consequences of leaving an ailment
untreated.
6 The patient should sign a consent form which, in itself, should be sufficiently
clear, indicating that the procedure has been fully explained in a language
that is comprehensible and there has been sufficient opportunity to ask
questions and reconsider consent prior to surgery.

Continuing medical education

Medical education does not and should not cease on appointment as a medical
or surgical consultant. The rate of progress in medical and surgical management
of ophthalmic cases is so swift that obsolescent practice is possible and not
uncommon. Continuing education, the perusal of current peer reviewed
literature and attendance and participation in peer group meetings and
symposia is an essential aspect of professional life. Internet discussion groups
help in the solution of problems that may be unique or problematical for the
individual practitioner, when a wide canvas of similar episodes can help in
patient management.
Thus there are various ways in which practitioners can be kept up to date.
Continuing education should not be a matter of statutory requirement but a
desire on the part of all physicians to participate in local, national and
international events for which time and effort must be apportioned.

209
 APPENDIX 2

STANDARDS OF VISION FOR VARIOUS

OCCUPATIONS AND ACTIVITIES

Visual acuity standards

The Royal Navy

Eyesight and colour perception standards
Introduction
1 Eyesight standards for the RN have been comprehensively reviewed and the
resulting revised standards agreed by the Navy Board. The imperatives for
this review are diverse and include a better basis for improved recruiting
and retention, improvements in aids to vision, and the fact that eyesight
deteriorates with age. This DCI promulgates the revised standards and their
applicability to all branches and specialisations.
2 The new standards are effective from 1 January 1995. A copy of this DCI should
be retained within the covers of BR 1750A until the next amendment issue.
3 Seaman Officers whose eyesight is known to be below the old standard will
be contacted by the Naval Secretary. In general, it is anticipated that
submission to a Medical Board of Survey (MBOS) will only be necessary for

211
 Ophthalmology

those who fall below the following revised standards. All outstanding cases
should be referred to the Naval Ophthalmic Consultant Adviser for
assessment and referral to MBOS for determination of permanent medical
category if required.
Radial keratotomy and photorefractive keratectomy (PRK)
4 Personnel are to be informed that these procedures are not available from
service sources, and, if carried out privately, could have an adverse effect on
their future service career by rendering them unfit for duty.
5 Service personnel who have had corneal surgery carried out are to be referred
to the Service Consultant Ophthalmologist for assessment. The highest
medical category awarded will normally be P3. In selected cases a higher
category may be appropriate.
6 Full details are contained in BR 1750A article 0510 and DCI 269/93 (until
incorporated into BR 1750A).
Eyesight and colour perception standards
7 The table at annex A defines the visual acuity and colour perception required
for service in the designated specialisations.
Revised visual acuity (VA) standards
8 Revised VA standards are given in annex B. It should be noted that these are
entry standards. The methods of testing and recording VA are given in BR
175A articles 0503 and 0504.
Colour perception (CP) standards
9 The standards, methods of testing and recording of CP have not been revised
and remain as given in BR 175A articles 0506, 0507 and 0508. However it
should be noted that the Martin lantern is no longer used.
Spectacles and contact lenses
10 There is in general no restriction on the wearing of spectacles or contact lenses
to improve visual efficiency provided that the required corrected standards
of visual acuity are met. Defence spectacles are provided from public funds if
required for the efficient performance of duties but contact lenses are not
currently provided from public funds. Those who choose to wear contact
lenses must also have a pair of Defence spectacles to wear as an alternative.
Instructions for the use of contact lenses are at annex C.
Deterioration of eyesight in service
11 Officers with bridge watch-keeping responsibilities are required to remain
within VA standard II (corrected) and should be tested annually to ensure
that this standard is maintained. Officers in any of the following categories
must be referred to the Consultant Adviser in Ophthalmology and thence to
the Medical Board of Survey to determine permanent medical category:
(a) those whose VA cannot be corrected to VA II;
(b) those who require greater than 6.0 dioptres correction to achieve VA II;
(c) those whose uncorrected vision is worse than 6/60 in either eye.
12 Aircrew who are found for the first time to require corrective lenses are to be
refracted and then referred to the Central Air Medical Board (CAMB) for
assessment of their flying medical category.

212
 Appendix 2

13 Submarine seaman specialists whose correction is greater that ±3 dioptres (ie

outside the range of periscope optical correction) are to be referred for an
ophthalmic opinion and thence to the Submarine Flotilla Medical Officer to
determine their fitness for submarine service.
14 Seaman ratings—applicants for entry must meet visual standard II. However, OM
ratings for AW/AWW specialisation must achieve visual standard I in service.
15 Royal Marine Officers and other ranks—Royal Marine personnel specialising in
aircrew, bridge watch-keeping and other specialist duties must achieve the
standards set out in annex A.
16 Any serving personnel whose unaided vision in the better eye falls below 6/60,
or who requires correction of greater than ±6.0 dioptres is to be referred for
an ophthalmic opinion and thence to the MBOS for determination of permanent
medical category.

Annex A

213
 Ophthalmology

Annex B
The three standards of visual acuity are:
Standard I

Annex C
Instructions for the use of contact lenses
1 Contact lenses may well provide visual advantages over spectacles
enhancing peripheral vision and reducing reflection and aberration. They
are also more compatible than spectacles with specialist equipment such as
night-vision goggles. Gas-permeable hard contact lenses cannot be
recommended for military use as they cannot be worn on an extended wear
basis should the need arise. Tinted lenses are also not permissible. The
decision whether or not to wear contact lenses must remain with the
individual. The individual must also be responsible for ensuring proper care
of contact lenses. The vast majority of complications and ocular pathology
arising from contact lens wear are associated with inadequate care of contact

214
 Appendix 2

lenses. Lenses must be of a soft type and are to be used on a daily wear basis
but to have the facility for extended wear if required. That is to say that in
normal working they should be inserted at the start of the working day and
removed before any periods of sleep but could be left in for an extended
period should the operational need arise. This extended period should not
be for more than seven days.
2 In addition submariners are allowed to wear contact lenses.
3 At all times a pair of spectacles of up-to-date prescription must be available
to the individual. If either eye becomes red or painful the individual must
remove the lens.

The Army

Visual standards applicable in the Army.

Minimum visual standards
(a) Candidates for the Royal Military, Sandhurst, Army scholarships and
urtiversity cadetships require a minimum visual acuity with spectacles of 6/
6 in one eye and not less than 6/36 in the other. Some Arms/Caps require the
right eye to be 6/6.
NB. Failure to achieve colour perception grade 3 (see below) will restrict entry
to certain Arms and Services.
(b) Most regiments and corps require a corrected visual acuity of 6/6 with the
right eye and 6/36 with the left eye. Entrants to the Royal Corps of Transport
as a driver require an uncorrected acuity of 6/60 in each eye, correcting to 6/
9 in the (R) eye and 6/12 in the (L).
Failure to achieve colour perception grade 3 will restrict employment to certain
trades.
(c) Myopia exceeding 7 dioptres in any meridian in either eye or hypermetropia
exceeding 8 dioptres precludes acceptance even if vision is correctable to the
required standard.
Diseases of the eye
Any pathological condition is liable to be a cause of rejection of military service.
Colour perception (CP) standards
Three classifications are applied:
(a) CP2—no errors made on Ishihara plates in daylight or using artificial light
source of equivalent quality;
(b) CP3—ability to recognise signal colours on the approved lantern test; this is
normally the Holmes-Wright lantern; and
(c) CP4—inability to achieve grade 3.
These notes are for guidance only. Each case must be judged on its merits and the
final decision as to a candidate’s fitness will be made by the appropriate Army
Medical Board.

215
 Ophthalmology

Royal Air Force

Visual standards for acceptance for flying and non-flying personnel.
The following are the minimum standards for acceptance for service in the Royal
Air Force. These standards are under regular review and are subject to alteration
without notice and no responsibility for consequences arising as a result of these
changes can be accepted by the Ministry of Defence (Air). The decision as to the
individual’s fitness is the prerogative of the Medical Board which examines him/her.
Flying Personnel
Distant vision
(a) Pilot entry 6/12 in each eye separately correctable to 6/6 and is in the refraction
range–0.75 to +3.0 in any meridian. The astigmatic element must not be greater
than +1.25.
(b) Navigator entry 6/24 in each eye correctable to 6/6 and is in the refraction
range–1.25 to +3.0 in any meridian. The astigmatic element must not be greater
than +1.25.
(c) Loadmaster I (including SAR helicopter duties) entry 6/9 in each eye
correctable to 6/6 and is in the refraction range–0.25 to +3.0 in any meridian.
The astigmatic element must not be greater than +1.25.
(d) Loadmaster II (excluding SAR helicopter duties) entry 6/24 in each eye
correctable to 6/6 and is in the refraction range–1.5 to +3.0 in any meridian.
The astigmatic element must not be greater than +1.25.
(e) Other aircrew entry 6/60 in each eye correctable to 6/6 and is in the refraction
range–2.00 to +3.00 in any meridian. The astigmatic element must not be
greater than +1.25.
(f) The refraction range is defined as the power of the lens determined by
retinoscopy without cycloplegia with which the candidate can accurately and
quickly read the 6/6 line of type, all astigmatic lens notations being in the
plus cylinder transposition.

Near vision
Able to read N5 type with each eye separately at the appropriate distance for age,
with spectacles if applicable, as determined from the accepted Duane scale or
RAF binocular gauge test. This does not mean with ageing aircrew that spectacles
should enable the examinee to achieve this standard in practice. The spectacles
prescribed for use should enable the examinee to achieve an adequate standard
of near vision for the aircraft he operates.
Ocular muscle balance
(a) Pilot
Distance Maddox Rod Eso 6⌬ to Exo 8⌬
Not more than 1⌬ vertical deviation
Near Maddox Rod Eso 6⌬ to Exo 16⌬
Not more than 1⌬ vertical deviation
Convergence 10cm or better objectively
Any manifest strabismus disqualified.

216
 Appendix 2

(b) Navigator
As for pilot except that an alternating strabismus which is cosmetically
satisfactory and does not affect the vision may be accepted.
(c) Other aircrew
No standard required unless diplopia or other symptoms of ocular muscle
imbalance are present. A unilateral manifest strabismus will disqualify as the
deviating eye will be amblyopic, but an alternating strabismus which is
cosmetically acceptable, or which has been corrected surgically, and which
does not affect visual acuity, may be accepted if required.
(d) No candidate for piloting duties with a symptomless heterophoria outside
the limits recommended should be rejected without full orthoptic examination.
Such symptomless candidates may be accepted if the range of fusion is within
acceptable limits.
(e) Cases of convergence insufficiency may be re-assessed after a course of
orthoptic training.
Media and fundi
(a) Any active pathological condition or a congenital or static condition interfering
with vision disqualifies.
(b) Small, healed unilateral lesions in the retinal periphery may be accepted
subject to consultant adviser opinion.
Colour perception—CP2 or CP3
Definitions of colour perception:
CP2 No errors are made using Ishihara plates in daylight or artificial light of
equivalent quality. Tests carried out under normal tungsten or fluorescent
lighting are not acceptable except where the Adlake lamp is used.
CP3 Although errors are made using Ishihara plates the candidate is readily
able to recognise the colours used in aviation. At present the Holmes-
Wright lantern is the only recognised test.
CP4 Unable to pass standard 3
Non-flying personnel
The minimum uncorrected acuity for entry for most non-flying personnel may be
less than 6/60, 6/60, provided that it is correctable to 6/9, 6/9, and:
(a) the fundi are normal;
(b) no other ophthalmic pathological condition is present; and
(c) considering each eye separately, the spherical correction lies between the
range of–8 and–7 dioptres, and the astigmatic correction is not greater than 5
dioptres. Candidates with one amblyopic eye may, under certain
circumstances, be accepted.
Officers
Visual acuity
Correctable to 6/9, 6/9, is acceptable for the majority of ground branches.

217
 Ophthalmology

Colour perception
CP4 with the following exceptions:
• engineer, photographic interpreter—CP2 (engineer applicants who are CFP4
may be appointed but will be required to accept certain limitations in
employment); and
• physical education (including parachute instructor), aircraft control, fighter
control—CP3.
Other ranks
Visual acuity
Correctable to 6/9, 6/9, is acceptable for the majority of ground grades.
Colour perception
CP with the following exceptions:
• electrical, radio, most aircraft engineering trades, electronic engineering (air
and ground), some general engineering trades, aerospace systems operators,
safety and surface trades, photographic trades, some marine trades, some
supply and movements personnel, air stewards—CP2; and
• physical training instructors, air traffic controllers, RAF regiment firemen,
MT drivers, police, most movements personnel, air stewards—CP3.

Civil Aviation Authority

Visual requirements for licences applicable to professional pilots, licensed air
crew, air traffic control officers, student and private pilots.
ICAO has 184 contracting states; the UK is one. Each of these states exercises its
sovereignty by issuing national regulations for aviation, including medical
requirements for licensing. So does the UK. ICAO’s international standards
(see below) are minimum requirements which all contracting states shall
respect, but all states are free to set higher national standards as they like.
Actually, a state may set a lower national standard too, if it so wishes, provided
it informs ICAO of this difference. These are the international minimum
requirements but a would-be pilot may, depending on his nationality or where
he lives, have to meet somewhat higher medical requirements in order to obtain
a pilot’s licence.

ICAO International Standards and Recommended Practices

Personnel licensing
Note 1—Guidance material to assist licensing authorities and medical examiners
is published separately in the current edition of the ICAO Manual of Civil
Aviation Medicine (doc 8984).
Note 2—The standards and recommended practices established in this chapter
cannot, on their own, be sufficiently detailed to cover all possible individual
situations. Of necessity many decisions relating to the evaluation of medical

218
 Appendix 2

fitness must be left to the judgement and discretion of the individual

designated medical examiner. The evaluation must, therefore, be based on a
medical examination conducted throughout in accordance with the high
standards of medical practice. Due regard must be given to the privileges
granted by the licence applied for or held by the applicant for the medical
assessment, and the conditions under which the licence holder is going to
exercise those privileges in carrying out assigned duties.
Note 3—Attention is called to the administrative clause in 1.2.4.8 dealing with
accredited medical conclusion.
Medical assessment—general
Three classes of medical assessment shall be established as follows:
Class 1 medical assessment—applies to applicants for, and holder of: commercial
pilot licences (aeroplane and helicopter); airline transport pilot licences
(aeroplane and helicopter); flight navigator licences; flight engineer
licences.
Class 2 medical assessment—applies to applicants for, and holders of: private
pilot licences (aeroplane and helicopter); glider pilot licences; free balloon
pilot licences.
Class 3 medical assessment—applies to applicants for, and holders of, air traffic
controller licences.
The applicant for a medical assessment shall provide the medical examiner with
a personally certified statement of medical facts concerning personal, familial
and hereditary history. The applicant shall be made aware of the necessity
for giving a statement that is as complete and accurate as the applicant’s
knowledge permits, and any false statement shall be dealt with in accordance
with 1.2.4.5.1.
The medical examiner shall report to the licensing authority any individual case
where, in the examiner’s judgement, an applicant’s failure to meet any requirement,
whether numerical or otherwise, is such that exercise of the privileges of the licence
being applied for, or held, is not likely to jeopardise flight safety.
The requirements to be met for the renewal of a medical assessment are the
same as those for the initial assessment except where otherwise specifically
stated.
Requirements for medical assessment
Visual requirements—The methods in use for the measurement of visual acuity
are likely to lead to differing evaluations. To achieve uniformity, therefore,
contracting states shall ensure that equivalence in the evaluation of methods
be obtained.
Recommendation—The following should be adopted for tests of visual acuity:
(a) For a visual acuity test in a lighted room a test illumination level of
approximately 50 lux normally corresponding to a brightness of 30
candelas per sq. metre should be adopted. The light level of the room
should be approximately one-fifth of the test level illumination.

219
 Ophthalmology

(b) For a visual acuity test in a darkened or semi-darkened room a test

illumination level of approximately 15 lux normally corresponding to a
brightness of 10 candelas per sq. metre should be adopted.
(c) Visual acuity should be measured by means of a series of optotypes of
Landolt or similar optotypes placed at a distance of 6m from the applicant
or 5m as appropriate to the method of testing adopted.
Colour perception requirements—Contacting states shall use such methods of
examination as will guarantee reliable testing of colour perception.
The applicant shall be required to demonstrate the ability to perceive readily
those colours the perception of which is necessary for the safe performance
of duties.
The applicant shall be tested for the ability to identify correctly a series of
pseudo-isochromatic plates (tables) in daylight or in artificial light of the same
colour temperature such as that provided by illuminant ‘C’ or ‘D’ as specified
by the International Commission on Illumination (ICI).
Recommendation—An applicant obtaining a satisfactory score as prescribed
by the licensing authority should be assessed as fit. An applicant failing to
obtain a satisfactory score in such a test may nevertheless be assessed as fit
provided the applicant is able to readily and correctly identify aviation
coloured lights displayed by means of a recognised colour perception lantern.
Class 1 Medical Assessment
Assessment issue and renewal—An applicant for a commercial pilot licence
(aeroplane or helicopter), an airline transport pilot licence (aeroplane or
helicopter), a flight engineer licence or a flight navigator licence, shall
undergo an initial medical examination for the issue of a class 1 medical
assessment.
Except where otherwise states in this section, holders of commercial pilot
licences (aeroplane or helicopter), airline transport pilot licences (aeroplane
or helicopter), flight engineer licences or flight navigator licences, shall have
their class 1 medical assessments renewed at intervals not exceeding those
specified in 1.2.5.2.
When the licensing authority is satisfied that the requirements of this section
and the general provisions have been met, a class 1 medical assessment shall
be issued to the applicant.
Visual requirements—The medical examination shall be based on the following
requirements.
The function of the eyes and their adnexae shall be normal. There shall be
no active pathological condition, acute or chronic, of either eye or adnexae
which is likely to interfere with its proper function to an extent that would
interfere with the safe exercise of the applicant’s licence and rating
privileges.
The applicant shall be required to have normal fields of vision.
The applicant shall be required to have a distant visual acuity of not less
than 6/9 (20/30, 0.7) in each eye separately, with or without the use of

220
 Appendix 2

correcting lenses. Where this standard of visual acuity can be obtained

only with correcting lenses, the applicant may be assessed as fit provided
that:
(a) the applicant possesses a visual acuity without correction in each eye
separately, not less than 6/60 (20/200, 0.1) or the refractive error falls
within the range of ±3 dioptres (equivalent spherical error);
(b) such correcting lenses are worn when exercising the privileges of the
licence or rating applied for or held;
(c) a spare set of suitable correcting lenses shall be readily available when
exercising the privileges of the applicant’s licence.
An applicant accepted as meeting those provisions which refer to refractive
error is deemed to continue to do so unless there is reason to suspect otherwise
in which case refraction is repeated at the discretion of the licensing authority.
The uncorrected and corrected visual acuity is measured and recorded at each
re-examination. Conditions which indicate a need to re-determine the
refractive error include: a refractive state close to the limit of acceptability, a
substantial decrease in the uncorrected visual acuity and the occurrence of
eye disease, eye injury or eye surgery.
The applicant shall be required to have the ability to read the N5 chart or its
equivalent at a distance selected by him in the range 30–50cm (12–20in) and
the ability to read the N14 chart or its equivalent at a distance of 100cm
(40in). If this requirement is met only by the use of correcting lenses, the
applicant may be assessed as fit provided that such lenses are available for
immediate use when exercising the privileges of the licence. No more than
one pair of correcting lenses shall be used in demonstrating compliance
with this visual requirement. Single vision near correction shall not be
acceptable.
N5 and N14 refer to ‘Times Roman’ type-face.
An applicant who needs correction to meet the requirements will require
‘lookover’, bifocal or perhaps trifocal lenses in order to read the instruments
and a chart or manual held in the hand, and also to make use of distant vision
through the windscreen without removing the lenses. Single vision near
correction (full lenses of one power only, appropriate to reading) significantly
reduces distant visual acuity. Whenever there is a requirement to obtain or
renew correcting lenses, an applicant is expected to advise the refractionist
of reading distances for the visual flight deck relevant to the types of aircraft
in which the applicant is likely to function.
Recommendation—An applicant should have a near point of accommodation of
30cm (12in) while wearing the correcting lenses for distant vision. An applicant
who does not meet this provision may nevertheless be assessed as fit provided
he produces evidence, satisfactory to the licensing authority, of having been
fitted with correction for near and intermediate-range vision or that he does
not at present require such correction. Such an applicant should be required
to wear the correction needed for near and intermediate range vision, in
addition to any correcting required for distant vision while exercising the
privileges of his licence.

221
 Ophthalmology

Class 2 medical assessment

Assessment issue and renewal—An applicant for a private pilot licence (aeroplane
or helicopter), a glider pilot licence or a free balloon pilot licence shall
undergo an initial medical examination for the issue of a class 2 medical
assessment.
Except where otherwise stated in this section, holders of private pilot licences
(aeroplane or helicopter), glider pilot licences or free balloon pilot licences,
shall have their class 2 medical assessments renewed at intervals not exceeding
those specified in 1.2.5.2.
When the licensing authority is satisfied that the requirements of this section
and the general provisions have been met, a class 2 medical assessment shall
be issued to the applicant.
Visual requirements—The medical examination shall be based on the following
requirements.
The function of the eyes and their adnexae shall be normal. There shall be no
active pathological condition, acute or chronic, of either eye or adnexae which
is likely to interfere with its proper function to an extent that would interfere
with the safe exercise of the applicant’s licence and rating privileges.
The applicant shall be required to have normal fields of vision.
The applicant shall be required to have a distant visual acuity of not less than
6/12 (20/40, 0.5) in each eye separately, with or without the use of correcting
lenses. Where this standard of visual acuity can be obtained only with
correcting lenses, the applicant may be assessed as fit provided that:
(a) such correcting lenses are worn when exercising the privileges of the
licence or rating applied for or held; and
(b) a spare set of suitable correcting lenses readily available when exercising
the privileges of the applicant’s licence.
Recommendation—If the visual acuity required above is obtained only by the use
of correcting lenses and the uncorrected visual acuity in either eye is less
than 6/60 (20/200, 0.1) applicants whose refractive error in each eye falls
within the range of ±5 dioptres (equivalent spherical error) may be assessed
as fit. Applicants whose refractive error in either eye falls outside the range
of ±5 dioptres (equivalent spherical error) may however be accepted as fit
according to accredited medical conclusion.
An applicant accepted as meeting those provisions is deemed to continue to
do so unless there is reason to suspect otherwise, in which case refraction is
repeated at the discretion of the licensing authority. The uncorrected visual
acuity is measured and recorded at each reexamination. Conditions which
indicate a need to re-determine the refractive error include: a refractive state
close to the limit of acceptability, a substantial decrease in the uncorrected
visual acuity, and the occurrence of eye disease, eye injury or eye surgery.
The applicant shall have the ability to read the N5 chart or its equivalent at
a distance selected by that applicant in the range 30–50cm (12–20in). If this

222
 Appendix 2

requirement is met only by the use of correcting lenses, the applicant may
be assessed as fit provided that such lenses are available for immediate use
when exercising the privileges of the licence. No more than one pair of
correcting lenses shall be used in demonstrating compliance with this
visual requirement. vision. Single vision near correction shall not be
acceptable.
Note 1—Single vision near correction (full lenses of one power only,
appropriate to reading) significantly reduces distant visual acuity.
Note 2—Whenever there is a requirement to obtain or renew correcting lenses,
an applicant is expected to advise the refractionist of the reading distances
for the visual flight deck tasks relevant to the types of aircraft in which
the applicant is likely to function.
Class 3 medical assessment
Assessment issue and renewal—An applicant for an air traffic controller licence
shall undergo an initial medical examination for the issue of a class 3 medical
assessment.
Except where otherwise stated in this section, holders of air traffic controller
licences shall have their class 3 medical assessments renewed at intervals not
exceeding those specified in 1.2.5.2.
When the licensing authority is satisfied that the requirements of this section
and the general provisions of the above have been met, a class 3 medical
assessment shall be issued to the applicant.
Visual requirements—The medical examination shall be based on the following
requirements.
The function of the eyes and their adnexae shall be normal. There shall be no
active pathological condition, acute or chronic, of either eye or adnexae which
is likely to interfere with its proper function to an extent that would interfere
with the safe exercise of the applicant’s licence privileges.
The applicant shall be required to have normal fields of vision.
The applicant shall be required to have a distant visual acuity of not less than
6/9 (20/30, 0.7) in each eye separately, with or without the use of correcting
lenses. Where this standard of visual acuity can be obtained only with
correcting lenses the applicant may be assessed as fit provided that:
(a) the applicant possesses a visual acuity without correction in each eye
separately, not less than 6/60 (20/200, 0.1) or the refractive error falls
within the range of ±3 dioptres (equivalent spherical error);
(b) such correcting lenses are worn when exercising the privileges of the
licence or rating applied for or held; and
(c) a spare set of suitable correcting lenses is readily available when
exercising the privileges of the applicant’s licence.
Note—An applicant accepted as meeting these provisions above which refer
to refractive error is deemed to continue to do so unless there is reason
to suspect otherwise, in which case refraction is repeated at the
discretion of the licensing authority. The uncorrected visual acuity is

223
 Ophthalmology

measured and recorded at each re-examination. Conditions which

indicate a need to re-determine the refractive error include: a refractive
state close to the limit of acceptability, a substantial decrease in the
uncorrected visual acuity, and the occurrence of eye disease, eye injury
or eye surgery.
The applicant shall have the ability to read the N5 chart or its equivalent at a
distance selected by that applicant in the range 30–50cm (12–20in) and the
ability to read the N14 chart or its equivalent at a distance of 100cm. If this
requirement is met only by the use of correcting lenses, the applicant may be
assessed as fit provided that such correction is available for immediate use
when exercising the privileges of the licence. Not more that one pair of
correcting lenses shall be used in demonstrating compliance with this visual
requirement.
Note 1–N5 and N14 refer to Times Roman’ type-face.
Note 2–Single vision near correction may be acceptable for certain air traffic
control duties. However, it should be realised that single vision near
correction (full lenses of one power only, appropriate to reading)
significantly reduces distant visual acuity. Whenever there is a
requirement to obtain or renew correcting lenses, an applicant is expected
to advise the refractionist of reading distances for the air traffic duties
the applicant is likely to perform.
Recommendation—An applicant should have a near point of accommodation
of 30cm while wearing the correcting lenses, if any, required by the above.
An applicant who does not meet this provision may nevertheless be
assessed as fit if able to produce evidence, satisfactory to the licensing
authority, of having been fitted with correction for near and intermediate-
range vision, or of not requiring such correction at present. Such an
applicant should be required to wear the correction needed for near and
intermediate-range vision, in addition to any correction required by the
above, while exercising the privileges of the licence.
Photorefractive keratectomy (PRK) and radial keratotomy (RK)
Class 1/2—Individuals must be reviewed by a CAA consultant
ophthalmologist at 6 months and 12 months post-operatively and
annually thereafter. A pre-operative limit of -5 dioptres ESE applies and
a best visual acuity of 6/6 or better (with correction if necessary) must
be achieved. Suitable cases will be returned to flying 12 months after
operation.
Class 3—Applicants who have a pre-operative refractive error of -5 dioptres
ESE or less may be assessed by a local ophthalmologist with an
anticipated return to flying no earlier than 6 months post-operative in
the case of PRK, and 12 months post-operative for RK. If best visual acuity
is 6/9 or better, the eye is stable and there is no evidence of any problems
from glare, an unrestricted class 3 certificate may be issued, subject to
annual ophthalmological follow-up.

224
 Appendix 2

If an individual has a pre-operative refraction of over -5 dioptres ESE, he

must be reviewed by a CAA consultant ophthalmologist 12 months post-
operation. Glare testing may be required.
The CAA does not recommend eye surgery for certification purposes.
All applicants must be referred to medical division for any certificatory
decision.
NB—the proposed European standards with which the UK will be required to
harmonise in 1996 do not currently permit refractive surgery in initial class 1
applicants. Individuals should be aware that if a medical certificate is issued
by the UK CAA, it could be valid for a UK licence only, not a JAA one, post-
harmonisation.
The Joint Aviation Authorities inform us that JAR-FCL part 3 (medical),
which includes the European Aviation Medicine Manual, was adopted by
JAA on the 8 October 1996. Requirements contained therein will be
applicable on 1 July 1999. A final version of the requirements is not yet
available but will soon be published by the Printing and Publication Services
of the United Kingdom Civil Aviation Authority, from whom copies may be
ordered.

Merchant Navy

Eyesight standards for the Merchant Navy.

Industrial standards
1 Officers, Apprentices, Cadets and Ratings should not be passed as fit for
training or sea service if they are suffering from any morbid condition of
either eye, or the lids of either eye, which is liable to the risk of aggravation of
recurrence.
2 In all cases where glasses or contact lenses are required for the efficient
performance of duties, a spare pair of glasses (and, if different glasses are
used for distant and near vision, a spare pair of each) must be carried when
seafaring.
3 Colour vision for Deck Officers and Ratings may be regarded as normal if
plates 1, 11, 15, 22 and 23 in Ishihara’s charts are read correctly, or if the
Department of Trade lantern test is passed. It is important to realise, however,
that these numbers refer to plates in the ‘38 plate edition’ and which differ
from those in the ‘24 plate edition’ when the corresponding numbers are 1, 8,
11, 16 and 17.
New entrants to the Deck Department may wear glasses or contact lenses
both for the Industry Entrant Medical Examination and the Department’s
letter and lantern test.
Where aids to vision are used the following standards now apply:

225
 Ophthalmology

These entrant visual standards will also apply to general purpose ratings where
look-out duties are required.
M1144 has been superseded by notice M1331 issued 1988 (see following page).
Section III
General
1 A fee (plus VAT at the standard rate, except when the sight test is taken
in conjunction with the examination for a statutory marine qualification at
an inclusive fee), payable to the Superintendent of a Marine Office, is
charged for conducting a sight test at one of the Department of Transport offices.
2 Candidates other than new entrants who have previously failed to pass the
sight test either locally or at a special appeal test conducted by the Principal
Examiner of Masters and Mates or his Deputy may, provided aids to vision
have not been worn at any of these previous tests, apply to take the test again
locally with aids on payment of a further fee plus VAT.
3 Candidates who have taken a previous test without aids and have failed in
the letter test but did not proceed to the lantern (or having proceeded to the
lantern, passed the lantern test) may be re-examined locally, without aids,
after a period of one month.
4 Candidates who have taken a previous test with aids and have failed in the
letter test but did not proceed to the lantern (or having proceeded to the
lantern, passed the lantern test) may be re-examined locally, with aids, after a
period of not less than one month.

226
 Appendix 2

5 A list showing the ports where sight tests are held is shown below.
Applications for appointments should be made to the sight test examiner at
the Department of Transport Marine Office at the port concerned.
6 Unless other indicated sight tests are conducted between 9.30am and 12.30pm
on the listed days. A candidate who lives a distance from the port and cannot
attend during the hours at which sight tests are normally conducted at the
port should apply in writing to the Examiner at the sight test centre for a
special appointment. Sight tests are not held on Saturdays, Sundays or public
holidays.
Aberdeen Every Friday by appointment
Belfast Every Monday. Other days by appointment
Cardiff Every Monday
Glasgow Every Wednesday (9.30am-12noon).
Other days by appointment
Great Yarmouth By appointment
Grimsby By appointment
Hull Every Friday
Leith Every Tuesday (9.00am-l 1.30am)
Liverpool Every Thursday and Friday
London Tuesdays, Wednesdays, Fridays by appointment
Newcastle Every Friday
Plymouth Every Monday
Southampton Every Friday
Stornoway (Custom House) By appointment

Motor drivers
Regulations governing eyesight
The 1988 Road Traffic Act places an obligation on all British driving licence holders
to notify the Licensing Centre at Swansea as soon as they become aware that they
are suffering from any condition which might affect safe driving either now or in
the future. This requirement is printed on every British driving licence together
with the address to which the notification has to be sent. Failure to notify a disability
can have important motor insurance consequences.
Visual acuity
All British driving licence holders must meet a standard equating to the number
plate test whenever they are driving. Failure to meet that standard at any time
when driving is an offence (s 96 of the Road Traffic Act 1988). The number plate
test equates approximately to 6/10 Snellen (Drasdo and Haggerty 1977).
In precise terms a person is barred from holding a driving licence if she is unable
to read, in good daylight (with the aid of glasses if worn), a registration mark
fitted to a motor vehicle and containing letters and Figures 79.4mm high at a
distance of 20.5m.

227
 Ophthalmology

In the matter of advising patients on their visual fitness to drive a private vehicle,
the College of Ophthalmologists recommends (faculty of ophthalmology of the
Royal College of Surgeons of England Annual Report 1977) that the form of
wording used in ophthalmic reports on the examination of patients’ vision for
driving should avoid actual certification of visual fitness to drive. It is better to
adhere in the report to the actual findings and, if appropriate, to add a comment
that the visual findings are thought either to meet or not to meet present legal
requirements.
Visual fields
The College of Ophthalmologists has now advised that the minimum visual field
for safe driving should be at least 12° on the horizontal measured by the Goldmann
perimeter using the 114e settings, or equivalent perimetry. In addition there should
be no significant field defect in the binocular field which encroaches within 20° of
fixation, either above or below the horizontal meridian. By these means
homonymous or bi-temporal defects which come close to fixation whether
hemianopic or quadrantonopic are not accepted as safe for driving. Isolated
scotomata represented in the binocular field near to central fixation may also be
inconsistent with safe driving.
Colour vision
There are no restrictions on driving in relation to defective colour vision.
Night vision defects
The more marked degrees of night vision defect occurring in diseases such as
retinitis pigmentosa and advanced choroidal retinitis are normally regarded as a
bar to driving and must be notified to the Licensing Centre.
Note
Facsimile of number plates reduced so as to be equivalent to a full size plate at
20.5m [22.9m (75ft) for characters of 88.9mm (3.5in)] may underestimate the visual
acuity required to meet the number plate in good daylight.
Visual disorders
The law states that: a licence holder or applicant is suffering a prescribed disability
if unable to meet the eyesight requirements, ie to read in good daylight (with the
aid of glasses or contact lenses if worn) a registration mark fixed to a motor vehicle
and containing letters and figures 79.4mm high at a distance of 20.5m. If unable to
meet this standard, the licence must be refused or revoked, and the driver must
not drive.

228
 Appendix 2

Field of vision requirement for the holding of group 1 licence entitlement

The standards of the minimum field of vision for safe driving is designed as ‘a
field of at least 120° on the horizontal measured by the Goldmann perimeter using
1114e settings (or equivalent perimetry)’. In addition there should be no significant
defect in the binocular field which encroaches within 20° of fixation above or below
the horizontal meridian.
The standard is not equipment specific and permits other equivalent perimeters,
including auto perimeters where the programmes are easily specified and not
time consuming. The following (not exclusive) list will satisfy the standard.
(a) Older manual perimeters (Lister, etc) using 3mm targets one-third of a metre
distance.
(b) The Gultron Biotronics Autofield 1 and the Fieldmaster perimeters using their
basic programmes.
(c) The Humphrey perimeter (3-zone 61-points programme).
(d) The Dicon perimeter AP 2000 (target 25,000 Asb bowl 31.5 Ash).
(e) The Octopus perimeter 500 EZ (programme no 7).
(f) The Tubinger TAP 2000ct (programme no 6).

229
 Ophthalmology

(g) Ederhenson perimeter 4000 (full field strategy).

(h) The Esterman test. This can be monocular or binocular and can be
programmed into perimeters such as Dicon, Henson and Humphrey. It can
test 130° field with some enhancement of the binocular field as naturally
occurs. While the test can be exactly related to the Goldmann 1114c settings it
is probably the least stringent test which will satisfy the standard.
The binocular field of vision obtained by testing with both eyes open is generally
acceptable. Although testing individual eyes is useful as this indicates the
extent of the field in each eye and is preferable with bi-temporal visual field
defects.
Group 2—large goods vehicles (LGV) and passenger carrying vehicles (PCV)
1 The expected standard is a visual acuity of at least 6/9 in one eye and a visual
acuity of at least 6/12 in the other eye and a visual acuity not worse than 3/
60 uncorrected in each.
2 If (a) a person has never held a group 2 licence or (b) his first group 2 licence
was issued after 1 March 1992 or (c) his last group 2 licence expired before 1
April 1991, he must satisfy all three conditions quoted above. If he cannot
satisfy all three he may not drive vocationally.
3 If a person had a group 2 licence valid on 1 April 1991 or 1 March 1992 and
does not meet the expected standard he may qualify to drive
vocationally unless his visual acuity is worse than 6/9 in the better eye and
worse than 6/12 in the other eye and worse than 3/60 uncorrected in each
eye. Advice should be sought from the Drivers Medical Unit, DVLA, Swansea
SA99.
4 If a person had a group 2 licence valid on 1 January 1983 and 1 April 1991 and
did not meet the expected standard he may qualify to drive vocationally unless
his visual acuity is worse than 6/12 in the better eye and worse than 6/36 in
the other eye and worse than 3/60 uncorrected in each eye. Advice should be
sought from the Drivers Medical Unit, DVLA, Swansea SA99.
5 Monocular drivers can qualify provided the Traffic Commissioner had been
made aware of the monocularity before 1 January 1991 and issued a licence.
In which case a driver who held a valid group 2 at 1 January 1983 and 1 April
1991 must have a visual acuity of at least 6/12 and a driver who held a valid
group 2 at 1 April 1991 only must have a visual of at least 6/9.
6 Group 2 licence applicants who apply for a first licence after the 1 April 1991
may not be granted it if they suffer from monocularity. Indeed if the licence
holder becomes monocular after 1 April 1991, the Licensing Authority will
revoke the entitlement to drive.
7 Unless the visual acuity specifies uncorrected the standards can be met with
the aid of glasses or contact lenses if worn.
8 Diplopia if insuperable is a bar to vocational driving. If follows that if the
diplopia is corrected with a patch of prism the driver will become effectively
monocular, this may lead to the revocation of the licence.
9 There must be no pathological visual field defect.
10 If his eyesight falls below these standards at paragraph 1 but is above the
standard at paragraph 3 or 4 he should contact the Medical Section at DVLA

230
 Appendix 2

for advice. The address to write is Drivers Medical Branch, Oldway Centre,
Orchard Street, Swansea, SA99 1TU, tel 01792–304000.
‘Grandfather rights’
Currently, because of the wording of the second EC directive, if correction is used
the uncorrected visual acuity in one eye only must be at least 3/60. In January
1997 this will be changed to comply with the second EC Directive and the 3/60
must be achieved in each eye. Those who can satisfy the current standards, but
who will not be able to satisfy the new standards in January, will be permitted to
retain their licences. However there are a number of people who were taken into
the system at varying times, some prior to 1983, who were required only to achieve
6/12, 6/36, and there was no uncorrected visual acuity standard. Some time later
an uncorrected visual acuity of 6/60 was introduced and then in 1991 the new
regulations. All these people will be permitted to continue to drive but they will
be required to produce evidence that they have driven regularly for a minimum
of six months and that, if they have been involved in an accident, they must produce
a certificate to indicate that this was unlikely to have been due to eyesight problems.
These new conditions will begin to operate from January 1997, and how exactly
they will operate is at the moment unclear. So the regulations from 1 January 1997
will be 6/9, 6/12, 3/60 in each eye, that is a corrected visual acuity of 6/9 in one
eye, 6/12 in the other eye and 3/60 in each eye uncorrected. ‘Grandfather rights’
will be permitted providing there has been no deterioration in the eyesight since
the licence was issued and the licence holder can provide that he or she has been
driving regularly over the previous six months.

231
 Ophthalmology

Drivers of metropolitan motor cabs

All patients who have monocular vision or diplopia or pathological or binocular
field defects (such as bi-temporal or homonymous hemianopia) should be
regarded as unfit to drive HGVs or PSVs (note—the Assistant Commissioner of
the Metropolitan Police, as Licensing Authority for cab drivers in London,
expects the same standard of vision from a cab driver as from a PSV or HGV
driver).
Visual acuity—The following policy is adopted by the Vocational Licensing
Authorities in Great Britain. Persons commencing a career and those same persons
on renewal of their vocational licence are required to meet a Snellen standard of
visual acuity of 6/9 in the better eye and 6/12 in the other eye with corrective
lenses including contact lenses if worn. They must also meet an uncorrected
standard of static acuity of 6/60 in both eyes separately. Patients who have had a
cataract extraction will normally fail the uncorrected standard but they may be
permitted to drive heavy goods or public service vehicles if they have had a
successful lens implant and can meet the 6/60 standard.
The Licensing Authorities at their discretion apply a lower standard of vision for
persons who have held a vocational licence prior to 1 January 1983. This standard
requires a Snellen acuity of 6/12 in the better eye and 6/36 in the other eye with
corrective lenses other than contact lenses if worn. An existing licence holder who
has had a cataract operation or wears contact lenses should be advised against
driving unless the visual acuity in both eyes separately is at least 6/60
uncorrected.

The Post Office

Candidates for appointment—The standards of vision required depend
primarily upon the type of occupation in which the employee is placed. Any
visual defect is therefore considered in relation to this, to its cause and its
prognosis. Any employee on driving duties is expected to meet HGV/PSV
visual standards.

Civil Service
Candidates for appointment—Except for a few special posts where specific
visual standards are required, prospective candidates with visual problems are
assessed on an individual basis with regard to the requirements of the proposed
appointment and the appropriateness of wearing corrective spectacles or using
aids to vision.
Employees who have driving duties are expected to meet the current
standards laid down by the appropriate licensing authority.

232
 Appendix 2

Firefighter eyesight standards

Standards of vision
We considered it essential that a fire-fighter’s vision should be sufficient to enable
him to work efficiently and safely on operational duties. This necessitated a high
standard at entry which could permit some later deterioration. We also considered
that a minimum level should be set below which a fire-fighter’s eyesight must not
fall, however experienced he might be. The level adopted for this standard was
reached after full discussion with the Visual Standards Subcommittee and takes
into account both operational and medical considerations. It is hoped that the
more stringent entry standard may minimise or eventually eliminate the number
of fire-fighters reaching or falling below the new fallback standard.
Conclusion and recommendations
(a) On entry—the fire-fighter’s uncorrected visual acuity, measured by the method
known as the Snellen test, should be 6/6, 6/6. His unaided visual function,
including his colour vision, is such as to enable him to undertake firefighting duties
and that he does not have any abnormality or suffer from any disease which in
either case would be likely to affect such visual function temporarily or
permanently so as to incapacitate him for the performance of the said duties. The
maximum degree of manifest hypermetropia permissible at entry is +1.50 dioptres.
The maximum degree of myopia permissible at entry is–0.25 dioptres sphere
or–0.50 cylinder.
(b) A history of night blindness would be a bar to entry.
(c) Colour vision should be tested with the Ishihara plates. Two errors of
identification permitted in the set of plates. No substitute test of colour vision
should be accepted.
(d) Subsequently—The minimum unaided visual acuities of the firefighter should
normally be 6/18, 6/18 correctable to 6/9, 6/12. This must in no case fall
below 6/18, 6/24 correctable to 6/9, 6/12 and any decision should be taken
after consideration of the firefighter’s operational ability and other aspects
of visual function. In cases of doubt or where medical discharge is under
consideration the examining doctor might wish to consult an ophthalmologist.
It should be noted that the term ‘correctable’ does not imply that such
correction should be allowed for operational duties but rather that such
correction is possible.
(e) Contact lenses should not be permitted. Pseudophakia is acceptable provided
visual standards are met.
(f) Spectacles should not be permitted operationally in view of the lack of any
certification of a BA set compatible with their use and insufficient research
into the safety of firefighters with aids to vision generally, although they
should continue to be worn if required when driving appliances or at the fire
station.
(g) Examination—It is considered that the assessment of visual function is an
essential part of the assessment of general medical fitness for fire service
duties and requires close liaison between the fire service medical adviser
and the examining ophthalmologist who should make the ophthalmological

233
 Ophthalmology

assessment on entry. Subsequently it is recommended that referral for

ophthalmological advice is left to the discretion of the fire service medical
adviser.
(h) Hypermetropia (long-sightedness)—When the subject is found to be
hypermetropic, a manifest hypermetropia in either eye greater than +1.25
dioptres sphere is a bar to entry. (In practical terms the intention is that if the
subject can perceive, with each eye separately, an acuity of 6/6 with a +1.5
dioptres sphere before each eye, then he is visually disqualified by his manifest
hypermetropia.)
(i) Myopia—Applicants who are able to achieve an acuity of 6/6 in each eye
unassisted but who on retinoscopy are found to have greater than-0.25
dioptres sphere or-0.50 cylinder are disqualified.
(j) Near vision—Near vision is only likely to become a problem with the
hypermetropic entrant when the age of 40 or more has been reached. At this
time unaided distance acuity should be as set out in recommendation (d)
above. It is not though necessary routinely to test near vision. The normal
loss of accommodative power in the eye over the age of 40 should not prove
a disqualification for operational firefighting.
(k) Astigmatism—The maximum astigmatic error permissible in myopia is-0.5
dioptres cylinder and the maximum permitted astigmatic error in
hypermetropia is +1.5 dioptres cylinder. The astigmatic lens notation must
be in the plus cylinder transposition.
NB. A research project under the aegis of the Home Office is in progress within
the Fire Service nationally as regards the use in future of artificial aids to vision by
operational fire-fighters. This research was due to be completed in May but it
may be some while after before any amendments are made to the eyesight
standards.
Pending the outcome of this research, the Central Fire Brigades Advisory Council
has determined that serving members of fire brigades whose eyesight is below
the prescribed standard are to be retained in the service on light duties
rather than being retired as they would have been formerly, pending the final
agreement on the detail of the new standards and the obtaining of the equipment
necessary.

British Railways
1 Traincrew
Train (wo)men, Drivers, Conductors and Senior Conductors
On entry as Train (wo)man—No pathological condition of the eyes to be
present. 6/9, 6/12 or better with or without glasses. If glasses are worn,
unaided vision not to be worse than 6/12, 6/18 (Train (wo)men D) or 6/60,
6/60 (other Traincrew). Bifocal glasses permitted. Near vision to be N8 or
better with or without correction. Tinted or photochromatic prescription lenses
not acceptable for the purpose of meeting this standard. Contact lenses
prohibited. Normal colour vision tested by Ishihara plates required.

234
 Appendix 2

Serving staff (except Traincrews operating the Eurostar (UK) Ltd’s Eurostar
trains)—6/9, 6/12 or better with or without glasses. Near vision to be N8 or
better with or without correction. Normal colour vision on Ishihara test. No
pathological condition of the eyes should be present.
Drivers are provided with standard sunglasses to British Rail colour
transmission specification.
Traincrew needing glasses to meet the standards must provide one pair of
glasses at their own expense to be carried as a spare pair and are provided
with standard British Rail glasses for duty purposes. British Rail standard
glasses are ordered by the Board’s Medical Officers through local opticians
using a British Rail official order form.
Visual standards for Traincrews operating the European Passenger Services’
Eurostar Trains through the Channel Tunnel—(a) 6/6, 6/9 distance and N8
near vision, or better, with spectacles if worn; (b) if spectacles are worn,
unaided vision not to be worse than 6/12, 6/18 for Drivers and 6/60, 6/60
for Train Managers; (c) no pathological condition of the eyes to be present;
(d) history of surgical correction of short sight, eg laser excimetry, excludes
acceptance; (e) bifocal spectacles permitted; (f) contact lenses prohibited; (g)
tinted and photochromic prescription lenses prohibited. (These are examined
annually.)
Colour vision—colour vision must be normal, as assessed by the Ishihara
plates test;
2 Other operational staff
On entry—No pathological condition of the eyes to be present. 6/9, 6/12 or
better with or without glasses. If glasses worn, unaided vision not to be worse
than 6/60, 6/60. Bifocal glasses permitted. Tinted or photochromic
prescription lenses not acceptable for the purpose of meeting the standard.
Contact lenses prohibited. Normal colour vision on Ishihara test required,
when accurate colour perception is a requirement of the post.
Serving staff—Operational staff working on running lines are examined
periodically and the above standard is required to be met excluding the
minimum unaided vision clause.
3 Professional, technical staff, working on running lines
As in section 2 above but contact lenses permitted.
4 Clerical and non-operational staff
On entry—6/12, 6/36 or better without glasses (discretion may be exercised
bearing in mind the nature of the task to be performed). Near vision N5 or
better. Bifocal glasses permitted. Contact lenses permitted. Normal colour
vision not required.
Serving staff—There are no arrangements for periodic examinations of this
category of staff.

235
 Ophthalmology

The police
Entry requirements vary between forces, but all demand a high standard of
eyesight. Applicants are required to produce a certificate from a registered
optician issued within the preceding 12 months (6 months in Cheshire). No
force can accept candidates with only one eye, those unable to distinguish the
principal colours, or those who suffer from squint or other morbid conditions of
the eyes or the lids of either eye which is liable to the risk of aggravation or
recurrence.
The normal standard of vision requirements and the higher standards
required by some police forces are set out below. It is intended as a general guide
only and further information can be obtained from the chief officers of the local
force.

Normal standards of vision

An unaided distant vision of not less than 6/18 in each eye is required (Snellen’s
test). The distant vision should be correctable with approved vision aids to a
standard 6/6 in one eye, 6/12 in the other and 6/6 binocularly. The test for near
vision with approved vision aids should be in accordance with the standards set
by the College of Ophthalmologists.

Forces requiring higher standard of eyesight

Cheshire—An unaided distant vision of not less than 6/18 in each eye. The distant
vision should be correctable with approved vision aids to a standard 6/6 in
one eye, 6/12 in the other and 6/6 binocularly.
Dorset, Merseyside, Wiltshire and Sussex—An unaided distant vision of not less
than 6/6 in one eye and 6/12 in the other and 6/6 binocularly.
Gwent—An unaided distant vision of not less than 6/18 in each eye correctable
with approved vision aids to 6/6 in one eye, 6/12 in the other and 6/6
binocularly. Candidates should also be able to distinguish the principle colours.
Norfolk, Hampshire and Northamptonshire—An unaided distant vision of 6/6
in each eye.
North Yorkshire—An unaided distant vision of not less than 6/24. Aided vision
6/6 in one eye and 6/12 in the other and 6/6 binocularly. The above force
should be contacted, re colour vision acceptance.
Derbyshire—An unaided distant vision of not less than 6/18 in each eye (Snellen’s
test), which should be correctable with vision aids to a standard 6/6 in one
eye, 6/12 in the other and 6/6 binocularly. Candidates with only one eye and
those who suffer from a squint or other morbid conditions of the eye or lids of
either eye liable to the risk of aggravation or recurrence will not be accepted.

236
 Appendix 2

Staffordshire—An unaided distant vision of not less than 6/18 in one eye, 6/60
in the other correctable with approved vision aids to a standard of not less
than 6/6 in one eye, 6/12 in the other and 6/6 binocularly.
West Yorkshire—An unaided distant vision of not less than 6/6 in one eye, 6/12
in the other and 6/6 binocularly and unaided of at least 6/18 in each eye.
Candidates should be able to distinguish the principal colours.
West Midlands—An unaided distant vision of not less than 6/18 in one eye, 6/
60 in the other and 6/60 binocularly.
Cleveland—Applicants should have unaided vision of not less than 6/18 in each
eye (Snellen’s test); the distant vision should be correctable with approved
aids (spectacles or contact lenses) to a standard of 6/6 in one eye, 6/12 in the
other and 6/6 binocularly.
Lancashire

The test for near vision with approved vision aids should be in accordance
with the standards set out by the College of Ophthalmologists. The following
will not be accepted: candidates who are unable to distinguish principle colours.
Those who only have one eye or those who suffer from squint or other morbid
conditions of the eyes or the lids of either eye liable to the risk of aggravation or
recurrence.

237
 Ophthalmology

Most, but not all, forces accept applicants who wear contact lenses or glasses.
The exceptions are as follows:

• The following forces accept contact lenses but not glasses—Durham, Gwent
and West Mercia.
• The following forces accept glasses but not contact lenses—South Yorkshire
and Bedfordshire.
• The following forces do not accept glasses or contact lenses—Dorset,
Lancashire, Northamptonshire and Sussex.
• The following forces accept contact lenses and glasses only in special
circumstances—Greater Manchester, Merseyside, North Yorkshire, West
Midlands, Lincolnshire and West Yorkshire.

An ‘action pack’ covering the examination report and dispensing of optical

appliances for police constables is available to police authorities.
There is a variable recommendation in terms of visual acuity. Chief constables
have the right to set their own standards; for example at the RUC where
everybody is required to be fit to use firearms and the candidate has to have 6/
6 in each eye at recruitment. However, the majority of forces use 6/18.

Metropolitan Police Force

Requirements for Constables
1 Unaided vision—first three lines with each eye separately and both eyes
together. Right—6/24; left—6/24; both—6/24. Unaided vision is one eye
6/6 either eye 6/12 and both 6/6 or better vision aids are not required.
2 Aided vision should be able to read penultimate line with at least one eye
and both eyes together and aided vision in other eye can be as 4th line, ie
one eye 6/6, either eye 6/12 and both 6/6.

Prison officers
1 Visual acuity of 6/24 (Snellen) in each eye without glasses as long as they
eyes correct to 6/12 or better with contact lenses or glasses; or
2 Normal sight in one eye and up to 6/36 in the other corrected to 6/12 or
better with glasses or contact lenses.

It must be considered in assessing candidates who require to wear glasses or

contact lenses that should these be displaced or knocked off, would the subject
be able to defend himself and be able to identify positively the assailant?

238
 Appendix 2

Teaching profession
Visual standards for candidates for the teaching profession.
Impaired hearing and impaired eyesight
Neither a severe hearing loss nor a severe visual impairment is, of itself, a bar to
teaching. It is, however, a relevant factor in considering a candidate’s capacity to
give effective service as a teacher in the maintained system as a whole for a
reasonable period into the future. This includes the ability to participate fully in
school activities, including the supervision of practical work. A severe visual or
hearing impairment is likely to be a particularly important consideration in the
admission of candidates intending to teach physical education or other subjects
such as science and craft, design and technology (CDT) where physical hazards
are present and pupils are particularly mobile.
The final decision whether or not to admit a candidate with impaired hearing or
eyesight rests with the training institution. In considering the capacity of such a
candidate to give effective service as a teacher, an institution might wish to arrange
for the candidate to spend a day or two in a school as part of the selection procedure,
and to obtain advice from the school on whether or not the impairment is likely to
prove a serious obstacle to a successful teaching career. The candidate too might
fine it helpful to obtain advice from the school, particularly if considering
specialising in a highly practical subject, The secretary of state’s criteria for the
approval of initial teacher training courses require that schoolteachers are involved
in the selection of students.
When doubt arises about the capacity of a candidate with impaired hearing to
understand speech satisfactorily, or the visual capacity of a candidate with
impaired eyesight, the medical examiner or adviser may wish to obtain a
specialist’s report. For example, on the basis of an educational specialist’s advice
the medical adviser might explore with the candidate ways in which he or she can
respond competently in an educational setting and overcome any difficulties which
may arise in the teaching situation.
In the case of a candidate with impaired hearing, if ordinary conversational speech
cannot be understood at about 6m, even with an individual hearing aid, the medical
examiner or adviser may wish to obtain the opinion of an otologist who should
include a series of audiograms among the information provided on the candidate.
Wherever possible, due weight should be given to the results of any operative
treatment, eg for ostosclerosis.
In the case of a candidate whose best corrected vision does not attain 6/12 Snellen
in at least one eye, the medical examiner or adviser may wish to obtain from a
consultant ophthalmologist an opinion on the nature and extent of the impairment
and the prognosis. A specialist’s report will be particularly important where a
candidate intends to teach subjects such as physical education, science or CDT, or
where he or she has a colour vision abnormality and intends to specialise in
teaching art.
This guidance does not constitute an authoritative legal interpretation of the
provisions of the Education Acts or other enactments and regulations; that is
exclusively a matter for the courts (DFE circular 13/93).

239
 Ophthalmology

Visual display units

Introduction
The introduction of VDUs into offices and the home is increasing considerably,
and people are spending more time looking at VDU screens.
There is evidence to indicate that prolonged use of VDUs can cause symptoms
such as eye strain, blurred vision and headaches, in addition to postural problems
such as neck and backache as well as other pains.
There is little or no evidence that operators who have worked on VDUs for
many years show any permanent damage to their eyes. The evidence, however,
suggests that the use of VDUs leads to problems of discomfort rather than
problems of health. Many different studies have shown that VDU operators have
reported the following symptoms of eye strain or eye fatigue: loss of visual
sharpness; difficulty in focusing; seeing colour fringes; double vision; grittiness;
dryness; burning; redness; watering; and aching.
The use of a VDU for any length of time may present all the difficulties
associated with close work. It is important to recognise that the screen is likely
to be situated at a distance which differs from a normal working distance and
will certainly be higher than the normal reading position. Care is, therefore,
required in decisions about the type of lenses advised and clearly types of multi-
focal lenses will not be suitable.
Glare from the VDU screens is reported as a common problem and this is
particularly so with older VDUs. Anti glare filters may be of value but advice
about the brightness of the screen should be provided. External lighting is critical
since reflections from the screen can be very disturbing. Advice about the position
of lighting is important.
The Health and Safety Display Screen Regulations give employees a right
to a normal sight test as defined in the Opticians Act 1989 and related
regulations. The sight test, referred to from now on as an eye examination, will
reveal whether there is any defect of sight which may adversely affect the
employee’s ability to carry out work at the VDU. If, in the course of the
examination, a defect of sight is discovered which requires correction for
purposes other than VDU use, but which might also include VDU use, the law
does not require the employer to pay for any spectacles prescribed. The
intention of the regulations is not the free supply of spectacles to all VDU
users, rather that people with special needs related to their use of a VDU as
part of their employment should receive the necessary appliance at no cost to
themselves. The experience of large companies, with work forces ranging
across all age groups, shows that there are likely to be 5–10% of employees
who will require a correction specifically for VDU work.

240
 Appendix 2

Good practice
When an employee takes up her entitlement under the regulations, perhaps as a
result of visual problems when using VDU, it is necessary for the
ophthalmologist or optometrist to carry out a full eye examination to determine
the cause and to give appropriate advice. As part of the examination, the
employee should be asked to describe the work station and its environment.
On completion of the eye examination, the ophthalmologist or optometrist
is required by law to hand over to every patient a prescription or a written
statement saying that no prescription is needed. He is also required by law to
refer for medical advice those patients in whom he has discovered any sign of
abnormality or disease. These obligations remain unchanged whether or not the
eye examination is being carried out under the terms of the Health and Safety
Regulations, and the prescription or written statement is the property of the
patient.
For the purpose of these regulations, a report should also be made to the
employer, with a copy to the employee, which should state clearly whether or
not the employee needs a corrective appliance specifically for her work at the
VDU. The prescription for the corrective appliance for VDU work, if prescribed,
may be included in the report provided that the employee’s consent has been
obtained. The report should also contain a recommendation as to when the
employee should be re-examined under the terms of these regulations. Not only
should advice be given in relation to spectacles but also in relation to aspects of
the work station which might be affecting the employee’s vision at the screen.
This information should be passed to the employer by the optometrist as part of
his report.
Confidentiality of clinical information about the employee must be
maintained at all times and clinical information should only be divulged to an
employer if it is relevant to the employee’s work at the VDU, and only with the
patient’s consent.
The workers shall be provided with special glasses tested for the work
concerned if an ophthalmological or optometric examination shows that
they are required, and that glasses intended for normal purposes cannot be
used.
The following standards are generally recommended for VDU operators:

1 the ability to read N6 at a distance of two-thirds of a metre down to one-

third of a metre;
2 monocular vision or good binocular vision;
3 near phorias to be corrected if over-0.5⌬ vertically 2⌬ esophoria 8⌬ exophoria
(unless well compensated or deep suppression is present);
4 no central (20°) field defects in the dominant eye;
5 near point of convergence—normal; and
6 clear ocular media.

241
 Ophthalmology

If there are any deficiencies in muscle balance, near and intermediate acuity,
accommodation, central visual field, or convergence it is likely that patients using
VDUs will suffer symptoms as it will highlight these weaknesses; continued use
of the VDU will not of course cause them to weaken.
The new regulations will place an obligation on employers to evaluate safety
and health risks to employees, and to take appropriate measures to eliminate
the risks found.
Brussels had planned to delay imposition of minimum safety requirements
for two years after the introduction on 1 January 1993 of the new legislation, but
has now accepted the view of Euro-MPs that the rules should apply immediately
to new work stations brought into service. Employers have two years to bring
existing work stations up to standard.
The legislation lays down that workers will receive adequate training, not
only before beginning work at a VDU, but also whenever the organisation of the
work station is substantially modified. Employers will also be obliged to give
workers information about ‘possible effects on their eyes and physical or mental
problems’ and give workers or their representatives a say in deciding how daily
working time on VDUs should be divided up.

242
 Appendix 2

The above information was supplied by:

The Royal Navy, including WRNS and QARNS—Royal Navy Hospital,
Haslar, Gosport, Hampshire PO12 2AA. 4 March 1995.
The Army, including WRAC and QARANC—Ministry of Defence, Health 4,
Room 113, Lacon House, Theobalds Road, London WC1X 8RY. 29 March
1995.
The Royal Air Force, including PMRAFNS and WRAF—Ministry of Defence
(RAF). 15 March 1994.
Merchant Navy—Chamber of Shipping, Carthusian Court, 12 Carthusian Street,
London EC1M 6EB. 27 April 1995.
Civil Aviation Authority—Medical Department, Aviation House, South Area,
Gatwick Airport, Gatwick, West Sussex RH6 0YR. 22 March 1995.
The Police—(The Chief Officer of the Local Force). May 1995.
Constables of the Metropolitan Police Force—Metropolitan Police Office,
Medical Branch, Wellington House, 67–73 Buckingham Gate, London SW1E
6BE. 28 April 1995.
Prison Officers—Cleland House, Page Street, London SW1P 4LN. 14 March 1995.
Motor Drivers—Drivers’ Medical Unit, DVLA, Longview Road, Morriston,
Swansea, SA99 1TU. 31 March 1995.
Drivers of Metropolitan Licensed Taxi Cabs—Metropolitan Police, Public
Carriage Office, 15 Penton Street, London N1 9PU. 1 May 1995.
British Railways—British Railways Board, The Medical Centre, 1st Floor, West
Colonade, Euston, London NW1 2HS. 2 May 1995.
The Post Office—Post Office Headquarters, 7th Floor, Charles House, 148 Great
Charles Street, Birmingham B3 3HT. 15 March 1994.
Civil Service—Civil Service Commission, 18–20 Hill Street, Edinburgh EH2 5NB.
3 May 1995.
Teaching Profession—Department of Education and Science, Sanctuary
Buildings, Great Smith Street, Westminster, London SW1P 5BT. 20 March
1995.
London Fire and Civil Defence Authority—Queensborough House, 12–18 Albert
Embankment, London SE1 7SD. 20 March 1995.
Health and Safety Executive—Broad Lane, Sheffield S3 7HQ. 24 April 1993.
Department of Health—501 Hannibal House, Elephant and Castle, London. 9
July 1993.

243
 APPENDIX 3

ABBREVIATIONS AND NOTATIONS IN COMMON

USAGE BY OPHTHALMIC MEDICAL
PRACTITIONERS AND OPTOMETRISTS

Note-taking by ophthalmic professionals utilises a common shorthand. For the

lawyer who wishes to unravel entries in patient’s records, the following guide
may be helpful. (The abbreviations and notations in this appendix should be
used in conjunction with the appendix on ocular terminology.)
AC—anterior chamber of the eye
All—allergies
APD—afferent pupillary defect
AT—applanation tonometry (intra-ocular pressure measurement)
C—cornea
CC—current complaint
C/D—ratio of central cup diameter to overall diameter of the optic disc
Cells±flare—inflammatory cells±protein in the aqueous humour (signs of
intra-ocular inflammation)
Conf—confrontation (visual field)
Conj—conjunctiva
Corn—cornea
CWS—cotton wool spots
DD—disc diameters (optic disc), a form of reference for measurements within
the eye as viewed ophthalmoscopically in the living eye
Disc—optic disc
Ext—external examination
F—fundus
Fund—fundus
GH—general health
HPC—history present complaint
HPI—history presenting illness
Hyph—hyphaema
Hypop—hypopyon
KP—keratic precipitates
Mac—macula

245
 Ophthalmology

Meds—current medications
Mot—ocular motility (eye movements)
Nys—nystagmus
OD—oculus dexter (right eye)
ONH—optic nerve head
oRAPD—no relative afferent pupillary defect
OS—oculus sinister (left eye)
OU—oculi uterque (both eyes)
PC—present complaint
Perla—pupils’ equal reaction to light and accommodation
PMH—past medical history
POH—past ocular history
PP—posterior pole of the fundus
Pup—pupil
RAPD—relative afferent pupillary defect
ROS—review of systems
Scl—sclera
Sens—drug sensitivities
S/L—slit-lamp microscope
V— vitreous
VA—visual acuity
VF—visual field
Vit—vitreous

Measurement of vision—notations and abbreviations

BCVA—best corrected visual acuity
BE—both eyes
D—distance vision
DC—dioptre cylinder (unit used to measure astigmatic lens power)
DS—dioptre sphere (unit used to measure spherical lens power)
J—Jaeger type (near vision test, J1=small print, J2 slightly lager, J3, etc)
LE—left eye
N—near vision
N—near test type (N5=news print, N8=large-print books, etc)
NI—no improvement (in visual acuity on refraction)
OD—oculus dexter (right eye)
OS—oculus sinister (left eye)

246
 Appendix 3

OU—oculi uterque (both eyes)

PC—present correction
PH—pinhole (visual acuity)
RE—right eye
Ref—refraction
VA—visual acuity
s—without correction (glasses, contact lenses)
c—with appropriate correction
(Snellen eye test chart, see Chapter 5)
6/5, 6/6, 6/9, 6/12, 6/18, 6/24, 6/36, 6/60, 6/120
VA less than above:
CF 5—counting fingers at 5ft
CF1—counting fingers at 1ft
HM—aware of hand movements
LP proj—aware of light projection
PL/LP—aware of light perception
NPL/NLP—no light perception
WRS— spectacle prescription
+ -convex lenses used to correct hyperopia or far-sighted eyes (magnify)
- - concave lenses used to correct myopic or short-sighted eyes (minify)

Infants’ and illiterate children’s visual acuity test

AMB—amblyopia (lazy eye)
CSM—central, steady and maintained fixation on an object (object size is clue to
visual function)
E—illiterate E-test for visual acuity
F+F—fixate and follow
GCM—good, central maintained fixation
Nys—nystagmus
Pics—illiterate picture test for assessment of infant’s visual acuity

Eye measurements
ACD—anterior chamber depth
AT—applanation tonometry (intra-ocular pressure measurement)
Axl—axial length of the eyeball
Biom—biometry (eyeball-dimension measurements)

247
 Ophthalmology

ECC—endothelial cell count (corneal endothelial-cell layer)

ECCE—Extra-capsular cataract extraction
IOL—intra-ocular lens implant (power or dioptric strength, eg 21 dioptres)
IOP—intra-ocular pressure
Ks—keratometer readings (central 3mm corneal curvature)
NCT—non-contact tonometer (intra-ocular pressure measurement)
Pachym—pachymetry, the measurement of corneal thickness
Topog—corneal topography or corneal mapping or videokeratography of the
cornea

Ocular motility abbreviations and notations

A—A-syndrome, eyes convergent on up-gaze but divergent on down-gaze
AC—accommodation
DVD—dissociated vertical deviation
EOM—extra-ocular muscles
Eso—esophoria (latent convergence)
Exo—exophoria (latent divergence)
Esot—esotropia (convergent squint)
Exot—exotropia (divergent squint)
LIO—left inferior oblique muscle
LIR—left inferior rectus muscle
LLR—left lateral rectus muscle
LMR—left medial rectus muscle
LSO—left superior oblique muscle
LSR—left superior rectus muscle
PD—interpupillary distance
RSR—right superior rectus muscle
RLR—right lateral rectus muscle
RIR—right inferior rectus muscle
RMR—right medial rectus muscle
RSO—right superior oblique muscle
RIO—right inferior oblique muscle

248
 Appendix 3

Visual acuity reference chart—multi-system

Visual acuity—international system equivalents

Refractive surgery abbreviations

-ACIOL—Baikoff or Worst-Fechner high minus IOL anterior chamber located
lens implant for the correction of higher degrees of myopic refractive errors
AK—astigmatic keratotomy or arcuate keratotomy incisions
ALK—lamellar corneal surgery (keratomileusis) or automated lamellar
keratectomy
ALK+PRK—Lasik
Cat/IOL—cataract extraction and lens implantation
CLE+IOL—clear lens extraction with intra-ocular lens implantation
HK—hyperopic holmium keratoplasty
ICL—internal contact lens, a copolymer minus-power intra-ocular lens that is
placed onto the crystalline lens for the correction of higher degrees of myopia
ICL—implantable contact lens
ICR™—intrastromal corneal ring

249
 Ophthalmology

Lasik—laser-assisted intrastromal keratectomy

Park—excimer-laser photorefractive astigmatic keratectomy
PRK—excimer-laser photorefractive keratectomy
RK—radial keratotomy incisions
RK+AK—combined radial keratotomy and astigmatic keratotomy incisions
SAOZ—surface ablation of the optical zone of the cornea
TK—transverse keratotomy incisions

General clinical notes abbreviations

AC/A—convergence/accommodation
Aids—acquired immunodeficiency syndrome
ALT—argon-laser trabeculoplasty
AMPPE—acute posterior multifocal placoid pigment epitheliopathy
APCT—alternating prism cover test
bd—twice daily
BRVO—branch retinal-vein occlusion
CMV—cytomegalo virus
CN—congenital nystagmus
CNS—central nervous system
CPEO—chronic progressive external ophthalmoplegia
CPL—chloramphenicol (broad-spectrum antibiotic eye drops)
CRVO—central retinal-vein occlusion
CSF—cerebrospinal fluid
CT—computerised tomography
DD—disc diameter
DRS—diabetic retinopathy study
ENT—ear, nose and throat
EOG—electro-oculography
ERG—electroretinogram
ESR—erythrocyte sedimentation rate
ETDRS—early treatment diabetic retinopathy study
FFA—fundus fluorescein angiography
(F)T3—(free) tri-iodothyronine
5FU—5-fluorouracil
GCA—giant cell arteritis

250
 Appendix 3

HEMA—hydroxymethylmethacrylate
HIV—human immunodeficiency virus
ICE—iridocorneal endothelial syndrome
INO—internuclear ophthalmoplegia
IOP—intra-ocular pressure
IRMA—intraretinal microvascular anomaly
iv—intravenous
JCA—juvenile chronic arthritis
KC—keratoconjunctivitis
KCS—keratoconjunctivitis sicca
Laser—light amplification by stimulated emission of radiation
LTG—low-tension glaucoma
MG—myasthenia gravis
MRI—magnetic resonance imaging
MS—multiple sclerosis
(N)IDDM—(non-)insulin-dependent diabetes melitus
NSAIDs—non-steroidal anti-inflammatory drugs
NVD—new vessels at the optic disc
NVE—new vessels elsewhere
OA—optic atrophy
od—once daily
OHT—ocular hypertension
OIS—ocular ischaemic syndrome
PAS—peripheral anterior synechiae
PDR—proliferative diabetic retinopathy
PI—peripheral iridotomy, peripheral iridectomy
PMMA—polymethylmethacrylate
POAG—primary open-angle glaucoma
PRK—photorefractive keratectomy
PRP—pan-retinal photocoagulation
PVD—posterior vitreous detachment

251
 GLOSSARY

Ocular terminology including some ophthalmic disorders and

syndromes
Absolute scotoma—total blind spot in that area (scotoma—an area of loss of
sensitivity in the visual field).
Acanthamoeba—acanthamoeba keratitis is a corneal infection associated
predominately with soft contact lens wear, wherein the superficial layers
and the deeper layers of the cornea are involved in the infected process
(Chapter 18).
Accommodation—the process of increasing the refractive power of the crystalline
lens in the eye. It facilitates the ability of an eye to bring near objects (eg
reading matter) into focus. It is a function of the crystalline lens whose natural
elasticity is modulated by traction on its suspensory ligament, the zonule
(see below). Contraction of the ciliary muscle reduces the diameter of the
circle and relaxes the tension in the zonular fibres, causing the natural
elasticity in the crystalline lens to become more spherical and therefore bend
rays of light from near objects into focus on the retina.
A-constant—a lens-implant constant specific to the make and design of an intra-
ocular lens implant that is used in the formula for the power of the
replacement lens implant following removal of the lens or cataract.
Aids—acquired immunodeficiency syndrome. Ocular manifestations include
cytomegalo-virus (CMV) retinopathy a necrotising disorder that obliterates
retinal function, uveitis both anterior and posterior and optic neuropathy.
The affected patients have minimal resistance to infection and opportunistic
infecting agents such as the CMV are consequently destructive.
AK—astigmatic keratotomy or arcuate keratotomy incisions (see Chapter 17 on
refractive surgery).
Amaurosis fugax—monocular blurring of vision or loss of vision developing
within a 30sec period and lasting up to 2h. It is caused by embolic
phenomenon, ie material within small retinal blood vessels blocking the flow
of blood temporarily. Also known as fleeting loss of vision.
Amblyopia—a (usually unilateral but sometimes bilateral) reduction of the
expected best-corrected central-visual acuity in the absence of a visible
organic lesion, ie the inability of an eye to achieve normal visual acuity in
spite of normal structural appearances. It is a consequence of the failure of
visual development which takes place in the early years of life. It may be a
consequence of a poor focussing system (ametropia), ie different between
the two eyes, or the presence of a squint or strabismus. During development,
when the image from the two eyes is different because of focussing errors or

253
 Ophthalmology

because of alignment problems, the brain suppresses the image from one eye,
the squinting eye or the one with the more significant refractive error. In a
psycho-optical and neurological sense the development of vision relies on the
registration of data from each eye in the visual cortex, the occipital cortex of
the brain. Unless the sharp image is transmitted during the developmental
period, data registration fails and the eye becomes permanently defective in
visual acuity terms. To illustrate the process most graphically, if an eye were
to be artificially covered from birth for experimental purposes (theoretically)
or naturally by a congenital cataract, then failure of visual development will
be absolute. That eye would be for ever blind.
Amiodarone—see corneal opacification.
Angioid streaks—and ocular manifestation of pseudo-xanthoma elasticum—a
systemic disorder of elastic tissue associated with vascular disease (arterial
blood vessels contain elastic tissue) and gastric haemorrhage and skin
abnormalities due to shrinkage of elastic tissue in the skin. Other ocular
manifestations include, macular degeneration and sub-retinal haemorrhage
with serious visual consequences. Angioid streaks are seen in a number of
other ocular disorders including Paget’s disease.
Angle of anterior chamber—the angle form between the periphery of the cornea
internally and the periphery of the iris diaphragm, through 360° of the
anterior chamber of the eye, is the location of drainage of the aqueous humour
out of the eye. Within the angle there is a fine sieve-like trabecular meshwork
which filters the aqueous humour back into the blood circulation for
recycling.
Anisocoria—a disparity in size between the pupil in each eye under normal
lighting conditions or any variation thereof.
Anisometropia—a difference in refractive error between the two eyes. This may
be any combination of refractive error, myopia (short sight), hyperopic (far
sight), astigmatism or any combination of refractive errors that produces a
different focus between the two eyes.
Anophthalmos—no eye; usually congenital absence of the eye globe.
Anterior chamber—that space within the eye bounded in front by the posterior
surface of the cornea and behind by the iris diaphragm and the pupil.
Anticholinergic—a class of drugs which opposes the action of cholinergic
compounds. They dilate the pupil and paralyse the ciliary muscle which
effects accommodation (atropine-like drugs).
Applanation tonometer—an instrument which measures intra-ocular pressure
by applanation or touch on the surface of the cornea. The cornea is flexible
and, if the intra-ocular pressure is high, the force required to applanate a
specific area on the surface of the cornea by the contact prism is measurably
higher than if the intra-ocular pressure was low. Intra-ocular pressure is
measured in millimetres of mercury (mmHg). The applanation tonometer is

254
 Glossary

calibrated so that the force required to flatten a tiny area on the cornea is
interpreted in mmHg intra-ocular pressure.
A-scan—a form of ultrasonographic tracing of the echoes from the eye using
ultrasonic signals. A-scan is a time amplitude display that is a one-
dimensional display, where echoes occur as vertical deflections from a base-
line on the screen of an ultrasound instrument.
Astigmatism—the refractive power of the eye is not the same in all meridians.
There are two forms of astigmatism. Regular astigmatism means the eye has
two points of focus and is correctable by a sphero-cylindrical combination
in the refracting lens, eg in spectacle lenses. Conceptually it is best envisaged
that the surface of the cornea, rather than being spherical like a football,
would be shaped more like the side of a barrel or rugby ball. In one meridian
the radius of curvature is steep while at right angles to that meridian the
radius of curvature is flatter. Thus, if a rugby ball is placed in a vertical fashion
as when it is placed for a goal kick, its flat meridian extends from the point
at the top to the point in the ground and its steep meridian is at right angles
to it (see Figure 38, page 176).
B-scan—a form of ultrasound scanning of the eye to provide a two-dimensional
display where echoes occur as dots on the screen of an ultrasound instrument.
It provides a brightness-intensity-modulated display.
Band keratopathy, band degeneration of the cornea—see corneal opacification.
This refers to an anterior plaque on the cornea stretching across the mid-
cornea in the area of the palpebral fissure (between the eyelids). Holes are
often present in the plaque which will contain calcium, commonly giving it
a Swiss-cheese appearance. Usually begins at the 3 and 9 o’clock positions
adjacent the limbus, and extends across the cornea.
Behcet’s disease—a chronic multi-system disorder first described by Hulusi
Behcet in 1937. It involved a clinical triad of ocular involvement—uveitis
with oral and genital ulceration. It is a relapsing, inflammatory process of
unknown cause. Ocular manifestations include an anterior uveitis with a
recurrent heavy cell accumulation in the aqueous humour (hypopyon). This
may lead to cataract, retinal oedema, retinal vasculitis, retinal new-blood-
vessel formation, secondary glaucoma and blindness. The systemic disease
may cause involvement to the extra-ocular muscles through involvement of
the supply in cranial nerves. It is estimated that 70% of patients suffering
from Behcet’s disease have some ocular involvement. Treatment, from the
ocular point of view, includes a combination of topical and systemic
cortico-steroid therapy given in conjunction with other agents including
cyclosporin and azathioprine.
Blepharitis—indicates infection of the margin of the eyelids, usually deep seated
in the roots of the eyelashes.
Blepharoconjunctivitis—inflammation of the ocular surface (eyelid and
conjuctiva).

255
 Ophthalmology

Blepharo-keratoconjunctivitis—inflammation of the ocular surface (eyelid,

conjuctiva and cornea).
Blepharospasm—is characterised by uncontrolled blinking, twitching and
closure of the eyelids bilaterally due to episodic, involuntary contraction of
the orbicularis oculi muscles.
Blindness—legal definition in the UK is as defined on form BD8 (see page 61);
of partial sight. Registration of a person who is blind or partially sighted
opens up the assistance of social services for the visually disabled.
Blind spot—that area of the visual field of an eye corresponding to the projection
into space of the optic nerve head; no vision exists there as it contains no
light receptors. The optic nerve conducts impulses from the light receptors
in the retina to the visual apparatus in the brain. The nerve head is some 15°
to the temporal side of fixation on the horizontal meridian, and therefore
the blind spot in the visual field is 15° from the fixation point.
Blow-out fracture—fracture of the wall or walls of the orbital eye socket in
response to a blunt injury causing compression of the contents of the orbit
with the resultant fracture of the weaker wall, usually the floor of the orbit,
but it can also affect the medial or nasal wall of the orbit. It results in restriction
of eye movements and enophthalmos and hypo-ophthalmos. Other
associations may occur including subcutaneous or conjunctival emphysema
and hypaesthesia (the loss of sensation) in the distribution of the intra-orbital
nerve, ipsilateral cheek and upper lip (see Chapter 2 on trauma).
Branch retinal artery occlusion—in this case a branch of the central retinal artery
is affected with corresponding infarction or death of the area of blood supply
(quadrant of the retina); see central retinal artery occlusion.
Branch retinal vein occlusion—one branch of the central retinal vein is occluded
to cause quadrantic defects; see central retinal vein occlusion.
Bulbar conjunctiva—that portion of the conjunctival mucous membrane lying
on the surface of the eye globe. It is a freely-moveable tissue which forms
the most superficial covering of the eye and is contiguous with the conjuntiva
that lines the back of the eyelids (sub-tarsal conjunctiva).
Bullous keratopathy—corneal oedema with microcysts or bullae giving the
cornea a hazy appearance associated with dramatic visual loss and light
sensitivity. Usually the result of corneal endothelial damage by trauma or
surgical procedures.
Bull’s eye maculopathy—see chloroquine.
Buphthalmos—(‘ox-eye’) distension of the globe in response to elevated intra-
ocular pressure in infancy, also known as congenital glaucoma. The corneo-
scleral wall of the eye is soft and malleable in infancy and is stretched by
raised intra-ocular pressure which occurs in the infantile form of glaucoma.
Canaliculus—the fine tube that connects the lacrimal punctum, the opening of
the tear drainage apparatus at the inner margin of the eyelid, to the tear sac

256
 Glossary

sitting in its pouch at the side of the nose connecting with the naso-lacrimal
duct through to the nasal cavity.
Carotid occlusive disease—is relevant to ophthalmic interests as the carotid
artery is the main arterial route to the eye. Carotid artery occlusive disease
may result in ocular ischaemia or transient ischaemic attacks (TIA) with
obscurations of vision. The disease itself is part of the hardening-of-the-
arteries syndrome, otherwise known as atherosclerosis or arteriosclerosis.
TIAs occur when fragments of debris from the sclerosing wall of the carotid
artery (plaques of cholesterol material) lodge in the end-arterial system of
the retina. While most body tissues have alternative blood supply options in
the event of obstruction to one source, the retina has a single system rendering
it vulnerable to occlusion of its small calibre vessels; see central retinal artery
occlusion.
Cataract—refers to opacification within the crystalline lens and includes localised
change of refractive power, eg due to a nuclear or oil-drop cataract (see section
on cataracts).
Central retinal artery occlusion—a unilateral, painless, acute loss of vision as a
result of embolic, thrombotic or other causes of obstruction to the flow of
blood through the central retinal artery.
Central retinal vein occlusion—a painless, usually unilateral loss of vision
characterised by diffuse superficial retinal haemorrhages (flame shaped) in
all quadrants of the retina with dilated tortuous retinal veins. A condition
seen in association with raised systemic blood pressure (hypertension),
systemic conditions that affect the walls of blood vessels with inflammation
(vasculitis), or due to compression of the central retinal vein by thickening
of hardening of an adjacent central retinal artery because of their anatomical
association.
Central serous chorioretinopathy—condition in which the retinal-pigment
epithelial layer, which lies between the choroid on its outer aspect and the
retinal light receptors on its inner aspect, loses its fluid barrier effect. As a
consequence, fluid leaks underneath the retina causing a localised, serous
detachment of the retina (a micro-blister) with consequential blurring of
vision characterised by localised darkening and micropsia (minification of
the image).
Chalazion—also known as hordeolum. It is a cystic nodule within the eyelid,
the consequence of a blocked meibomian gland orifice. It causes localised
eyelid tenderness and, if infected, may be associated with a swollen regional
lymph gland (pre-auricular node in front of the ear). It is also known as an
internal stye and it requires surgical incision from the internal aspect of the
eyelid to release its contents.
Chemosis—oedema or water logging of the conjunctiva.
Chloroquine—a drug used in the treatment of rheumatoid arthritis and malaria.

257
 Ophthalmology

In toxic doses (by accumulation) it causes macular degeneration (Bull’s eye

maculopathy) and is also deposited in the cornea (see corneal opacification).
Cholinergic—a class of drugs simulating the action of acetylcholine, a natural
compound that effects transmission in the autonomic nervous system. In
the eye it causes pupillary constriction and affects production of the aqueous
humour by the ciliary body and its drainage through the trabecular
meshwork in the angle of the anterior chamber.
Choroid—the vascular supporting layer of the retina. It consists of arteries, a
spongy capillary network, draining veins and cells containing the pigment
melanin which minimises light scatter within the eye to aid visual function.
It is the vascular coat of the eye.
Choroidal rupture—a rupture of the sub-retinal vascular layer, the choroid,
associated with trauma. The clinical signs are a yellow or white crescent-
shaped sub-retinal streak which is generally concentric with the optic nerve
head. Single or multiple lesions may be manifest. In the acute phase the
rupture may be obscured by sub-retinal accumulation of blood, but when
this clears a characteristic crescent-shaped scar with central-whitening
peripheral pigmentation is obvious. It is usually associated with a visual
defect, particularly if the rupture occurs between the optic nerve head and
the macula. There is no specific treatment.
Coats’ disease—a condition in which a congenital retina vascular abnormality
becomes associated with a yellowish mass of exudate.
Coloboma—congenital absence of eye structures may affect the eyelid, the cornea,
the iris diaphragm, the lens, the retina, the choroid and the optic nerve head.
It is a result of developmental failure and fusion processes in the embryonic
eye.
Commotio retinae—bruising of the retina as a result of blunt trauma. Symptoms
depend on location of the defect. If it is central then there is a significant
drop in visual acuity. If it is peripheral it may be asymptomatic but would
correspond to a visual field defect. Clinically-confluent areas of whitening
of the retina are seen in its acute phase, giving way to a mottled appearance
of the retina due to pigment migration and clumping of the retinal-pigment
epithelial layer associated with destruction of neuro-sensory elements, ie
rods and cones, the cause of visual defect. There is no treatment. The
condition will heal spontaneously but invariably with a corresponding
visual defect.
Computerised video-keratography—see corneal topography.
Conjunctivitis—inflammation of the conjunctiva which may be caused by
infection (bacterial, viral or parasitic organisms), allergies (environmental,
cosmetics, foodstuffs, etc) and inflammation secondary to chemicals, physical
agents or ionising and non-ionising radiation (including UV light). If
associated with corneal inflammation the term keratoconjunctivitis is

258
 Glossary

applicable. If associated with inflammation of the eyelid blepharocon-

junctivitis is the applicable term.
Cortical blindness—a severe or complete loss of vision usually due to infarction
(death) of the visual cortex in the occipital lobes of the brain.
Corneal opacification—may be congenital or acquired in origin. As the cornea
is the main refracting surface of the eye its function may be compromised by
opacification due to numerous causes (Chapter 18).
Corneal ulceration—infectious corneal ulceration is a serious problem causing
chronic morbidity or blindness. Effective medical management is important
to reduce the risks of severe visual defects. Fortified preparations of antibiotics
should be used in the initial treatment of severe infectious keratitis; therapy
should include consideration of the results of culture and sensitivity tests of
corneal scrapings. However, it is not unusual for ophthalmologists to treat
ulcers without the benefit of culture using commercial preparations of topical
antibiotics and antibiotic-corticosteroid combinations such as gentamycin,
cefazolin, neomycin-dexamethasone, and sulfacetamide ophthalmic
solutions. Their uncontrolled use violates the principle of effective, broad-
spectrum, antimicrobial coverage. Culture and sensitivity data is a
prerequisite for controlled therapy, and microscopy of corneal scrapes may
reveal fungal infections which would not be expected to respond to any
antibacterial regimen. The majority of infectious ulcers will respond
favourably to outpatient management. Broad-spectrum treatment is usually
appropriate but resistant organisms and fungal contaminants must be
identified.
Cotton-wool spot—refers to localised retinal infarction, death of tissue which
appears as a fluffy white lesion obscuring the retinal vessels in the region. It
is due to swelling of nerve tissue following the localised loss of its blood
supply.
Crowding phenomenon—refers to an eye that can read individual letters better
than a whole line. It is a sign found in amblyopic eyes.
CT-scanning—(computed tomography scanning) uses thin X-ray beams to obtain
tissue density values, from which cross-sectional images of the body are
derived. It is a technique particularly used in the evaluation of the brain,
orbit and eye. It is a safe and rapid, non-invasive technique which has
revolutionised improvements in neuro-ophthalmic diagnosis. Techniques
have progressed to the point where high resolution and contrast facilitates
detailed examination of the intra-cranial and orbital structures and, to some
extent, within the eye. Certainly the optic nerve eye muscles and optic canal
can yield computer-derived reconstruction, an x-ray technique and a primary
procedure for diagnosing orbital disorders.
Cycloplegic—a drug that causes paralysis of the ciliary muscle and therefore
paralyses accommodation, ie making it difficult or impossible to focus on

259
 Ophthalmology

near objects. Cycloplegic drugs are used both for diagnosis and treatment.
They dilate the pupil as well as paralysing the ciliary muscle, enabling the
posterior segment of the eye to be examined. They are also used to relax or
rest the ciliary muscle.
Cystoid macular oedema—an accumulation of fluid within the macular region
of the retina due to abnormal permeability of the retinal capillaries in that
region, associated with many disorders and causing either transient or
permanent blurring of vision.
Dacryo-adenitis—inflammation of the lacrimal gland, the tear-producing gland
of the eye.
Dacryops—cyst of the lacrimal gland.
Dark adaptation—the change in retinal sensitivity to improve the vision of an
eye in dim light.
Delayed hypersensitivity reaction—may result as a response to infection by
Staphylococcus tuberculosis (TB) or other infectious agents elsewhere in the
body (very rare).
Dellen—corneal thinning in the peripheral cornea near to the limbus; ellipsoid
in shape and accompanied by focal conjunctival or corneal elevation
occurring as a response to stasis of the tear film status.
Demyelination—loss of the myelin nerve sheath in the eye and only refers to
the optic nerve retrobulbar portion. Occurs in multiple sclerosis or can be an
isolated event of unknown cause.
Dendritic ulcer—the branching or dendriform ulceration on the cornea in herpes
simplex keratitis.
Dermoid cyst—a congenital, benign tumour usually occurring under the bulbar
conjunctiva on the globe of the eye, usually on its temporal aspect.
Descemet’s membrane—one of the inner posterior layers of the cornea.
Descemetocele—the cyst-like bulging of the inner corneal layers through
deficient outer layers.
Diplopia—double vision.
Disciform—a pathological response to inflammation of the cornea (disciform
keratitis) or a healing response to central retinal/macular degeneration
(disciform macular degeneration).
Distichiasis—abnormal extra row of eyelashes.
Double vision—(diplopia) awareness of two images. The result of either
binocular defect (the eyes are not aligned) or monocular defect (a defect or
opacity in the anterior ocular media that causes image splitting in the optical
pathway).
Drusen—the amorphous collection of colloid material into smaller or larger white

260
 Glossary

spots under the retina which can occur centrally and peripherally. Spots
may become calcified and have a crystalline or refractile appearance. Can
occur naturally (familial) or as a response to the ageing process.
Dry eye syndrome—to be distinguished from eyes feeling dry. The syndrome
requires loss of some or all of the components of tears with corresponding
clinical signs, essentially dryness and roughness of the ocular surface.
Echogram—the returning echo displayed on the screen of an ultrasound
instrument; also known as a scan or sonogram.
Enophthalmos—a measurable depression of the globe within the bony eye socket
or orbit.
Ectropion iridis/ectropion uvea—eversion of the iris at the pupillary rim so that
the pigmented posterior aspect of the iris can be seen.
Electro-diagnostic tests—see electroretinography, electro-oculography and
visually evoked response.
Electro-oculography (EOG)—computer-assisted tomography. A difference in
electrical potential occurs between the cornea and the posterior part of the
eye which is known as the corneo-retinal potential or resting potential.
Though it is difficult to measure the actual resting potential, the problem is
resolved by placing electrodes on the skin on either side of the eye at the
medial and lateral canthi. The patient then makes horizontal eye movements
of a constant size. These rotations of the eye induce a change in the resting
potential which is picked up by the electrodes and revealed as the electro-
oculogram, the changes in potential related to the resting potential if the eye
movements are constant. The EOG is affected by the state of light or dark
adaptation of the eye. With light adaptation there is a progressive rise in
amplitude of the waves whereas with dark adaptation there is a fall. Thus,
the ratio between the maximum amplitude achieved in light adaptation (the
light peak) and the minimum of amplitude achieved in dark adaptation (dark
trough) is determined to evaluate the response. Normal patients have EOG
ratios of 1:60 or greater. It is believed that the EOG largely reflects the
metabolic activity of the retinal-pigment epithelium, and thus the technique
can be used to provide an evaluation of some aspects of the condition of the
retina. The technique can also be used to monitor eye movements such as in
nystagmus, lazy eye conditions (amblyopia) and with abnormal fixation of
objects by the retina (eccentric fixation).
As a test for retinal function the EOG compliments the ERG, and together
they provide some information about a portion of the ocular apparatus. While
pathological processes in the eye that cause alteration in one response also
cause similar responses in the other technique, there are some exceptions.
For example, in juvenile macular disease, Best’s disease or vitelliform macular
dystrophy, the EOG ratio is abnormal, not only at an early stage in those
affected by the disorder but also in those who carry the gene for the disorder.

261
 Ophthalmology

In these patients the ERG is normal. In retinitis pigmentosa in its later stages
the EOG and the ERG tend to parallel each other, but there are variations in
some of the specific forms of the disease.
Electro-retinography—the normal retina creates electrical changes when exposed
to light. The measurement of the changes in the electrical potential in the
retina under the influence of light is known as the electro-retinography and
the output is known as an electro-retinogram. The ERG indicates the
difference in electrical potential between an electrode in a corneal contact
lens and a electrode on the forehead. The ERG is a waveform response with
multiple elements which result from several superimposed events. There
are four principle waves:
A-wave—the initial negative response after a latent period following the
light stimulus; it originates in the photoreceptor cell layer (rods and cones);
B-wave—the quality of deflection emanating from electrical changes in the
bipolar cell layer, ie the layer of the neural or the nerve layer of the retina
that connects the light-sensitive elements, rods and cones to the retinal nerve
fibres; this is followed by
C-wave—a slight positive deflection in the wave; and finally
D-wave—(the effect of removing the light) producing a positive potential.
The value of electroretinography is in the valuation of retinal function in
eyes where the optical media are obscured or where there is no clinical
evidence to support the patient’s contention that the eye cannot see. Recent
developments in the technique of electroretinography allow discreet areas
of the retina, eg the macula, to be targeted to elucidate further their function.
Endophthalmitis—infection within the eye (see Chapter 14).
Enophthalmos—a measurable depression of the globe within the bony eye socket
or orbit.
Enucleation—removal of an eye.
Epicanthus—a fold of skin at the inner aspect of the eyelids which may conceal
part of the white of the eye to create an illusion that a child is suffering from
a convergent squint. It generally disappears with facial growth.
Episcleritis—inflammation of the external surface of the sclera beneath the
conjunctiva.
Esophoria—the same as above, but the non-fixating eye is turned inwards.
Esotropia—ocular misalignment in which the non-fixing eye is turned inwards
(convergent squint).
Excimer-laser photorefractive keratectomy (PRK)—a process to ablate and
therefore change the shape of the central cornea. Used principally to effect
reduction of myopia (short-sight). New generation lasers have the capability
of treating hyperopia and astigmatism. Complications of therapy include
loss of best-corrected acuity, corneal haze and irregularity (see Chapter 17).

262
 Glossary

Excimer-laser photorefractive astigmatic keratectomy (Park)—a process to

ablate and therefore change the shape of the central cornea. Used principally
to effect reduction of myopia (short sight). New generation lasers have the
capabiliiy of treating and astigmatism (see Chapter 17).
Exotropia—ocular misalignment in which the non-fixing eye is turned outwards
(divergent squint).
Exophthalmos—a measurable protrusion of the globe from the bony eye socket
or orbit.
Exophoria—a latent tendency to divergence of the eyes demonstrated when one
eye is covered and binocular fixation of an object is lost.
Fuch’s corneal endothelial dystrophy—see corneal opacification.
Flare—increased protein in the aqueous humour in the anterior chamber
visualised by directing a pin-point beam from the slit-lamp by a microscope
(like a ray of light penetrating a foggy atmosphere).
Giant papillary conjunctivitis (GPC)—a severe allergic response by the
subconjuctival lymphoid tissue to form irritating giant papules or papillae.
Typical of vernal conjunctivitis or Spring catarrh, a malady especially
affecting young people. Secondary effects include corneal abrasions and
ulcerations with later scarring and vascularisation.
Ghost vessels—corneal stromal blood vessels which contain no blood; indicative
of ocular syphilis as well as former syphilitic keratopathy; rarely seen in the
other conditions.
Goldmann tonometer—an applanation tonometer which uses corneal flattening
to measures intra-ocular pressure (IOP). The higher the IOP the more force
is required to flatten a measured portion of the cornea. The force required is
calibrated to provide a read out of the IOP.
Gonioscopy—a method of viewing the anterior chamber angle through a special
contact lens placed on the anaesthetised eye. The contact lens contains a
mirror allowing the observer to evaluate the status of the drainage through
a bio-microscope. This particular examination utilised in cases of glaucoma
provides more accurate diagnostic information, allowing a sub-classification,
eg pigmentary glaucoma and chronic closed-angle glaucoma.
Gram staining—the procedure for identifying bacteria and certain other microbes
according to whether they retain crystal violet dye after washing with alcohol
or other solvents (gram-positive) or lose the stain after washing (gram-
negative).
Granuloma—a firm collection of a specific kind of inflammatory cell.
Graves’ disease—hyperthyroidism, a condition of unknown origin which
involves the thyroid gland and causes the soft tissues surrounding the globe
to swell.

263
 Ophthalmology

Guttata (corneal)—droplet-like excrescence on the posterior surface of

Descemet’s membrane visible on high-powered corneal microscopy and
specular corneal microscopy.
Haemorrhage—accumulation of blood from a broken blood vessel.
Haemostasis—control of bleeding.
Haptics—the elements of an intra-ocular lens implant which secures the optic
within the eye. They usually take the form of C-shaped extrusions from the
optic in a one-piece lens made of Perspex or polymethylmethacrylate
(PMMA), or in a three-piece. The haptics, made either of Perspex or
polypropylene, are fused into the optic during construction of the lens.
Hard retinal exudates—refers to the deposition of fatty (lipid) substances deep
in the retina. The exudates are the result of localised permeability of retinal
capillaries allowing blood products to accumulate in the retina. They are
engulfed by macrophages (white cells) but have difficulty in escaping from
the retinal tissue and thus become deposited. They often have a glistening
appearance.
Hemianopia—the type of visual field defect in which the right or left half of the
field in one eye is missing.
Herpes simplex virus—type I (HSV-1) is a virus that causes recurrent fever
blisters on the lips and mouth and, if introduced into the eye, blepharo-
keratoconjunctivitis; type 2 (HSV-2) is similar to HSV-1 except that it more
commonly infects the genital region and is spread by sexual contact.
Herpes zoster and chickenpox—related viral infections with ocular
manifestations. Herpes zoster ophthalmicus (HZO) may produce ocular
problems from the eyelids back to the optic nerve. Anaesthesia of the cornea,
corneal ulceration and scarring and post-herpetic neuralgia are the most
common complications and persistent ones. Uveitis, cataract formation,
secondary glaucoma and posterior inflammation of choroid and retina are
also known.
Heterochromia—is a difference in colouration between the two irides in a person.
This may be congenital heterochromia or acquired. In the latter form, deep
pigmentation of the iris may occur in chronic inflammatory disease
(heterochromic cyclitis).
HIV—human immunodeficiency virus (see below).
Holmium keratoplasty (HK)—a method of corneal shrinkage to effect hyperopic
shift in the focus of the eye effected by punctate applications of the holmium
laser.
Homonymous hemianopia—the type of visual field defect in which the right or
left half of the field in both eyes is missing.
Hordeolum—see internal hordeolum or stye.

264
 Glossary

Host—plant in which a microbe lives as a parasite, gaining nutrients and the

conditions for survival and reproduction.
Hruby lens—contact lens attached to the slit-lamp microscope to enable
examination of the optic nerve head, posterior retina and vitreous.
HSV-1—see herpes simplex virus type 1.
HSV-2—see herpes simplex virus type 2.
Human immunodeficiency virus (HIV)—a virus that causes a deficiency of the
immune system, making the patient susceptible to a variety of opportunistic
infections of various tissues, including the retina.
Hydrophilic—refers to the property of combining with or attracting water.
Hydrophobic—refers to the property of resisting or repelling water.
Hyperopia (far-sightedness)—a condition in which the focussing system of the
eye, ie its refractive power, is insufficient to bring distant objects into clear
focus. In effect the eyeball is too short. The refractive problem is overcome
by provision of a convex focussing lens on or in front of the eye.
Hypertension—raised pressure. Systemic hypertension is raised blood pressure
with retinal complications of arterial thickening, occlusion and retinal tissue
death or infarction. A swollen optic nerve head is papilloedema, qv a
differential diagnosis in raised intracranial pressure. Ocular hypertension is
raised intra-ocular pressure, ie greater than 21mmHg, the accepted upper
limit for normal eyes. Unlike glaucoma, ocular hypertension has no
damaging effects.
Hyphaema—refers to blood in the anterior chamber. If blood is present in quantity
in the anterior chamber the red cells settle and form a small meniscus with a
horizontal surface at the base of the anterior chamber. It rarely occurs
spontaneously and is usually the result of trauma. If a hyphaema is total,
with the aqueous humour full of blood, this will lead to blood staining of
the cornea with permanent corneal light-transmission damage.
Hypopyon—a layer of white blood cells in the lower recesses of the anterior
chamber of the eye representing the response to inflammation, be it sterile
or infective (pus in the anterior chamber).
Hypotony—abnormally-low, intra-ocular pressure, usually below 6mmHg.
Hypoxia—reduced oxygen saturation in tissues.
Intraretinal microvascular abnormalities (IRMA)—dilated, (telangiectatic)
retinal capillaries that act as shunts between arterioles and venules, and a
particular feature of retinal vascular abnormalities in diabetic retinopathy.
Internal contact lens (ICL)—a copolymer minus-power intra-ocular lens that is
placed onto the crystalline lens for the correction of higher degrees of myopia.
Intrastromal corneal ring (ICR™)—a surgical device for the correction of lower
degrees of myopia

265
 Ophthalmology

IOL constant—a value assigned by the manufacturer of a lens implant which

corresponds to the anticipated position of the lens implant within the eye.
This is dependent on lens size, in particular the angulation between the
supporting haptics, that portion of the intra-ocular lens which fixes the
implant in the eye, and the optic.
Iritis—anterior uveitis, iridocyclitis or (cyclitis) inflammation of the iris ciliary
body or both structures.
Immune reaction—the body’s response to infection; antibodies are manufactured
to neutralise the infecting micro-organism and perhaps prevent recurrence
of the infection.
Incision—a surgical cut produced by a steel or diamond knife in ophthalmic
surgery.
Inclusion—a microcolony of organisms within an infected cell.
Indentation—a form of tonometry in which the amount of corneal indentation
produced by a fixed weight is measured.
Indirect-contact transmission—the form of infection transmission involving an
intermediate, inanimate object.
Indirect ophthalmoscope—an instrument which affords an inverted but wider
view of the fundus than does the direct ophthalmoscope.
Indirect ophthalmoscopy—the use of a focussing lens, usually 20–30 dioptres
in power, located between the patient and the observer and which enables
the observer to have a wide field view of the fundus of the eye. It is
particularly valuable in penetrating cloudy media which make direct
ophthalmoscopy difficult. Excellent for providing an overview of the retina
and examination of the peripheral retina, particularly with scleral
indentations or depression, a technique by which indentation of the
peripheral retina is combined with the indirect ophthalmoscopy to bring
the peripheral retina into view.
Infection—the invasion and multiplication of harmful micro-organisms in
biological tissues. A local bacterial or fungal infection begins in the tissues
immediately, surrounding the micro-organism’s point of entry. If unchecked
the infection may spread to surrounding tissues, thereby becoming diffuse.
Infectious corneal ulceration—see corneal ulceration.
Inferior oblique muscle—the extra-ocular muscle that rotates the eye upward
and away from the nose.
Inferior rectus muscle—the extra-ocular muscle primarily responsible for turning
the eye downward.
Intra-retinal microvascular abnormalities (IRMA)—dilated retinal capillaries
that are abnormal and provide shunts between arterioles and venules (small
arteries and small draining veins) usually found in vascular retinopathies
such as diabetes and hypertension.

266
 Glossary

IOL optic—that portion of an intra-ocular lens implant which transmits light to

the retina.
Iritis—also known as anterior uveitis iridocyclitis or cyclitis; inflammation of
the iris ciliary body or both.
Ischaemic optic neuropathy—a painless, non-progressive problem which causes
unilateral visual loss. In older patients (over 60) it is associated with
inflammation of arteries (giant cell arteritis).
Javal-Schiotz keratometer—an instrument for measuring the central radii of
curvature of the cornea.
Juvenile retinoschisis—an X-linked inherited disorder characterised by splitting
of the retina.
Juvenile rheumatoid arthritis—associated with an ocular triad of corneal band
degeneration, uveitis and cataract formation. A serious ocular condition.
Juvenile xanthogranuloma—age group below 15 years present with a
spontaneous bleed into the anterior chamber (hyphaema), yellow-grey,
poorly-demarcated, iris nodular lesions and associated orange-yellow skin
lesions.
K-reading—the measurement of the curvature of the anterior corneal surface
using a keratometer.
Keratometry—a technique used to measure the curvature of the anterior corneal
surface.
Keratometer—the instrument used to perform keratometry.
Keratitis—(corneal inflammation) due to infection by bacterial, viral or parasitic
organisms. Trauma is by chemical or physical agents or ionising or non-
ionising radiation (including UV light) or combinations thereof.
Keratoconjunctivitis—inflammation of the ocular surface (conjuctiva and
cornea).
Keratic precipitates—cellular aggregates that form on the corneal endothelium
(in aligning of the cornea), usually in a base-down triangular pattern on the
inferior aspect of the cornea.
Keratoconjunctivitis sicca—dry eyes; Sjogren’s syndrome, includes a dryness
of the mouth due to a failure of tear and saliva secretions.
Keratoconus—a degenerative corneal disease in which there is thinning of its
stroma causing it to assume the shape of a cone, seriously affecting vision.
Keratometer—an instrument used to measure corneal curvature.
Keratometry—the measurement of corneal curvature.
Keratomileusis—corneal lamellar surgery, wherein a procedure is performed
which flattens the cornea. Used in the treatment of myopia; see Lasik.
Kinetic perimetry—the type of visual field estimation which uses a moving test

267
 Ophthalmology

object of a predetermined size and brightness; of static perimetry, which

uses a fixed target.
Koeppe lens—a high-plus contact lens used in gonioscopy to examine the angle
structures directly with a hand-held light source and microscope.
Lacrimal apparatus—the structures of the eye which produce tears and the duct
which drains the excess fluid from the front of the eyes into the nose.
Lacrimal gland—the gland which produces the watery component of the middle
layer of the tear film; located under the lateral aspect of the orbital rim.
Lacrimal probe—an instrument for exploring and clearing an obstruction of the
tear duct.
Lacrimal sac—the sac which holds tears after they pass through the canaliculi
connecting the lacrimal punctum to the orifice at the inner aspect of both
upper and lower eyelids on their marginal surface, which empty in turn
into the naso-lacrimal duct leading into the nasal cavity where the tears are
finally absorbed or discharged with nasal secretions.
Lagophthalmos—a condition in which the globe is not completely covered when
the eyelids are closed; may be caused by a 7th cranial nerve (facial-nerve)
paralysis or by an enlarged or protruding eye.
Lamellar corneal surgery—(keratomileusis) or automated lamellar keratectomy
(ALK).
Lasik—Laser-assisted intrastromal keratectomy (ALK+PRK).
Lateral canthus—the outer aspect of the palpebral aperture (the window on the
world between the eyelids).
Lateral geniculate body—that part of the brain where optic nerve fibres connect
(synapse) to the optic radiations and transmit visual impulses to the visual
(occipital) cortex of the brain.
Lateral rectus muscle—the extra-ocular muscle which rotates the eye outward
toward the temple.
Legal blindness—a best-corrected visual acuity of 6/60 or less or a visual field
reduced to 20° or less in the better-seeing eye.
Lens—the crystalline lens is the second focussing lens in the twin-lens system of
the eye. It provides one-third of the total focussing power, the corneal tear
film the other two-thirds. It lies immediately behind the iris.
Lens meter—an instrument for measuring the prescription of eyeglass lenses or
the power of rigid contact lenses.
Leucocoria—(grossly visible white pupil) any intra-ocular pathology which
prevents normal light reflection from the retina and choroid and which
naturally give the pupil a black colour or red (if light is directly reflected as
in the red eye photograph). The main causes of a white pupil are cataract
formation (mature cataract) or in infants a retinoblastoma (malignant tumour
of the retina) or inflammatory mass as in Coat’s disease.

268
 Glossary

Limbal dermoid—a congenital, benign tumour usually located in the infero-

temporal quadrant of the limbus (junction between cornea and sclera).
Lyme disease—a serious systemic disorder consequent upon infection with the
Rickettsia borrelia burgdorferi transmitted by a tick bite. Symptoms include
diplopia, blurred vision, ocular pain, plus headache, malaise and fever. It
may cause inflammation of any or all ocular structures including the optic
nerve and extra-ocular muscles
Lymphangioma—usually a congenital lesion that does not become apparent until
some years after birth. It is a slowly progressive multi-cystic lesion.
Macula—an area of three to four optic disc diameters in size at the centre of the
posterior part of the retina which provides our sharp (central) vision and
colour vision.
Macular hole—a partial or full thickness hole in the central retina,
characteristically seen in middle-aged or elderly women and associated with
loss of central vision, usually to the order of 6/60. It is due to degeneration
of the inner retinal layers and often associated with cystoid maculopathy.
Magnetic resonance imaging (MRI)—proton magnetic resonance imaging with
the utilisation of surface coils produces high-level resolution of body tissues.
It is a modern, non-invasive technique which provides rapid insight into
brain and orbital problems in relation to ophthalmic and neuro-ophthalmic
disorders. As MRI scans do not utilise X-rays or ionising radiation, they are
not harmful to biological tissues or systems. Tumours, fat, blood, nerve tissue
and bone are examples of body materials which have a characteristic MRI
appearance. The scans may also be enhanced by coupling the technique with
contrast media.
Malignant melanoma of the choroid—a primary, pigmented tumour arising in
the choroidal layer at the back of the eye, appearing grey-green or brown.
An expanding mass which causes symptoms according to its location as it
creates a detachment of the retina as the mass expands. There are varying
degrees of malignancy. Tumours may be destroyed by photocoagulation or
radiotherapy. They can sometimes be removed locally, or if they are too large
the eye is removed.
Megalocornea—a larger than normal but functional cornea (above 13mm
diameter).
Meibomian glands—exist in the tarsal plate of the eyelids and produce the oily
component of the tear secretions.
Meibomianitis—inflammation of the meibomian glands which exist in the tarsal
plate of the eyelids.
Meridians, horizontal and vertical—the radial meridians which divide the
circular visual field into to quarters.
Metastases—malignant tumours that have spread to other parts of the body.

269
 Ophthalmology

Thus a malignant melanoma of the choroid in the eye may spread

(metastasise) to the liver. A cancer of the breast may metastasise to the choroid
in the eye.
Microcornea—a smaller than normal but functional cornea (below 9mm
diameter).
Microphthalmos—congenitally-small, disorganised eye.
Miosis—constriction of the pupil.
Mires—the perpendicular crossed lines in a lens meter.
Mucinous—sticky.
Mucopurulent discharge—a thick fluid containing mucous and pus,
symptomatic of a bacterial infection.
Multifocal lens—a lens with more than two planes of focus (see bifocal and
trifocal lens).
Mydriasis—dilatation of the pupil.
Mydriatic—a drug which dilates the pupil.
Myopia—short sight; a refractive condition of the eye wherein the image is
focussed somewhere in front of the retina dependent upon the degree of
myopia. It occurs because of a mismatch between the focussing power of
the cornea/lens combination and the length of the eyeball.
Naevi—(singular: naevus) literally, freckles; common tumours appearing on the
bulbar conjunctiva and appearing as yellowish-pink or brown areas on the
conjunctiva or skin.
Nanophthalmos—a congenitally-small but otherwise normal eye.
Nasal step—one type of visual defect which, when plotted, appears as a steplike
loss of vision at the outer limit of the nasal field.
Nasolacrimal duct—the duct through which tears pass from the lacrimal sac
into the nasal cavity.
Near add—the additional convex lens power added to a distance spectacle
prescription to allow reading matter to be focussed within arms length.
Near visual acuity—the ability to see clearly at a normal reading distance.
Negative lens—a concave lens, ie of negative power (makes images smaller).
Neoplasm—a new growth of different or abnormal tissue, such as a tumour
which may be benign or malignant, or a wart.
Neovascularisation—growth of new blood vessels of abnormal architecture in
abnormal locations, usually with adverse effects on local anatomy and
physiology.
Neurofibromatosis (Von Recklinghausen’s disease)—benign space-occupying
tumours arising out of neural tissue characterised by multiple lesions on the
skin, in the brain, in the eye and optic nerve. May take a plexiform

270
 Glossary

configuration resulting in gross distortion of the face and/or eyelids,

compromising ocular function and possible requiring drastic surgery.
Inherited in an autosomal dominant pattern with incomplete penetration.
Neutralisation—(see lensometry) the measurement of the refractive power of a
spectacle or other lens by matching it with a lens of opposite power, ie a
convex and concave lens combination. It allows assessment of spectacle-
lens power without a lens meter,
Neutralisation point—the lens power that is the approximate correction for a
refractive error.
Normal flora—micro-organisms that colonise part of a host’s tissue without
producing disease.
Nystagmus—repetitive oscillations of the eye either horizontally, vertically or
in a rotary direction. There are two forms. Jerky nystagmus is where the eye
slowly drifts in one direction with an abrupt return to its original position,
each move being known as the slow or fast phase (a problem with a
continuous cycle). Pendular forms of nystagmus cause a pendulum-like drift
of the eyes from one side to another with a smooth movement, in contrast to
the jerky nystagmus.
Nystagmus may be congenital in origin when it is associated with albinism
(no pigment), aniridia (bilateral absence of the iris from birth) and other
causes. Acquired nystagmus may be optical, ie due to loss of vision (a
searching movement) associated with dense cataract, trauma, retinal
dystrophies or being toxic in origin due to a variety of drugs and chemicals,
or due to disorders of the central nervous system, whether by haemorrhage,
vessel occlusion (stroke), space-occupying lesions, injuries or trauma and
multiple sclerosis.
Optokinetic nystagmus describes the physiological reaction of the eyes to
passing objects. The eyes follow the object to the end point of gaze before
flicking back to the usual position, following again. It is easily seen if one’s
eyes are observed when watching a passing car or train.
Objective refractometry—(see retinoscopy) the assessment of the refractive
power of an eye by judging images from the eye seen through a focussing
lens and an instrument, the retinoscope.
Occlusion—blockage of a vessel, eg artery, vein, capillary or anatomical tube
such as the tear drainage system.
Ocularist—an ophthalmic paramedical professional who measures and fits
patients with an artificial eye (prosthesis) to replace the absent eye or cover
an unsightly one.
Ocular media—the transparent components of the eye’s optical system, ie cornea,
aqueous humour, crystalline lens and vitreous humour.

271
 Ophthalmology

Ocular histoplasmosis syndrome—a condition characterised by painless loss

or distortion of vision due to lesions in the retina, classically yellow-white,
pushed-out, round spots with a sub-retinal neovascular membrane in the
macular region and peripapillary atrophy or scarring (the areas next to the
optic nerve head), thought to be due to infection with the histoplasma
organism.
Ocular surface—(corneal and conjunctival) especially as it interfaces with the
external environment, is commonly subject to inflammation, infection,
lubrication disorders, degeneration and trauma as well as rarer pathological
incidents such as tumours. Pathological events may compromise the corneal
surface and/or the conjunctival surface. Ocular lubrication disorders affect
all surfaces, these being variably due to failures of the secretions of the
lacrimal gland (watery component of tears), meibomian gland (oily
component of tears) and mucous-secreting-cells gland (mucous component
of tears). Corneal pathology includes pain, blurring of vision, watering of
the eye (epiphora) and often severe and redness of the eye. Conjunctival
pathology includes redness of the eye, epiphora, sticky discharge (mucous
and pus—muco-purulent discharge) and variable discomfort—irritation or
pain. There is chronic irritability of the eyelid margins.
Oculist—an obsolete term for an ophthalmologist or ophthalmic surgeon.
Optical zone—the true centre of the cornea from which keratometer readings
for intra-ocular lens power calculations are obtained.
Osmotic agents—eg mannitol, reduce IOP by the osmotic suction of fluid out of
the eye.
Oscillopsia—a symptom that causes the patient to have the perception that the
environment is moving back and forth.
Ora serrata—the most peripheral portion of the retina.
Optic neuritis—inflammation of the optic nerve, also includes demyelination
(loss of whiter nerve sheath of myelin) seen in multiple sclerosis.
Ophthalmoplegia—paralysis of the ocular muscles (external ophthalmoplegia—
if total all eye movements are paralysed).
Pachymetry—the measurement of corneal thickness. This can be performed by
optical methods or by use of ultrasound systems. It is used clinically in
refractive surgery of the cornea and to monitor the corneal response to injury
and/or surgery.
Palpebral conjunctiva—the conjunctiva lining the underside of the eyelids.
Palbebral fissure—the aperture between the upper and lower eyelids.
Palsy—a weakness or incomplete paralysis of a muscle or muscles.
Papillitis—inflammatory swelling of the optic-nerve feed.
Papilloma—benign growths which occur on the eyelid or the conjunctiva, either
of viral origin or non-viral, and which may be pre-cancerous.

272
 Glossary

Papilloedema—a swelling of the optic nerve head produced by an increase in

the pressure within the skull (raised intracranial pressure). The specific term
papilloedema is usually reserved for that swelling caused by raised
intracranial pressure. The optic nerve sheath contains cerebrospinal fluid. If
intracranial pressure is raised, this is transmitted to the optic nerve sheath
causing nerve compression and venous congestion as drainage of circulating
blood is impaired. The fluid exudation (oedema) haemorrhage and nerve
swelling contribute to the overall elevation of the nerve head. It is a vital
clinical sign.
Paracentral scotoma—a relatively-blind area in the visual field near to the fixation
point, either above, below, to the nasal side or the temporal side.
Paraxial—parallel light rays from a distance source which enter the eye (the
cornea) at any point other than the centre.
Pathogenic—disease-causing pathogens, micro-organisms which disrupt normal
light processes to cause disease.
Pathological—abnormal.
PD (pupillary or inter-pupillary distance)—distance from the centre of the pupil
in one eye to the centre of the pupil in the fellow eye.
Perimetry—is the measurement of the expanse and sensitivity of peripheral
vision (peripheral visual field) in order to provide a record of normality or
defects.
Peripheral iridectomy—removal of a portion of the peripheral iris used to
provide an alternative pathway for aqueous humour to course from the
posterior chamber between iris and crystalline lens and the anterior chamber
between iris and cornea.
Peripapillary—surrounding the optic disc.
Peripheral anterior synechia (PAS)—adhesions between the peripheral iris and
the peripheral cornea which may obstruct the drainage angle of the anterior
chamber.
Peripheral vision—the visual perception of objects and space which surround
the direct line of sight.
Pharmacology—a study of the use of medicines and actions of drugs.
Phenathiazines—drugs used in the treatment of psychiatric disorders which
have potential ocular effects including dryness of the eyes and pupillary
dilatation due to the mild anticholinergic effect. Other potential, toxic effects
include blurring of vision, poor night vision or brownish discolouration of
vision associated with: thioridazine (melleril) with abnormal pigmentation
in the central retina; and thorazine (chlorpromazine) with blurring of vision
and abnormal pigmentation of the eyelids, cornea and conjunctiva, with a
pigmentary retinopathy.

273
 Ophthalmology

Phoria—the tendency of eyes to deviate. It is prevented under normal visual

circumstances by the ability of the brain to fuse the two images. However,
on covering one eye (cover test) one eye will deviate either centrally
(esophoria) or temporally (exophoria), or move upwards (hyperphoria) or
downward (hypophoria).
Phoropter—an instrument for determining a corrective lens prescription. It is a
device which stores a range of trial lenses that are dialled into position.
Photochromic—refers to spectacle lenses made of crown glass that is specially
manufactured with pigments sensitive to UV light, so that the lens darkens
in sunlight and the process reverses when out of sunlight.
Photocoagulation—the surgical welding with the laser or high intensity light
beams of tissue within the eye.
Photophobia—light sensitivity.
Photopsia—sensation of instantaneous flashes of light often occurring in the
presence of a retinal traction or vitreous detachment.
Photoreceptor—a light-sensitive nerve ending found in the retina and of which
there are two types: the rods, which are sensitive to monochromatic light;
and the cones, which are sensitive to colour, in particular red, blue and green.
Photorefractive keratectomy (PRK)—refractive surgery that employs laser light
to re-shape the cornea.
Physiological blind spot—refers to the blank area or scotoma in the normal
visual field which corresponds to the position of the optic disc or nerve head.
Piezo-electric element—is a component of an ultrasound probe which converts
electrical energy to mechanical, and vice versa.
Pigment epithelium—(retinal-pigment epithelium) the outer layer of the retina
which separates the photoreceptors from the vascular tissue of the choroid.
It is a layer that is responsible for the maintenance, repair and rejuvenation
of the photoreceptor cells.
Pinguecula—is a benign, small, yellowish-white mass of degenerate tissue lying
beneath the bulbar conjunctiva in the palpebral aperture, either nasal or
temporal to the limbus.
Pinhole occluder—a hand-held device which completely covers one eye and
allows the other to visualise a visual acuity chart through a pinhole or tiny
central opening. As the pinhole effect virtually eliminates refractive errors,
the test is a quick means of determining whether or not the visual disability
of an eye is due to a refractive error or a more profound medical cause.
Pneumo-retinopexy—a surgical procedure for correcting a retinal detachment
by injecting gas into the eye, which has the effect of pushing the retina back
into place where it is secured against the underlying choroid with other
adjuncts used in retinal detachment surgery, eg cryotherapy.

274
 Glossary

Polycoria—presence of many openings in the iris.

Polymethylmethacrylate (PMMA)—a substance otherwise known as Perspex,
or Plexiglas in the US, in clinical quality, ie very pure forms. It is used to
manufacture intra-ocular lenses.
Posterior synechia—refers to adhesions occurring between the iris at the pupil
and the anterior lens capsule.
Posterior vitreous detachment (PVD)—separation of the posterior hyaloid
membrane and normal anatomical attachments of the vitreous gel,
particularly at the optic nerve head. Usually age related or traumatic in origin
and associated with symptoms of floating spots in front of the eyes and
occasional flashes of light.
Potential acuity meter (PAM)—is a device which determines potential visual
acuity in the eye despite the presence of opacities in the ocular media. It
may be used to predict the outcome of cataract surgery.
Presbyopia—the progressive loss of the ability to accommodate, due to the
natural process of ageing in the lens, which becomes thicker and thus elastic
with advancing age. Its typical onset is over 40 years of age. Treatment is to
provide magnifying lenses to supplement the failing power of the crystalline
lens in the eye.
Primary angle-closure glaucoma—a form of glaucoma in which the natural age-
related increase in the size of the crystalline lens blocks the flow of aqueous
humour through the pupil. This causes a gradual forward bowing of the iris
(iris bombée) until its outer edge blocks the aqueous outflow channels and
the anterior-chamber angle to cause an acute rise in intra-ocular pressure
(see Chapter 8).
Primary open-angle glaucoma—a form of glaucoma in which the pressure inside
the eye is elevated because of increased resistance to the drainage of aqueous
humour within the outflow channels in the angle of the anterior chamber.
Principle axis—the pathway of a light ray that strikes the centre of a lens of any
shape and passes undeviated through the lens material.
Principle meridian—refers to the maximum and minimum meridia of corneal
curvature which are denoted in the prescription for astigmatism.
Prism—a triangular refractive object, either glass of plastic, with flat sides and
apex under the base.
Prismatic effect—an optical distortion in which images are displaced from their
normal position. It occurs if the distance between optical centres fails to
correspond to the interpupillary distance. It is more noticeable when the
spectacle correction reaches higher levels.
Prism cover test—for measuring the extent of the deviation of an eye from parallel
alignment with the fellow eye; used in ocular motility evaluation.

275
 Ophthalmology

Prism dioptre—a unit of measure of the refractive power of a prism, used in

spectacle corrections which incorporate a prismatic element. Also referred
to in ocular motility reports to denote the deviation of an eye from the parallel.
Prognosis—the prediction of the outcome of a medical condition.
Proptosis—a condition characterised by protrusion of an eyeball caused by an
increase in the volume of the orbital contents. When both eyes are involved
it is known as exophthalmos, seen typically in dysthyroid conditions.
Pseudo-hypopyon—a layered collection of non-inflammatory cells in the anterior
chamber occurring when there is an intra-ocular tumour such as a
retinoblastoma.
Pseudo-isochromatic colour plates—used to test colour vision. They consist of
displayed patterns of colours and grey dots; also known as Ishihara colour
plates.
Pseudophakia—the use of an intra-ocular lens to correct the vision in an aphakic
eye, ie an eye in which the crystalline or natural lens has been removed.
Pseudo-xanthoma elasticum—a systemic disorder of elastic tissue associated
with vascular disease (arterial blood vessels contain elastic tissue), gastric
haemorrhage and skin abnormalities due to shrinkage of elastic tissue in the
skin. The ocular manifestations include angioid streaks, macular
degeneration and sub-retinal haemorrhage with serious visual consequences.
Pterygium—a wedge-shaped growth on the bulbar conjunctiva which shows
progressive growth onto the surface of the cornea and penetrates into the
anterior substance.
Ptosis (blepharoptosis)—the drooping of, or an inability to raise, the upper eyelid.
Punctum—(plural: puncta) refers to the tiny opening on the eyelid margins at
the inner aspect near the nose, through which tears pass into the tear-drainage
apparatus leading from the punctum into the nasal cavity. There are four
puncta, two on each upper lid and two on each lower lid.
Pupil—the opening of the centre of the iris diaphragm which enlarges to admit
more light or constricts to reduce the amount of light entering the eye.
Pupillary block—a term used to describe the condition within the eye when
aqueous humour is prevented from flowing from the posterior chamber
(behind the iris) into the anterior chamber (between the iris and cornea).
Quadrant—one of four quarters of the visual field: upper left, upper right, lower
left, and lower right.
Quadrantanopia—loss of a quadrant of visual field in matching aspects of the
visual field in each eye, eg by temporal quadrantanopia, which would
indicate the prospect of a lesion affecting the optic chiasma.
Quiet eye—a non-inflamed eye, ie one with no inflammatory activity. A term
used to describe a post-operative eye or a post-inflamed eye.

276
 Glossary

Radial keratotomy—a form of incisional refractive surgery in which radial

incisions are made deep into the cornea so as to flatten its central optical
zone in the treatment of myopia.
Radiation retinopathy—the response of the retina, in particular its circulation
to trauma by physical radiation such as X-rays. It is characterised by
inflammation of retinal blood vessels, in particular causing leakage of blood
contents into the retina with consequential effects on visual processes.
Refraction—in eye care, is the process of measuring a patient’s refractive error
and thereby determining the optical correction required.
Refractive error—a deficiency in the eye’s optical system causing a failure to
bring distant images into focus on the central retina (fovea).
Refractive index—the ratio of the speed of light in a vacuum to its speed through
a specific substance.
Refractive surgery—see Chapter 17.
Regression formula—a formula which produces the desired power of an intra-
ocular lens implant to replace the natural lens following cataract surgery.
This formula, which is empirical, is based on the retrospective analysis of
actual, post-operative, refractive data.
Regular astigmatism—that form of astigmatism (two principle planes of focus)
which can be corrected by a sphero-cylindrical spectacle lens.
Relative scotoma—visual imaging is diminished in that area (scotoma—an area
of loss of sensitivity in the visual field).
Retina—the light-sensitive layer at the back of the eye composed of the light-
sensitive nerve endings (rods and cones) and their supporting nerve and
connective tissues (see Chapter 3).
Retinal detachment—a detachment of the retina occurring as a result of a retinal
break, either a hole, a tear or a disinsertion of the retina (see Chapter 10).
Retinitis pigmentosa—hereditary, progressive, retinal degeneration which may
lead to severe visual disability or blindness. It is characterised by typical
changes in the retina, wherein there is pigment migration in the formation
of spider-shaped clusters of pigment. There is often coincident attenuation
or thinning of retinal blood vessels and serious visual field defects.
Night blindness is an early characteristic feature as the neurosensory
receptors, the rods, often deteriorate first. There may be associated cataract
formation.
Retinoschisis—an X-linked inherited disorder characterised by splitting of the
retina which also occurs in adult forms. It may be asymptomatic or cause
visual loss by progression. It may be difficult to arrest, but retinal detachment-
type surgical procedures are used.
Retinoscopy—a technique in which the reflex from a streak of light shining

277
 Ophthalmology

through the eye onto the retina is used to estimate the refractive error of the
eye in conjunction with convex or concave lenses.
Retinitis—inflammation of the retina; relative afferent pupillary defect. A
decreased pupillary constriction to light in one eye as compared to the other
eye using the swinging/flash light test (see Chapter 6).
Retinal vascular disorders—any syndrome which involves pathological changes
in the retinal circulation. Used as a general term to cover disorders including
retinal artery and vein occlusive disorders, diabetic and hypertensive
retinopathies, etc.
Retrobulbar—inflammation of the optic nerve behind the eye, eg retrobulbar
neuritis.
Rosacea keratitis—acne rosacea is a skin disorder which may spread to the cornea
to cause inflammation and destructive changes. It has a tendency to become
bilateral and to progress in intermittent attacks, with intermissions lasting
several years. Each attack involves much pain and disability and every attack
brings the patient nearer to visual incapacity (see Chapter 18).
Rubeosis iridis—new vessel formation on the iris diaphragm, a sign of ocular
ischaemia or deprivation of blood supply to the anterior or posterior
segments of the eye, especially retinal ischaemia. The condition is usually
accompanied by secondary glaucoma.
Schiotz tonometer—an indentation contact tonometer which uses weights to
determine intra-ocular pressure. It was used in the detection of glaucoma
before more sophisticated devices such as applanation tonometer and non-
contact tonometers were devised.
Schirmer test—uses strips of filter paper to measure a patient’s tear output. It is
used in the diagnosis of dry eye conditions. The irritating effect of the filter
paper stimulates the production of tears, and the soaking of the strip in a
five minute period is measured to give an objective evaluation of the state of
the watering component of tear production.
Schlemm’s canal—a structure that drains the aqueous humour from the anterior
chamber after it has flowed through the trabecular meshwork. The sclera is
the white tissue surrounding the cornea and forming the wall of the eye to
protect the intra-ocular contents.
Sclera—wall of the eye consisting of white collagenous tissue.
Scleral buckle—a surgical procedure for correcting retinal detachment, which
involves placing a block of silicone or other material on the wall of the eye
to indent the structure and bring the torn element of the retina into apposition
with the underlying choroid, which is usually treated by freezing or
cryotherapy, to provide a sticky medium that will cause a healing scar.
Scleritis—inflammation of the sclera.
Scotoma—an area within the visual field where vision is reduced (relative
scotoma or absent absolute scotoma).

278
 Glossary

Secondary glaucoma—glaucoma occurring secondary to another primary

disease; see Chapter 12.
Sjogren’s syndrome—includes a dryness of the mouth due to a failure of tear
and saliva secretions.
Slit-lamp microscope—the main instrument used for close examination of all
aspects of the eye. It has a beam whose intensity can be varied, and an image
which can be conformed into a slit to help the observer to appreciate the
relationship between objects within the eye and to detect diseased processes.
It is also called the slit-lamp biomicroscope.
Snellen acuity chart—a measurement of visual acuity by testing the ability to
read characters at a standard distance on a target known as the Snellen chart,
which consists of Snellen opto-types, specially formed letters of the alphabet
arranged in rows of decreasing letter size (see Chapter 6).
Specular microscope—a method of microscopic examination and/or imaging
by photography of the endothelial cells on the posterior aspect of the cornea.
The system uses high magnification, allowing the form and number of cells
in a specific area to be annotated.
Spirochaetes—spiral or corkscrew-shaped bacteria, of which the best known is
the one which causes syphilis.
Squint—see strabismus.
Staphyloma—out-pouching of the wall of the eye where it involves the sclera,
retina and uvea. It causes elongation of the eyeball and myopic consequences,
ie the eye becomes very short-sighted.
Static perimetry—a test of the visual field using static targets (pin-point lights
switched on and off) to detect active or missing areas in the visual field.
Stereopsis—three-dimensional vision, a function of binocular vision.
Steroid—anti-inflammatory drugs based on the natural adrenocortical hormones.
Strabismus—misalignment of the eyes, also known as squint.
Strabismic amblyopia—failure of visual development due to misalignment of the
eyes in infancy, causing suppression of the image of the strabismic eye to avoid
double vision and thereby preventing the cementing of the communication
between eye and brain that must occur in the early years of life.
Stroma (corneal)—the substance of the cornea bounded at the back by the
endothelium and at the front by epithelium (see Chapter 4).
Sub-conjunctival haemorrhage—bleeding under the conjunctiva. It may look
bad but is rarely other than of cosmetic significance.
Superior oblique muscle—one of the six external ocular muscles. Innervated
by the 4th cranial nerve, it causes the eye to rotate and look down.
Suprathreshold static perimetry—a type of static perimetry which utilises a
light or target of a specific size, so that the patient will visualise it at a
particular site in the visual field.
Stye or external hordoleum—infection in the root of eyelashes.

279
 Ophthalmology

Synapse—joining area between nerve fibres.

Syndrome—a collection of symptoms and signs that fit a disease pattern.
Syneresis—exudation of a liquid from a gel. In ophthalmology this refers to the
age-related or disease-related breakdown of the gel of the vitreous humour.
Tangent screen test—a type of kinetic perimetry (moving target) used for
qualifying visual field defects within a 15° radius of fixation.
Tarsal plate (tarsus)—the semi-rigid, connective-tissue, cresentic plate which
gives the eyelids their relative rigidity.
Tarsorrhaphy—joining together, either partially or completely, of the upper and
lower eyelids by a surgical process.
Threshold static perimetry—that type of static perimetry in which the threshold
stimulus is at a level of brightness which allows the patient to detect it 50%
of the time.
Thyroid eye disease—over-action of the thyroid gland (thyrotoxicosis), treated
by thyroidectomy, which can be performed medically using radioactive
iodine or surgically. The activity of the thyroid gland is controlled by the
thyroid stimulating hormone (TSH) secreted by the pituitary gland using a
feedback system. As the concentration of thyroxine (the hormone of the
thyroid gland) in the blood stream falls, the pituitary gland is stimulated to
produce more TSH. With the reaction of the thyroid gland limited by its
reduced capacity, more TSH is produced. A side effect of excess TSH is to
promote fluid and cellular aggregation in the eye socket or orbit. This increase
in orbital material pushes the eye forwards—proptosis (one eye) or
exophthalmos (both eyes)—a characteristic sign of dysthyroid disease
(abnormal thyroid gland activity). The extracellular content in orbital tissues
(inflammatory cells) may infiltrate the extra-ocular muscles to cause
weakness and abnormal eye movements with consequential diplopia (double
vision). Treatment is to apply anti-inflammatory drugs such as cortisone by
mouth, although surgical enlargement of the orbit by removing some or all
of its bony walls may be necessary to prevent severe protrusion of the eyes,
which causes exposure problems. Strabismic complications are treated
optically with prismatic corrections in the spectacles or strabismic surgery.
Severe cases may require occlusion of one eye to overcome intractable
diplopia.
Titmus stereopsis test—a test of the quality of stereoscopic vision which
differentiates between fine and course depth perception.
Tonometer—a device used to measure intra-ocular pressure.
Tonometry—measurement of intra-ocular pressure.
Topical application of drugs—eye drops (guttae).
Toric cornea—one in which the surface is not uniform (shaped like the side of a
barrel).

280
 Glossary

Toxin—a poison secreted by an organism, usually with reference to bacterial

enzymes.
Trabecular meshwork—the meshwork system in the angle of the anterior
chamber between corneal periphery and the root of the iris diaphragm,
through which aqueous humour drains out of the eye (see Chapter 4 on
structure).
Trabeculectomy—one of the surgical techniques used to improve aqueous
outflow in glaucoma patients by creating a valve in the scleral wall of the
eye.
Transposition—a term used to describe movement of an extra-ocular muscle, in
whole or in part, to the site of an inactive or paralysed extra-ocular muscle
to effect eye movement in a direction of gaze missing through muscle
paralysis.
Triage—the screening of patients (in person or by telephone) to ensure that
patients with the most serious complaints receive prompt attention.
Trichiasis—in-growing eyelashes which are treated by epilation (pulling them
out with forceps or by electrolysis, to effect a permanent loss of the lash and
producing a follicle in the margin of the eyelid).
Tropia—permanent misalignment of the eyes (strabismus or squint).
UGH syndrome—(uveitis-glaucoma-hyphaema syndrome) results from
inflammation initiated by early designs of the intraocular lens implants
utilised in cataract surgery. Poor design and poor finish of the lens implant
caused uveal tissue irritation with resultant inflammation, bleeding
(hyphaema) and secondary glaucoma.
Ultrasonography—see page 53.
Uveal tract—the iris diaphragm, ciliary body and choroid.
Uveitis—inflammation of the uveal tract (iris diaphragm, ciliary body and
choroid), classified by location and cause: anterior uveitis (of which iritis
comprises the majority of unknown aetiology) which is related to arthritis;
posterior uveitis infections (choroiditis) due to post-operation toxoplasmosis,
toxocariasis or sarcoidosis; and generalised uveitis or pan-uveitis (anterior
and posterior) due to all of the above and including sympathetic ophthalmitis
(see Chapter 15).
Varicella zoster virus (VZV)—see herpes zoster or chickenpox.
Vertex distance—from the back surface of a spectacle lens to the front surface of
the cornea (the further away from the cornea a lens is placed, the greater its
effective power (magnification).
Virtual image—the image formed by a concave lens when the paraxial (see
above) rays from a distant source are refracted and diverged.
Visual cortex—that area of the brain in the occipital region responsible for the

281
 Ophthalmology

initial conscious registration of visual information. It is the destination of

the nerve-end pulses from the retina.
Vitreous opacification—light-blocking opacities in the vitreous humour, usually
blood or blood derivatives.
Visco-elastic agents—adjuncts to intra-ocular surgery, especially in the anterior
segment; major application in cataract surgery. The viscosity of the agent, of
which the one used most is sodium hyaluronate, is very high and maintains
the space in the narrow confines of the anterior chamber of the eye to offer
the vulnerable structures protection and the surgeon time and space to
perform manoeuvres. They are one of the major ophthalmic innovations of
the past 15 years.
Visual acuity—a measure of the ability of an eye and the visual system to
discriminate detail. Measured usually by a Snellen acuity chart and a near
vision chart (see Chapter 5).
Visual cortex—that part of the brain concerned with vision. Connected to the
eyes by the visual pathways, the visual cortex is located in the occipital region
at the back of the brain. Each visual cortex (left and right) receives images
from each eye. The temporal field of the right eye and the nasal filed of the
left eye are connected to the left hemisphere’s visual cortex, and vice
versa.
Visual evoked response (VER) or visual evoked potential (VEP)—when a flash
of light reaches the retina it causes the omission of a volley of nerve impulses
which are transmitted along the neural visual pathways to the posterior
aspect of the brain, where the visual cortex resides in the occipital region.
The response of the brain to the light stimulus can be recognised by placing
electrodes over that portion of the brain and using computer programmes
to eliminate other brain activity. The technique is of great value in providing
objective evidence of the function of the optic pathways. By stimulating each
eye separately, nerve lesions can be recognised by the absence of a response
on one side or the other, identifying the affected nerve. Similarly, partial
lesions of the optic nerve will result in delay of conduction and a reduction
in the amplitude of the response. It is therefore an important tool in the
objective investigation of the visual system in non-responsive patients such
as infants and attempted malingerers.
Visual field—the representation of the retinal ability to see space, usually
approximately 150° wide and 120° degrees high (see Chapter 5).
Visual pathway—comprises the link between the eyes and the brain: optic nerves,
chiasma, optic tracts, optic radiations leading into the visual cortex (see
Chapter 3).
Vitreous—the clear gel that lies behind the crystalline lens and in front of
the retina, bound by the hyaloid membranes anterior and posterior (see
Chapter 3).

282
 Glossary

Vitrectomy—removal of the vitreous gel to clear an opaque medium or to release

traction on the retina.
Vitritis—inflammation of the vitreous gel.
Von Hippel-Lindau syndrome—(retinocerebellar capillary haemangiomatosis)
a congenital vascular anomaly which may cause visual and neurological
problems due to late enlargement of the lesions in the 2nd, 3rd and 4th
decades of life.
Warpage—refers to a change in corneal shape induced by contact lenses.
Worth four-dot test—a test for ocular alignment, as well as brain suppression of
the image from one eye.
Xanthogranuloma juvenile—age group below 15 years present with a
spontaneous bleed into the anterior chamber (hyphaema), yellow-grey
poorly-demarcated iris, nodular lesions and associated orange-yellow skin
lesions.
Xanthelasma—flat, yellow, sharply-demarcated lipid deposits in the inner aspect
of the upper eyelids. It may be related to a high blood lipid level.
Xylocaine—a local anaesthetic administered by injection.
Zonule—the ligament which supports the crystalline lens by connecting it to
the ciliary body. It consists of hundreds of fibres attached to the equator of
the lens and nearby to its anterior and posterior surfaces. It transmits the
forces that allow the crystalline lens to accommodate according to the state
of contraction of the ciliary muscle.
Zovirax (acyclovir)—anti-viral medication for specific action against the herpes
simplex virus.
Zonule—the suspensory ligament of the crystalline lens connecting it to the ciliary
muscle through 360°.
Zoster—see herpes zoster.

283
 BIBLIOGRAPHY

USEFUL SOURCES OF FURTHER READING

Complications in ophthalmic surgery, T Krupin and AE Kolker (eds) (1993) Wolfe,

London.
Hazards of light, ES Rosen, J Marshall and J Cronly-Dillon (eds) (1989) Pergamon
Press, Oxford.
Immediate eye care, NK Ragge and DL Easty (1990) Wolfe Publishing Ltd, London.
Intra-ocular lens implantation, DJ Apple, N Mamalis, RJ Olson and MC Kingave
(1989) Williams and Wilkins, London; intra-ocular lenses, evolution, designs,
complications and pathology.
Intra-ocular lens implantation, E Rosen, WM Haining and EJ Arnott (eds) (1979)
Mosby Co, New York.
Ocular emergencies, RA Catalano (1992) WB Saunders and Co, London.
Ophthalmic drug facts 1995, Wolters Kluwer Co, St Louis, US; facts and
comparisons.
Ophthalmology, M Yanoff and J Duker (eds) (to be published in 1997) Mosby,
London and New York; this will provide a very comprehensive textbook on
modern ophthalmology.
Refractive eye surgery, LD Bores (1993) Blackwell Scientific Publications.
Textbook of ophthalmology, SM Bodos and M Yanoff (eds); in 12 volumes, Mosby
Co, London.
Visco-elastic materials, ES Rosen and J Cronly-Dillon (1989) Pergamon Press,
Oxford.

Current literature

American Journal of Ophthalmology

Archives of Ophthalmology
British Journal of Ophthalmology, published monthly by the British Medical
Association.
Eye, journal of the Royal College of Ophthalmologists, published monthly.
Journal of Cataract and Refractive Surgery, a monthly publication of the American
Society of Cataract and Refractive Surgery and the European Society of
Cataract and Refractive Surgeons.
Journal of Refractive Surgery
Ophthalmology, journal of the American Academy of Ophthalmology, published
monthly.

285
 INDEX

Abbreviations, 245–52 Applanation tonometry, 50

Acanthamoeba keratitis, 145–46 Aqueous humour, 22–23, 25, 26
Acne, 146–47, 193 drainage, 50
Acquired disorders, 78 examination, 50
Age, 69–70 glaucoma, 111–15,
blindness, 62, 64–65 118–21, 124–29
cataracts, 64, 82, 83, 87 haemorrhage, 155–56
cornea, 19–20 laser treatment, 202
diabetic retinography, 64 Arcuate keratotomy, 184, 188
eyelids, 17 Army, 215
glaucoma, 64, 69, 113 Arteritis, 195, 196
lens, 69, 70 Arthritis, 148
macular degeneration, 64, 70, Astigmatism
105, 109 arcuate keratotomy, 188
optometrists, 69 cataracts, 90
presbyopia, 25, 66, 67, 69 cornea, 177
refractive surgery, 174 glasses, 66
scleral coat, 20 refractive surgery, 174, 176–77,
regeneration, 70 180, 183–84, 188
repair, 70 retina, 176
retina, 27, 64, 69–70 vision, 176
vision, 70
visual acuity, 70 Bacteria, 75, 77
zonular fibres, 25 cataracts, 93, 94
AIDS/HIV, 76 conjunctivitis, 144
Alignment, 10, 49 endophthalmitis, 93, 149–50
Alpha-adrenergic agonist, 127 Beta-blockers, 115, 125, 127
Amblyopia, 49, 67–68 Biomicroscope, 52
children, 68, 166–70 Bi-temporal hemianopia, 48
congenital stabimus, 67–68 Blepharitis, 41, 144
relative, 67 Blindness
squints, 68 age, 62, 64–65
visual acuity, 67–68 cataracts, 64, 81, 82, 86
Ametropia, 174, 177–78 causes, 64–65
Amsler grid test, 49 certification, 62
Anaesthesia, 73, 92 children, 64–65, 169, 170
Angiography, 52, 54 complications, 103
diabetic retinopathy, 134, 136 definition, 61–62
macular degeneration, 107–09 developing countries, 86
Anatomy, 71, 82, 133, 143–44 diabetic retinopathy, 64, 133–34
Anterior capsular, 84 examination, 61–62, 65
Antibiotics, 94–95, 150 glaucoma, 64, 123
Anti-metabolites, 129–30 macular degeneration, 64, 109

287
 Ophthalmology

optometrists, 65 extracapsular cataract

race, 64 extraction, 88–90
red eyes, 144 eye drops, 94
retinal detachment, 102, 103 eyelids, 93–94
sudden and unexplained, 196–99 fibrous metaplasia, 84
sympathetic glare, 47
ophthalmitis, 153 glasses, 67, 87
trachoma, 76, 147 glaucoma, 96, 118, 130
uveitis, 148 infection, 91, 93
visual acuity, 65 inflammation, 84, 90,
Blinking, 153 91, 92, 95
Blow-out fracture of intracapsular cataract
the orbital wall, 158–59 extraction, 88–89
Bolam test, 3–4 intra-ocular lens implants, 91
Bruch’s membrane, 28–29 investigations, 86–87
Bruising, 156–57, 158 iris, 82, 88, 90, 92
iritis, 88, 92
Cataracts, 81–97 irrigation, 94
age, 64, 82, 83, 87 laser treatment, 202
anaesthesia, 92 lens, 23, 81, 82–84,
anatomy, 82 85, 87–94, 179
anterior capsular, 84 lifestyle, 83
anterior hyaloid ligament, 93
membrane, 27 macula, 95, 96
antibiotics, 94–95 medical negligence, 82
antiseptic, 94 morphology, 83
astigmatism, 90 natural history, 87
bacteria, 93, 94 neonates, 97
bilateral, 91, 97 nuclear, 83
blindness, 64, 81, 82, 86 nutrition, 83
causes, 83, 96–97 opafication, 81, 82
clinical signs, 83 outcome, 92
complications, 90, 91, 92–96 pathophysiology, 82–83
congenital, 96–97 perforation of globe, 92
contact lenses, 87, 97 phacoemulsification, 90–91
cornea, 86, 92, 96 prevention, 94–95
cortical, 84 pupils, 82
cystoid maculopathy, 95 race, 64
deterioration, 87 referrals, 87
developing countries, 82, 86 refraction, 86, 87
diabetic retinopathy, 133, 140–41 refractive surgery, 173, 174,
drugs, 86, 94 189–90
endophthalmitis, 93, 150–51 rehabilitation, 90–91
extracapsular cataract retina, 84, 91, 96
expansion, 81 retrobulbar haemorrhage, 92

288
 Index

risk, 83, 84, 86 contact lenses, 97

study, 84–85 counselling, 165
surgery, 81, 82, development, 166
85–97, 130–31 diagnosis, 168, 169
symptoms, 83 diseases, 165, 167
therapy, 85–96 drugs, 165
training, 89 examinations, 64–65, 170–71
trauma, 82, 84, 87, glasses, 67
90, 92–93, 96 glaucoma, 121
treatment, 87 inflammation, 169
ultrasonography, 86 lens, 67
ultasound, 89 leucocoria, 169
unilateral, 97 neonates, 97, 170
uveitis, 84, 95 paramedics, 168
visual acuity, 47, 87 partially sighted, 63
vitrectomy, 92 premature babies, 170–71
Cerebro-vascular pseudostrabismus, 168, 169
accidents, 48, 196–97, 200 retina, 166, 170–71
Chemical injuries, 145, 160–63 retinoblastoma, 169
alkaline substances, 160, 161, 162 retinopathy of
classification, 161–62 prematurity, 170–71
clinical signs, 163 screening, 68, 170–71
complications, 163 specialists, 168
conjunctiva, 161, 163 strabismus, 167–68
cornea, 160, 161, 162
surgery, 167–68
definition, 160
symptoms, 169
infections, 163
toxacara, 169
inflammation, 160
treatment, 168, 169, 171
irrigation, 160, 162, 163
tumours, 169
mistakes, 163
vision, 167, 171
natural history, 161
visual acuity test, 45
omissions, 163
Chlamydia, 75–76
outcome, 163
Cholinesterase inhibitors, 125
pathophysiology, 160
Choroid, 29–32, 77, 105, 157
referrals, 161
Ciliary body, 22–23, 25
surgery, 162
symptoms, 161 Circulation, 27
treatment, 160, 161, 162 Civil Aviation Authority, 218–25
Chemosis, 144 Civil Service, 232
Children, 165–71 Colour, 29–30, 51
acquired problems, 165 Complications
amblyopia, 166–67 anaesthesia, 73, 92
arthritis, 148 blindness, 103
blindness, 169, 170 blow-out fracture of
congenital injuries, 165 the orbital wall, 159

289
 Ophthalmology

cataracts, 90, 91, 92–96 Cornea, 8, 10, 11, 18–20

chemical injuries, 163 abrasions, 154
glaucoma, 118, 119, 122 age, 19–20
refractive surgery, 190 anterior chamber, 41
retinal detachment, 102, 103 astigmatism, 177
uveitis, 148 biomicroscope, 52
Computed tomography, 59 cataracts, 86, 92, 96
Congenital disorders, 78 chemical injuries, 160, 161, 162
cataracts, 96–97 conjunctival epithelium, 19
children, 165 conjunctivitis, 144, 145
corneal opafication, 193 corneal epithelium, 19, 51–52
eyelids, 18 corneal opacification, 193–94
glaucoma, 111, 113, 124 degeneration, 20, 194
myopia, 175 Descemet’s membrane, 19
retina, 31 examination, 41
Conjunctiva, 8 eyelids, 17
See also Conjunctivitis function, 10
chemical injuries, 161, 163 glaucoma, 112, 119, 120,
eyelids, 17 121, 122, 124
ocular surface, 18 gonioscopy, 41
red eyes, 143 intrastomal corneal ring, 189
scleral coat, 20 keratitis, 145–47
Conjunctivitis, 76 laser treatment, 202
bacteria, 144 lens, 19
chemicals, 145 light, 10–11, 61
chemosis, 144 mapping, 55
cornea, 144, 145 measurement, 51
definition, 144 ocular surface, 18
eyelids, 144 oedema, 194
inflammation, 144 pachymetry, 51
keratoconjunctivitis, 144–45 photorefractive
red eyes, 144–45 keratectomy, 188–89
trachoma, 147 pinhole test, 44
vernal, 144 radial keratotomy, 186–87
viral, 144 refraction, 55–56
Consent informed, 74, 96, refractive surgery, 178, 180, 181,
180, 207–09 184–87, 189, 192
medical negligence, 74 replacement, 147
professional standards, 207–09 reshaping, 86
refractive surgery, 180 retina, 10, 19
Constriction, 22, 50, 156 retinal detachment, 101
Consultants, 1 shape, 19, 20
Contact lenses, 67, 87, 97, 146 specular microscopy, 51–52
Contrast sensitivity, 47 structure, 19

290
 Index

surgery, 51, 56, 96 pathophysiology, 133–34

tonometry, 50 photography, 139
topography, 55–56, 190 prevalence, 133
trauma, 20, 91 race, 64
visual acuity test, 44 referrals, 138–39
visual defects, 61 retinal detachment, 135, 139
Cryotherapy, 102 retinography, 64, 133–41
Crystalline lens. See Lens classifications, 134–35
CT scanning, 59 end-stage, 135
Cystoid maculopathy, 95 proliferative, 135
Cysts, 77 pro-proliferative, 135
Cytomegalovirus retinitis, 76 risk, 138
screening, 139
Delay, 5, 65, 74 specialists, 139
Descemet’s membrane, 19 surgery, 139, 140–41
Diabetic eye disease, 133–41 symptoms, 138
age, 64 treatment, 139–40
anatomy, 133 uveitis, 135
angiography, 134, 136 vision, 135, 140
blindness, 133–34 Diagnosis. See also
cataracts, 133, 140–41 Examination, Symptoms
commission, 140 chemical injuries, 165, 167
diagnosis, 138 corneal abrasion, 154
general delay, 5, 65
diabetic retinopathy, 138
ophthalmologists, 138–39
electro, 57–58
general practitioners, 138–39
endophthalmitis, 151
glasses, 67
general practitioners, 204
glaucoma, 135
glaucoma, 113, 116,
haemorrhages, 134
121–22, 131
intra-retinal microangiopathy,
haemorrhage, 155
134
history, 37, 65
iris, 133
professional standards, 206, 207
kidney failure, 138
red eyes, 143
laser treatment, 139, 140, 202
retinal detachment, 101
lens, 133, 141
screening, 65, 68
macula, 135, 137–38, 140 trauma, 153
mistakes, 140 traumatic mydriasis, 156
natural history, 137–38 Dilation, 22, 49, 156
neuropathy, 133 Diplopia, 10, 49
omission, 140 Disease
ophthalmoscopy, 139 anaesthesia, 73
optic nerve, 133 anatomy, 71
optometrists, 138–39 classification, 78–79
outcome, 140 clinical signs, 72

291
 Ophthalmology

commission, 74 Electro-retinography, 57–58

complications, 73 Endophthalmilitis, 93, 149–51
consent, 74 Episclera, 20
corneal opacification, 193–94 Examination, 41–59
diagnosis, 71, 72 anterior chamber, 41
drugs, 73 blindness, 61–62
general practitioners, 72 blow-out fracture of
investigations, 72 the orbital wall, 158
management errors, 74 cataracts, 86–87
natural history, 72, 73 children, 64–65, 170–71
omission, 74 colour vision testing, 51
optometrists, 72 computed tomography, 59
outcome, 73 contrast sensitivity, 47
pathology, 72 corneal topography, 55–56
pathophysiology, 71 diseases, 70
prognosis, 72, 73 electro-diagnosis, 57–58
referrals, 72 external, 41
remission, 72 frequency, 65
surgery, 72, 73, 74 glaucoma, 114
symptoms, 71 gonioscopy, 41
systemtic approach to, 71–74 history, 37–38, 65
treatment, 73–74 intra-ocular pressure
Distance acuity test, 42–43, 45–46 measurement, 50
Double vision, 10, 49, 158–59 lifestyle, 65
Driving, 63, 227–32 magnetic resonance
Drugs. See also Eye drops imaging, 59
alpha-adrenergic ocular alignment and
argonist, 127 motility, 49
cataracts, 86, 94 ophthalmic photography, 52–53
children, 165 ophthalmoscopy, 42
cholinesterase inhibitors, 125 pachymetry, 51
corneal opacification, 193 pupils, 49–50
diseases, 73 refraction, 53–55, 66
glaucoma, 115, 121, screening, 65
124, 125–28 specular microscopy, 51–52
haemorrhage, 156 tonometry, 50
hyperosmotic agents, 127 ultrasonography, 53
keratitis, 146 visual acuity, 42–47, 65–66
sympathomimetic drugs, 125 visual defects, 61–62, 65–66
treatment, 73 visual display units, 241
uveitis, 148 visual field
examination, 47–49, 66
E-test, 44–45 Experts, 206
Electro-diagnosis, 57–58 Exposure injuries, 154–55
Electro-oculography, 57–58 Extracapsular cataract expansion, 81

292
 Index

Extracapsular cataract 15-Hue Fransworth-Munsell-D-15

extraction, 88–90 test, 51
Eye drops Fibrous metaplasia, 84
adrenaline, 115–16 Firefighters, 233–34
beta-blockers, 115, 125, 127 Foreign bodies, 159
cataracts, 94 Fracture of orbital wall, 158–59
corneal abrasion, 154 Fungi, 76
glaucoma, 115–16, Fundus camera, 42, 52, 54
124, 125
haemorrhage, 156 Gamma-radiation, 78
keratitis, 146 General ophthalmologists, 1, 103,
prostaglandins, 116, 125, 128 138–39
Eyeballs, 9–10 General Optical Council, 204–05
Eyelids, 17–18 General practitioners
age, 17 diabetic retinopathy, 138–39
blepharitis, 44, 144 diagnosis, 204
cataracts, 93–94 diseases, 72
composition, 17 glaucoma, 123–24
congenital anomalies, 18 referrals, 101, 103,
conjunctiva, 8, 17 123–24, 204
conjunctivitis, 144 retinal detachment, 103
cornea, 17 standard of care, 204
cross-section, 8 Glare, 47, 240
examination, 41 Glasses, 64–65
exposure injuries, 154 See also Presbyopia
function, 17–18 age, 66–67
iris, 17 astigmatism, 66–67
muscles, 17 cataracts, 87
palpebral aperture, 17 children, 67
ptosis, 18 dependency, 66–67
retina, 17 hyperopia, 66
tarsal plate, 17 myopia, 175
watering, 18 prescriptions, 67
Eyes visual display units, 240, 241
anterior chamber, 12 Glaucoma, 22, 23, 111–31
colour, 11, 21 acquired, 113–21
front view, 7 acute, 120, 122, 124
movement, 10, 49, 58 adrenaline, 115, 125
overview, 7–15 age, 64, 69, 113
side-view, 9 alpha-adrenergic
strain, 195, 240 agonist, 127
vascular system, 13 anterior chamber, 41
vitreous gel, 13 anti-metabolites, 129–30
aphakic, 118
Far-sightedness. See aqueous humour, 111–15,
Hyperopia 118–21, 124–29
293
 Ophthalmology

beta-blockers, 115, 125, 127 optic nerve, 111–14, 122–23

blind spots, 123 optometrists, 123–24
blindness, 64, 111 pathophysiology, 111–12
causes, 119 patients, 127
cataracts, 96, 118, 130 phacolytic, 118
children, 21 pigmentary, 117
cholinesterase inhibitors, 125 prostaglandin eye
chronic close-angle, 121 drops, 116, 125, 128
chromic open-angle, 113–16, pseudo-exfoliative, 117
121–22, 128 race, 64, 113, 129
clinical management, 114, referrals, 123–24
118, 119, retina, 111, 123
120–21, 125–27 risk, 124
clinical signs, 114, 119, 120, 122 science of, 112–13
complications, 118, 119, 122 screening, 113, 121–22
congenital disorder, 111, 113, 124 secondary, 117–18, 122
cornea, 112, 119, 120, side effects, 131
121, 122, 124 specialists, 123–24
definition, 111, 116 steroids, 117, 119, 122
diabetic retinopathy, 135 surgery, 96, 115, 118,
diagnosis, 113, 116, 124, 128–31
121–22, 131 sympathomimetic
drugs, 115, 121, agents, 125
124, 125–28 symptoms, 113, 117,
eye drops, 115–16, 124, 125 119, 120–21
examination, 114 systemic medication, 115
general practitioners, 123–24 trabeculectomy, 115, 119, 130
gonioscopy, 122, 123 trabeculoplasty, 116, 128
headaches, 194 treatment, 115, 117,
history, 114 124, 127–31
hyperosmotic agents, 127 compliance, 127–28
implants, 130 tube/shunt procedure, 130
infections, 129 uveitis glaucoma
inflammation, 117, 121, 124 hyphaema syndrome, 118
investigations, 122–23 vision, 121
iris, 112, 119, visual acuity, 111, 121
120, 124 Globe
laser treatment, 116, 128–29 conjunctiva, 8
lens, 112, 118, 120–21 lacerations, 159
low-tension, 116–17 macular degeneration, 8, 41
malignant, 121 examination, 41
motics, 115 Glossary, 253–83
myopia, 113 Gonioscopy, 41, 122, 123
neo-vascular, 119
normal-tension, 116–17 Haemorrhage

294
 Index

aqueous humour, 155–56 irrigation, 77

blow-out fracture of keratitis, 146
the orbital wall, 158–59 protozoa, 77
choroidal rupture, 157 sterilisation, 77–78
definition, 155 trachoma, 76
diabetic retinopathy, 134 uveitis, 148
diagnosis, 155 viruses, 76
drugs, 156 Inflammation
eye drops, 156 cataracts, 84, 90, 91, 92, 95
red eyes, 143 chemical injuries, 160
retina, 30, 31 children, 169
surgery, 156 corneal opacification, 193
symptoms, 155 glaucoma, 117, 121, 124
traumatic hyphaema, 155–56 meningitis, 197
treatment, 155–56 red eyes, 143, 145
Headaches, 194–96, 197 retinal detachment, 102
Health and safety at work, 240–42 scleral coat, 20–21
Hemianopia, 200 sympathetic
Herpes zoster ophthlalmicus, 195 ophthalmitis, 153–54
Homonymous hemianopia, 48 trachoma, 147
Hospital ophthalmology, 1 uvea, 21
Hyperopia, 66, 174, uveitis, 84, 148
175–76, 180 Intracapsular cataract
Hyperosmotic agents, 127 extraction, 88–89
Hypertension, 195, 197 Intra-ocular pressure
Immune system, 75, 76, 148, 153 measurement, 50
Implants, 91, 130 Intra-retinal micro-angiopathy, 134
Infections, 74–77 Intrastomal corneal ring, 189
See also Bacteria Investigations. See Examinations
AIDS/HIV, 76 Iris, 11, 21
blow-out fracture of anterior chamber, 41
the orbital wall, 159 aqueous humour, 23
cataracts, 91, 93 cataracts, 82, 88, 90, 92
chemical injuries, 163 diabetic retinopathy, 133
chlamydia, 75–76 examination, 41, 50
choroido-retinitis, 77 eyelids, 17
conjunctivitis, 65 glaucoma, 112, 119, 120, 124
cysts, 77 iritis, 88, 92
disinfection, 77 laser treatment, 202
endophthalmitis, 149–50 melanin, 11, 21
fungi, 76 pupil, 21, 50
glaucoma, 129 sphincter muscle, 50
headaches, 194 uvea, 21
herpes zoster ophthalmicus, 195 Irrigation, 77, 94, 160, 162, 163
immune system, 75, 76

295
 Ophthalmology

Jaeger notation, 44 children, 67

components, 25
Keratitis, 145–47
cornea, 19
Keratoconjunctivitis, 144–45
crystalline, 23–25
Keratectomy, 46, 181, 185,
development, 23–24
188–89, 191
diabetic retinopathy, 133, 141
Keratotomy
diagram, 24
arcuate, 184, 188
examination, 41
occupational visual
fibres, 24
standards, 191
function, 23
radial, 181, 182–83,
glasses, 64
186–88, 190–91
glaucoma, 112, 118, 120–21
Kidney failure, 138
growth, 24–25
Lacerations, 159 laser treatment, 202
Laser treatment, 200–02 presbyopia, 177
application, 201–02 red eyes, 143
aqueous humour, 202 refraction, 55
cataracts, 202 removal, 88, 90
choroidal rupture, 157 replacement, 88, 120–21
cornea, 202 retina, 11–12
diabetic retinopathy, 139, 140, 202 retinal detachment, 101
diode, 202 refractive surgery, 74, 180,
glaucoma, 116, 128 189, 192
iris, 202 shape, 24
lasik, 185, 189 structure, 23
lens, 202 zonular fibres, 25
light, 201 Leucocoria, 169
macular degeneration, 108 Lifestyle, 65, 83
photocoagulation, 139 Light
photorefractive cornea, 10–11, 61
keratectomy, 188 electro-oculography, 57–58
refractive surgery, 173, 185, 192 laser treatment, 201
retina, 200–01, 202 optic nerve, 32
specifications, 201–02 pupil, 21–22, 50
surgery, 128 red eyes, 144
trabeculoplasiy, 128 retina, 29–30, 58, 61
Lasik, 185, 189 swinging light test, 50
Lazy eye. See Amblyopia visual acuity test, 47
Lens. See Contact lenses visual defects, 61
age, 24–25, 70 visual evoked response, 58
anterior chamber, 41 visual evoked potential, 58
aqueous humour, 25 Logmar test, 46, 47
cataracts, 23, 81, 82–84,
85, 87–94, 179 Macula, 13–14

296
 Index

age, 64, 70, 105, 109 Melanin, 11, 21, 28, 31

angiography, 107–08 Meningitis, 197
blindness, 64, 109 Merchant Navy, 225–27
cataracts, 95, 96 Microscopy, 51–52
degeneration, 64, 105–09 Migraine, 195, 197
definition, 105 Mistakes
detachment, 103–04 blow-out fracture of
diabetic retinopathy, 135, the orbital wall, 159
137–38, 140 chemical injuries, 163
laser treatment, 108 diabetic retinopathy, 140
macular oedema, 96 keratitis, 146
opthalmoscopy, 42 retinal detachment, 103
pathophysiology, 105 Molecular membrane, 26–27
race, 64 Morphology, 83
refractive surgery, 174 Motility, 10, 49
retina, 105–08 Motor drivers, 227–32
retinal detachment, 102, 103–04 Mucous membrane, 8–9, 18
surgery, 96 Mydriasis, 156
symptoms, 108 Myopia
treatment, 105–09 congenital, 175
vision, 105, 108, 109 glasses, 67, 175
glaucoma, 113
visual acuity, 105
optic nerves, 35
visual aids, 109
pathological, 175
Macular oedema, 27
physiological, 175
Magnetic resonance imaging, 59
refractive surgery, 173–75,
Magnifying glasses, 109
180–81,
Measurement, 45–47
183, 185, 191
Medical assistants, 1
scleral coat, 21
Medical negligence. See
also Vicarious liability
Navy, 191, 211–15, 225–27
Bolam test, 3
Near acuity test, 44, 45
burden of proof, 5
Negligence. See Medical
cataracts, 82
negligence
causation, 5
Neuropathy, 133
commission, 74
Notations, 245–51
consent, 74
Nutrition, 22–23, 83
guidelines, 206–07
medical reports, 3–4 Occupational vision
omission, 74 standards, 3, 211–43
opinions, 1 See also Particular professions
professional standards, 206–07 photorefractive keratectomy, 191
Medical reports, 3–4 radial keratotomy, 191
Medical treatment. refractive surgery, 91–192
See Treatment Ocular fundus photography, 52–53

297
 Ophthalmology

Ocular surface, 18 Orbital wall, 158–59

Omissions
Pachymetry, 51
blow-out fracture of
Paediatric problems. See Children
the orbital wall, 159
Panophthalmitis, 149
chemical injuries, 163
Papilloedema, 32, 35, 196–97, 199
delay, 74
Paramedics, 1, 168
diabetic retinopathy, 140
Partial sight, 61–63
referrals, 72
Pathophysiology
Opafication, 81, 82, 193
blow-out fracture of
Ophthalmic disorders, 37–40, 65 the orbital wall, 158
Ophthalmologists. See cataracts, 82–83
General ophthalmologists, chemical injuries, 160
Specialists diabetic retinopathy, 139
Ophthalmoscopy, 42, 100–01, 139 diseases, 71
Opinions, 1–3, 203 glaucoma, 111–12
Optic nerves, 9, 14, 32–35 (figs) macular degeneration, 105
atrophy, 32 red eyes, 144–47
colour, 51 Phacoemulsification, 90–91
computed tomography, 59 Photorefractive keratectomy, 46,
diabetic retinopathy, 133 181, 185,
examination, 50 188–89, 191, 202
glaucoma, 111–14, 122–23 Phototherapeutic keratectomy, 202
head, 32–35 Photography, 52–54
malfunction, 50 Pilots, 216–25
myopia, 35 Pinhole acuity test, 44
opthalmoscopy, 42 Police, 236–38
papilloedema, 32, 35, Post Office, 232
196–97, 199 Posterior hyaloid membrane, 30
pathology, 32 Presbyopia, 25, 64, 66
pupils, 50 See also Glasses
retina, 15, 30, 32 age, 25, 66, 67
scotomata, 31 lens, 177
visual defects, 61 refractive surgery, 173–74,
Optometrists, 204–05 177, 181
age, 69 Professional standards, 206–09
diabetic retinopathy, 138–39 consent, 207–09
General Optical Council, 204–05 diagnosis, 206, 207
glaucoma, 123–24 disclosure, 207
referrals, 72, 101, experts, 206
103, 123–24, guidelines, 206–07
138–39, 203–05 medical negligence, 206–07
retinal detachment, 101, 103 patient education, 208–09
visual acuity, 65 risks, 207–08
Orbital cellulitis, 149 training, 209

298
 Index

treatment, 207–08 103, 123–24,

Prostoglandins, 116, 125, 128 138–39, 204
Protozoa, 77 glaucoma, 123–24
Pseudo-isochromatic keratitis, 146
colour plates, 51 omissions, 72
Pseudostrabismus, 168–69 optometrists, 72, 101, 103,
Ptosis, 18 123–24, 203–05
Pupils, 11, 21–22 refractive surgery, 204
abnormalities, 49 retinal detachment, 101, 103
aqueous humour, 23 specialists, 103, 123–24,
cataracts, 82 138–39, 158, 204
children, 169 standard of care, 204
constriction, 22, 50, 156 Refraction. See also
dilation, 22, 49, 156 Refractive surgery
examination, 49–50 autorefractors, 54
iris, 21, 49–50 cataracts, 86, 87
light, 21–22, 50 cornea, 55–56
optic nerve, 50 correction, 66
reaction, 50 errors, 10, 53–55
size, 50 examination, 53–55
traumatic-loss pupil lenses, 55
constriction and measurement, 53
dilation, 156 retinoscopy, 54
visual acuity test, 46 test, 53
white, 169 Refractive surgery, 87, 173–92
age, 174
Quadrantinopia, 48 ametropia, 177–78
arcuate keratotomy, 184, 188
Race, 64, 113, 129 astigmatism, 174, 176–77,
Radial keratotomy, 181, 182–83, 180, 183–84, 188
186–88, 190–91 cataracts, 173, 174, 189–90
Radiation, 78 complications, 190
Railways, 234–35 consent, 180
Rectus muscles, 9–10 cornea, 178, 180, 181,
Red eyes, 143–51 184–87, 189, 192
Referrals, 203–04 definition, 173–78
blow-out fracture of evolution, 179
the orbital wall, 158 future, 192
cataracts, 87
hyperopia, 174, 175–76, 180
chemical injuries, 161
intrastomal corneal
diabetic retinopathy, 138–39
ring, 189
direct, 204
laser treatment, 173, 185, 192
diseases, 72
lasik, 185, 189
general ophthalmologists, 103
lens, 174, 180, 189, 192
general practitioners, 72, 101,

299
 Ophthalmology

macula, 174 definition, 99

myopia, 173–75, 180–81, diabetes, 64, 133–41, 202
183, 185, 191 electro-retinography, 57
normal vision, 173–74 eyelids, 17
occupational visual standards, function, 13–14, 30
191–92 glaucoma, 111, 123
options, 180–85, 188 haemorrhage, 30–31
photorefractive laser treatment, 200–01, 202
keratectomy, 181, 185, lesions, 49
188–89, 191 light, 29, 58, 61
presbyopia, 173–74, 177, 181 macula, 13–14
radial keratotomy, 181, 182–83, degeneration, 105–08
186–88, 190–91 melanin, 28
refractive errors, 174 molecular membrane, 27
refractive surgery, 204 nerve cells, 30
retina, 174 opthalmoscopy, 42
scope, 180 optic nerve, 15, 30, 31, 32
screening, 190 pathological, 26
topography, 186 pathophysiology, 29
Repair pigment epithelium, 27–29, 105
age, 70 posterior hyaloid
lacerations, 159 membrane, 30
retina, 105 red eyes, 143
scleral coat, 21 refraction, 54
trauma, 153 refractive surgery, 174
Regeneration, 70, 105 regeneration, 105
Reports. See Medical reports repair, 105
Retina, 13 replacement, 105
See also Retinal detachment retinal disorders, 78–79
age, 27, 29, 64, 69–70 retinoscopy, 54
astigmatism, 176 rod receptors, 29–30, 105
blindness, 64 scotomata, 31
blood vessels, 31 uvea, 21
bruising, 156–57 vascular circulation, 27, 29, 30
Bruch’s membrane, 28–29 vision, 29–31, 49
cataracts, 84, 91, 96 visual defects, 61
children, 166, 170–71 visual evoked potential, 58
choroid, 29, 30, 105 visual evoked response, 58
colour, 29–30, 51 vitreous humour, 30
commotio retinae, 156–57 Retinal detachment, 27, 29, 99–104
cones, 29–30, 105 blindness, 102, 103
congenital disorders, 29, 31 cataracts, 91
cornea, 10, 19 children, 170, 171
crystalline lens, 11–12 clinical signs, 100–01

300
 Index

complications, 102, 103 Screening, 65, 68, 113, 121–22,

cornea, 101 139, 170–71, 190
cryotherapy, 102 Senate of Royal Colleges. 1
diagnosis, 101 Sinuses, 9
general ophthalmologists, 103 Snellen chart, 43–44, 47, 62, 63
general practitioners, 101, 103 Socket, 7, 9, 10, 41, 153
inflammation, 102 Specialists, 1, 203
investigations, 101 See also Refractive surgery
lens, 101 blow-out fracture of
macula, 102, 103–04 the orbital wall, 158
mistakes, 103 children, 168
natural history, 101 diabetic retinopathy, 139
ophthalmoscope, 100–01 opinions, 1, 203
optometrist, 101, 103 glaucoma, 123–24
outcome, 102–03 orbital, 158
referrals, 101, 103 referrals, 123–24, 138–39,
risk, 102 158, 204
specialists, 103 retinal detachment, 102
surgery, 96, 101–03 vitreo-retinal, 103, 139–40
symptoms, 99 Specular microscopy, 51–52
treatment, 101–03 Squint, 10, 167–69
vision, 99–100, 103 Standard of care, 2, 3
visual acuity, 100, 103–04 See also Professional
Retinoblastoma, 169 standards
Retinopathy of prematurity, 170–71 employment, 3
Retrobulbar haemorrhages, 92 general practitioners, 204
Retrolental fibroplasia, 170–71 inexperience, 5
Risk professional standards, 206
cataracts, 83, 84, 86 reasonableness, 206
diabetic retinopathy, 138 treatment, 74
diseases, 72 Standards. See Occupational
glaucoma, 124 visual standards
outcome, 73 Sterilisation, 77–78, 94–95
professional standards, 207–08 Steroids, 117, 119, 122, 154
retinal detachment, 102 Strabismus, 167–68
surgery, 72 Strain, 195, 240
Rosacea keratitis, 145 Strokes. See Cerebro-vascular
Royal Air Force, 216–18 accidents
Royal Navy, 191, 211–15 Surgery.
See also Refractive
Schirmer’s test, 41 surgery
Scleral coat, 20–21 anaesthesia, 73
Scleritis, 21 blow-out fracture of
Scotomata, 31 the orbital wall, 158–59

301
 Ophthalmology

cataracts, 81, 82, Topography, 55–56, 186, 190

95–97, 130–31 Toxacara, 169
chemical injuries, 162 Traberolectomy, 115, 119, 130
children, 167–68 Traberoloplasty, 116, 128
cornea, 51, 56, 96 Trachoma, 76, 147
diabetic retinopathy, 139, 140–41 Training
diseases, 72, 73 cataracts, 89
endophthalmitis, 149–51 consultants, 1
glaucoma, 96, 115, 118, continuing education, 1, 89, 209
124, 128–31 professional standards, 209
laser, 128 visual display units, 242
macular oedema, 96 surgeons, 1
pachymetry, 51 Trauma, 2, 153–63
refraction, 87 blinking, 153
retinal detachment, 96, 101–03 blow-out fracture of
risk, 72 the orbital wall, 158–59
treatment, 73 cataracts, 82, 84, 87,
uveitis, 148 90, 92–93, 96
visual acuity test, 47 chemicals, 153, 160–63
vitreo-retinal, 103, 139–40 children, 167
Sympathaminetic agents, 125 choroidal rupture, 157
Sympathetic ophthalmitis, 153–54 cornea, 20, 91
Symptoms, 38–40 corneal opacification, 193
blow-out fracture of diagnosis, 153
the orbital wall, 158 endophthalmitis, 151
cataracts, 83 eye injuries, 153–63
chemical injuries, 161 globe, 153, 159
children, 169 haemorrhage, 155–56
choroidal rupture, 157 repair, 153
commotio retinae, 156–57 socket, 153
corneal abrasion, 154 sympathetic
delay, 65 ophthalmitis, 153–54
diabetic retinopathy, 138 traumatic mydriasis, 156
diseases, 71 treatment, 153
glaucoma, 113, 117, vision, 153
119, 120–21 Treatment. See also Drugs,
haemorrhage, 155 Glasses, Surgery
red eyes, 143 blow-out fracture of
traumatic mydriasis, 156 the orbital wall, 158–59
cataracts, 87
Teachers, 239–40
chemical injuries, 160, 161, 162
Tear glands, 7–8, 18, 41
children, 168, 169, 171
Testing. See Examination
choroidal rupture, 157
Tomography, 59
Tonometry, 50 commotio retinae, 156–57

302
 Index

compliance, 127–29 blind spots, 15

corneal abrasion, 154 children, 167, 171
delay, 74 choroidal rupture, 157
diabetic retinopathy, 139–40 central, 49, 157
diseases, 73 colour, 30, 51
drugs, 73 contrast sensitivity, 47
endophthalmitis, 151 diabetic retinopathy, 135, 140
haemorrhage, 155–56 double, 10, 49, 158–59
historical perspective, 74, 103 electro-diagnosis, 57–58
keratitis, 146, 147 hemianopia, 200
laser, 108 macular degeneration, 105,
macular degeneration, 105–09 108, 109
professional standards, 207, 208 night, 29
retinal detachment, 101–03 normal, 173–74
standard of care, 74 peripheral field, 14, 48–49
surgery, 73 red eyes, 143
trauma, 153 retina, 29–30, 49
traumatic mydriasis, 156 retinal detachment, 99–100, 103
uveitis, 148 sharp, 30
Tumours stereoscopic, 31, 49
children, 169 sudden and unexplained
headaches, 195–96 loss of, 196–99
loss of vision, 197 trauma, 153
optic chiasma, 48 visual evoked response, 58
pituarity, 48 visual evoked potential, 58
retinoblastoma, 169 visual field
examination, 47–49,
Ultrasonography, 53, 86 66, 114–15, 157
Uveitis, 84, 95, 135, 147–49 Visual acuity
Uvea, 21 age, 70
amblyopia, 49
Vascular circulation, 27 cataracts, 47
Vicarious liability, 5 children, 45
Videokeratoscopy, 55–56 commotio retinae, 156–57
Viruses, 76 cornea, 44
Visacuity, 87 distance acuity test, 42–43, 45–46
Visual display units, 240–42 E-test, 44–45
Vision, 14–15 environmental
See also Occupational visual conditions, 46–47
standards, Visual examination, 42–47, 65–66
acuity, Visual defects glare visual acuity test, 47
age, 70 international systems, 45
Amsler grid test, 49 Jaeger notation, 44
astigmatism, 176 light, 47

303
 Ophthalmology

Logmar visual acuity test, 46, 47 amblyopia, 67–68

macular degeneration, 105 blindness, 61
measurement, 45–47 children, 68
near acuity test, 44, 45 contact lenses, 67
occupational vision cornea, 61
standards, 211–42 examination, 61–62, 65–66
optometrists, 65 glasses, 64–65, 66–68
pinhole acuity test, 44 hyperopia, 66
pupils, 46 light, 61
retinal detachment, 100, 103–04 optic nerve, 61
Snellen chart, 43–44, 47, 62 partially sighted, 61–63
surgery, 47 presbyopia, 66
visual defects, 61–62 retina, 61
Visual aids, 109 test, 62
See also Contact lenses, Vitrectomy, 92
Glasses Vitreous body, 26–27, 30
Visual defects, 61–68
age, 62, 66 Zonular fibres, 25

304