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Oxford Specialty Training:
Training in Ophthalmology
Second Edition
Oxford Specialty Training:
Training in Ophthalmology
Second Edition

Edited by
Venki Sundaram
Consultant Ophthalmic Surgeon
Luton and Dunstable University Hospital
UCL Partners, UK

Allon Barsam
Consultant Ophthalmic Surgeon
Luton and Dunstable University Hospital
UCL Partners, UK

Lucy Barker
Consultant Ophthalmic Surgeon
Rwanda International Institute of Ophthalmology
Dr Agarwal’s Eye Hospital, Rwanda

Sir Peng Tee Khaw

Professor of Glaucoma and Ocular Healing, and Consultant Ophthalmic Surgeon
NIHR Biomedical Research Centre at Moorfields Eye Hospital and UCL Institute of Ophthalmology
London, UK

Series Editor
Matthew D. Gardiner
Specialty Trainee in Plastic Surgery, Imperial College London
Honorary Clinical Lecturer in Plastic Surgery, Kennedy Institute of Rheumatology, University of Oxford

1
1
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© Oxford University Press 2016
The moral rights of the authors have been asserted
First Edition published in 2009
Second Edition published in 2016
Impression: 1
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ISBN 978–0–19–967251–6
Printed in Great Britain by
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Oxford University Press makes no representation, express or implied, that the
drug dosages in this book are correct. Readers must therefore always check
the product information and clinical procedures with the most up-to-date
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and the most recent codes of conduct and safety regulations. The authors and
the publishers do not accept responsibility or legal liability for any errors in the
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 To my wife Champa, our boys Jay and Krish
and our families.
Venki Sundaram

To Sarah, Aron, Ezekiel, Raphael, and Joseph and

our families.
Allon Barsam

To my boys, Will and Rufus.

Lucy Barker

To Peggy, Ruth and Rachel.

Peng Khaw
 Foreword

Training in Ophthalmology sets out a beautifully practical way to learn clinical ophthalmology. The experience of
the authors translates into a welcome, much needed addition to the general ophthalmology text books genre
and it deserves its place as an ‘essential read’—not simply a new library book.
Each chapter covers the essentials—starting with basic sciences which are necessary to understand the sub-
sequent clinical content in a meaningful way. Relevant clinical conditions and diagnoses are then drawn to-
gether in a combination of bullet points, clear descriptive text, tables, and illustrations. This extensive factual
information is then supplemented by methods of clinical assessment which need to be mastered in order to
elicit the appropriate clinical signs: and finally there are sections on practical and surgical skills which are a
goldmine of tips and tricks to ensure that there is little room for error. The comprehensive content includes
illustrations which are a mixture of high-quality clinical photographs, demonstrating relevant signs succinctly,
and figures annotating critical detail—working well to complement the text.
Advances and newer treatments do not always feature in a teaching text, but these are reflected in the
various chapters, such as refractive surgery, and it does not fail to omit the ‘softer’ professional skills, such as
communication, governance, and understanding research, which are so important for everyone involved in
patient care. The way that ophthalmology is delivered and taught is changing and this book demonstrates how
this can be done effectively.
Although aimed at those in training—particularly, but not exclusively, ophthalmologists—the strength of this
vi book is that it has something for everyone with an interest in this fascinating specialty and its layout and con-
tent make it eminently readable and pertinent. The authors are to be congratulated for this work which will
help to shape the ophthalmic team of tomorrow.
Carrie MacEwen
Foreword: A Trainee’s Perspective

Having thoroughly dissected the first edition of this book as a junior trainee and whilst preparing for my Col-
lege exams, I am delighted to welcome this latest iteration.
Following on from its initial success as a bespoke training manual for UK trainees, this latest edition brings a
fresh perspective that keeps up to date with the current curriculum and adds concise practical guidance in a
number of key clinical and surgical skills. These summaries and protocols will be invaluable to the developing
trainee learning new techniques and will also aid in the completion of work-based assessments.
Ophthalmic investigations and therapeutics have rapidly advanced in recent years and this new edition
keeps up to date with these trends, summarising the latest evidence that not only emphasizes current clinical
practice but also provides an important template for examination learning.
The last chapter covers important professional and practical skills that are typically not covered in other
textbooks but form a growing part of our curriculum whilst new chapters in refractive surgery and microsur-
gical skills offer a unique perspective not commonly addressed in this format.
This book is wonderfully presented and easy to read with beautiful illustrations. It is a comprehensive yet
compact text that mirrors the UK curriculum and will play a key role both as a daily reference and in preparing
for College examinations. Being conveniently concise and portable, it is a book that belongs in the satchel of
all budding ophthalmologists, as well as interested allied specialists and GPs

Oliver Bowes vii

Chairman, Ophthalmologists in Training Group (OTG),
Royal College of Ophthalmologists
 Preface

We are pleased to introduce the second edition of Training in Ophthalmology. We introduced the first edition
of this textbook to address the needs of ophthalmic trainees and relevant allied specialities, with particu-
lar emphasis on changes in ophthalmology training that occurred following the introduction of Modernising
Medical Careers and the new Ophthalmic Specialist Training (OST) curriculum from the Royal College of
Ophthalmologists.
With the relative lack of ophthalmology teaching at medical school and the often inconsistent formal teach-
ing of fundamental examination and clinical techniques during initial posts, ophthalmology trainees often feel
they are being ‘thrown in at the deep end’ early on in their career. In addition, trainees are now expected to
clearly demonstrate evidence of having acquired the expected knowledge, clinical, technical, and surgical skills
at each stage of their training in order to progress.
This book aims to help address these issues by mapping the stages of the OST curriculum and providing
trainees with the core knowledge and clinical skills they will require to succeed. In this updated edition, we
have included two new chapters, Refractive surgery (Chapter 4) and Microsurgical skills (Chapter 12), as well
as expanding the strabismus section to create a dedicated paediatric ophthalmology and strabismus chapter
(Chapter 9); and included additional practical and surgical skills that are required to be demonstrated in the
final years of training.
As before, each chapter covers relevant basic science, history and examination techniques, and pertinent
viii clinical conditions for each sub-speciality. Practical skills are highlighted with particular emphasis on the core
competencies of the OST curriculum and we have provided an overview of the non-clinical yet increasingly
important elements of ‘being a doctor’ in the professional skills chapter (Chapter 13).
Although this book is primarily aimed at trainees at all stages of their training, it will also be appealing for
medical students, general practitioners, more senior ophthalmologists, optometrists, orthoptists, and other
healthcare professionals with an interest in ophthalmology.
We hope that you enjoy and benefit from reading this book and we welcome any feedback on how it may
be improved for the future.
VS
AB
LB
PTK
Acknowledgements

We would like to thank Fiona Richardson and Rachel Goldsworthy at OUP for their help and guidance
throughout producing this book.

Thank you to all the chapter authors for their hard work and cooperation.

ix
 Contents

Contributors xii
Contributors to the First Edition xiv
Abbreviations xv

1 Oculoplastics 1
Tarang Gupta and Daniel Ezra

2 Cornea and conjunctiva 39

Georgia Cleary, Allon Barsam, and Stephen Tuft

3 Cataract 107
Georgia Cleary and Allon Barsam

4 Refractive surgery 139 xi

Georgia Cleary, Allon Barsam, and Eric Donnenfeld

5 Vitreoretinal surgery 155

Sidath E. Liyanage, Fred K. Chen, and James W. Bainbridge

6 Medical retina 195

Venki Sundaram and Michel Michaelides

7 Uveitis and medical ophthalmology 241

Edward Hughes, Miles Stanford, and Dania Qatarneh

8 Glaucoma 289
Andrew Tatham and Peng Tee Khaw

9 Paediatric ophthalmology and strabismus 353

Lucy Barker, Kelly MacKenzie, Joanne Hancox, Wanda Kozlowska, and Andrew Tatham

10 Neuro-ophthalmology 419
Lucy Barker, Gordon T. Plant, and Indran Davagnanam

11 Orbit 465
Tarang Gupta and Daniel Ezra

12 Microsurgical skills 493

Ronald Kam and Paul Sullivan

13 Professional skills and behaviour 513

Lucy Barker, Ameenat Lola Solebo, Melanie Hingorani, and John Bladen

Index 537
 Contributors

James W. Bainbridge Joanne Hancox

Professor of Ophthalmology Consultant Ophthalmic Surgeon
UCL Institute of Ophthalmology and Moorfields Moorfields Eye Hospital
Eye Hospital London, UK
London, UK Chapter 9
Chapter 5
Melanie Hingorani
Lucy Barker Consultant Ophthalmologist
Consultant Ophthalmic Surgeon Moorfields Eye Hospital
Rwanda International Institute of Ophthalmology London, UK
Dr Agarwal’s Eye Hospital, Rwanda Chapter 13
Chapters 9, 10, 13
Edward Hughes
Allon Barsam Consultant Ophthalmologist
Consultant Ophthalmic Surgeon Sussex Eye Hospital
Luton and Dunstable University Hospital Brighton, UK
UCL Partners, UK Chapter 7
Chapters 2–4
xii Ronald Kam
John Bladen Specialty Registrar
Trainee and Medical Student Mentoring Scheme Moorfields Eye Hospital
Faculty of Medical Leadership and Management London, UK
London, UK Chapter 12
Section 13.9
Sir Peng Tee Khaw
Fred K. Chen Professor of Glaucoma and Ocular Healing, and
Consultant Ophthalmologist Consultant Ophthalmic Surgeon
Perth, Australia NIHR Biomedical Research Centre at
Chapter 5 Moorfields Eye Hospital and UCL Institute of Ophthalmology
London, UK
Georgia Cleary
Chapter 8
Specialty Registrar
London Deanery, UK Wanda Kozlowska
Chapters 2–4 Consultant in Paediatric Respiratory Medicine
King’s College Hospital
Indran Davagnanam
London, UK
Consultant Neuroradiologist
Section 9.22
The National Hospital for Neurology and
Neurosurgery and Moorfields Eye Hospital Sidath E. Liyanage
London, UK Vitreoretinal Department
Section 10.7 Moorfields Eye Hospital
London, UK
Eric Donnenfeld
Chapter 5
Professor of Ophthalmology
New York University Kelly MacKenzie
New York, NY, USA and Senior Orthoptist
Ophthalmic Consultants of Long Island Moorfields Eye Hospital
New York, NY, USA London, UK
Chapter 4 Chapter 9
Daniel Ezra Michel Michaelides
Consultant Ophthalmic Surgeon Professor of Ophthalmology and Consultant Ophthalmic
Moorfields Eye Hospital Surgeon
London, UK UCL Institute of Ophthalmology and Moorfields Eye Hospital
Chapters 1 and 11 London, UK
Chapter 6
Tarang Gupta
Locum Consultant Ophthalmic Surgeon, Dania Qatarneh
Moorfields Eye Hospital Consultant Ophthalmologist
London, UK Alfred Hospital
Chapters 1 and 11 Melbourne, Australia
Chapter 7
Gordon T. Plant Venki Sundaram

Contributors
Consultant Neurologist, The National Hospital for Neurology and Consultant Ophthalmic Surgeon
Neurosurgery and Moorfields Eye Hospital Luton and Dunstable University Hospital
London, UK UCL Partners, UK
Chapter 10 Chapter 6
Ameenat Lola Solebo Andrew Tatham
NIHR Academic Clinical Lecturer, Consultant Eye Surgeon
UCL Institute of Child Health and UCL Institute Princess Alexandra Eye Pavilion
of Ophthalmology Edinburgh, UK
London, UK Chapter 8, Section 9.26
Chapter 13
Stephen Tuft
Miles Stanford Consultant Ophthalmologist
Professor of Ophthalmology Moorfields Eye Hospital
St Thomas Hospital London, UK
London, UK Chapter 2
Chapter 7
Paul Sullivan
Consultant Ophthalmologist
Moorfields Eye Hospital
London, UK
Chapter 12

xiii
 Contributors to the First Edition

Amar Alwitry Saurabh Goyal

Consultant Ophthalmologist Glaucoma Clinical Fellow
Derby Hospitals NHS Foundation Trust Moorfields Eye Hospital
Derby London
Simon D.M. Chen Julie Huntbach
Retina Specialist Specialist Registrar in Ophthalmology
Vision Eye Institute Queens Medical Centre
Sydney Nottingham
New South Wales
Moneesh Patel
Australia
Specialist Registrar in Ophthalmology
Claire Daniel Derby Hospitals NHS Trust
Adnexal Fellow Derby
Moorfields Eye Hospital
Bheema Patil
London
Advanced Specialist Trainee in Ophthalmology
John Elston Nottingham University Hospital
xiv Consultant Ophthalmologist (paediatrics and neuro- Nottingham
ophthalmology)
Pankaj Puri
Oxford Eye Hospital
Consultant Ophthalmologist
John Radcliffe Hospital, Oxford
Derbyshire Royal Infirmary
Rebecca Ford Derby
Specialist Registrar in Ophthalmology
David Spalton
Moorfields Eye Hospital
Consultant Ophthalmic Surgeon
London
St Thomas’ Hospital
Matthew Gardiner London
Clinical Research Fellow in Plastic and Reconstructive Surgery
Jimmy Uddin
Kennedy Institute of Rheumatology
Consultant Ophthalmologist
Imperial College London
Moorfields Eye Hospital
London
London
 Abbreviations

AC/A ratio accommodative convergence/accommodation EBV Epstein–Barr virus

ratio ECCE extracapsular cataract extraction
ACE angiotensin-converting enzyme EOG electro-oculogram
ACHM achromatopsia Epi-LASIK epithelial laser-assisted in situ keratomileusis
AIDS acquired immunodeficiency syndrome EPR electronic patient records
AION anterior ischaemic optic neuropathy ERG electroretinography
AKC atopic keratoconjunctivitis ESR erythrocyte sedimentation rate
ALPI argon laser peripheral iridoplasty ETDRS Early Treatment Diabetic Retinopathy Study
ALT argon laser trabeculoplasty ETROP Early Treatment for Retinopathy of Prematurity
AMD age-related macular degeneration FAF fundus autofluorescence
ANA anti-nuclear antibody FBC full blood count
ANCA anti-neutrophil cytoplasmic antibody FFA fundus fluorescein angiography
AR autosomal recessive FOV field of view
AREDS Age-Related Eye Disease Study GA geographic atrophy
AVM arteriovenous malformations GAT Goldmann applanation tonometry
xv
BCC basal cell carcinoma GCC ganglion cell complex
BIO binocular indirect ophthalmoscopy GDD glaucoma drainage devices
BRAO branch retinal artery occlusion GI gastrointestinal
BRVO branch retinal vein occlusion GCA giant cell arteritis
BSS balanced salt solution GMC General Medical Council
CCC continuous curvilinear capsulorrhexis GPS glaucoma probability score
CCF carotid–cavernous fistula GVHD graft-versus-host disease
CCT central corneal thickness HAART highly active antiretroviral therapy
CDB corneal dystrophy of Bowman’s layer HIV human immunodeficiency virus
CDR cup/disc ratio HLA human leucocyte antigen
CHED congenital hereditary endothelial dystrophy HRT Heidelberg retinal tomograph
CHRPE congenital hypertrophy of retinal pigment HSCA Health and Social Care Act
epithelium
HSK herpes simplex keratitis
CIN conjunctival intraepithelial neoplasia
HSV herpes simplex virus
CMV cytomegalovirus
HZO herpes zoster ophthalmicus
CNS central nervous system
HZV herpes zoster virus
CNV choroidal neovascularization
ICG indocyanine green
CPEO chronic progressive external ophthalmoplegia
IFIS intraoperative floppy iris syndrome
CRAO central retinal artery occlusion
IL-1 interleukin 1
CRION chronic relapsing inflammatory optic neuropathy
IL-2 interleukin 2
CRP C-reactive protein
IOL intraocular lens
CRVO central retinal vein occlusion
IOP intraocular pressure
CSCR central serous chorioretinopathy
IPD interpupillary diameter
CSF cerebrospinal spinal fluid
IR inferior rectus
CSMO clinically significant diabetic macular oedema
IRMA intraretinal microvascular abnormalities
CT computed tomography
ITC iridotrabecular contact
CXR chest X-ray
JIA juvenile idiopathic arthritis
DEXA dual-energy X-ray absorptiometry
LASEK laser-assisted subepithelial keratomileusis
DR diabetic retinopathy
LASIK laser-assisted stromal in situ keratomileusis
DSAEK Descemet's stripping automated endothelial
LCD limbal chamber depth
keratoplasty
LE left eye
DSEK Descemets stripping endothelial keratoplasty
LogMAR logarithm of the mean angle of resolution
DVD dissociated vertical deviation
 LPS levator palpebrae superioris PUK peripheral ulcerative keratitis
Abbreviations

LR lateral rectus PVD posterior vitreous detachment

LSM laser spot magnification PVR proliferative vitreoretinopathy
MHC major histocompatibility complex PXF pseudoexfoliation syndrome
MLF medial longitudinal fasciculus RAPD relative afferent pupillary defect
MMP mucous membrane pemphigoid RD retinal detachment
MR medial rectus RE right eye
MRA Moorfields regression analysis RGC retinal ganglion cell
MRI magnetic resonance imaging RNFL retinal nerve fibre layer
NHS National Health Service ROP retinopathy of prematurity
NICE National Institute of Clinical Excellence RP retinitis pigmentosa
NMO neuromyelitis optica RPE retinal pigment epithelium
NPDR non-proliferative diabetic retinopathy RRD rhegmatogenous retinal detachment
NSAID non-steroidal anti-inflammatory drug SAC seasonal allergic conjunctivitis
NSR neurosensory retina SAP standard automated perimetry
NVD neovascularization of the optic disc SD-OCT spectral domain optical coherence
NVE new vessels elsewhere tomography
OCA oculocutaneous albinism SITA Swedish Interactive Thresholding Algorithm
OCT optical coherence tomography SLT selective laser trabeculoplasty
OHT ocular hypertension SO superior oblique
xvi OKN optokinetic nystagmus SP small pupil
ONTT Optic Neuritis Treatment Trial SR superior rectus
OPP ocular perfusion pressure SS-OCT swept source optical coherence tomography
OTG Ophthalmic Trainees’ Group STGD Stargardt disease
PAC perennial allergic conjunctivitis SWAP short-wavelength automated perimetry
PACG primary angle closure glaucoma TD-OCT time domain optical coherence tomography
PACS primary angle closure suspect TGF transforming growth factor
PAS peripheral anterior synechiae TIGR trabecular-meshwork-inducible glucocorticoid
response
PCO posterior capsule opacification
TM trabecular meshwork
PCR polymerase chain reaction
TNF tumour necrosis factor
PCT prism cover test
tPA tissue plasminogen activator
PDR proliferative diabetic retinopathy
TPMT thiopurine methyltransferase
PDS pigment dispersion syndrome
TSH thyroid-stimulating hormone
PDT photodynamic therapy
UBM ultrasound biomicroscopy
PED pigment epithelial detachment
UKPDS UK Prospective Diabetes Study
PHPV persistent hyperplastic primary vitreous
VDRL Venereal Disease Research Laboratory
PI peripheral iridotomy
VEGF vascular endothelial growth factor
PM pathological myopia
VEP visual evoked potential
POAG primary open-angle glaucoma
VFI visual field index
PORN progressive outer retinal necrosis
VKC vernal keratoconjunctivitis
PP posterior pole
VN vestibular nucleus
PPRF paramedian pontine reticular formation
VZV varicella-zoster virus
PR peripheral retina
WD working distance
PRK photorefractive keratectomy
PRP pan-retinal photocoagulation
 Chapter 1

Oculoplastics
Tarang Gupta and Daniel Ezra

Basic sciences Surgical skills

1.1 Eyelid and nasolacrimal system a­ natomy 2 DCR technique 27
Surgical repair of lid trauma 34
Clinical knowledge Lateral tarsorraphy 35
Emergency lateral canthotomy/
1.2 Lash abnormality 5
cantholysis 35
1.3 Entropion 8
1.4 Ectropion 10
1.5 Ptosis I 12
1.6 Ptosis II 14
1.7 Benign lid lesions 16 1
1.8 Premalignant lesions 19
1.9 Malignant lid lesions I 20
1.10 Malignant lid lesions II 22
1.11 Epiphora 24
1.12 Acquired nasolacrimal system
­abnormalities 26
1.13 Congenital abnormalities 30
1.14 Miscellaneous 32
1.15 Practical skills in oculoplastics 34

Clinical Assessment
Ptosis examination 12
Evaluation of the patient with acquired
epiphora 24

Practical skills
Incision and curettage of chalazion 16
Syringing and probing 25
Using diathermy safely 34
Removing sutures 34
Preparing a biopsy sample 34
Botulinum-toxin injection 34
 1.1 Eyelid and nasolacrimal system anatomy
Eyelid anatomy
The primary function of the eyelids is to protect the globe from
injury, and the retina from excessive light. They also assist in
the distribution of tears across the ocular surface during blink-
ing. Additionally, the eyelids provide mechanical support for the
globe, the lacrimal canaliculi, and the punctae that form part of
the tear drainage system.
The upper and lower eyelids extend from the lateral to the
medial canthi. The distance between the upper and lower lids
is called the palpebral aperture and exhibits considerable racial
variation. The eyelid consists of many layers, the most anterior
being skin, which is followed by subcutaneous tissue and the or-
bicularis oculi muscle fibres, which together form the anterior
lamella. The posterior lamella is formed by the tarsal plate and
conjunctiva. The division of the eyelid into anterior and poster-
ior lamellae is useful clinically as these structures are easily div-
ided by a convenient surgical cleavage plane.
Skin
The eyelid skin is the thinnest in the body (<1 mm). Loose sub-
2 cutaneous areolar tissue separates the skin from the underlying
orbicularis. A plane can potentially form beneath the skin during
local anaesthetic infiltration. Subcutaneous fat is sparse, and it is
absent beneath the pretarsal skin.
Orbicularis oculi
The orbicularis oculi is one of the muscles of facial expression
and may be divided into orbital, preseptal, and pretarsal por-
tions (see Figure 1.1). These anatomical divisions also reflect
functional and physiological differences. The pretarsal part is
responsible for fast blink (90% of the muscle consists of Type 1
fast-twitch fibres). In contrast, the peripheral orbital part is re-
sponsible for forced sphincter closure. Orbital orbicularis oculi
fibres interdigitate with those of the frontalis, the procerus, and
the corrugator supercilii muscles superiorly and the lip elevators
inferiorly.
Sweeping fibres of the orbicularis oculi run in a circular fash-
ion from the medial canthal tendon inferiorly and superiorly, to
join at the lateral palpebral ligament. Specialized fibres of the
medial pretarsal orbicularis invest the canaliculi and insert into
the lacrimal sac fascia. These fibres are known as Horners mus-
cle, which is thought to mediate the lacrimal pump. The nerve
supply of the orbicularis muscle is from the facial nerve (tempo-
ral and zygomatic branches).
Orbital septum
The orbital septum is a connective tissue extension of the thick-
ened periosteum at the orbital rim (the arcus marginalis). It is a
multi-laminated barrier between the eyelid and the orbit. The
septum fuses with the levator aponeurosis near the eyelid mar-
gin (see Figure 1.2).
Tarsal plate
The tarsal plate forms the fibrous skeleton of the lids. The
upper tarsal plate measures 10–12 mm centrally, and the lower
tarsal plate measures about 5 mm. Both tarsal plates are at-
tached to the orbital rim by medial and lateral palpebral liga-
ments. Each tarsus is 1 mm thick and contains approximately 30
meibomian glands. These glands produce a holocrine sebaceous
secretion that constitutes the outer lipid layer of the precorneal
tear film. The openings are located posterior to the grey line
and just anterior to the mucocutaneous junction. The eyelash
roots lie against the anterior surface of the tarsus and exit the
skin at the anterior lid margin. The glands of Moll are modified
sweat glands that open onto the lid margin between the lashes
or into a lash follicle. The glands of Zeiss are sebaceous glands
that open into each lash follicle.
Medial palpebral ligament
The medial palpebral ligament is formed by condensations
of the pretarsal and preseptal orbicularis muscles. A superfi-
cial head inserts onto the frontal process of the maxilla whilst
a deep head inserts into the lacrimal sac and posterior lacrimal
crest.
Lateral palpebral ligament
The lateral palpebral ligament is a broad dense fibrous tissue
that passes laterally, deep to the orbital septum, to insert into
Whitnalls tubercle, 1.5 mm posterior to the orbital rim.
Upper lid elevators
Levator palpebrae superioris
The levator palpebrae superioris (LPS), a striated muscle,
originates from the lesser wing of the sphenoid at the orbital
apex. It shares a developmental origin and fibrous attach-
ments with the superior rectus, which it passes above (see
Figure 1.2). It then fans out, ending in an aponeurosis 10 mm
behind the orbital septum. The muscle fibres change orienta-
tion from horizontal to vertical at Whitnalls ligament, which
runs from the lacrimal gland fascia to the trochlea. The le-
vator aponeurosis expands laterally and medially into horns
which attach to Whitnalls tubercle and the posterior lacrimal
crest, respectively. The levator aponeurosis inserts centrally
into the upper third of the anterior surface of the tarsal plate.
The LPS is supplied by the superior division of the oculomo-
tor nerve.
Müllers muscle
This smooth muscle augments the action of the levator. It arises
from the inferior aspect of the levator aponeurosis and inserts
into the superior border of the tarsal plate. The peripheral vas-
cular arcade is adherent to the lower border of Müllers muscle.
It is innervated by sympathetic fibres from the superior cervical
ganglion.
Lower lid retractors
There is no inferior equivalent to the levator. The lower lid re-
tractors are connective tissue condensations that originate from
the fascial sheath of the inferior rectus tendon. This sheath is
continuous with Lockwoods suspensory ligament and extends
anteriorly to envelop the inferior oblique muscle, ending at the
inferior border of the inferior tarsus (see Figure 1.3).
Blood supply and lymphatic drainage
Arterial blood supply to the eyelids is provided by a mar-
ginal and peripheral arcade formed from the medial and lateral
palpebral arteries. Venous drainage occurs medially into the
ophthalmic and angular veins and laterally into the superior
temporal vein. Lymphatic drainage from the lateral two-
thirds of the upper and lower lids is to the superficial parotid
(preauricular) lymph nodes, and lymphatic draining from the
medial third is to the submandibular nodes.
Nasolacrimal system anatomy
The aqueous component of the tear film is produced by the lac-
rimal gland in the supero-lateral orbit. This gland comprises a
large orbital lobe and a much smaller palpebral lobe. Tiny acces-
sory lacrimal glands are also located in the conjunctival fornix.
The nasolacrimal drainage system is a conduit for the flow of
tears from the external surface of the eye to the nasal cavity across the ocular surface and across the tear strips on the upper

(see Figure 1.4).
Lacrimal puncta
These are small openings that lie on the medial aspects of the
upper and lower lids. Each punctum sits on an elevated pale
mound called the papilla lacrimalis. The punctae are normally
directed so as to be in contact with the tear meniscus.
Oculoplastics
and lower lid margins by capillarity. The contribution made by
each canaliculus to total tear draining capacity is not known, but
estimates vary from 50% to 80% for lower canalicular drainage.
When the eyelids close during blinking, the Horners muscle fi-
bres of the orbicularis muscle contract, causing expansion of
the lacrimal sac. Negative pressure sucks tears into the canaliculi
and sac. When the eyelids open, positive pressure within the

CHAPTER 1
Lacrimal canaliculi sac then forces the tears down the nasolacrimal duct. This cycle
The canaliculi begin at the punctum and pass vertically for 2 mm is known as the lacrimal pump and becomes ineffective with in-
before turning through 90° to pass horizontally and medially for creasing eyelid laxity.
8 mm before meeting at the common canaliculus. The common
canaliculus continues medially to enter the lacrimal sac obliquely
through the valve of Rosenmuller at the lateral wall of the lacri-
mal sac. Palpebral
ral part Preseptal Orbital part of
of orbicularis
cularis Pretarsal orbicularis muscle
Lacrimal sac
The lacrimal sac is located in the lacrimal fossa in the anterior
part of the medial orbital wall, between the anterior and pos-
terior lacrimal crests formed by the frontal process of the max-
illa and lacrimal bones, respectively. The sac measures 12 mm in
length and is enclosed in fascia.
Nasolacrimal duct
The nasolacrimal duct connects the lower portion of the lac-
rimal sac with the nasal cavity. The duct passes inferiorly,
posteriorly and laterally. The maxilla, lacrimal bone, uncinate
3
process, and inferior turbinate form the canal. The duct opens
into the inferior meatus of the nose. A flap of mucous mem-
brane, called the valve of Hasner, prevents retrograde reflux of
nasal contents and is commonly imperforate at birth, leading to
Terminal branches of the zygomatic
epiphora.
division of the facial nerve
Fig 1.1 The orbicularis oculi muscle and the terminal branches
Physiology of the facial nerve
The main and accessory lacrimal glands secrete the tears, 10%– Reproduced from Colour Atlas of Ophthalmic Plastic Surgery, 2008; A.G.Tyers and
20% of which are lost through evaporation. The remainder pass J.R.O. Collin p8 Butterworth Heinemann, copyright Elsevier

Whitnall’s
ligament
Pre-aponeurotic
fat pad
Levator muscle
Common sheath
Arcus marginale
Orbital septum
Orbicularis muscle

Preseptal space
Levator aponeurosis
Post-aponeurotic space
Accessory
Levator aponeurotic lacrimal Superiror rectus
insertion into orbicularis glands muscle
Levator aponeurotic Müller’s muscle
insertion into tarsus

Muscle of Riolan

Fig 1.2 Vertical section of the upper eyelid

Reproduced from Colour Atlas of Ophthalmic Plastic Surgery, 2008; A.G.Tyers and J.R.O. Collin p18 Butterworth Heinemann, copyright Elsevier
 Inferior tarsal muscles
Eyelid and nasolacrimal system anatomy

orbicularis muscle Inferior rectus muscles

Capsulopalpebral fascia
Capsulopalpebral head
Orbital septum
Inferior oblique muscle
Arcus marginale
Lockwood’s ligament
Fig 1.3 Cross section of lower eyelid
Reproduced from Gold D. and Lewis R., Clinical Eye Atlas, second edition, 2010, Fig. 1.5, p. 4, by permission of Oxford University Press, USA

Lacrimal sac Common canaliculus Punctum

12–15 mm
1.1

Ampulia 2 mm
Canaliculus
Anterior 8 mm
lacrimal crest Hiatus
Middle semilunaris
turbinate with sinus
Nasolacrimal ostia
duct
12–18 mm

Inferior
turbinate

Valve of
Hasner
Fig 1.4 Normal anatomy of the lacrimal excretory system
Measurements are for adults
1.2 Lash abnormality
Trichiasis
Trichiasis is an acquired misdirection of normally sited eye-
lashes towards the globe. The most common underlying patho-
logical process is posterior lamellae scarring but in children,
particularly in those of Asian origin, epiblepharon is a common
cause of trichiasis. Trichiasis is not to be confused with meta-
plastic lashes, which are aberrantly located lashes resulting from
chronic eyelid margin inflammation.
Aetiology
• Inflammatory: chronic blepharitis, vernal and atopic kera-
toconjunctivitis, mucous membrane pemphigoid, Stevens–
Johnson syndrome
• Infective: herpes zoster ophthalmicus, trachoma (can result
in upper lid entropion; see Figure 1.5)
• Traumatic: post eyelid surgery (particularly transconjunc-
tival approach), chemical (alkali burns, long-term eye drop
use) or thermal injuries
Morbidity
The misdirected eyelashes cause repeated corneal trauma re-
sulting in punctate epithelial erosions, microbial keratitis, and
corneal scarring in chronic cases.
Management
As well as including the treatment of any underlying conditions,
management is dictated by the pattern (segmental or diffuse) of
the trichiasis, and the quality of the posterior lamella. Lubricants
may reduce the irritation caused by lash contact but are often
unsatisfactory if used in isolation.
In cases of focal trichiasis, lash follicle destruction is preferable,
whereas diffuse trichiasis is best treated with lash repositioning.
Mechanical epilation
The initial treatment for a few misdirected lashes is removal
with fine forceps at the slit lamp. Lash regrowth normally recurs
in 3–4 weeks and the short, stiff lash cilia can be more irritating
to the cornea than mature longer lashes.
Electrolysis
Modern electrolysis is delivered via a radio frequency probe to
ablate the lash follicle. The probe should be inserted perpen-
dicular to the eyelid margin, with sufficient depth to reach the
follicle root (2.4 mm in the upper lid, 1.4 mm in the lower lid).
The lash should fall away easily if sufficiently ablated. A direct
cut-down and visualization of the follicle root prior to the appli-
cation of electrolysis may be more effective with less collateral
damage than electrolysis alone.
Repeated treatments can lead to scarring of the conjunctival
surface, particularly in the presence of inflammatory conditions.
To be most effective, treatment needs to be delivered at a time
in the lash growth cycle when the lashes are actively growing.
Cryotherapy
This approach can be useful in segmental trichiasis. A grey line
split is made in the area to be treated. A solid nitrous oxide
cryoprobe is then applied in a double-freeze-thaw technique.
The anterior lamella can be reattached with a double-armed
6–0 Vicryl suture through partial thickness tarsus and then out
through the orbicularis and the skin and tied. Possible side ef-
fects include skin depigmentation, notching of the lid margin,
and meibomian gland damage.
Surgery
Full-thickness wedge resection may be useful for segmental
trichiasis. Generalized trichiasis may require anterior lamellar
Oculoplastics
repositioning with or without a grey line split. This method does
not disturb the conjunctival surface and may be preferable in
mucous membrane pemphigoid.
CHAPTER 1
Distichiasis
This relatively uncommon condition consists of an abnormal row
of lashes originating from the meibomian gland orifices, poste-
rior to the grey line (Figure 1.6). The lashes are often shorter
and finer than normal lashes and tend to be directed towards the
globe. Treatment options are similar to those for trichiasis. Con-
genital distichiasis is a rare autosomal dominant condition. It may
be isolated or associated with ptosis, strabismus, chronic lym-
phoedema, spinal arachnoid cysts, and congenital heart defects.
Metaplastic lashes
Sometimes referred to as acquired distichiasis, this condition
consists of aberrant, posteriorly directed lashes which result
from chronic inflammation to the eyelid margin. The most com-
mon cause of metaplastic lashes is blepharoconjunctivitis, but
other forms of cicatrizing conjunctivitis such as Stevens–Johnson
syndrome and mucous membrane pemphigoid can also result in 5
metaplastic lashes.
Madarosis
Madarosis is a complete loss or decrease in the number of
lashes (see Figure 1.7). Causes include:
• Ocular: chronic blepharitis, infiltrating eyelid tumours
• Traumatic: chemical injuries, thermal injuries, trichotilloma-
nia (psychiatric disorder of habitual hair removal)
• Iatrogenic: following treatment of trichiasis or distichiasis;
radiotherapy or cryotherapy of eyelid and surrounding facial
tumours
• Systemic: psoriasis, generalized alopecia, hypothyroid-
ism, lepromatous leprosy, syphilis, systemic or discoid lupus
erythematosus
Eyelash ptosis
Eyelash ptosis is a downward misdirection of normally sited
upper lid lashes, caused by anterior lamellar dissociation and
slippage (see Figure 1.8). This condition is normally age related
but can be associated with dermatochalasis, floppy eyelid syn-
drome, or facial nerve palsy. Treatment is with anterior lamellar
repositioning surgery, which may be combined with eyelid ptosis
correction where indicated.
Hypertrichosis
Hypertrichosis is a condition in which lashes are abnormally
long and thick (trichomegaly) or there are an excessive number
of lashes (polytrichosis). Causes may be congenital or pharma-
cological (prostaglandin analogues, ciclosporin, and phenytoin).
Poliosis
Poliosis is the premature whitening of hair and can involve the
eyelashes as well as the eyebrows. Causes include:
• Ocular: sympathetic ophthalmitis, chronic anterior
blepharitis
• Systemic: Vogt–Koyanagi–Harada syndrome, Waardenburg
syndrome
Lash abnormality
1.2

Fig 1.5 Trichiasis secondary to trachoma Fig 1.7 Madarosis secondary to a lower lid lesion
Note the associated corneal opacification
Courtesy of Matthew Burton

Fig 1.6 Distichiasis of the lower lid

Fig 1.8 Eyelash ptosis of the right eye
Courtesy of Geoff Rose
7

CHAPTER 1 Oculoplastics
 1.3 Entropion
Entropion is an abnormal, inward rotation of the eyelid mar-
gin towards the globe. It commonly affects the lower lid but
can also occur in the upper eyelid. Eyelash-corneal contact
can lead to significant discomfort and, in severe cases, ulcera-
tion and scarring. Patients with significant punctate staining
and poor corneal sensation or those who develop microbial
keratitis should be referred urgently for correction of the
entropion.
Aetiology
• Congenital
• Acute spastic
• Involutional
• Cicatricial
Congenital entropion
Congenital entropion is rare and should be distinguished from
epiblepharon (see Section 1.13). It may be due to dysgenesis of
8 the inferior retractors resulting in eyelid instability.
Treatment
Treatment involves excision of a strip of skin and orbicularis
and then fixation of the skin to the tarsus (Hotz procedure).
Acute spastic entropion
Ocular irritation causes sustained eyelid orbicularis contrac-
tion and resultant inward rotation of the eyelid margin. The
in-turned eyelashes cause a cycle of further irritation and orbic-
ularis contraction. This condition commonly occurs in conjunc-
tion with involutional changes. Treatment options are similar to
those for involutional entropion.
Involutional entropion
Several factors are thought to play a role in involutional entro-
pion (see Figure 1.9):
1. Horizontal eyelid laxity: this condition can be assessed
by using the ‘snap-back’ test, as follows. The eyelid is pulled
away (distracted) from the globe. In patients without signifi-
cant laxity the eyelid will ‘snap’ back to its original position. If
horizontal laxity is present, the eyelid remains distracted until
the patient blinks.
2. Attenuation or disinsertion of eyelid retractors: this
condition can be identified when the lower lid has reduced
downward excursion on down-gaze.
3. Preseptal orbicularis overriding pretarsal orbicula-
ris: this condition may be evident when the patient squeezes
the eyelids closed and can be elicited on instillation of topical
anaesthetic.
Treatment
• Eyelid taping may be used as a temporary measure whilst
awaiting definitive surgical repair.
• Botulinum toxin injection to the preseptal orbicularis mus-
cle can temporarily relieve both spastic and involutional
entropion. A low dose is injected just below the skin over-
lying the preseptal orbicularis muscle by using an insulin
syringe. Avoid injecting below the punctum to prevent
punctal ectropion. In cases where an alternative to surgery
is required, repeated injections are usually sufficient to re-
lieve symptoms.
• Everting suture techniques are quick and useful tempor-
ary measures that can be performed at the bedside if
needed (e.g. in intensive therapy unit patients). However,
when used alone, they are associated with a high recur-
rence rate. Infiltrate the lower lid with local anaesthetic.
Three double-armed 4–0 or 5–0 Vicryl sutures are passed
through the conjunctiva low in the fornix, exiting the skin
2 mm below the lashes (thus catching the inferior retrac-
tors). These sutures can be left to dissolve. The medial
suture should be placed lateral to the punctum to avoid
punctal ectropion.
• Horizontal eyelid tightening improves success rates and
can normally be effectively achieved with a range of lid
shortening procedures such as the lateral tarsal strip pro-
cedure, which involves shortening and fixation of the lat-
eral tarsus.
• Retractors can be strengthened and directed anteriorly with
retractor plication methods such as the Jones procedure. A
subciliary incision is made 3 mm below the lid margin. The
orbicularis is divided by blunt dissection, and the septum is
opened to reveal the inferior retractors, which lie just anterior
to the conjunctiva. Interrupted Vicryl sutures are then used to
reattach the retractors to the lower border of the inferior tar-
sus. The skin is then closed, creating a scar that forms a barrier
to prevent the preseptal orbicularis overriding the pretarsal
orbicularis.
Cicatricial entropion
This condition is caused by conjunctival scarring and vertical tar-
soconjunctival contracture. Causes include:
• Traumatic: chemical or thermal burns
• Inflammatory: Stevens–Johnson syndrome
• Autoimmune: mucous membrane pemphigoid
• Infectious: trachoma, herpes zoster
• Iatrogenic: post-enucleation, post-lid surgery (particularly
transconjunctival approaches)
Treatment
Depending on the underlying cause, cicatricial entropion normally
requires surgery; however, lubricating ointments and bandage
contact lenses can be useful adjuncts. Mild-to-moderate cases
may be treated with anterior lamellar rotation with retractor pli-
cation and a grey line split. Mucous membrane grafts or other
spacers may be used in cases of significant forniceal shallowing
due to symblepharon formation and scarring. Typically the graft is
harvested from buccal mucosa, but nasal septum mucosa and am-
niotic membrane are also used. The graft is sutured to the pos-
terior lamella once the symblepharons are divided. Care must be
taken when operating on the conjunctiva in patients with mucous
membrane pemphigoid, as it may trigger inflammation. Systemic
immunosuppression may be advisable if there is significant risk of
reactivation.
 Oculoplastics
CHAPTER 1
Fig 1.9 Right lower lid involutional entropion

9
 1.4 Ectropion
Ectropion is an outward turning of the eyelid margin away from
the globe. Corneal exposure and dryness can result in punctate
epithelial erosions. Exposure of the palpebral conjunctiva results
in keratinization.
Aetiology
• Congenital
• Paralytic
• Involutional
• Cicatricial
• Mechanical
Congenital ectropion
Congenital ectropion is rare and is usually associated with
blepharophimosis syndrome or with ichthyosis. Often the cause
is an underdeveloped anterior lamella. Treatment is therefore as
for cicatricial ectropion.
10 Paralytic ectropion
Paralytic ectropion usually follows facial nerve palsy (see Fig-
ure 1.10). Paralysis of the orbicularis muscle may also result in
lagophthalmos leading to corneal exposure (see Figure 1.10C).
Treatment
Regular lubrication and forced blinking can be used for mild or
temporary cases. Taping of the lid (where the taping is applied
horizontally) may also be useful for nocturnal lagophthalmos, as
is a moisture chamber (created by applying lubricating ointment
and then covering the eye with Clingfilm taped to the cheek and
forehead). Cases with significant corneal exposure or perman-
ent paralysis will need surgical treatment aimed at improving lid
closure. Tarsorraphy can be temporary or permanent. It is vital
to assess where the area of exposure is most profound when
planning surgery. Poor orbicularis function may be addressed
with levator recession or the insertion of a gold weight to aid
downward lid excursion on blinking and forced eyelid closure.
Lower lid ectropion and midface droop may require medial/lat-
eral canthoplasty or fascial slings.
Tarsorraphy
Tarsorraphy is a procedure to oppose the upper and lower eye-
lids. It may be lateral, central, or complete (see Section 1.15)
Involutional ectropion
Involutional ectropion results from tissue relaxation, usually
a combination of horizontal lid laxity and medial and lateral
canthal tendon laxity (see Figure 1.11). Inferior retractor dehis-
cence may also play a part. Clinical examination can distinguish
these entities as follows.
• Horizontal laxity can be assessed by the ‘snap-back’ test (see
Section 1.3).
• Medial canthal tendon laxity can be assessed by the degree
the punctum can be distracted laterally. In severe cases, the
punctum may be pulled past the pupil.
• Lateral canthal tendon laxity is present when the lower lid
can be pulled medially without significant resistance.
• Inferior retractor dehiscence can be identified when the
lower lid has reduced downward excursion on down-gaze.
Treatment
Horizontal lid laxity can be managed with a lateral canthal
strip procedure or a full-thickness wedge resection (see Sec-
tion 1.15). The tarsal strip procedure will simultaneously ad-
dress any lateral canthal tendon laxity. In cases of significant
punctal ectropion, a lid shortening procedure can be combined
with a medial spindle. The medial spindle procedure requires
the excision of a horizontal diamond of conjunctiva below the
punctum. The defect is then closed with a buried suture that
catches the inferior retractors.
Cicatricial ectropion
Cicatricial ectropion is due to shortening of the anterior lamella
(see Figure 1.12). It may occur secondary to a variety of causes,
including sun damage, rosacea, atopic dermatitis, thermal/
chemical burns, and trauma (including iatrogenic surgical trauma
such as lower lid blepharoplasty).
Treatment
Treatment involves addressing the underlying cause. In cases
of rosacea and dermatitis, liberal massage of the skin with an
emollient can have a striking effect on reducing the ectropion. In
localized cases due to scar formation, a relaxing procedure such
as Z plasty can be used. More generalized cases require anterior
lamellar lengthening using a skin graft, typically from the pre- or
post-auricular areas. A midface lift can also be used to recruit
more skin to the lower eyelid and has the advantage of not re-
quiring any grafted tissue.
Mechanical ectropion
Mechanical ectropion may be caused by bulky tumours on or at
the lid margin, or by poorly fitted spectacles.
 Oculoplastics
A

CHAPTER 1
Fig 1.11 Bilateral involutional lower lid ectropion

11

Fig 1.12 Right cicatricial ectropion secondary to a cheek basal

cell carcinoma

Fig 1.10
A Left lower motor neurone facial nerve palsy causing paralytic
ectropion
B Forced lid closure. Note that there is significant lagophthalmos
but a good Bells phenomenon
C On close inspection, it can be seen that a small amount of
cornea is exposed on forced closure. It is important to assess if
there are signs of corneal exposure
 1.5 Ptosis I
Ptosis refers to drooping of any anatomical structure. Strictly
speaking, the term blepharoptosis should be reserved specifi-
cally for an abnormally low position of the upper lid with re-
spect to the globe. In adults, the upper lid normally sits 1–2 mm
below the superior limbus. Ptosis is due to dysfunction of one
or both of the eyelid elevators (the LPS and Müllers muscle).
History
Always ask about the nature of onset. Any sudden-onset pto-
sis may indicate a neurological cause. Pain must always be iden-
tified, as ptosis due to oculomotor nerve compressions (by a
posterior communicating artery aneurysm) typically cause pain.
A history of diplopia should also direct the clinician to consider
any underlying neurological cause.
Ptosis examination
Introduction
Introduce yourself to the patient and explain the examination.
12 Observation
Look for:
• Scars (trauma, surgery)
• General facial asymmetry
• Anisocoria (third nerve palsy, Horner syndrome)
• Heterochromia (congenital Horner syndrome)
• Strabismus (myasthenia gravis, third nerve palsy)
• Frontalis overaction
• Chin lift (severe bilateral ptosis with superior visual field
defects)
• Abnormal facial features (blepharophimosis syndrome, myo-
tonic dystrophy)
If examining a child, ask them to chew and protrude their jaw to
look for Marcus Gunn jaw-winking syndrome.
Measure
Measure the following (see Figure 1.13):
• The palpebral aperture in the primary position; measuring
this aperture may require covering the other eye if the pa-
tient has a heterotropia as detected on cover test.
• The upper and lower marginal reflex distance (the distance
between the centre of a light shone on the pupil and the
upper and lower lid margin, respectively). Palpebral aperture
measurements alone can be misleading e.g. in the context of
lower lid ectropion or hypoglobus.
• The skin crease height (the distance between the lid crease
and the upper lid margin in down-gaze). The lid crease is
often high in aponeurotic dehiscence (see Figure 1.14).
• The upper lid show (the distance from the lid margin to the
upper lid skin fold). This value may be zero in patients with
significant dermatochalasis.
• Levator function (upper lid excursion as the patient is asked
to look from extreme down-gaze to extreme up-gaze). It is
important to prevent frontalis action during this measure-
ment by placing a thumb firmly across the brow.
Bells phenomenon
Bells phenomenon is identified by asking the patient to close
their eyes whilst the examiner holds the eyelid open. The phe-
nomenon is positive if the eye rolls up under the upper lid. It is
extremely useful in assessing the risk of post-operative corneal
exposure. Patients with a poor or absent Bells phenomenon
should have conservative lid raising to avoid corneal exposure.
Lid lift
Lift the ptotic eyelid to look for a contralateral ptosis being un-
masked. This is an important test which can predict whether the
fellow eyelid will become ptotic if the ptosis is corrected.
Fatigability
This test is performed by asking the patient to maintain up-gaze
for 30 seconds and then observing if the ptosis is worse (which
would suggest myasthenia gravis). After fatiguing the upper lid,
ask the patient to make a quick downwards saccade, then back
to primary position. An upward overshoot of the upper lid be-
fore taking up fixation occurs in myasthenia gravis (Cogans lid
twitch sign). The ice pack test can also be used to aid diagno-
sis of myasthenia gravis. An ice pack is placed over the ptotic
lid for 3 minutes. A rise in the lid position suggests myasthenia
gravis.
Additional examination
• Exophthalmometry, to exclude enophthalmos
• Cover test to exclude hypotropia
• Ocular motility to exclude third nerve palsy, myasthenia
gravis
• Pupillary reactions to exclude Horner syndrome, third nerve
palsy
• Corneal sensation is important when deciding how high to
surgically lift the eyelid.
• Evert the upper lid to exclude mechanical causes of ptosis,
such as giant papillae or masses.
• Jaw-winking.
Consider pseudoptosis
Pseudoptosis is an apparent eyelid drooping that should be dif-
ferentiated from true ptosis via:
• Ipsilateral hypotropia
• Contralateral hypertropia
• Contralateral upper lid retraction
• Volume deficiencies such as enophthalmos, microphthalmos,
and phthisis bulbi
• Brow ptosis
• Dermatochalasis (when excess upper eyelid skin overhangs
the eyelid margin and gives the appearance of a ptosis).
Treatment is with blepharoplasty.
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