Plastic Surgery

Shehan Hettiaratchy
Matthew Griffiths • Farida Ali
Jon Simmons
(Editors)

Plastic Surgery
A Problem Based Approach
Editors
Shehan Hettiaratchy, M.A. Matthew Griffiths, MBBS, FRCS,
(Oxon), BM BCh, FRCS(Eng), MD, FRCS (Plast)
DM, FRCS(Plast) Department of Plastic
Department of Plastic and Reconstructive Surgery
and Reconstructive Surgery Broomfield Hospital
Imperial College Healthcare Chelmsford, UK
NHS Trust, London
UK Jon Simmons, B.Sc., MBBS,
MRCS, M.Sc. FRCS (Plast)
Farida Ali, MB ChB, M.Sc., Department of Plastic
FRCS (Plast) and Reconstructive Surgery
Department of Plastic Imperial College Healthcare
and Reconstructive Surgery NHS Trust, London
St George’s Hospital UK
London, UK

ISBN 978-1-84882-115-6 e-ISBN 978-1-84882-116-3

DOI 10.1007/978-1-84882-116-3
Springer London Dordrecht Heidelberg New York
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© Springer-Verlag London Limited 2012
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Foreword

The surgical trainee is required to assimilate an ever increas-

ing amount of knowledge and for the plastic surgeon this
covers a wide area. Consequently, it can sometimes be diffi-
cult to maintain attention on the fundamentals of patient
assessment. This book aims to bring the focus back on the
patient by providing an algorithmic approach to taking a his-
tory, examination and formulating a management plan. This
refreshingly different clinical problem-based style makes it
easy to read. At the end of every chapter the authors provide
some key references for further reading.
The book should appeal to the early years trainee as well
as to those preparing for clinical examinations

v
Preface

Plastic surgery is a big subject and the size of traditional text-

books reflects this. This book was conceived as something
different. Instead of a top-down, subject-by-subject approach,
we wanted a bottom-up approach, with the starting point
being a patient with a problem. The stimulus for this method
was lack of any decent texts for the clinical sections of the
professional exams in plastic surgery FRCS Plast in the UK,
boards in the USA and their equivalents in other parts of the
world). The chapters were written with the concept of a
patient sitting in front of the reader, as there would be in the
exam situation. However the same approach works when one
first sees a patient in the clinic. We aimed to provide the
reader with the structure and information necessary to be
successful in their careers. We have used our experience to
ensure the text is as succinct and relevant as possible. We
hope we have achieved this in some way and that this book
forms a useful adjunct to more traditional texts.
Many have contributed to the book and we would like to
thank them for their hard work and effort. SH would particu-
larly like to thank Jon Simmons for getting us across the fin-
ish line; it would not have happened without him and his
dogged determination. Finally, we would like to thank our
patients from whom we have learnt everything that is in this
book.

Shehan Hettiaratchy
Jon Simmons

vii
Acknowledgements

The Editors would specifically like to thank the following for

providing the artwork in this book:

Simon Mackey
Specialist Registrar, Plastic and Reconstructive Surgery
Pan-Thames Training Scheme
London, UK

ix
Contents

1 Abdominoplasty ............................................................. 1
Robert Caulfield and Shehan Hettiaratchy

2 Blepharoplasty ............................................................... 9
Robert Caulfield

3 Breast Reconstruction ................................................... 17

Robert Caulfield and Matthew Griffiths

4 Large Breasts/Reduction............................................... 25
Robert Caulfield and Matthew Griffiths

5 Ptotic Breasts/Mastopexy ............................................. 33

Robert Caulfield and Matthew Griffiths

6 Burns Contracture ......................................................... 41

Farida Ali and Jon Simmons

7 Burns ............................................................................... 47
Farida Ali, Abhilash Jain, and Jon Simmons

8 Cleft Lip and Palate ....................................................... 57

Ivo Gwanmesia, Matthew Griffiths,
and Jon Simmons

9 Congenital Hand ............................................................ 65

Shehan Hettiaratchy and Jon Simmons

10 Craniosynostosis............................................................. 73
Ivo Gwanmesia and Matthew Griffiths
xi
xii Contents

11 Dupuytren’s Disease ...................................................... 79

Shehan Hettiaratchy and Jon Simmons

12 Facial Palsy...................................................................... 87
Ivo Gwanmesia, Farida Ali, and Jon Simmons

13 Maxillofacial Trauma ..................................................... 93

Farida Ali, Ivo Gwanmesia, and Jon Simmons

14 Gynaecomastia ............................................................... 103

Robert Caulfield and Jon Simmons

15 Hand with Nerve Palsy .................................................. 109

Shehan Hettiaratchy and Jon Simmons

16 Hand with Inflammatory Arthropathy ........................ 117

Shehan Hettiaratchy, Abhilash Jain,
and Jon Simmons

17 Hypospadiat .................................................................... 125

Ivo Gwanmesia and Matthew Griffiths

18 Lower Limb Trauma ...................................................... 131

Shehan Hettiaratchy, Abhilash Jain,
and Jon Simmons

19 Lump in the Neck .......................................................... 137

Farida Ali, Ivo Gwanmesia, and Jon Simmons

20 Complex Wounds: Pressure Sore ................................. 143

Jon Simmons and Matthew Griffiths

21 Abnormal Ear ................................................................ 149

Ivo Gwanmesia, Matthew Griffiths,
and Jon Simmons

22 Management of the Pigmented Lesion ....................... 157

Fiona Harper
 Contents xiii

23 Aged Face: Facelifting ................................................... 165

Shehan Hettiaratchy

24 Nerve Compression ....................................................... 175

Shehan Hettiaratchy, Abhilash Jain,
and Jon Simmons

25 Severe Soft Tissue Infection.......................................... 181

Jon Simmons, Shehan Hettiaratchy,
and Carolyn Hemsley

26 Rhinoplasty ..................................................................... 187

John Henton and Jon Simmons

Appendix: FRCS Plast Classification Systems ................. 197

Index...................................................................................... 235
Contributors

Farida Ali, MB, ChB, MSc, FRCS (Plast)

Department of Plastic and Reconstructive Surgery,
St George’s Hospital, London, UK

Robert Caulfield, MB, BCh, BAO (NUI), AFRCSI, MD,

FRCSI (Plast)
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme, London, UK

Matthew Griffiths, MBBS, FRCS, MD, FRCS (Plast)

Department of Plastic and Reconstructive Surgery,
Broomfield Hospital, Chelmsford, UK

Ivo Gwanmesia, BSc, MSc, MBChB, MRCS, FRCS (Plast)

Department of Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

Fiona Harper, BSc, MBBS, MSc, FRCS (Plast)

Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

Carolyn Hemsley, MA, (Oxon), PhD, MRCP (UK),

FRCPath Directorate of Infections
Guy’s and St Thomas’ NHS Foundation Trust,
London, UK

xv
xvi Contributors

John Henton, BSc, MBBS, MRCS (Eng)

Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust, London, UK

Shehan Hettiaratchy, MA, (Oxon), BM BCh, FRCS (Eng),

DM, FRCS (Plast) Department of Plastic and
Reconstructive Surgery, Imperial College Healthcare
NHS Trust, London, UK

Abhilash Jain, MBBS, MRCS (Eng), MSc, PhD,

FRCS (Plast) Department of Plastic and Reconstructive
Surgery, Imperial College Healthcare NHS Trust London,
London, UK

Jon Simmons, BSc, MBBS, MRCS, MSc, FRCS (Plast)

Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust, London, UK
Abbreviations

a-FP Alpha-Fetoprotein
ADL Activities of Daily Living
AP Antero-Posterior
ATLS Advanced Trauma Life Support
BAHA Bone Anchored Hearing Aid
BCC Basal Cell Carcinoma
BMI Body Mass Index
BOS Base of Skull
BPI Brachial Plexus Injury
BRCA 1/2 Breast Cancer Susceptibility Protein (type 1
or 2)
CMCJ Carpometacarpal Joint
CP Cerebral Palsy
CRS Constriction Ring Syndrome
CSF Cerebrospinal Fluid
DBUN Dorsal Branch of Ulnar Nerve
DCIS Ductal Carcinoma In-Situ
DIC Disseminated Intravascular
Coagulopathy
DIEP Deep Inferior Epigastric Artery
Perforator
DM Diabetes Mellitus
DN Digital Nerve
DRUJ Distal Radio-Ulnar Joint
DVT Deep Venous Thrombosis
EAM External Auditory Meatus
ECG Electro-Cardiograph
EPL Extensor Policis Longus
FBC Full Blood Count
FCU Flexor Carpi Ulnaris
xvii
xviii Abbreviations

FDP Flexor Digitorum Profundus

FDS Flexor Digitorum Superficialis
FHx Family History
FNA(C) Fine Needle Aspiration (Cytology)
FPL Flexor Policis Longus
FSH Follicle Stimulating Hormone
FTSG Full Thickness Skin Graft
FTT Failure to Thrive
g-GT Gamma-Glytamyl Transpeptidase
GA General Anaesthetic
GI Gastro-Intestinal
GnRH Gonadotropin Releasing Hormone
hCG Human Chorionic Gonadotropin
HLA Human Leukocyte Antigen
IDDM Insulin Dependant Diabetes Mellitus
IGAP Inferior Gluteal Artery Perforator
IMF Inframammary Fold
IPJ Interphalangeal Joint
IVDU Intravenous Drug User
IVI Intravenous Infusion
Lat Lateral
LH Luteinising Hormone
LMN Lower Motor Neuron
LS Lichen Sclerosus
MCN Musculocutaneous Nerve
MPJ/MCPJ Metacarpophalangeal Joint
MRD Marginal Reflex Distance
NAC Nipple Areolar Complex
NSAID Non Steroidal Anti Inflammatory Drugs
NVB Neurovascular Bundle
OPG Orthopantomogram
ORIF Open Reduction and Internal Fixation
PCMN Palmar Cutaneous Branch of Median Nerve
PE Pulmonary Embolus
PET Positron Emission Tomography
PIPJ Proximal Interphalangeal Joint
PIN Posterior Interosseous Nerve
PVD Peripheral Vascular Disease
 Abbreviations xix

RCT Randomised Controlled Trial

ROM Range of Movement
SCC Squamous Cell Carcinoma
SGAP Superior Gluteal Artery Perforator
SSG Split Skin Graft
T4 Thyroxine
TMG Transverse Myocutaneous Gracilis Flap
TNF Tumour Necrosis Factor
TOCS Thoracic Outlet Compression
Syndrome
TPF Temperoparietal Fascia
TRAM Transverse Rectus Abdominis
Myocutaneous
TSH Thyroid Stimulating Hormone
U+E Urea and Electrolytes
UCL Ulnar Collateral Ligament
UMN Upper Motor Neuron
USS Ultrasound Scan
VAC Vacuum Assisted Closure
XR X-Ray
Chapter 1
Abdominoplasty
Robert Caulfield and Shehan Hettiaratchy

Refers to excision of excess skin and subcutaneous fat from

anterior abdominal wall +/− rectus plication.

Recognition
Cosmetic patients are usually female, middle aged, or present
post pregnancy with abdominal striae and excess skin.
Massive weight loss patients can be either male or female and
any age (Fig. 1.1).

History
General introduction
Age, occupation, recent pregnancy/childbirth, interference
with lifestyle, relationships, clothing and occupation, diabetes,
hypothyroidism.
Specific abdomen
• Is patient’s weight stable? (only operate if weight definitely
stable)
• Have they achieved their target weight/BMI?

R. Caulfield ()
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 1

DOI 10.1007/978-1-84882-116-3_1,
© Springer-Verlag London Limited 2012
2 R. Caulfield and S. Hettiaratchy

Figure 1.1 Pre-operative candidate for abdominoplasty

• Any previous abdominal surgery: Laparoscopy, laparotomy,

hernia repair, appendix, open cholecystectomy, hysterec-
tomy, etc.
• Any previous cosmetic abdominal surgery (beware, often
these patients will have had previous aesthetic abdominal
procedures, e.g., extensive liposuction (implications for
blood supply to abdominal pannus) or previous abdomi-
noplasty and will come to clinic with high aesthetic
expectations).
• Previous pregnancies, with particular emphasis on whether
normal delivery or c-section
• Any current symptoms/signs of abdominal herniae
• Psychological effects of excess abdominal tissue
• Patient’s expectations of outcome achieved by surgery
• Awareness of risks and complications associated with
surgery
 Chapter 1. Abdominoplasty 3

Risk factors
• Multiple previous pregnancies, particularly if more than
one c-section (with multiple pregnancies the abdominal
wall layers may be very loose/stretched, thus reducing
effectiveness and outcome possible with surgery; also risk
of bowel/bladder injury with multiple c-sections in the
past)
• Previous aesthetic abdominal surgery, particularly exten-
sive liposuction (quite common in these patients, hence
risk to blood supply of abdominal pannus)
• Any history of GI or respiratory problems (this can poten-
tially interfere with post-op recovery/mobilisation and
increase risk of complications)
• Smoking
• Medication (aspirin, NSAIDs, herbal medications,
anticoagulants
• Bleeding tendencies
• Hypertension
• Diabetes
• BMI >30 (known association with increased complications –
so used by NHS trusts to rationalise treatment)

General
Full medical and drug history
• Must consider co-existing morbidities relative to risks of
procedure (as essentially a cosmetic procedure, in both the
pure aesthetic and the massive weight loss cases)
• Family completed or whether planning further children
(particularly if you plicate the rectus. Although Menz, PRS
1996 implies that pregnancy is still possible, but requires
close monitoring. Need to discuss this carefully with
pre-menopausal female patients pre-op)
• Any psychological issues (i.e., is patient requesting surgery
for genuine reasons, as above)
• Occupation and sporting hobbies (as this may interfere
with these)
4 R. Caulfield and S. Hettiaratchy

• Any drug allergies

• Medications (as above)
• BMI (weight must be stable)
• Smoking (associated with increased risk of wound break-
down/delayed healing)

AIM: By the end of history you should know

1. Extent of patient’s symptoms from the excess abdominal
pannus
2. Need for additional investigations/ treatment of any
co-morbidities prior to GA
3. Patient’s awareness of risks/complications
4. What the patient hopes to achieve
5. Chances of surgery meeting these objectives

Examination
Look
Evidence of general obesity. Any overt signs of other signifi-
cant co-morbidities
• Skin quality and laxity
• Any striae (particularly if supraumbilical, as patient needs
to be informed that these will still be present post-op)
• Any scars from previous surgery or c-section. (N.B. make
sure to check for very small laparoscopic scars around
umbilicus, as these will potentially compromise viability of
umbilicus and often patients do not volunteer details
about previous laparoscopy – as they consider it a test/
investigation rather than surgery)
• Obvious hernia and bulges
• Whether significant supraumbilical component of excess
tissue (i.e., possible Fleur De Lys approach required)

Feel/move
Need to have an idea about the different components of
abdominal wall and how you will approach them
 Chapter 1. Abdominoplasty 5

• Skin quality and laxity, including scars (both above and

below umbilicus)
• Fascial system laxity, i.e., adherence of skin fat to anterior
rectus sheath – as this will influence outcome achieved by
surgery (both above and below umbilicus)
• Distribution of fat (whether liposuction also required –
both above and below umbilicus)
• Tone of abdominal wall, including divarication of recti and
any herniae (both above and below umbilicus)

AIM: By the end of examination

1. Identified any previous unknown abdominal pathology
which may require investigation/treatment
2. Have decided on most appropriate technique/combination
of techniques
3. Have an idea of any problem areas patient wishes to
address
4. Awareness of patient’s expectations about outcome
5. Willingness of patient to accept downtime and scar matu-
ration period

Investigations
• Routine bloods: FBC, U + E’s, Coag, Group and Save
• Depending on co-morbidities, may also need chest X-ray,
ECG, etc.

Treatment/Surgical Technique
Depends on examination findings and patient’s expectations
about outcome, downtime and willingness to accept risks/
complications.
Bearing this in mind the surgical options generally depend
on the amount each of the different components of abdomi-
nal wall are contributing to the overall problem (Matarasso
classification), as in examination section above. Surgeon
6 R. Caulfield and S. Hettiaratchy

preference for scar placement, plication technique and simul-

taneous liposuction also play a role.
Contribution according to
abdominal wall components Treatment options
Excess fat only Nothing or liposuction
alone
Mild excess skin and fat, no fascial Mini-abdominoplasty +/−
laxity, +/− divarication below umbilicus plication
Moderate excess skin, fat, +/− fascial Full abdominoplasty and
laxity +/− divarication above and/or plication +/− liposuction
below umbilicus
Significant excess skin, fat, fascial Full abdominoplasty and
laxity and divarication plication +/− liposuction

Risks/Complications
General
• Risks of GA including DVT/PE/chest infection
• Haematoma
• Drains

Specific

• Wound breakdown/delayed healing

• Decreased or increased sensation in abdominal skin
• Asymmetry, inadequate correction of excess pannus
• Bowel injury (unlikely – but take care when blindly plicat-
ing, particularly with round bodied needle)
• Hypertrophic scars (particularly centrally due to excess
tension in closure)
• Keloid scars (should avoid these by counselling patient
pre-op against surgery)
• Dog ears (particularly laterally – this is often due to
deficiencies in pre-op markings, most surgeons will try to
address this intra-op with either excision or liposuction)
 Chapter 1. Abdominoplasty 7

Post-operative Management
• Expected in-patient stay (2–3 days, but depends on drains)
• Many surgeons advise abdominal binder for the initial
post operative period
• Compression garment, such as high cycling shorts for
6 weeks
• Downtime: can be back at sedentary occupation after
2 weeks
• Avoid driving for 2 weeks minimum, even then only short
distances for 6 weeks
• Once healed (usually at 2 weeks) can begin massage and
moisturisation of scars
• Leave any minor revisions, such as dog ears, for at least
3 months to allow to settle first
• Counsel about duration of 12–18 months for scar
maturation
Chapter 2
Blepharoplasty
Robert Caulfield

Refers to adjustment or re-shaping of the appearance of the

upper or lower eyelids. Beware the lower lid, skin shortage and
ectropion.

Recognition
In the upper lid, patients often present with a degree of cutane-
ous hooding concealing all or part of the upper eyelid itself in
forward gaze. In the lower lid, they present with ‘bags’, i.e., post-
septal fat pads bulging behind a weakened septum. (N.B. Must be
aware of co-existing ptosis, as surgical correction is different, as
well as any compensated brow ptosis, which may require brow-
lifting prior to any upper lid blepharoplasty) (Fig. 2.1).

History
General introduction
Age, occupation, psychological reasons, interference with
lifestyle, relationships. General medical conditions such as
diabetes and thyroid disease which may also affect the eyes.

R. Caulfield
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 9

DOI 10.1007/978-1-84882-116-3_2,
© Springer-Verlag London Limited 2012
10 R. Caulfield

Figure 2.1 Pre-operative blepharoplasty candidate

Specific eyes
• Any pre-existing eye disease or defect
• Does the patient wear glasses, contact lenses or combina-
tion of both? (N.B. Contact lenses are commonest cause
of ptosis in young adults, due to stretching of levator
aponeurosis)
• Any history of glaucoma
• Dry eyes
• Excessive tearing (epiphora)
• Redness/soreness
• Double vision (diplopia)
• Any previous aesthetic lid surgery
• Family history: As puffy lower eyelids are often familial and
such patients may seek advice at a relatively young age
• Patient’s expectations of outcome achieved by surgery
• Awareness of risks and complications associated with
surgery
Risk factors
• Any pre-existing eye disease must be documented very
clearly pre-op in terms of visual function and fields
• Any significant past medical history of cardiac, GI or respi-
ratory problems (this can potentially interfere with post-op
recovery/mobilisation and increase risk of complications)
• Smoking
 Chapter 2. Blepharoplasty 11

• Medication (aspirin, NSAIDs, herbal medications,

anticoagulants)
• Bleeding tendencies (increased risk of bleeding following
post-septal fat excision – risk of retro-orbital haematoma
and blindness)
• Hypertension
• Diabetes
General
Full medical and drug history
• Must consider co-existing morbidities relative to risks of
procedure (as essentially a cosmetic procedure)
• Full list of medications such as aspirin, NSAIDs, herbal
medications, anticoagulants – which can result in cata-
strophic retro-orbital haematoma (as above)
• Any psychological issues (i.e., is patient requesting surgery
for genuine reasons)
• Occupation and sporting hobbies
• Any drug allergies
• Smoking (associated with increased risk of wound break-
down/delayed healing)

AIM: By the end of history you should know

1. Extent of patient’s symptoms, e.g., hooding causing inter-
ference with visual fields or purely aesthetic reasons
2. Need for additional investigations/treatment of any
co-morbidities prior to surgery
3. Patient’s awareness of risks/complications
4. What the patient hopes to achieve
5. Chances of surgery meeting these objectives

Examination
Note: Should always have routine assessment by ophthalmolo-
gist of patient’s visual fields and visual acuity (both with and
without glasses and contact lenses) prior to any surgery.
12 R. Caulfield

N.B. Patient and examiner should sit opposite each other with
their eyes at a similar height and the patient in direct forward
gaze.

Look
Eyes
• Any obvious eyelid pathology, e.g., BCCs, SCCs, skin tags,
cysts
• Any pre-existing scars
• Skin quality of both upper and lower lids and any wrin-
kling, particularly at rest
• Orbital asymmetries (dystopia)
• Asymmetries of brow height (brow ptosis – if present will
need to be corrected prior to upper lid blepharoplasty, as
otherwise will get more noticeable brow ptosis post
blepharoplasty)
• Presence of lagophthalmos (inability to close eyes) – if
present pre-op, this is an absolute contraindication to aes-
thetic blepharoplasty
• Position of upper lid (supratarsal) skin crease and any
asymmetries between both eyes
• Position of medial and lateral canthi relative to each
other
• Any ectropion or entropion
• Any scleral show
• Relationship of globe of eye to orbital margin (vector) –
less complications with +ve:
Negative vector: eye protruding beyond inferior orbital
margin
Positive vector: eye protected by lying behind inferior
orbital margin
Feel/move/measure
Examine for brow ptosis, i.e., measure the distance between
the mid-pupil and brow apex with callipers: on average is
approximately 2.5 cm in adult female. Measure distance from
brow apex to anterior frontal hairline: on average is 4.5–6 cm.
Thus – if mid-pupil to brow apex height is <2.5 cm and brow
apex to hairline height is >6 cm, then you have brow ptosis.
 Chapter 2. Blepharoplasty 13

• Check for compensatory brow ptosis, i.e., the brow rises

and falls as you open and close the eye.
• Assess for upper lid ptosis: Need to measure MRD1 and
MRD2 (marginal reflex distance) and levator function:
MRD1 = distance from mid-pupillary point to upper lid
margin (normal = 5 mm)
MRD2 = distance from mid-pupillary point to lower lid
margin (normal = 5 mm)

Measure levator function (Normal = 15–18 mm)

Subsequent surgical treatment of ptosis depends on
amount of ptosis (mild, 1–2 mm; moderate, 2–3 mm; severe,
4 mm or more) and levator function (good if >10 mm and
poor if <10 mm).
Assess lower lid laxity and lateral canthal tension using
snap test: any delay indicates lack of lower lid support (man-
dating a transcanthal canthopexy or perhaps canthoplasty).
Location and size of fat pads and degree of prolapse is
assessed in both upper and lower lids, simply by gentle pres-
sure on the globe itself.
Assess for presence of Bell’s phenomenon, i.e., upward
movement of globe on eyelid closure. As absence of Bell’s
will increase the risk of corneal exposure post-op, particularly
if there is any degree of lagophthalmos.

AIM: By the end of the exam

1. Identified any previous unknown eyelid pathology which
may require investigation/treatment
2. Determined from ophthalmology report the pre-op status
of visual fields and visual acuity
3. Assessed for brow ptosis and compensated brow ptosis
4. Assessed for upper lid ptosis
5. Determined lower lid laxity and lateral canthal tension
6. Confirmed presence of Bell’s phenomenon
7. Have decided on most appropriate technique/combination
of techniques
8. Have an idea of any problem areas patient wishes to address
9. Awareness of patients expectations about outcome
14 R. Caulfield

Investigations

• Opthalmologist assessment of visual fields and visual acuity

• If GA: Routine bloods: FBC, U + E’s, Coagulation screen
• If GA and depending on co-morbidities, may also need
chest X-ray, ECG etc.

Treatment/Surgical Technique
Depends on examination findings and patient’s expectations
re outcome, downtime and willingness to accept risks/
complications.
Upper lid blepharoplasty:
Can be done under local (infiltration and eye drops) and seda-
tion (much faster recovery and less expensive) or under GA.
Excise skin only first (pinch amount with Adson forceps),
then excise partial upper strip of orbicularis (but full width strip
laterally – as lateral orbicularis acts as depressor of brow).
Do not disrupt septum or take medial fat pad unless
patient specifically requests (while initially looks good, this
can hollow when patient ages and there is no way of correct-
ing this).

Lower lid blepharoplasty:

Can be done under local (infiltration and eye drops) and
sedation (much faster recovery and less expensive) or
under GA.
Always go for transconjunctival approach if possible as
much better results (if experienced in the technique) and less
complications than subciliary incision.
Transconjunctival: Be careful about removing too much
fat. Patients should expect much more conjunctival oedema
following this approach.
Transcutaneous/subciliary: Should always simultaneously
perform a transcanthal canthopexy to prevent ectropion in
immediate post-op period.
 Chapter 2. Blepharoplasty 15

Risks/Complications
General

• If under GA include DVT/PE/chest infection

Specific to eye
• Retro-orbital haematoma (rare: approximately 1 in 40,000
if untreated can cause blindness)
• Ectropion, i.e., resulting from overcorrection with lower lid
blepharoplasty (avoid by taking minimal amount of lower
lid skin and always performing transcanthal canthopexy)
• Excessive scleral show (again avoid in same way as for
ectropion)
• Over-correction with upper lid blepharoplasty resulting in
lagophthalmos (always store the excised skin, but be aware
of Human Tissue Act in this regard)
• Under-correction with upper lid blepharoplasty with resid-
ual hooding
• Under-correction with lower lid blepharoplasty fat exci-
sion with residual prominent ‘bags’
• Corneal abrasions (treat with contact lens dressing for
5–7 days)

Post-operative Management

• If done under local and sedation, then can go home same day
• Avoid any strenuous activity, heavy lifting, sports for mini-
mum of 2 weeks
• Downtime: can be back at sedentary occupation after
2 weeks
• Sutures out at 5 days
• Warn about appearance of elevated lateral canthus if tran-
scanthal canthopexy performed along with lower lid
blepharoplasty
• Counsel about duration of 12–18 months for scar
maturation
16 R. Caulfield

Anatomy of the Lids (Fig. 2.2)

Orbital septum
Pre-aponeurotic fat

Pre-septal
orbicularis oculi

Levator

Levator
aponeurosis
Mullers muscle
Pre-tarsal
orbicularis Sub-aponeurotic space
oculi
Tarsal plate

Conjunctiva

Tarsal plate

Conjunctiva
Inferior lid retractors

Inferior oblique muscle

Septum

Orbicularis oculi

Inferior rectus
muscle
Fat
Arcus marginalis

Figure 2.2 Top: upper lid anatomy, Bottom: lower lid anatomy
Chapter 3
Breast Reconstruction
Robert Caulfield and Matthew Griffiths

Occurs most commonly as either immediate or delayed

reconstruction following mastectomy +/− axillary dissection.
Recently, oncoplastic techniques are being used to optimise
aesthetic results following wide local excision of breast lumps.

Recognition
Often in combination with general/breast surgeons in joint
clinics prior to tumour removal or following referral from
them for either immediate or delayed reconstruction. Type
and extent of reconstruction depends on tumour treatment
(particularly adjuvant therapy such as radiotherapy), patient
choice/expectations and experience/capability of reconstruc-
tive team (Fig. 3.1).

R. Caulfield ()
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 17

DOI 10.1007/978-1-84882-116-3_3,
© Springer-Verlag London Limited 2012
18 R. Caulfield and M.Griffiths

Figure. 3.1 Patient post DIEP breast reconstruction pre-symmetrization

History
General
Age, occupation, recent pregnancy/childbirth/family completed.
Detailed past medical history (as co-morbidities will impact
significantly on choice of reconstruction), social history,
medications and smoking.

Specific breast cancer

• Family history of breast cancer
• Any genetic high risk, e.g., BRCA1 or BRAC2
• Personal history of previous/current lumps, nipple dis-
charge, skin retraction, inverted nipples
• Any previous breast investigations and the results
• Any pre-op therapy planned, e.g., chemotherapy
• Surgical management plan by general breast surgeons
• Post-op adjuvant therapy planned, e.g., radiotherapy
or chemotherapy (Must be aware of exact timings)
Risk factors
• Tumour grade/extent/stage
• Age: may influence reconstructive options
 Chapter 3. Breast Reconstruction 19

• Multiple co-morbidities
• General obesity: Will be associated with significant increase
of complications
• Family history of breast cancer (as above)
• Smoking: Associated with wound healing problems, poor
vessels/blood flow in free flaps and increase in anaesthetic
related complications, e.g., chest infection, DVT PE
• Medication (aspirin, NSAIDs, herbal medications, antico-
agulants)
• Bleeding tendencies
• Hypertension
• Diabetes
• BMI >30
Breast reconstruction history
• Current breast size/shape
• Patient desire for post-op size/shape
• Patient’s awareness of reconstructive options and specific
requests for particular reconstruction
• Patient willingness to have symmetrisation procedures on
the other side
• Past surgical history, particularly abdominal surgery (be
aware that increasingly units are being more expansive in
their approach to such cases and often they can be consid-
ered as relative contraindications or considered as ‘more
complex’ rather than absolute contraindications)
• Patient’s weight stable (as otherwise DIEP/TRAM recon-
struction will change as weight changes)
• Patient’s occupation, hobbies, sports
• Acceptance of donor site morbidity and outcome
AIM: by the end of history you should know
1. Patient’s expected treatment plan
2. Tumour related factors that may influence type of
reconstruction
3. Patient related factors that may influence type of
reconstruction
4. Patient’s choice/request for specific reconstruction
20 R. Caulfield and M.Griffiths

5. Patient awareness of reconstructive pathway, risks/compli-

cations, duration and timing
6. Chances of reconstructive surgery meeting patient’s
objectives

Examination
Look
Evidence of general obesity, any overt signs of other signifi-
cant co-morbidities.
Breast
Cancer exam first
In immediate cases, will already be well documented by gen-
eral breast surgeon, but will help in planning size, shape and
inset of flap/reconstruction.
In delayed cases, will identify any previously unknown
problems on unaffected side, as well as assisting in planning
size, shape and inset of flap/reconstruction
• Look for symmetry (immediate cases), lumps, skin retrac-
tion, inverted nipples, nipple discharge
• Examine standing or sitting up: first arms by side, then on
hips flexing pectoralis major and then arms above head
• Examine both breasts for abnormal lumps (NAC, four
quadrants and tail of breast) with patient lying down and
arm above head for each side
• Examine both axillae for any nodes
Aesthetic exam
• Examine with patient standing up, looking straight ahead
and hands on hips
• In delayed cases, examine with bra on, as this allows you to
gauge volume/size of reconstruction required (particularly
if patient does not want any symmetrisation on normal
side post-op)
• In delayed cases: need to assess volume of tissue required and
amount of skin and ptosis required to match opposite side
 Chapter 3. Breast Reconstruction 21

• Assess suitability of opposite side for subsequent masto-

pexy/reduction procedure
• Measure sternal notch to nipple distance and nipple to
IMF on normal side and correlate with ideal position on
side to be reconstructed
• Skin quality (particularly if previous radiotherapy and if
previous smoker or other co-morbidities)
• Presence of any scars
Abdomen (DIEP/TRAM donor site)
• Extent of available abdominal pannus
• Presence of divarication of recti or any hernia
• Any abdominal scars, e.g., appendix, laparoscopy, laparo-
tomy, c-section/pfannenstiel, hysterectomy, Kocher’s, etc.
(as noted in breast reconstruction history – are now con-
sidered more complex cases or relative contraindications,
rather than absolute contraindications)
Back (latissimus dorsi donor site)
• Presence or absence of lat. dorsi (N.B. Poland’s syndrome)
• Volume of adipose tissue
• Amount of excess skin
• Presence of pre-existing scars
Thigh (TMG donor site)
• Volume of adipose tissue
• Amount of excess skin
• Presence of pre-existing scars
Buttock (SGAP/IGAP donor site)
• Volume of adipose tissue
• Amount of excess skin
• Presence of pre-existing scars
AIM: by the end of exam
1. Identified most appropriate donor site for reconstruction
2. Have secondary ‘back-up’ donor in case of problems with
first choice
3. Have an idea of any problem areas patient wishes to address
22 R. Caulfield and M.Griffiths

4. Awareness of patient’s expectations about outcome and

reconstruction pathway
5. Willingness of patient to accept downtime and subsequent
symmetrisation and adjustment phase of reconstruction

Investigations
Routine bloods: FBC, U + E’s, coag, group and crossmatch
CT angiogram (not routine in every unit, but increasingly
used to plan pre-op for DIEPs).
Additional radiological/cytological/histological investiga-
tions only if clinical suspicion:
• Radiology: Ultrasound breast (if < 35 years old)
• Mammogram breast (if > 35 years old and suspicious lump
or if > 50 years old and > 1 year since last mammogram)
• Ultrasound axillae (if palpable axillary nodes)
• Cytology/Histology: i.e., FNA or Trucut biopsy of suspi-
cious lumps or nodes

Treatment/Surgical Technique
Depends if immediate or delayed reconstruction, any pre-op
therapy, post-op radiotherapy/chemotherapy, as well as exam-
ination findings, suitable donors to provide optimal recon-
struction and patient’s expectations.
Ultimately tumour treatment and patient survival is most
important, so reconstruction should not interfere in any way
with this. Remember low grade DCIS patients can survive for
a long time, and high grade tumours often have limited prog-
nosis (so simpler, less complicated reconstructions may be
more appropriate).
Considering all of the above, rigid reconstruction rules do
not apply (apart from avoiding implant based reconstructions
 Chapter 3. Breast Reconstruction 23

if post-op radiotherapy is planned). So any reconstruction

can be any one or combination of those below.
Note: Autologous reconstructions can include:
Extended Lat Dorsi, DIEP/TRAM, SGAP/IGAP, TMG.
An example of a reasonable general approach and options
for reconstruction:
Young, fit and Old and
well Radiotherapy infirm
Small 1. Expander 1. Autologous 1. Expander
breast 2. Lat. dorsi and 2. Lat.
implant dorsi and
3. Autologous implant

Moderate 1. Expander and 1. Autologous 1. Expander

breast mastopexy/
reduction
2. Lat. dorsi and
implant and
mastopexy/
reduction
3. Autologous
Large breast 1. Nothing 1. Nothing 1. Nothing
2. Expander and 2. Lat. dorsi 2. Expander
reduction and implant and
3. Lat. dorsi and and reduction reduction
implant and 3. Autologous
reduction
4. Autologous

Risks/Complications
General
• Risks of GA including DVT/PE/Chest infection
• Haematoma
• Drains
24 R. Caulfield and M.Griffiths

Specific
Flap problems:
• Flap loss/failure
• Partial flap loss/fat necrosis
• Delayed wound healing/wound breakdown (can delay
start of adjuvant therapy)
Donor problems:
• Haematoma
• Hernia/bowel injury (with DIEP/TRAM – but very low
risk with modern techniques)
• Delayed wound healing/wound breakdown (can delay
start of adjuvant therapy)
Implant/expander problems:
• Haematoma
• Infection
• Extrusion
• Delayed wound healing/wound breakdown (can delay
start of adjuvant therapy)
• Capsular contraction and pain

Post-operative Management
Depends on:
• Type of reconstruction performed
• Immediate post-op complications
• Unit protocol for post-op care and discharge of flap
reconstructions
• Timing of any planned adjuvant therapy
Chapter 4
Large Breasts/Reduction
Robert Caulfield and Matthew Griffiths

Bilateral mammary hypertrophy/hyperplasia. Often asym-

metrical. Can also be associated with significant ptosis – so be
aware of overlap of reduction approach/techniques with
mastopexy approach/techniques.

Recognition
Can present at any age post puberty: But usually young females
in early 20s or women in 40s after completion of family.
Recognise by excess of breast tissue +/− excess skin, +/− ptosis,
combined with presenting symptoms (see below) (Fig. 4.1).

History
General introduction
Age, symptoms and duration, occupation, N.B. interference
with lifestyle, relationships, clothing and occupation. Neck
pain and shoulder pain (N.B. warn patients that neck/shoul-
der pain may be due to other causes and may not resolve
post-op). Diabetes, hypothyroidism.

R. Caulfield ()
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 25

DOI 10.1007/978-1-84882-116-3_4,
© Springer-Verlag London Limited 2012
26 R. Caulfield and M. Griffiths

Figure 4.1 Candidate for breast reduction

Specific breast
• Grooving
• Intertrigo/maceration
• Requirement to wear bra at night
• Psychological effects
• Pain (Must make sure patient is wearing correct bra size
(see below) – commonest cause of breast pain )
• Family history of breast cancer
• Personal history of previous/current lumps, discharge, skin
retraction, inverted nipples
• Any previous breast investigations and the results: FNAs,
biopsies, ultrasound, mammogram
Risk factors
• Family history of breast cancer
• General obesity: In younger women – associated with
oestrogen induced increase in dense glandular tissue; in
older women – associated with increase in fatty/adipose
content of breast
• Smoking
• Medication
• Bleeding tendencies
 Chapter 4. Large Breasts/Reduction 27

• Hypertension
• Diabetes
• BMI > 30 (known association with increased complications –
so used by NHS trusts to rationalise treatment)

General
Full medical and drug history
• Must consider co-morbidities in risk/benefit analysis
• Family completed or whether planning further children
(implications for breast feeding)
• Any psychological issues (i.e. is patient requesting surgery
for genuine reasons)
• Any drug allergies
• Medications (as above)
• BMI (weight must be stable)
• Smoking (associated with increased risk of wound break-
down/delayed healing)

AIM: by the end of history you should know

1. Extent of patient’s symptoms
2. Need for additional investigations/treatment of any
intrinsic breast lump/problem
3. Patient’s awareness of risks and complications
4. What the patient hopes to achieve
5. Chances of surgery meeting these expectations

Examination
Look
Evidence of general obesity. Any overt signs of other signifi-
cant co-morbidities.

Breast – cancer exam first

• Look for symmetry, lumps, skin retraction, inverted nip-
ples, nipple discharge
• Examine standing or sitting up: first arms by side, then on
hips flexing pec. major and then arms above head
28 R. Caulfield and M. Griffiths

• Examine both breasts for abnormal lumps (NAC, four

quadrants and tail of breast) with patient lying down and
arm above head for each side
• Examine both axillae for any nodes
Aesthetic breast exam
• Initially examine with bra on: to determine if correct size/
possible cause of breast pain (particularly if pain is the
patient’s main reason for requesting a reduction)
• Examine with patient standing up, looking straight ahead
and hands on hips
• Assess approximate cup size and asymmetry:
Measure chest circumference at IMF level:
If even number: add 4 in. This gives the bra size
If odd number: add 5 in. i.e., 34 or 36 etc.
Measure breast circumference at most prominent part of
breast:
If equal to IMF measurement – then AA cup
If 2 cm (1 in.) more – then A cup
If 4 cm (2 in.) more – then B cup etc.
• Grade of ptosis (see mastopexy chapter)
• Measure sternal notch to nipple distance
• Measure nipple to IMF distance
• Inspect for stretch marks
• Skin quality
• Presence of any scars: N.B. previous wide local excision for
breast lump (will need to consider altering skin excision
technique to possibly include scar); previous duct excision
for benign nipple discharge (will have partial periareolar
scar, but significant risk to nipple viability if pedicle is
based in same area, so will need to change location of der-
moglandular pedicle).

AIM: by the end of exam

1. Identifyied any previous unknown breast pathology
2. Have an idea of any problem areas patient wishes to
address
 Chapter 4. Large Breasts/Reduction 29

3. Have decided on most appropriate technique

4. Awareness of patient’s expectations
5. Willingness of patient to accept downtime and scar matu-
ration period

Investigations
• Routine bloods: FBC, U + E’s, coag
• Cytology/Histology: i.e. FNA or Trucut biopsy of suspi-
cious lumps or nodes
• Additional radiological/cytological/histological investiga-
tions only if clinical suspicion:
− Radiology: Ultrasound breast (if < 35 years old)
− Mammogram breast (if > 35 years old and suspicious
lump or if > 50 years old and >1 year since last
mammogram)
− Ultrasound axillae (if palpable axillary nodes)

Treatment/Surgical Technique
Depends on examination findings and patient’s expectations
about outcome and willingness to accept risks/complications:
• Amount of expected tissue to be resected from each side:
• 32–34 in. chest – one cup size = 100 g
• 36 in. chest or > − one cup size = 180–200 g
• Skin quality and amount of excess skin
• Degree of ptosis
• Nipple to IMF distance
• Patient’s age: younger patient’s skin more elastic (better
results with vertical scar than older patient)
• Smoker/ex-smoker/non-smoker
Technique
All based on dermoglandular pedicle: Can be inferior, super-
omedial or central superior depending on surgeon’s prefer-
ence and experience.
Some general guidelines (but considerable variation in
approach depending on surgeon’s preference and experience):
30 R. Caulfield and M. Griffiths

1. Very small reduction: Liposuction only. Easier in

older atrophic, less glandular
breasts
2. Ptosis only: Mastopexy technique (see
mastopexy chapter)
3. Sternal notch to nipple distance:
• Less than 30 cm Vertical scar technique (but
only if young, good quality
elastic skin and non-smoker)
• Greater than 30 cm Wise pattern technique of your
choice
• Greater than 40 cm Warn of risk of free nipple graft

Risks/Complications
General
• Risks of GA including DVT/PE/Chest infection
• Haematoma
Specific
Nipples:
• Nipple loss/necrosis (partial or complete)
• Decreased or increased sensation
• De-pigmentation of NAC
Wound:
• Delayed healing
• T junction breakdown
Scar:
• Hypertrophic scars (particularly at medial and lateral
extent of wounds
• Keloid scars (very important to counsel at risk patients
adequately pre-operatively)
• Dog ears (particularly laterally – this is often due to defi-
ciencies in pre-op markings)
 Chapter 4. Large Breasts/Reduction 31

Gland:
• Loss of ability to breastfeed (should have identified preop-
eratively whether family complete; however up to 70%
can still lactate post-op)
• Residual asymmetry

Post-operative Management
• Expected in-patient stay (1–3 days, but depends on drains – a
lot of surgeons routinely do not use drains with reductions
anymore, so can often discharge day after surgery)
• Downtime: can be back at sedentary occupation within 2
weeks
• Avoid driving for 2 weeks
• Wear sports bra day and night for 6 weeks
• Once healed (usually at 2 weeks) can begin massage and
moisturisation of scars
• Counsel about duration of 12–18 months for scar
maturation
Chapter 5
Ptotic Breasts/Mastopexy
Robert Caulfield and Matthew Griffiths

Pure ptosis refers to descent of NAC and breast tissue below

the IMF (see grading below). Often asymmetrical. Often asso-
ciated with mammary hypertrophy/hyperplasia – so be aware
of overlap of mastopexy approach/techniques with reduction
approach/techniques.

Recognition
Usually patients present post childbirth with post-pregnancy
involutional changes, volume loss, striae, etc. (N.B. These
cases often require augment-mastopexy approach; assess
very carefully pre-op) But usually women in 40s or older with
moderate ptosis. Often associated with excess breast tissue
and asymmetrical, so take care to assess in detail pre-op
about all aspects, i.e., skin, breast, NAC and most importantly
patient’s expectations about outcome (Fig. 5.1).

R. Caulfield ()
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 33

DOI 10.1007/978-1-84882-116-3_5,
© Springer-Verlag London Limited 2012
34 R. Caulfield and M. Griffiths

Figure 5.1 Patient with ptotic breasts

History
General introduction
Age, duration of problem and symptoms, occupation, recent
pregnancy/childbirth, is family complete, interference with
lifestyle, relationships, clothing and occupation, diabetes,
hypothyroidism. (Neck pain and shoulder pain are usually
not an issue in pure mastopexy cases, unless associated with
significant mammary hypertrophy/hyperplasia).
Specific: Breast
• Recent changes in bra size (hence breast volume)
• Any previous aesthetic breast surgery (these patients
often have high aesthetic expectations – must know details
of surgery)
• Grooving
• Intertrigo/maceration
• Requirement to wear bra at night
• Psychological effects
• Pain (must make sure patient is wearing correct bra size –
commonest cause of breast pain)
• Family history of breast cancer
• Personal history of previous/current lumps, discharge, skin
retraction, inverted nipples
• Any previous breast investigations and the results: FNAs,
biopsies, ultrasound, mammogram
 Chapter 5. Ptotic Breasts/Mastopexy 35

Risk factors
• Multiple previous pregnancies (hence significant involu-
tional volume loss and striae, poor skin quality)
• Previous aesthetic breast surgery (see above)
• General obesity in younger women, much denser breast,
hence get good results with mastopexy alone, often verti-
cal scar possible
• General obesity in older women, more fatty breast and less easy
to get good projection, so often require augment-mastopexy).
• Family history of breast cancer
• Smoking
• Medication
• Bleeding tendencies
• Hypertension
• Diabetes
• BMI > 30 (known association with increased complica-
tions – so used by NHS trusts to rationalise treatment)
General
Full medical and drug history
• Must consider co-existing morbidities relative to risks of
procedure (as essentially a cosmetic procedure)
• Family completed or whether planning further kids (impli-
cations for breast feeding and postpartum shape/volume
changes)
• Any psychological issues (i.e., is patient requesting surgery
for genuine reasons, as above)
• If augment-mastopexy required, does patient wish for one
stage procedure, or happy to have two stage (implications
for cost (if private) and also downtime). Also awareness of
future implant related ops.
• Any drug allergies
• Medications (as above)
• BMI (weight must be stable)
• Smoking (associated with increased risk of wound break-
down/delayed healing)
AIM: by the end of history you should know
1. Extent of patient’s symptoms
2. Need for additional investigations/treatment of any intrin-
sic breast lump/problem
36 R. Caulfield and M. Griffiths

3. Patient’s awareness of risks/complications

4. What the patient hopes to achieve
5. One stage or two stage preferred by surgeon and/or by patient
6. Chances of surgery meeting these objectives

Examination
Look
Evidence of general obesity. Any overt signs of other
significant co-morbidities.
Breast
Cancer exam first
• Look for symmetry, lumps, skin retraction, inverted nip-
ples, nipple discharge
• Examine standing or sitting up: first arms by side, then on
hips flexing pec major and then arms above head
• Examine both breasts for abnormal lumps (NAC, four
quadrants and tail of breast) with patient lying down and
arm above head for each side
• Examine both axillae for any nodes
Aesthetic exam
• Initially examine with bra on: to determine if correct size-
possible cause of breast pain
• Examine with patient standing up, looking straight ahead
and hands on hips
• Particularly important to assess upper pole breast volume
– pinch test:
If > 2 in. breast tissue upper pole can go subglandular
If < 2 in. breast tissue upper pole must go submuscular
• Assess grade of ptosis (Regnault):
− Normal breast: NAC above IMF, breast tissue at or
above IMF
− Grade 1: Nipple at IMF and above most dependent
breast tissue
 Chapter 5. Ptotic Breasts/Mastopexy 37

Figure 5.2 Grades 1–3 ptosis

− Grade 2: Top of NAC at IMF and above most depen-

dent breast tissue
− Grade 3: NAC below IMF and below most dependent
breast tissue
− Pseudoptosis: NAC above IMF, but breast tissue below
IMF (usually post reduction) (Fig. 5.2)
• Measure sternal notch to nipple distance
• Measure nipple to IMF distance
• Stretch marks/striae
• Skin quality (particularly if previous smoker or other
co-morbidities)
• Presence of any scars

AIM: by the end of exam

1. Identified any previous unknown breast pathology/sus-
pected cancer which may require investigation/treatment
2. Have decided on most appropriate technique/combination
of techniques
3. If augment-mastopexy required: whether one stage or two
stage (surgeon preference versus patient preference)
4. Have an idea of any problem areas patient wishes to address
5. Awareness of patient’s expectations about outcome
38 R. Caulfield and M. Griffiths

Investigations
• Routine bloods: FBC, U + E’s
• Additional radiological/cytological/histological investiga-
tions only if clinical suspicion.

Treatment/Surgical Technique
Depends on examination findings and patient’s expectations
about outcome, downtime and willingness to accept risks/
complications.
• If mastopexy alone, which skin excision technique will give
best results in terms of breast tissue re-modelling, as well
as most appropriate skin resection to give optimum pro-
jection and shape
• If augment-mastopexy, whether one stage or two stage and
how to manage patient’s expectations about results and
downtime, particularly if two stage approach

Technique
As described above, technique can be mastopexy alone, or
augment-mastopexy, which can in turn be one or two stages
(if two stages should do augment first, followed by mastopexy
a minimum of 3 months later).
Mastopexy alone techniques:
All based on same approach taken to reduction cases.
Skin excision:
• Periareolar: but take care, these scars can stretch badly and
often leave visible white scar as result
• Vertical scar: Rule of thumb, only if young, good elastic
skin quality, non-smoker and only need to lift nipple less
than 10 cm, i.e., most tend to be grade 1 or 2 ptosis
• Wise pattern: Tend to need in most cases, as the self-selecting
patient population are older, poor skin quality, often
smokers/ex-smokers, and anyone with grade 3 ptosis
 Chapter 5. Ptotic Breasts/Mastopexy 39

Breast tissue re-modelling:

Use a dermoglandular pedicle (as with reduction cases),
which can be inferior, superomedial or central superior
depending on surgeon’s preference and experience. Rather
than excise tissue (unless needed), you simply re-position/
re-mould tissue to give ideal projection and shape.

Augment-mastopexy techniques:
As noted above, can be one or two stage

If one stage:
• Do augment first (either subglandular or submuscular –
see ‘Examination’ section)
• Then mastopexy, using most appropriate combination of
skin excision and breast re-modelling techniques as
above

If two stage:
• Same approach as one stage, except separate by 3 months,
which allows the subsequent mastopexy to be more
effective (but must carefully manage patient’s expec-
tations).

Risks/Complications
General
• Risks of GA: DVT/PE/chest infection
• Haematoma
• Drains (often not used in pure mastopexy cases)

Specific
Nipples:
• Nipple loss/necrosis (partial or complete – again less likely
than in reduction cases)
• Decreased or increased sensation
• Depigmentation of NAC
40 R. Caulfield and M. Griffiths

Wound:
• Delayed healing
• T junction breakdown

Scar:
• Hypertrophic scars (particularly at medial and lateral extent
of wound)
• Keloid scars (Ensure susceptible patients are properly
counselled about the potential risks)
• Dog ears (particularly laterally)

Gland:
• Lack of projection
• Insufficient volume in upper pole
• Loss of ability to breastfeed (Patients should be coun-
selled about this pre-operatively if family incomplete -
approximately 70% can still lactate post-op)
• Residual asymmetry

Post-operative Management
• Expected in-patient stay (2–3 days, but depends on drains –
a lot of surgeons routinely do not use drains anymore, so can
often discharge day after surgery)
• Downtime: can be back at sedentary occupation within
2 weeks
• Avoid driving for 2 weeks
• Wear sports bra day and night for 6 weeks
• Once healed (usually at 2 weeks) can begin massage and
moisturising scars
• If two stage augment-mastopexy, counsel about expecta-
tions after first op (augment) and need for 3 month delay
before second stage
• Counsel about duration of 12–18 months for scar
maturation
Chapter 6
Burns Contracture
Farida Ali and Jon Simmons

Prevention is better than cure. Children, in particular, who

have sustained burns should be followed up regularly to allow
early identification of problematic scars.

Recognition
Burn scar contracture can result in both functional and aes-
thetic problems. The aim of treatment should firstly be to
improve function, particularly in vital areas such as perior-
bital, hand or perioral (Fig. 6.1).

History
General introduction
Age, occupation, handedness, interference with lifestyle, rela-
tionships, smoking and occupation. Co-morbidities and
medication.

F. Ali ()
Department of Plastic and Reconstructive Surgery,
St George’s Hospital,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 41

DOI 10.1007/978-1-84882-116-3_6,
© Springer-Verlag London Limited 2012
42 F. Ali and J. Simmons

Figure 6.1 Burn contracture

Specific burn history

• Mechanism of burn
• How long ago
• Initial treatment
• Time to healing (>3/52 higher risk of problematic scars)
• Complications such as infection
• Length of time in hospital: to give an idea of the complex-
ity of the burn
Define the problem
• What is the patient’s assessment of any problems
• Unstable skin, ulceration and bleeding, pain and itching
• Facial: asymmetry, scarring, think about cosmetic units
• Periorbital scars: eye opening or closure, watering
• Perioral scars: microsomia, inability to close mouth?
• Neck: restricted range of movement. Does it pull down/
distort the mouth upon movement?
 Chapter 6. Burns Contracture 43

• Breast: abnormal breast development (especially with

burns sustained in prepubertal girls)?
• Joints
− Axillary contracture. Limitation of arm and shoulder
movement? Ask about any difficulty dressing (doing up
a bra, fastening buttons), personal care, e.g., brushing
hair
− Popliteal fossa: limited leg extension? Difficulty
walking?
− Feet: hyperextension of the toes – problems with
footwear?
− Hands: Is the wrist affected? Limitation of finger exten-
sion more common. Can prevent or restrict coarse and
fine grip

AIM: by the end of the history you should

1. Have a full understanding of the history of the burn and its
cause and initial treatment
2. Understand how long different areas of the burn took to
heal and any complications
3. Have a thorough understanding of the patient’s functional
level
4. Understand what the patient hopes to achieve from any
further treatment
5. Know any factors which might influence treatment:
co-morbidities, occupation, etc.

Examination
Look
• Assess the patient’s skin from head to toe, then concen-
trate on the problem areas
• Where is it?
• Does it cross joints or cosmetic units?
44 F. Ali and J. Simmons

• Is there distortion at rest?

• What is the morphology of the burn: linear scar or large
confluence?
• Is the scar mature or immature, keloid or hypertrophic?
• What is the quality of the burn tissue and surrounding
tissues?
Move
• Take the patient through the range of movement specific
to that area.
• Note any limitation in movement and distortion of neigh-
bouring structures as they go through their range of
motion.
• Ask the patient to perform simple activities that demon-
strate the degree (and impact) of such limitation.
− Put your chin on your chest
− Look up to the ceiling
− Look over your left/right shoulder
− Close your eyes
− Smile
− Close your mouth (with and without neck extension)
− Put your hands behind your head/back
− Lift your arms above your head
− Straighten your arm
− Put your hands flat on the table
− Make a fist
• Ask them to walk noting any deviation from the normal
gait cycle.
• Examine the neighbouring tissues to evaluate the poten-
tial use in the reconstructive options.
AIM: by the end of the examination you should
1. Understand any functional or cosmetic implications of the
burn
2. Have assessed surrounding tissues for local treatment
options
 Chapter 6. Burns Contracture 45

3. Have assessed remote sites for potential donor sites

4. Have formulated some plans for treatment

Investigations
• Routine bloods: FBC, U + E’s, Coagulation, Group and
Save
• Depending on co-morbidities, may also need chest X-ray,
ECG etc.
• If joints are involved, relevant x-rays

Treatment
Early
• Pressure therapy: need to work closely with the OT who
need to ensure the pressure garment fits well and is
changed as necessary to allow growth
• Splint: Resting and night splints to prevent/minimise
deformity
• Physiotherapy: to preserve as much range of motion as
possible
• Surgery rarely indicated but may be required to protect eye
Surgical treatment is usually only considered in mature scars.
Local flaps: The use of local flaps alone requires adequate
tissue laxity in the surrounding skin and soft tissue
• Z plasty
• Y–V flaps
Tissue expansion
• With second stage local flap (advancement, transposition,
rotation)
• Beware the lower limb where expansion is fraught with
difficulties
46 F. Ali and J. Simmons

Resurfacing
• FTSG: better than STSG because of less contraction and
better colour match. Maybe useful in burn contractures of
the neck. Not so useful in contractures around joints,
which require durable tissue.
• Distant flap: includes fasciocutaneous and musculocutane-
ous flaps, e.g., latissimus dorsi flap for axillary scar release,
TFL flap for groin
• Free flaps
• Skin substitutes
Chapter 7
Burns
Farida Ali, Abhilash Jain, and Jon Simmons

As with all trauma, burns patients should be managed accord-

ing to ATLS guidelines. Types: minor, major and burns in
special sites.

Recognition
Establish the history early as facial and/or airway swelling
may make this difficult later on. Flame burns and chemical
burns are most common in adults. In children and the elderly,
scalds are more common. For this group, non-accidental
injury must also be considered.

Referral to a burns unit

National Burn Care Review Group guidelines:
• Major burns (>10% in children, >20% in adults)
• Full thickness burns >5% TBSA
• Inhalational injury
• Specific mechanisms (chemical burns (esp. hydrofluoric
acid), high tension electrical burns)
• Special sites (facial, hands, feet, perineum, flexor surfaces,
circumferential burns)

F. Ali ()
Department of Plastic and Reconstructive Surgery,
St George’s Hospital,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 47

DOI 10.1007/978-1-84882-116-3_7,
© Springer-Verlag London Limited 2012
48 F. Ali et al.

Figure 7.1 Acute chemical burn

• Special groups (the elderly (>60), very young (<5), NAI)

• Concomitant injury/coexisting disease (Fig. 7.1)

History
Specific
The type of burn:
• Flame: flash burn, explosion, clothes on fire, extinguished,
enclosed space, first aid measures
• Scalds: immersion or spill, source (boiled water, with or
without milk, other (e.g., oil – deeper burns), bath water)
• Electrical: high tension or domestic, lightening strike, arc-
ing, collapse (cardiac arrest/arrhythmia), contact time
• Chemical: acid or alkali, time of exposure, irrigation,
neutralisation
• Contact: temperature, industrial (much higher tempera-
tures) versus domestic
Respiratory complications: 10–20% of patients admitted for
major burns have an associated inhalational injury. Consider
the possibility of direct injury to the airways, smoke inhalation,
blast injury (mechanical trauma to the lungs/alveolae, ARDS).
The timings:
Time of burn itself
Exposure time
 Chapter 7. Burns 49

Time first aid measures commenced

Length of time of cooling/irrigation
Time fluids started (if any)

Circumstances of burn:
Accidental, non-accidental, self-inflicted? Self-inflicted inju-
ries often obvious. Non-accidental injuries (NAI) however
can be difficult to identify but are extremely important to
recognise. Consider in all burns in children and the elderly.
Check ‘at risk’ register. If any suggestion of NAI, child pro-
tection services need to be involved. Although distressing for
the family, primary concern is patient safety. Suspect if any of
the following are present:

• Delayed presentation
• Changing history
• History/signs of previous injuries of varying age
• Inappropriate reactions (over the top or no interest)
• Inappropriate interaction between involved parties

Concomitant injuries:
Did they need to jump out of a building? Was there an explo-
sion? With high-tension electrical injuries, patients can be
thrown a significant distance, sustaining mechanical trauma
in addition to the burn injury. Blast injury?

Other:
Co-morbidities/smoker? This will affect the carboxyhaemo-
globin result.
Drug history/allergies

Examination

As per ATLS guidelines

Airway (with Cx Spine control):
If conscious, is the patient talking? Airway burns are those
above the level of the vocal cords. Facial/oral/mucosal burns/
oedema. Singeing of nasal hairs. Carbonaceous sputum.
Stridor. Hoarse voice.
50 F. Ali et al.

Breathing (with 100% oxygen via a non-rebreather bag):

Signs include: tachypnoea, dyspnoea. Abnormal chest move-
ments (circumferential deep dermal/full thickness burns of
the torso or associated mechanical trauma). Crepitations.
Pulmonary oedema. Signs of ARDS. Reduced oxygen satura-
tions (may be falsely high in carboxyhaemoglobin toxicity).
Arterial blood gas analysis may reveal hypoxia or raised car-
boxyhaemoglobin (>25–30% in a non-smoker is an indica-
tion for ventilation).
ANY concerns about actual or potential airway or breath-
ing complications should initiate anaesthetic input to assess
the patient, securing a protected airway and providing respi-
ratory support where indicated. Intubation is indicated in all
patients prior to transfer to a burns unit where there is poten-
tial for respiratory compromise, irrespective of whether they
show signs or not at the referring hospital.

Circulation (with IV access and fluids):

Heart rate. Blood pressure. Hypovolaemia uncommon in
initial stages of burn injury (if present, suspect delayed pre-
sentation, occult injury or cardiac disease). Peripheral tem-
perature. Capillary refill. IV access preferably through
unburnt skin (interosseous route may be required in chil-
dren). Blood tests: FBC, U&Es, glucose, clotting screen, G&S.
ECG/cardiac enzymes in high-tension electrical burns. ECG
abnormalities more common if history of collapse/cardiac
arrest associated with the injury. These patients require car-
diac monitoring for 24 h.

Disability:
GCS/AVPU/ Pupillary reaction. If compromised, consider
hypoxia, hypovolaemia or other injury (including head
injury).

Exposure (with environment control):

Examine entire patient to estimate the percentage of total
body surface area (TBSA) of the burn and check for con-
comitant injury. Prevent unnecessary/prolonged exposure,
which can lead to hypothermia and burn depth extension.
 Chapter 7. Burns 51

Methods of percentage TBSA estimation:

1. Lund and Browder charts
The younger the child, the greater the surface area of the
head in proportion to the body. Use the relevant paediatric
charts as necessary.
2. Rule of Nines
Head 9%, arm 2 × 9%, torso 2 × 18% front and back,
leg 2 × 18%, perineum 1%.
3. Palm of the (patient’s) hand = 1%
More useful for small or irregular burns.
Assessment of burn depth:
Superficial +/− Blisters.Underlying tissue sensate (painful!)
with bright red appearance. Blanching on
digital pressure (painful procedure). Think
sunburn!
Deeper Overlying epidermis and superficial dermis
partial lost. Cherry red appearance of underlying
thickness dermis with punctate lesions. Fixed capillary
staining on digital pressure with deeper dermal
burns. Painful!
Full Eschar (thick/white +/− charring of
thickness surrounding tissues (flame burn) or leathery
in appearance). Insensate. No bleeding to
pinprick. Circumferential burns may impair
limb circulation or restrict chest wall excursion.
Electrical Arborisation pattern on skin. May have
burns significant deep muscle injury with relatively
normal looking overlying skin.Rhabdomyolysis,
myoglobinuria

Fluid Resuscitation
Major burns associated with massive fluid loss, firstly, through
the burn wound itself and secondly, loss of circulating volume
(associated systemic inflammatory response). Fluid requirements
52 F. Ali et al.

calculated according to the percentage TSBA of burn. The British

Burns Association recommends the Parkland Formula to calcu-
late the crystalloid fluid requirements during the first 48 hours.
Parkland Formula: Resuscitation volume = 4 ml × wt
(kg) × %TBSA.
Half given in the first 8 hours and half in the next 16 h,
followed by the total amount in the second 24-h period.

Maintenance Fluid
IV maintenance required for all children and those adults
unable to take oral fluids. NB limited glucose stores in chil-
dren therefore use dextrose. Children also at risk of cerebral
oedema so careful monitoring essential.
Hourly infusion rate for children = 4 ml/kg (first
10 kg) + 2 ml/kg (next 10 kg) + 1 ml/kg (every kg over 20).

Clinical Evaluation
Hourly heart rate, blood pressure, temperature and urine
output. Aim for urinary output of 0.5–1 ml/kg/h. Complicated
burns (e.g., high-tension electrical burns or inhalational
injury) require increased fluids (urine output 1–2 ml/kg/h).
The calculated fluid is a guide only and may require
adjustment.
Analgesia
IV analgesia (opiates) should be provided for all burns
patients.

Secondary survey
During this detailed examination of the patient, any other
concomitant injuries should be identified, investigated and
treated as appropriate.

Surgical Management of Burns

Immediate
Tracheostomy: This may be necessary to secure the airway.
Escharotomy: Should be performed in controlled environment in
theatre under general anaesthetic. Mid-axial incisions used,
 Chapter 7. Burns 53

carefully sited around joints and near superficial nerves (e.g., the
ulnar nerve at the medial epicondyle). Significant blood loss can
occur.
Fasciotomy: Bone has high resistance, therefore in high-
tension electrical burns, electrical energy is converted to heat
within myofascial compartments leading to myonecrosis.
Fasciotomies are required to relieve the pressure in these
compartments, limiting myonecrosis and therefore the risk of
acute tubular necrosis.

Burn excision
Early excision (<72h)
Early excision of the entire burn wound thought to limit systemic
inflammatory response and improve outcome. Significant blood
loss can occur. When considering early excision, determine car-
diovascular stability of the patient, operative risk and potential
morbidity of the wound itself if it were not removed rapidly. For
burn wounds <30% TBSA, usually sufficient donor sites. For
larger excisions, skin substitutes should be applied to remaining
wound until autologous skin available. As a guide, each procedure
should be limited to 2–3 h operative time. NB: Safer to perform a
number of moderate procedures rather than one massive one.

Delayed Excision
May be indicated where burn depth unclear. More common in
children. If burn shows little/no healing at 2 weeks, then excision
and grafting indicated (reduces risk of hypertrophic scars).

Techniques
Tangential excision
Shaving of burn wound until bleeding bed obtained.
Advantage: allows excision of the burn while preserving via-
ble deep dermis. Disadvantage: associated with increased
blood loss. Limit excisions to 18–25% TBSA at a time.

Fascial excision
Excision down to the underlying fascia. Advantages: Quick proce-
dure with less blood loss than tangential excision. Disadvantages:
poor appearance compared to tangential excision.
54 F. Ali et al.

Excision and direct closure

Only really indicated for small full thickness burns
Skin cover
Autologous
SSG Skin is usually meshed 1:1.5 but higher ratios
may be used for very large burns and limited
donor sites. The cosmetic appearance is inferior
but it aids wound closure
FTSG May be appropriate in small deep dermal or
full thickness burns, particularly on the face and
hands. Superior functional and cosmetic result
but limited by the size of the defect
Allogenic
Cadaveric (glycerol or cryopreserved)
May be of use as a temporising method of wound cover. Both
types require preparation before use. Glycerol preserved skin
must be repeatedly washed in normal saline. Cyropreserved
is gently warmed (less popular as theoretical infection risk).
Some of the dermal elements may become incorporated in
the recipient.

Xenograft
Pig skin. Temporising skin cover until other methods available.

Skin substitutes
Biobrane, Integra
Synthetic bilaminar skin substitutes, containing dermal com-
ponents, collagen and connective tissue elements (GAGs).
Varying degrees of incorporation into host bed.

Cultured keratinocytes
Spray delivery or sheet graft. Usually applied in combination
with widely meshed SSG or dermal substitute for deeper burns.
Dressings
Simple Jelonet, liquid paraffin (facial burns)
Silver containing Flammazine
Flammacerium
Aquacel Ag
 Chapter 7. Burns 55

The benefit of silver containing preparations is to promote a

sterile environment. They may however make burn depth assess-
ment difficult if this has not been done prior to application.

Outcome
Delayed healing (more than 3 weeks) associated with hyper-
trophic scars. Scar management should start as soon as
wounds healed to reduce risk of problematic hypertrophic
scars and scar contracture. Includes scar massage, rehydra-
tion, pressure therapy and splints. Custom-made masks avail-
able for facial burns. These interventions continue until scar
maturation has occurred (18–24/12). Follow up of patients in
particular the paediatric populations who have not finished
growth yet is vital.
Preservation of movement and function with vigorous
exercise regimes aim to reduce morbidity associated with
limited function.
Reduction in oedema with compression, movement, eleva-
tion and maximising lymphatic function.
Delayed surgical reconstruction aimed at resurfacing
burned areas to improve cosmesis and function.
Chapter 8
Cleft Lip and Palate
Ivo Gwanmesia, Matthew Griffiths,
and Jon Simmons

Cleft lip is a congenital abnormality of the primary palate

involving the lip, alveolus and hard palate anterior to the inci-
sive foramen. If the soft palate is involved, it is termed cleft lip
and palate. It has an incidence of 1 in 750 live births.

Recognition
Usually seen as infants in the setting of a cleft lip and palate
multidisciplinary team (Fig. 8.1).

History
When was the cleft diagnosed?
Where there any problems with the pregnancy?
Does the child have any feeding or breathing difficulties?
Are there any other congenital anomalies present?
Is there a family history of clefts?

I. Gwanmesia ()
Department of Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 57

DOI 10.1007/978-1-84882-116-3_8,
© Springer-Verlag London Limited 2012
58 I. Gwanmesia et al.

Figure 8.1 Complete cleft palate

AIM: by the end of history you should

1. Know about the general health of the child and any spe-
cific issues with breathing or feeding
2. Understand the extent of the cleft and structures involved
3. Identify any social/family factors that will require attention
4. Assess the parents understanding about the condition

Examination
Specific
Type of cleft: unilateral or bilateral, complete or incomplete,
primary or secondary, microform or forme fruste

Is the secondary palate involved?

Is the nose distorted?
Are the alveolar arches widely displaced? (The child may
require pre-surgical orthopaedics)
General
General body habitus
Normal weight for age – red book for height and weight
charts
 Chapter 8. Cleft Lip and Palate 59

Exclude presence of other congenital anomalies (their presence

may be an indication of a syndromic cleft)

AIM: by the end of exam you should have

1. Assessed and documented the type of cleft and its extent
2. Identified any other anomalies
3. Assessed the child to determine suitability for surgery
4. Formulated a treatment strategy and timeline for treatment
5. Identified factors which may require treatment or investi-
gation before surgery

Investigations
FBC, U&Es, group and save. Feeding assessment. Hearing
assessment.

Treatment
Best carried out within a multidisciplinary team. Treatment
requires surgical and non-surgical skills.
Non-surgical
Geneticist – screens for the presence of genetic conditions
within the affected family
Clinical nurse specialist – advises parents on any feeding or
breathing difficulties
Psychologist – to prepare older patient and family for
treatment
Audiologist – assesses child’s hearing
Surgical
An MDT involving – Plastic Surgeon, Maxillofacial Surgeon,
ENT Surgeon, Orthodontist
Cleft lip repair is commonly performed at 3 months of age
(or according to the rule of 10s; 10 kg, 10 g/dL of haemoglo-
bin, 10 weeks of age) when the anaesthetic risk is much
reduced. Primary rhinoplasty is also carried out at this time.
60 I. Gwanmesia et al.

Cleft lip repair methods

Millard rotation advancement method
Tennison-Randall method
Cleft palate repair methods
Cleft palate is usually repaired at 6 months. The patient is also
assessed for the need for grommets at this time. Other proto-
cols exist (Fig. 8.2).

Direct closure for narrow clefts

Von Langenbeck technique (Fig. 8.3)
Furlow’s double opposing Z-plasty

Figure 8.2 Millard technique for cleft lip repair

Figure 8.3 Von Langenbeck technique for palate repair

 Chapter 8. Cleft Lip and Palate 61

Veau-Wardill-Kilner technique
Intravelar veloplasty
Vomerine flaps

Complications of Repair
Infection
Dehiscence
Bleeding
Scarring
Whistle deformity of the lip
Breathing difficulties
Fistula formation of the palate
Velopharyngeal incompetence
Midfacial growth disturbance

Other Aspects of Cleft Lip and Palate Repair

Cleft lip and palate care varies from unit to unit, but the main
points for patient management following cleft lip and palate
repair include the following:
Speech and language assessment at 4–5 years
Alveolar bone grafting at 9–10 years (during the period of
mixed dentition)
Orthodontic assessment and surgery at 11–18 years
Secondary rhinoplasty at skeletal maturity (may also be per-
formed during growth)

Secondary Rhinoplasty
Cleft lip and palate patients usually still have residual defor-
mities of the midfacial area after primary rhinoplasty.
Treatment is carried out for functional and aesthetic reasons.
Treatment is best carried out once all orthodontic treatment
is completed. The patients would usually be between 16 and
19 years of age.
62 I. Gwanmesia et al.

Some of the factors leading to these deformities include:

Intrinsic nasal factors

Deformed and depressed lower lateral cartilage
Deviated septum
Asymmetric nasal tip
Deviated columella
Asymmetric nasal bones and nasal pyramid

Extrinsic skeletal factors

Maxillary hypoplasia
Maxillary cleft (if not already corrected)
Lack of bony support for nasal base
A comprehensive and systematic assessment of the cleft
deformity is necessary prior to initiating secondary rhino-
plasty. This comprises of carrying out an external and internal
examination of the nose.

External examination
Skeletal base support
Nasal base position (exclude retroposition)
Nasal base size and asymmetry
Columella length, shape and position
Size and shape of nostrils
Nasal dorsum
The degree of dorsal projection
Degree of asymmetry of the nasal pyramid
Degree of deviation of the nasal pyramid
The nasal width and length
Nasal tip and ala
Asymmetry in tip projection
Flattening of the ala on the affected side
Skin envelope
Position of any scars

Internal examination
The degree of septal cartilage deviation
 Chapter 8. Cleft Lip and Palate 63

Position of the footplates of the lower lateral cartilages

The size of the inferior turbinates
Is the caudal septum attached to the anterior nasal spine?
Are there any scars within the nasal vestibule?
Procedures carried out during secondary rhinoplasty include
the following:
Bone grafting of maxillary defects, nasal bone osteotomies,
submucous cartilaginous resection or septoplasty, the use of
various cartilage grafts to provide support for the columella
and to augment lower lateral cartilages, or as spreader grafts
to correct a collapsed internal valve, various suture tech-
niques to modify the position of the cartilages and skin flaps
to lengthen the columella.

Outcomes
Utilising proven techniques in the context of the multi-
disciplinary team, excellent cosmetic outcomes can and
should be achieved. Speech quality as influenced by palatal
development following repair requires treatment by speech and
language therapists to maximise the potential for clear speech.

Velopharyngeal Dysfunction
The velopharynx is a rectangular structure that acts as a valve
to separate the nasal and oral cavities during speech and
swallowing.
• Causes of velopharyngeal dysfunction are classified as
structural or neurologic impairment, and mechanical inter-
ference. It is seen in about 20% of cleft patients after
palatoplasty.
• Structural impairment can result from submucous cleft
palate, unrepaired cleft palate, short palate after palate
repair, palatal fistula and tissue deficiency.
• Neurologic impairment can be due to neurologic disorders
that impair the function of the muscular sphincter.
64 I. Gwanmesia et al.

• Mechanical interference can result from large adenoids

and tonsils.
Evaluation and Diagnosis
• Complete evaluation of velopharyngeal dysfunction
includes assessment of perceptual speech, anatomy and
physiology of the velopharyngeal complex.
• Assessment of perceptual speech is done by looking
for hypernasality, nasal emission and compensatory
articulation.
• Assessment of the anatomy of the velopharynx is through
the use of nasendoscopy and videofluoroscopy.
• Assessment of the physiology of the velopharyngeal com-
plex is performed by using nasometry.
Treatment
Treatment can be non-operative or operative.
• Non-operative treatment consists of speech therapy
alone.
• Operative treatment includes pharyngeal flaps, pharyngo-
plasty, posterior pharyngeal wall augmentation, palate
re-repair and velar muscle reconstruction (either through
intravelar veloplasty or Furlow palatoplasty).

Complications of Surgical Correction

of Velopharyngeal Dysfunction
These include postoperative bleeding, airway obstruction,
obstructive sleep apnoea and possibly restriction of facial
growth.
Chapter 9
Congenital Hand
Shehan Hettiaratchy and Jon Simmons

There is nothing a child with a congenital hand difference

should not be allowed to do. Their difference is normal to
them.

Recognition
Child with craniofacial syndrome with associated hand
anomaly – try and identify the syndrome to determine the
likely hand anomaly
Normal child with isolated limb difference
Normal child with multiple limb differences (Fig. 9.1)

History
Paediatric intro
Age, handedness if known
Pregnancy + delivery history
Growth and development
Associated medical problems and plan
Siblings/family history

S. Hettiaratchy ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 65

DOI 10.1007/978-1-84882-116-3_9,
© Springer-Verlag London Limited 2012
66 S. Hettiaratchy and J. Simmons

Figure 9.1 Syndactyly

Specific – Tailor this to what is age appropriate

When first noticed
Progression/worsening
Current state of hand function
Specific tasks unable to do
School performance
ADLs
Parents and child’s goals
Risk factors
Teratogens
Twins
Large baby
Oligohydramnios
Family history
 Chapter 9. Congenital Hand 67

AIM: by the end of history you should have an idea of

1. The impact of the hand difference on the child
2. What has been done/achieved so far
3. Child’s/parents’ goals

Examination
Look

• Craniofacial syndrome:
• Apert’s: complex syndactyly-varying degrees
• Crouzon’s
• Carpenter’s
• Pfeiffer’s: broad toes/thumbs

One or multiple limbs:

• Symmetrical cleft hands/feet – typical cleft
• Different levels with absence – Constriction Ring
Syndrome

Posture:

• Normal components abnormal posture – CP, BPI

Upper Limb normal posture:
• All components present
− Hypoplastic: Poland’s syndrome – check NAC/pectora-
lis major: Symbrachydactyly
− Hyperplastic: hemihypertrophy
• Part missing
− Hand present – intercalated
− Hand absent – no nubbins – transverse arrest
− Hand absent – nubbins – symbrachydactyly
• Hand present
− Deviated at wrist/forearm short-longitudinal deficiency,
check thumb as indicator if radial or ulnar
• Palm present
− Cleft in palm – cleft hand
68 S. Hettiaratchy and J. Simmons

• Fingers present
− All short – symbrachydactyly
− Some short – brachydactyly
− Radially deviated – little finger – clinodactyly
− PIPJ flexion – camptodactyly
− Fused – syndactyly
− Abnormal position – arthrogryposis
− Stiff – symphalangism
− Hyperplastic – macrodactyly
− Increase in number – radial/ulnar polydactyly – mirror hand
− Decrease in number – symbrachydactyly
• Thumb
− Small/absent – hypoplasia (Blauth)
− Flexed – clasped thumb – trigger thumb
Feel/move
Check specific joint ranges and stability as indicated
Need to think about:
• Joint stability/stiffness – from shoulder downwards
• Length discrepancies – flex elbow to see if arm is short
above or below/compare
• Correctability of any deviations – will influence the type of
procedure/success
• Functional task
− Holding pen/writing
− Grasping cup (wide grip)
− Handling toys

AIM: by the end of exam you should have an idea of

1. Specific functional limitations
2. Options, if any, for addressing them
3. Timing of any intervention given the age of the child

Investigations
Plain X-ray – after 6 months
 Chapter 9. Congenital Hand 69

Treatment
Principles
• Improve/preserve overall hand function, not individual
joint movements.
• Cosmesis should not be achieved at the expense of
function.
• For the child the hand is normal, how they adapt may
exceed what is expected.
• Timing is critical as an intervention too early may lead to
recurrence. Too late may not fully correct the problem.
What to treat
• To release abnormally joined structures (e.g., syndactyly)
• To join abnormally separated structures (e.g., cleft hand)
• To correct deviation (longitudinal deficiencies)
• To prevent future deviation (clinodactyly)
• To reconstruct a missing part
• To remove an extra/duplicated part
Options for treatment
Non-surgical
Physiotherapy
• May help stiffness/contractures/instability
• Splintage may be a useful adjunct for certain conditions
(longitudinal deficiencies)
Botox
May have a role in arthrogryposis to balance agonist/
antagonist
Surgical general timing
Techniques will depend on the condition being treated and
the intended aim. Timing:
<1 year: syndactyly where growth might be affected
>1 year: other syndactyly
>2 years: microvascular surgery
2–4 years: clinodactyly – physiolysis)
70 S. Hettiaratchy and J. Simmons

Specific procedures
Syndactyly release
Stage if both sides of a digit are involved
Various techniques – mainly interdigitating triangular
flaps for digits and some form of dorsal flap for commisure.
Buck-Gramcko paronychial flaps. Some form of skin grafting
often needed – tend to be FTSG.
First web release
Seen in association with clasped thumb/hypoplasia. Is it skin
or adductor? Splintage first.
If very tight may need surgery
• Skin – 4 flap z-plasty
• Adductor – release
Clinodactyly
Operate if >45°/progressing. Options:
• Physiolysis – if still growing (best done 2–4 years) then rely
on the finger growing straight and correcting
• Osteotomy – if no longer growing/physiolysis has not
worked
Trigger thumb
Often not diagnosed early (neonates clasp their thumb).
Palpate nodule in FPL (Notta’s node). May get stuck in flex-
ion or extension.
May resolve before 2 years old. Otherwise operate; release
radial part of A1 to avoid injury to the oblique pulley.
Clasped thumb
Splintage/therapy
If skin short may need transposition flap from radial border
of index finger
EPL reconstruction
Thumb hypoplasia
Critical is quality of CMCJ and stability.
If stable, then aim is to reconstruct around the CMCJ
(i.e., improve adductor function).
If unstable/missing may be better to pollicise.
 Chapter 9. Congenital Hand 71

Thumb duplication
Choose which is the better formed duplicate and use that as
basis for reconstruction. May need to reconstruct IPJ/MPJ
stability, FPL, EPL and delineate digital nerves (may need
interneural dissection).
Radial longitudinal deficiency
Targets for treatment are to improve wrist/hand position and
thumb reconstruction while maximising ulna growth. This can
often be conflicting – options to place the carpus on the end of the
radius may damage the ulnar physis and compromise growth.
Options:
• Centralisation
• Radialisation (Buck-Gramcko)
• Vascularised physis transfer (Vilkki) – 2nd MT taken as a free
flap
• Manipulation only (Ezaki)

Risks and Complications

These will depend on the surgery and timing. Recurrence of
the problem is often an issue in certain conditions.

Aetiology
Upper limb and hand development between the 4th and 12th
week of gestation initiated by fibroblast growth factors.
Development occurs along three axes. Proximal to distal
(Apical ectodermal ridge), anterior to posterior (zone of pola-
rising activity) and dorsal to ventral (wingless gene encoded
protein). Apoptosis is responsible for separating the digits.

Classifications
IFSSH Swanson classification
Blauth thumb hypoplasia Syndactyly
Bayne-Radial/Ulnar dysplasia
72 S. Hettiaratchy and J. Simmons

3 or 4 large flaps

Volar mirror dorsal flaps

Dorsal rectangular flap approx

2/3 distance from metacarpal
heads to PIPJ

Buck-Gramcko flaps can be used

to create nail folds

Figure 9.2 Syndactyly flap design. The commisural flap has many
variations

Controversies
Timing of treatment
Commisure flap design in syndactyly
FTSG vs. SSG vs. open finger technique in syndactyly (Fig. 9.2).
Chapter 10
Craniosynostosis
Ivo Gwanmesia and Matthew Griffiths

Craniosynostosis is the premature fusion of one or more cra-

nial sutures. It is classified according to the suture(s) involved.
It can be either syndromic or deformational. It has an inci-
dence of 1 in 2,000 live births.

Recognition
A child with an abnormal skull and face presenting to a cran-
iofacial multidisciplinary team (Fig. 10.1).

History
• When was the deformity initially noticed?
• Where there any problems with the pregnancy?
• Has there been an improvement in the shape of the head
over time?
• Is there a positive family history of abnormal head shapes?
• Is the child developing normally?
• Have there been any signs of raised intracranial pres-
sure? (Irritability, vomiting, tense fontanelles, seizures,
papilloedema)

I. Gwanmesia ()
Department of Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 73

DOI 10.1007/978-1-84882-116-3_10,
© Springer-Verlag London Limited 2012
74 I. Gwanmesia and M. Griffiths

Fused unilateral coronal suture

Figure 10.1 Plagiocephaly – fused coronal suture

Examination
Specific
Look
• What is the shape of the skull?
• Are the ears in a similar position?
• Are the orbits symmetrical? – Patients with unilateral
coronal synostosis typically have a wind-swept unilateral
orbit due to the anterior position of the sphenoid
• Is there any evidence of papilloedema?
• Are the cheeks symmetrical?
• Is the nose deviated?
• Is the chin in the midline?
Feel
• Is the anterior fontanelle open?
• Is the posterior fontanelle open?
• Is there a palpable ridge?
• Do the sternocleidomastoid muscles feel normal and is
there a full range of neck movement?
General
• Are they any abnormalities of the limbs?
• Are there any cardiac abnormalities?
 Chapter 10. Craniosynostosis 75

Investigations
• Plain X-ray – sufficient to identify the affected suture(s); the
beaten-copper appearance is an indication of raised intracra-
nial pressure.
• CT scan – gold standard for imaging, however comes with a
higher dose of radiation. Useful for detecting the presence of
Arnold-Chiari malformations seen in Crouzon syndrome.

Treatment
Always within the context of a multidisciplinary team.
Non-surgical
• Geneticist: Determines evidence of a potential syndromic
or a familial pattern of inheritance
• Neuropsychologist: determines patient’s underlying brain
function which serves as a benchmark for any postopera-
tive changes
• Paediatrician: assesses patient’s general well-being
• Paediatric ophthalmologist: excludes the presence of
papilloedema
Positioning and the use of orthotic devices are useful for posi-
tional plagiocephaly.
Surgical
Indications for surgery include significant cranial and facial
asymmetry, elevated intracranial pressure (ICP) and neurop-
sychologic disorders.
In most cases of single suture craniosynostosis, the indication
for surgery is the degree of cranial and/or facial asymmetry.
Trigonocephaly
Premature fusion of the metopic suture.
Has an incidence of 1 in 10,000 live births and account for
10–20% of all cases of single suture synotoses.
Affected patients usually present with a keel-shaped fore-
head with a palpable ridge and hypotelorism.
Surgical correction involves the elevation of a bifrontal flap,
excision of the synostoses, calvarial remodelling through the
76 I. Gwanmesia and M. Griffiths

use of kerfs with radial osteotomies and the use of bone

grafts if the defect is greater than 2 cm. Some units may in
addition use orthotic devices to assist with calvarial
remodelling.

Scaphocephaly
Most common form of unilateral craniosynostosis. It is the
premature fusion of the sagittal suture.
Has an incidence of 1 in 2,000 live births.
Patients present with a long head.
Surgical correction usually involves the elevation of frontal,
parietal and occipital bone flaps and remodelling of the flaps
by osteotomies.
Some units use orthotic devices to assist in achieving the
desired head shape.

Plagiocephaly
It is the premature fusion of a unilateral coronal suture.
It has an incidence of 1 in 4,500.
The features include a retropositioned forehead on the affected
side, a raised superior orbital ridge, a laterally positioned lat-
eral canthus, a nasal root deviated towards the affected orbit, a
prominent cheek on the affected side and the chin deviated
away from the affected orbit.
Surgical treatment involves the elevation of a bifrontal bone
flap and three-quarter orbital osteotomies. The orbits are
advanced unequally to correct the orbital deformity. Bone
grafts may or may not be used.

Brachycephaly
Premature fusion of the coronal sutures.
It has an incidence of 1 in 2,500 live births and accounts for
25% of single suture synostosis.
Patients present with a long head, flattening of the occiput,
skull widening and some have been described as tower head
‘turribrachycephaly’.
Surgical correction involves elevation of frontal and occipital
bone flaps and correction with radial osteotomies.
 Chapter 10. Craniosynostosis 77

Lambdoidal plagiocephaly
Premature fusion of a single lambdoid suture.
It is the least common of all the single suture synostosis,
accounting for less than 5% of all synostosis.
Patients present with a flattened occiput on the affected side, the
ear on the affected side is posterior compared to the contralateral
ear, and there is bossing of the forehead on the affected side.
Surgical correction involves the raising of an occipital bone
flap and radial osteotomies with or without the use of springs
to correct the head shape.
Surgical complications of calvarial remodelling
Complications are acute and delayed.
Acute complications include blood loss, dural tear with CSF
leak, infection and respiratory infections. Delayed complica-
tions are predominantly those of relapse and scalp scarring.

Syndromic Craniosynostosis
Apert syndrome (acrocephalosyndactyly type I)
Autosomal dominant inheritance
Incidence of 1 in 25,000 to 1 in 100,000
Typically present with bilateral coronal synostosis, with tur-
ribrachycephaly skull deformity, midface hypoplasia and
complex syndactyly

Crouzon syndrome (acrocephalosyndactyly type II)

Autosomal dominant inheritance
Incidence of 1 in 10,000 to 1 in 25,000
Typically present with bilateral coronal synostosis with severe
midface hypoplasia, exorbitism
There is no syndactyly
Saetre-Chotzen syndrome (acrocephalosyndactyly III)
Autosomal dominant inheritance
Incidence of 1 in 10,000
78 I. Gwanmesia and M. Griffiths

Features include unilateral coronal synostosis, low-set hair-

line, ear abnormalities and incomplete simple syndactyly of
the hands
Carpentar syndrome (acrocephalosyndactyly type IV)
Autosomal recessive inheritance
Incidence of 1 in 10,000
Features include sagittal or bicoronal synostosis, widely
spaced eyes, hydrocephalus, some have heart defects.
Pfeiffer syndrome (acrocephalosyndactyly V)
Autosomal dominant inheritance
Incidence of 1 in 15,000
Features include coronal synostosis, midface hypoplasia and
limb abnormalities including broad thumbs and toes
(Fig.10.2).

Frontal bones Metopic suture

Anterior fontanelle Coronal suture

Parietal bones Sagittal suture

Posterior fontanelle

Occipital bone Lambdoid suture

Figure 10.2 Sutures and bones of the normal skull

Chapter 11
Dupuytren’s Disease
Shehan Hettiaratchy and Jon Simmons

Benign fibroproliferative disease of unknown aetiology.

Important to identify the patient with a diathesis/aggressive
disease. The patient must realise that no interventions can cure,
they only buy a variable disease-free interval.

Recognition
Male patient over 50 with ulnar sided contracture of fingers.
Often bilateral, be aware of early onset, recurrent and extra-
palmar disease (Fig. 11.1).
Differentials include: ulnar nerve lesion, joint contracture,
scar contracture.

History
Hand intro – Age, occupation, handedness, hobbies, musical
instruments and interference with these.

S. Hettiaratchy ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 79

DOI 10.1007/978-1-84882-116-3_11,
© Springer-Verlag London Limited 2012
80 S. Hettiaratchy and J. Simmons

Figure 11.1 Dupuytrens disease

Disease specific
1. Specific problems the patients has, what cannot they do,
what do they want to achieve?
2. How long have they had it? Progression? Why are they
seeking treatment now?
3. Any pain/numbness/tingling?
4. Any previous treatment/surgery? When and what?
5. Any other sites affected? (extra palmar, feet-Lederhosen,
penis – Peyronie’s).

Risk factors
1. Family history – who, at what age, progression/treatment
2. Smoking – how much and for how long
3. EtOH – how much? How long?
4. IDDM
5. Epilepsy – what medications?
6. Diathesis – aggressive/young/FHx/ectopic
General – Previous medical history/drug history, especially
any anti-coagulants, aspirin, etc. social history including home
circumstances, support mechanisms
 Chapter 11. Dupuytren’s Disease 81

AIM: by the end of history you should have

1. Determined how aggressive the disease is (influences type
of surgery and outcome).
2. Assessed what the patient’s main complaint is and what
they want to do about it.
3. Assessed the practicality of surgery for the patient, and
suitability for surgery.

Examination
General – Sit across table, expose patients arms below the
elbow. Examine both hands together.
Look
• Palmar surface – Digits affected, previous scars (including
forearm), skin pits, obvious nodules
• Dorsal surface – Garrod’s pads any guttering or wasting of
first dorsal interosseous (ulnar nerve lesion)
• Table top test – Quick gross assessment of disease/amount
of MPJ/PIPJ contracture. Patients places hands as flat as
possible on the table, palms down.

Feel/move
Overview
One hand at a time. Palpate all cords under tension as it
makes them more obvious. Hyperextend fingers and look for
obvious cords. Quickly palpate palm, affected fingers, thumb,
first web space. Check first web and hand span (compare
both sides – limited span suggests involvement of the nata-
tory bands). Check palm for nodules.
Disease extent/configuration
Examine each affected digit in detail. Determine if it is only
palmar disease or disease in the finger. Identify affected
cords. Identify a spiral cord as it increases the risk of digital
nerve injury (displaces NVB).
82 S. Hettiaratchy and J. Simmons

Range of movement using Goniometer

Check ROM. Measure MPJ extension. Flex MPJ (elimi-
nates effect of short intrinsics) and measure PIPJ ROM.
Note active and passive range. Note attenuation of the
central slip (i.e., is passive extension of PIPJ greater than
active extension). Attenuation increases the risk of joint
contracture.
• Assess the skin in the affected digits – will a graft be
required?
• Check and comment on sensation

AIM: by the end of exam you should consider

1. Extent of disease
2. Type of surgery required (soft tissue/joints)
3. Whether FTSG will be required
4. If there is a spiral cord – potential risk to the nerves

Investigations
Only as indicated on the basis of clinical findings and history.
Blood work on the basis of co-morbidities. Nerve conduction
studies if considering peripheral nerve lesion.

Treatment
Options
1. Watch and wait
2. Non-surgical
3. Surgical

When to treat
1. PIPJ contracture – greater than 30° (McFarlane)
2. MPJ – no absolute figure, consider individual patient and
disease progression
3. Significant interference with activities
4. Aggressive disease
 Chapter 11. Dupuytren’s Disease 83

Non-surgical treatment
1. Splintage – no evidence of effect
2. Steroids (nodules) – not universally accepted
3. Collagenases – ?future. FDA approved for treatment.
Role and RCT awaited.

Surgical
1. Fasciotomy
Simple division of the cord; done under LA; best for pal-
mar disease
Advantages: quick, simple, effective
Disadvantages: high recurrence rate; risk of DN injury in
finger/thumb
Complications: DN injury; incomplete release
Indication: elderly patient, pre-tendinous cord, unfit for
surgery
2. Limited fasciectomy
Removal of affected tissue, leaving behind unaffected fascia
Advantage: lower recurrence rate than fasciotomy
Disadvantages: needs GA/regional block; higher recur-
rence than dermofasciectomy
Complications: wound problems, DN injury, recurrence
Indication: most primary, non-rapidly progressing disease
3. Dermofasciectomy
Removal of affected skin and underlying cords
Adv: lowest (if any) recurrence
Disadv: donor site/FTSG take
Complications: graft failure; donor site problems
Indications: recurrent disease; aggressive disease in the
young; extensive skin involvement

PIPJ management
Aggressive surgical release may cause more scarring and
limit movement.
Release check rein ligaments and accessory collateral liga-
ments in combination with gentle passive manipulation.
Approximately half the correction is usually lost over the
first 6 months. Recurrence is more likely if central slip attenu-
ated; correcting attenuation offers limited benefit.
84 S. Hettiaratchy and J. Simmons

Skin incisions
Bruner
Adv: start dissection in normal tissue, Y-V allows extra skin
to be imported
Disadv: tips of flap vulnerable, limited skin imported, does
not re-orientate dermal fascia
Skoog
Adv: multiple z-plasties importing skin, z-plasties realign der-
mal fascia
Disadv: harder to reopen, dissection started in abnormal
tissue
Palm is often left open (McCash technique)
Post-operative management
Fasciotomy Minimal dressing; nightsplint 6/12
Limited Palmar: nightsplint 6/12, Finger: splint
fasciectomy day and night 6/52 then night to 6/12
Dermofasciectomy Splint day and night 6/52 then night to 6/12

Risks/Complications
1–3% nerve injury depending on procedure
5% delayed healing
<1% ischaemia

Outcome
Fasciotomy – 100% by ??
Fasciectomy – 45% by 5 years
Dermofasciectomy – 0–35% by 5 years

History
First described by Astley Cooper in 1777. First released by
Baron Guillaume Dupuytren in 1831. Hueston described diath-
esis in 1961.
 Chapter 11. Dupuytren’s Disease 85

Anatomy
Dupuytren’s disease involves the normal fascial structures of
the palm and digits (Fig. 11.2)
Pre-tendinous band: Pre-tendinous cord
Natatory ligament: Natatory cord
Superficial volar fascia: Central cord
Lateral digital sheet: Lateral cord
Spiral cord is formed from proximal to distal by the pre-
tendinous band; oblique or spiral band; the lateral digital sheet;
Grayson’s ligament.

Central cord

Spiral cord

Natatory cord

Lateral cord

Figure 11.2 Dupuytrens cords

86 S. Hettiaratchy and J. Simmons

Pathophysiology
Luck described 3 phases; proliferative/involutional/residual
Proliferative
Random accumulation of fibroblasts in a whorl like pattern
– nodules
Involutional
Differentiating fibroblasts in the presence of tension causes
aggregation of fibroblasts along these tension lines causing
cords. Myofibroblast differentiation.
Residual
Cords become relatively acellular.

Key Evidence
Hueston, J.T. Limited fasciectomy for Dupuytren’s contracture. Plast.
Reconstr. Surg. 27:569, 1961.
McCash, R.The open palm technique in Dupuytren’s contracture. Br. J.
Plast. Surg. 17:271, 1964.
McFarlane, R.M. Clinical perspective on the origin and spread of
Dupuytren’s disease. J. Hand Surg. (Am.) 27:385, 2002.
Swartz, William M. M.D.; MOC-PS(SM) CME Article: Dupuytren’s
Disease; Plastic and Reconstructive Surgery; Volume 121(4) Supplement,
April 2008, pp 1–10.
Chapter 12
Facial Palsy
Ivo Gwanmesia, Farida Ali, and Jon Simmons

Facial palsy is the paralysis of the seventh (facial) cranial

nerve. It can be unilateral or bilateral. There are multiple
causes.

Recognition
Patient (adult or infant) presenting with facial weakness and
asymmetry (Fig. 12.1).

History
• When was the weakness/deformity initially noticed?
• Are there any known causes?
• Is there a history of associated trauma?
• Has the patient had any previous treatment?
• What problems is the patient having?

I. Gwanmesia ()
Department of Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 87

DOI 10.1007/978-1-84882-116-3_12,
© Springer-Verlag London Limited 2012
88 I. Gwanmesia et al.

Figure 12.1 Smiling demonstrating facial weakness

• Is there eye pain?

• Does the patient experience any difficulties with hearing?
• Does the patient experience any difficulties with speech
and feeding?

Examination
(Top to bottom examination of the face)
 Chapter 12. Facial Palsy 89

Specific
Look
• Hairline and position
• Forehead wrinkles
• Brow position
• Presence of nasal deviation with evidence of external
valve collapse
• Malar flattening and ptosis
• Increase in length of upper lip
• Asymmetry of the mouth
Feel
• Sensation along the ophthalmic, maxillary and mandibular
branches of the trigeminal nerve
• Palpate the temporalis muscle, asking the patient to bite
hard at the same time
Move
• Ask patient to elevate forehead and brows
• Ask patient to close eyes
• Ask patient to blow out cheeks
• Check for Cottle’s sign (in order to exclude internal valve
collapse)
• Ask patient to show his/her teeth
• Ask patient to contract the neck muscles
General
Complete general physical examination.

Investigations
Investigations are usually directed towards cause (if known).
They are broadly classified as etiologic, prognostic and
topographic
Aetiologic
Blood tests
• Serologic studies for: syphilis, diabetes, hyper- and
hypothyroidism
• Viral titres for: herpes, varicella zoster and Epstein Barr virus
90 I. Gwanmesia et al.

Imaging
• X-rays of the mastoid
• CT scan to detect intracranial, intratemporal and extratem-
poral tumours of the facial nerve
• MRI scan with Gadolinium will delineate the course of the
facial nerve

Prognostic
Used to determine if facial nerve regeneration has begun
Nerve Excitability Test – Performed with nerve stimulator.
A 3ma difference between the two sides of the face is
regarded as an abnormal result.
Maximal Stimulation Test – Also performed with nerve
stimulator. Abnormal test result is any difference in facial
movement between the two sides of the face.
Electroneurography – Current is delivered to the stylomas-
toid foramen, sufficient to evoke maximum response of the
facial muscles. A difference of 95% in the evoked compound
muscle action potential between the two sides of the face is
sufficient to indicate unsatisfactory return of facial function
following regeneration.
Electromyography – Should only be considered after 3 weeks
if no recovery is clinically apparent. Useful in detecting early
return of facial nerve function.
Topographic – CT and MRI scans: useful for locating the site
of a lesion.

Treatment
Treatment is broadly classified into watchful waiting, medical
and surgical
Watchful waiting
Indicated for mild cases of facial palsy. Eighty percent of
patients treated this way begin to recover within 3 weeks
 Chapter 12. Facial Palsy 91

Medical treatment
Corticosteroids – remains controversial but patients usually
recover facial movement to a House-Brackmann Grade 1 or 2
Surgical treatment
Direct Nerve Repair/transposition
Primary nerve repair (intracranial, intratemporal,
extratemporal)
Interpositional nerve graft (most commonly sural nerve)
Cross face nerve graft (sural nerve)
Hypoglossal facial nerve transfer
Hypoglossal facial nerve jump graft (sural nerve)
Free Muscle Transfer (with cross-face nerve graft)
Free muscle flap (gracilis, latissimus dorsi, pectoralis minor,
serratus anterior) with cross-face sural nerve graft
Regional Muscle Transposition
Temporalis muscle transposition
Masseter muscle transposition
Digastric muscle transposition
Static Facial Support
Browlift
Blepharoplasty
Upper lid gold weight
Lower lid repositioning and support
Lip and cheek support (fascia lata, Goretex)
Chapter 13
Maxillofacial Trauma
Farida Ali, Ivo Gwanmesia, and Jon Simmons

All cases should be managed as per ATLS guidelines.

The principles of management in facial fractures are accurate
diagnosis on clinical examination and radiography, followed
by early surgical treatment. It is no longer common practice
to wait for the swelling to settle before surgical treatment.

Recognition
Maxillofacial trauma may involve bony injury, soft tissue
injury or a combination. Though facial injuries themselves
are not usually life threatening, three life-threatening emer-
gencies may occur: respiratory obstruction, aspiration and
haemorrhage. Ten percent of patients with facial fractures
have an associated cervical spine injury and 10% have an
associated ocular injury. Early CT scanning is essential in
identifying the configuration of bony injury and planning
surgical intervention (Fig. 13.1).

F. Ali ()
Department of Plastic and Reconstructive Surgery,
St George’s Hospital,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 93

DOI 10.1007/978-1-84882-116-3_13,
© Springer-Verlag London Limited 2012
94 F. Ali et al.

Figure 13.1 Facial injuries

History
General
• The exact mechanism of injury – high-energy vs. low
energy, blunt or penetrating object, e.g., car, windscreen or
sharp object
• Loss of consciousness
• Neck pain (cervical spine injury in 10%)
• Alcohol intake (may mask head injury)
• General health
• Allergies/medications
• Smoking history
• Last oral intake

Specific
Upper third
• Frontal sinus and anterior cranial fossa: Ask about pain,
CSF rhinorrhoea
• Altered vision: Ask about loss of vision, blurred or double
vision (orbital floor, zygomatic fractures)
 Chapter 13. Maxillofacial Trauma 95

Middle third
• Orbits: Remember, ocular injury is present in 10% of
patients with facial fractures
• Zygoma: Swelling usually obvious
• Maxilla: Ask about dentition (missing/loose)
• Nose: Deformity/deviation (rule out a previous history of
fracture)

Lower third
• Mandible: Dentition
• Trismus: do they have pain on movement of the mandible?
Zygomatic arch fractures (impingement on coronoid pro-
cess) or mandibular fractures involving the coronoid process
• Occlusion: Is occlusion normal? Ask them if their teeth
meet normally anteriorly and posteriorly

Sensation
• Forehead numbness (supratrochlear and supraorbital
nerves)
• Upper lip and teeth (infraorbital nerve)
• Lower lip and teeth (mental nerve)

Facial lacerations
Ask about abnormal facial movement. The position of the
laceration will guide you to specific branches of the facial
nerve. The parotid duct may also be injured in lacerations of
the cheek.
Other injuries
This is particularly important with high-energy facial injuries.
Consider chest, abdominal and long bone injuries, all of
which may be a source of significant haemorrhage.
AIM: by the end of history you should have
1. Identified symptoms and correlated these with injuries
2. Understood the exact mechanism of injury and anticipated
likely injuries
3. Systematically considered different levels of injury
96 F. Ali et al.

Examination
Primary survey
You may be shown a photograph of a patient with major dis-
ruption of the face (e.g., gunshot, blast injury). Do not be
distracted by gross facial injuries. Approach the scenarios as
per ATLS guidelines!
Airway (with cervical spine control)
Airway obstruction: Blood, vomitus and/or foreign bodies
(including teeth) can obstruct the airway and should be
removed ASAP. Tongue may drop back if mandibular frac-
ture associated with a flail segment.
A protected airway should be secured as soon as possible.
Endo-tracheal intubation can be extremely difficult in patients
with major maxillofacial injury. Nasotracheal intubation
should be avoided in any patient that may have cribriform
plate fractures.
Breathing (with 100% oxygen via non-rebreather bag)
Patients unable to maintain oxygenation require intubation
and ventilation. Reduced conscious level, from intoxication
or head injury, may also impair respiratory effort. Patients
who have aspirated are at high risk and may well require
ventilatory support. Failure of intubation requires cricothy-
roidotomy, which is a temporary measure until a definitive
surgical airway can be secured.
Circulation (with IV access)
Obtain IV access with two large-bore cannulae and draw
blood for analysis.

Control of life threatening haemorrhage may include:

Manual reduction of the fractures (temporary measure)
Packing of the nasal and oral cavities
Foley catheters to control bleeding from the nasopharyngeal
region
Facial bandaging (not commonly used today)

Embolisation or ligation of the source arteries may be

required. If embolisation is not available, transantral ligation
 Chapter 13. Maxillofacial Trauma 97

of the internal maxillary arteries and ligation of the facial

arteries may help control bleeding. Ligation of the external
carotid artery has been used as a last resort.

Disability
GCS/AVPU/pupillary reaction.

Exposure
This should be a brief examination to rule out any concomi-
tant injury.

Secondary survey
Once the patient has been stabilised and the primary survey
completed, a detailed examination of the maxillofacial region
should be performed. Be systematic: start at the top and work
your way down.

Look
• Examine the patient from the front, from the top of the
head (bird’s eye view) and from below (worm’s eye view).

Face
• Lacerations and soft tissue
• Facial swelling, asymmetry or deformity
• Facial elongation – midface fractures
• Loss of malar prominence – most easily identified from
above – zygomatic arch fractures

Orbits
• Periorbital ecchymosis (bilateral or Panda eyes associated
with BOS fracture)
• Enophthalmos – may be more noticeable from above
• Orbital dystopia – vertical height discrepancy of the
globe – orbital blowout fracture (floor involved, rim
spared)
• Subconjunctival haemorrhage (posterior margin visi-
ble? If not, consider anterior cranial fossa /orbital
fractures)
98 F. Ali et al.

Nose
• Nasal deformity
• Septal haematoma
• CSF rhinorrhoea (base of skull (BOS) fracture)

Ears
• Haematoma (needs drainage to prevent cauliflower ear
deformity)
• Mastoid ecchymosis (Battle’s sign) associated with BOS
fracture. Usually occurs after days
• CSF otorrhoea (BOS fracture)

Intraoral
Do not forget to look inside the mouth for:
• Degree of mouth opening: limited with trismus. TMJ dislo-
cation/fracture
• Teeth: missing, loose, malocclusion
• Haematoma of the palate (maxillary fractures) or upper
buccal sulcus (zygomatic fractures)
• Intraoral lacerations
• Parotid duct injury (may see blood at Stenson’s duct
(opposite upper second molar)

Palpation
Start at the skull and work systematically, feeling for tender-
ness, steps, crepitus (sinus fractures) or abnormal movement
at suture lines.
Le Fort fractures of the midface (may be asymmetrical)
(Fig. 13.2).

I – maxilla only – floating palate

II – pyramidal fracture
III – craniofacial disassociation
Neurological examination
Motor
Check each branch of the facial nerve
 Chapter 13. Maxillofacial Trauma 99

Figure 13.2 Le Fort classification

Sensory
Forehead (supratrochlear and supraorbital)
Cheek, upper lip and upper teeth (infraorbital)
Lower lip and lower teeth (mental)

Vision
Relative Afferent Pupillary Defect (RAPD).
Visual acuity, HESS chart
Snellen chart, finger counting, perception of light
Visual fields
Extra-ocular eye movements
Limitation of upward gaze associated with diplopia suggests
entrapment of the inferior oblique muscle (orbital floor
fractures)

Investigations
Once life-threatening injuries have been addressed and the
patient has been stabilised, further investigations may be
performed.
100 F. Ali et al.

X-rays
Be guided by your clinical findings. There are many different
views that have been used to image the facial skeleton.
Waters: Oblique AP of orbital rims and maxilla. Panorex:
mandible, OPG.

CT
Most units managing maxillofacial trauma now use CT scan
(+/− 3D reconstruction) to accurately delineate complex
facial fractures and aid treatment planning.

Treatment
Medical
Broad-spectrum antibiotic cover (fractures open to oral cav-
ity, dog/human bites) and tetanus.

Surgical
Soft tissue injuries
Wound debridement (including scrubbing for road rash),
minimal wound margin excision, copious lavage and layered
repair should be performed.
Lacrimal duct
Should be performed by an experienced oculoplastic sur-
geon. Repair over a stent, (removed after minimum of
3/12).

Facial nerve injury

Nerve branches readily identifiable lateral to a vertical line
from the outer canthus and should be repaired directly under
magnification (loupe or microscope). Beyond this limit, there
is no indication for surgical repair (nerve branches small and
may have adequate crossover between except frontal and
mandibular branches).
Parotid duct laceration
Options include repair over a stent (removed after 2-3/52),
ligation or reimplantation into the buccal mucosa.
 Chapter 13. Maxillofacial Trauma 101

Maxillofacial fractures
Detailed management of specific fractures is outside the remit
of this book. The following addresses the basic principles:

1. Accurate diagnosis through thorough clinical examination

and radiographic evaluation
2. Early single stage surgery with
(a) Adequate exposure of bony fragments
(b) Rigid fixation and the immediate use of bone graft as
necessary
(c) Finally, re-suspension and reconstruction of the soft
tissues

Adequate exposure
Take advantage of any pre-existing lacerations, which
may be useful to approach fractures. However, additional
incisions may be required to aid visualisation, reduction and/
or fixation of fractures.
Methods of fixation
Intermaxillary fixation
Requires tooth-bearing segments of maxilla and mandible on
either side of the fracture fragments. May also act as a splint
to maintain the relative position of the maxilla and mandible
while a distant fracture heals.
Intraosseous wiring
Though not rigid, it may be of use at the ZF suture and
infraorbital rim.
Plate fixation
Low profile monocortical plates now generally advocated for
most fractures in the maxillofacial region.

Bone grafting
If >5 mm bone gap present, bone graft usually indicated. The
orbital floor also frequently requires bone graft to recon-
struct the bony orbit, reposition and support the globe. Donor
sites: calvarium (outer table; thin membranous bone; good for
orbital floor), rib, iliac crest.
102 F. Ali et al.

Re-suspension and reconstruction of the soft tissues

Re-suspension of the soft tissues reduces facial oedema, pre-
vents soft tissue contracture and therefore the risk of post-
operative asymmetry. Reconstruction of soft tissue defects
provides optimal environment for bone healing.
Condylar fractures of the mandible – treatment is
controversial
Conservative: Undisplaced fractures. Soft diet
Intermaxillary Adequate dentition required
fixation:
ORIF: Indicated with TMJ dislocation, significant
displacement or bilateral fractures with
anterior open bite
Chapter 14
Gynaecomastia
Robert Caulfield and Jon Simmons

Gynaecomastia is the abnormal breast development in the

male, with increase in ductal tissue and stroma.

Recognition
Can present at any age: neonatal, pubertal or senile gynaeco-
mastia (See history below). Recognised by excess of breast
tissue +/− excess skin, usually predominately subareolar in
location (Fig. 14.1).

History
General
Age, time of onset, duration, progression, occupation, inter-
ference with lifestyle and occupation.

R. Caulfield ()
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 103

DOI 10.1007/978-1-84882-116-3_14,
© Springer-Verlag London Limited 2012
104 R. Caulfield and J. Simmons

Figure 14.1 Gynaecomastia

Specific
These questions depend on age of patient (hence likely
cause).
• Age of onset ? (N.B. If pubertal: 75% of pubertal males
affected and 75% of these resolve within 2 years)
• Unilateral or bilateral?
• Area affected – central subareolar or diffuse breast
enlargement?
• Excess tissue firm (glandular) or soft (adipose)?
• Any previous treatment /surgery?
• Patient’s expectations about outcome vs. awareness of
limitations of treatment and risks

Risk factors
• Smoking (marijuana)
• Medications (Spironolactone, Cimetidine, Digoxin,
Metoclopramide, Tricyclics, Methyldopa, androgen block-
ers, e.g., Zoladex, Oestrogens)
• Alcohol consumption (Risk of cirrhosis – imbalance in
oestrogen metabolism)
• Weight gain /obesity (Increased production of oestrogen
in adipose tissue)
 Chapter 14. Gynaecomastia 105

• Pre-existing renal disease (Causes increased LH and

oestrogens)
• Pre-existing general disability (Interferes with pituitary-
hypothalamic axis, e.g., burns)
General
Full medical and drug history
• Pituitary disorders (causes decreased GnRH, FH and
LH)
• Symptoms/signs of thyroid disease (hyperthyroidism
causes increased serum binding globulin and less free
androgen – hence oestrogen/androgen imbalance)
• Male breast cancer (family history, specific breast lumps)
• Liver disease (cirrhosis)
• Renal disease (increased LH and oestrogens)
• Testes (seminomas, teratomas and choriocarcinomas cause
increased hCG; Leydig, Sertoli and granulosa theca cell
cause increased oestrogen)

AIM: by the end of history you should know

1. What the likely cause is: physiological, pathological or
pharmaceutical
2. Need for additional investigations/treatment of any patho-
logical causes
3. Treatment/progress to date
4. What the patient hopes to achieve
5. Chances of surgery meeting these objectives

Examination
Look
Evidence of general obesity. Any overt signs of hyperthyroid-
ism, cirrhosis, renal disease, testicular masses

Thyroid
Examine for goitre – diffuse/localised enlargement

Breast
Examine both breasts and axillae
106 R. Caulfield and J. Simmons

• Unilateral of bilateral
• Subareolar or diffuse enlargement (grade – see below)
• Specific breast lumps and any axillary nodes

Liver
Examine for evidence of cirrhosis and any other signs of liver
disease

Renal
Check for renal masses

Testes
Examine for testicular masses and groin nodes

AIM: by the end of exam you should have

1. Identified any non-breast pathology which may require
investigation/treatment
2. Idea about the grade/extent of gynaecomastia
3. Formulated likely treatment plan

Investigations
• Routine bloods: FBC, U + Es, LFTs, g-GT
• Special bloods (only if clinical suspicion): TSH, T4, a-fp,
testosterone
• Ultrasound (again only if clinical suspicion): thyroid,
breast, liver, testes (depending on history/examination)

Treatment
Depends on grade and patient’s acceptance of scarring,
downtime, etc. with different treatment options (Simon et al.
PRS 1973).
 Chapter 14. Gynaecomastia 107

Grade Clinical appearance Surgical treatment options

Grade 1 Small Liposuction alone +/−
enlargement excision of subareolar
(subareolar excess via periareolar
button) incision
No skin excess
Grade 2a Moderate Liposuction alone +/−
enlargement circumareolar excision of
No skin excess excess tissue (infra-areolar
incision = Webster’s)

Grade 2b Moderate enlargement Excision of excess tissue via

With moderate skin donut mastopexy technique +/−
excess liposuction to feather edges
Grade 3 Marked Formal breast reduction type
enlargement technique (type depends on
With marked skin skin excess, i.e., Wise pattern
excess or vertical scar).

Risks/Complications
Early
• Haematoma
• Infection
Late
• Dishing
• Inadequate correction of gland volume or skin excess
• Nipple stuck to chest wall
• Altered nipple sensation
• Obvious scars on male chest wall

Post-operative Management
• Pressure garment (usually cycling vest) for 6 weeks day
and night
• Once healed: massage and moisturisation for scars
108 R. Caulfield and J. Simmons

Further Reading
Fruhstorfer. BJPS 2003. Systematic approach to surgical treatment
of gynaecomastia.
Rohrich. PRS 2003. Classification and management of gynaecomastia:
defining the role of ulatrsound-assisted liposuction.
Chapter 15
Hand with Nerve Palsy
Shehan Hettiaratchy and Jon Simmons

Focus on addressing specific functional deficits, not trying to

recreate all of the nerve’s function.

Recognition
Recognise by hand posture:
• Ulnar – hypothenar flat/wasted; little and ring finger claw
(MPJ hyperextended +/− flexion of DIPJ/PIPJ depending
on high/low lesion) (Fig. 15.1)
• Median – thumb in plane of hand, thenar flat/wasted
• Median and ulnar – both of the above, hand looks flat
• Radial – wrist drop, fingers in flexion

History
General hand
Age, occupation, handedness, hobbies, musical instruments
and interference with these.

S. Hettiaratchy ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 109

DOI 10.1007/978-1-84882-116-3_15,
© Springer-Verlag London Limited 2012
110 S. Hettiaratchy and J.Simmons

Figure 15.1 Hand with nerve palsy

Specific
Cause: trauma or peripheral neuropathy
Time since onset and circumstances
Progression/improvement
Treatment to date both surgical and non-surgical
Current problems:
• Sensory – problems related to loss of sensation; any neuro-
pathic pain
• Motor – specific tasks that are difficult
What does the patient hope to gain?
General
Smoking, social setup, support
AIM: by the end of history you should know
1. What the cause was
2. Treatment/progress to date
3. What the patient hopes to achieve
4. Chances of surgery meeting these objectives

Examination
Look
Expose upper limb; scars – supraclavicular/axilla/upper arm/
forearm/hand – surgical or traumatic?
 Chapter 15 Hand with Nerve Palsy 111

Posture
Arm
• Flail: pan-plexus
• Internally rotated: upper root/trunk plexopathy or UMN
lesion
Elbow
• Flexed: UMN/central
− LMN to triceps/plexopathy with radial N
• Flail: C5/6 lesion – upper trunk/root plexopathy/MCN injury
Wrist
• Flexed: Central/UMN
Radial nerve LMN
Thumb
• Flat median nerve LMN
Fingers
• All flexed: radial nerve
• Ulnar flexed/MCPJ hyperextended (Sign of Benediction) –
ulnar nerve palsy
• Little finger abducted – Wartenberg’s sign for ulnar nerve
Feel and move
Not a global exam; test specific muscles for specific nerves
the confirm with a sensory exam.
Median:
Check sensory (index finger pad) – if PCMN is also involved
then lesion is proximal to the wrist.
Anterior Interosseus Nerve:
OK sign – (FPL is anterior interosseous nerve with FDP to index).
With an AIN lesion there is no sensory deficit and AbPB is intact.
Abductor Pollicis Brevis – test with thumb abduction perpen-
dicular to the palmar plane.
Ulnar:
FCU, FDP to little finger
Interossei (grip paper between fingers without flexing, criss-
cross fingers).
112 S. Hettiaratchy and J.Simmons

Adductor Pollicis (Froment’s sign - can they grip paper in 1st

web without flexing the thumb IPJ, i.e. using FPL).
Test sensation to little finger. (dorsal branch of ulnar nerve) –
if also involved then lesion is proximal to the wrist.
Radial/posterior interosseous nerve (PIN):
Radial nerve – Brachioradialis, Extensor Carpi Radialis
Longus/Brevis.
Wrist extensors, finger extensors, Extensor Pollicis Longus. If
you find a deficit, try and determine where in the radial nerve/
PIN If it is PIN then there is no sensory loss. If there is sensory
loss then it is either above the elbow or SBRN. It is – PIN – no
sensory loss; – above the elbow. The rest below the elbow
therefore after division into PIN. EIP tends to be last branch.
Sensory Sensory – first web.
AIM: by the end of exam you should have
1. Identified which nerves are affected
2. Idea about the level of the lesion (high or low)
3. Confirmed what muscles are working for transfer
4. Identified any previous surgery which may impact on your
plans

Treatment
The main aim of treatment is to correct deformity and regain
specific activities.
These are:
Median: Thumb opposition
Thumb flexion (if high)
FDP to index/middle (if high)
Ulnar: Correct claw
FDP to little/ring (if high lesion)
Thumb adductor – secondary priority
Index abductor – secondary priority
Radial: Wrist extension
/PIN Thumb/finger extension
 Chapter 15 Hand with Nerve Palsy 113

Timing
Non-surgical can be started at any time.
Transfers should only be performed when:
Chance for neurological recovery has passed
Soft tissue is stable and supple
Joints are mobile
Patient is psychologically ready

Options for treatment

Non-surgical
Physiotherapy
• Maintaining passive range of non-motile joints
• Stretching non-innervated muscles
• Softening scars/tissues in preparation for transfer

Splintage
• Helpful for correcting deformity and maintaining joints –
preventing capsular/collateral shortening
• Functional splinting (wrist drop) – either static or
dynamic

Surgical
Transfers
Remember principles of tendon transfer (APOSLE). May
not be able to stick to all of them depending on the clinical
situation but more achieved, the better the result.

Median nerve palsy

Opponensplasty: Huber – abductor digiti minimi
Bunnell – FDS ring finger
Camitz – Palmaris longus
Burkhalter – EIP
FPL function: Brachioradialis
FDP to middle/index: Buddy to FDP to ring/little
114 S. Hettiaratchy and J.Simmons

Ulnar nerve palsy

Claw Need to assess extensor function- if
correction(low): on examination have full extension
on correction of the claw then, static
procedure may suffice. If extension
limited, it will need augmenting with a
dynamic transfer
Static: Zancolli lasso
Dynamic: ECRL into extensor
mechanism using PL as interposition
grafts – can use as adductor
Thumb: Adductor: EIP through palm ?FDS4
FDP to little/ring: Buddy to FDP index/middle

Radial/PIN
Wrist extensor: PL to ECRB
Finger extensors: FCR to EDC
Thumb extensor: PL to EPL

Risks and Complications

1. Transfer failure
2. Infection
3. Inability to relearn movements

Post-operative Management
1. Immobilise 4-6/52 (protect repairs)
2. Therapy regime (active then passive) to attain transfer
function (initiation – get patient to try and reproduce the
original function then strengthening/range exercises to
increase function)
 Chapter 15 Hand with Nerve Palsy 115

Outcome
Depends on patient’s age and motivation but can get
reasonable function. Never as good as the original. Tensioning
is extremely important. Some transfers are more forgiving
than others.
Chapter 16
Hand with Inflammatory
Arthropathy
Shehan Hettiaratchy, Abhilash Jain,
and Jon Simmons

Surgery is the last resort once medical treatments have failed

but should not be shied away from.

Recognition
Typical arthropathic hand position, splints, walking aids.
Obvious synovitis, previous surgical procedures; scars over
MCPJ, CMCJ and dorsal wrist.
Involvement of other joints (neck/shoulders/knees/hips)
(Fig. 16.1).

History
General
Age, handedness, occupation, hobbies
Specific
What specific tasks are problematic? ‘I can’t open jars’

S. Hettiaratchy ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 117

DOI 10.1007/978-1-84882-116-3_16,
© Springer-Verlag London Limited 2012
118 S. Hettiaratchy et al.

Figure 16.1 Hand with arthropathy

What are their specific hand problems? ‘I can’t straighten my

fingers’
What medication are they on, how long have they been on it,
who is looking after their arthropathy (GP vs. rheumatologist)
Do they have pain?
Do they have any pins and needles? (occult nerve compressions)
How much of an interference is their hand with normal liv-
ing? Is it getting worse?
Risk factors
Rheumatoid
Sero-negative arthropathies
Psoriasis
Medication
Current analgesics and anti-inflammatory agents
Current and historic use of: immunosuppressives (e.g., steroids),
disease modifying drugs (e.g., methotrexate, gold, sulphasala-
zine), biological agents (TNF-alpha blockers, e.g., infliximab)
Social
Patients support package and social setup. Will they be able
to self-care after an operation.
 Chapter 16. Hand with Inflammatory Arthropathy 119

AIM: by the end of history you should

1. Is there an indication for surgery?
2. What does the patient want to achieve?
3. Are there any other issues that must be addressed first
(nerve compression, proximal joint problems, etc)?
4. Have identified any current treatment which would impact
on surgical timing, e.g., organising surgery to occur at the
midpoint between biological agent doses.

Examination
For efficiency, the examination is broken down into look, feel
and move, but combines all three as you work down the
upper limb. Before you start remember to ask the patient if
any of the joints are painful.

Neck
Bend your neck forwards and back (flexion/extension)
Turn your head to left/right (rotation)

Shoulder
Put your hands behind your head (external rotation and
abduction)
Put your hands behind your back and reach up as far as you
can on your spine (internal rotation and adduction)

Elbow
Bend your elbows – look/feel for nodules
Straighten your arms
Lock your elbows into your side – turn your palms up and
palms down

Wrist
Examine
Dorsal/volar synovitis
Classic wrist deformity – four components
120 S. Hettiaratchy et al.

1. Carpal supination (i.e., ulnar side of the wrist has dropped)

2. Volar translocation (carpus has moved volarly)
3. Ulnar translation (carpus has slid down the radius towards
the ulna)
4. Radial rotation (compensation for ulnar translation – wrist
is radially deviated)
Caput ulnae: prominent ulnar head – compare with other side

Move/feel
Palms together as if you are praying – raise your elbows
(extension)
Back of your hands together – push your elbows down
(flexion)
Hands out straight, palms down – point them out (ulnar
deviation), point them in (radial deviation)
Synovitis
DRUJ piano key-push down on ulna
Check for carpal tunnel syndrome

Thumb and fingers

Look
MPJ–ulnar deviation/volar subluxation/check ulnar intrinsics
to see if tight/check EDC to see if subluxed into intermeta-
carpal valleys
Fingers – boutonniere or swan neck
Thumb – type of deformity (Nalebuff):

• Type I: Boutonniere, flexed MCPJ

• Type II: Metacarpal adduction with flexed MCPJ
• Type III: Z-shaped thumb/swan neck deformity
• Type IV: CMCJ subluxation due to rupture or attenuation
of UCL

Move/feel
Passive joint ranges
Are deformities correctable?
Synovitis
Check extrinsic extensors/flexors (esp. EPL) for ruptures/
synovitis
 Chapter 16. Hand with Inflammatory Arthropathy 121

Overview
It may be of benefit to get the patient to demonstrate specific
tasks that are difficult as this may make the problem and
solution more obvious.
AIM: by the end of exam you should have
1. Identified the physical cause of the problem the patient
wants addressing
2. Idea of the surgical options and sequence to planned inter-
ventions (if any)
3. Idea of the contraindications/prerequisites for surgery
4. Assessed whether the patient is suitable for a surgical
inter

Treatment
Operative vs. non-operative
When to treat – Commonly agreed indications for treatment
are:
I. Addressing pain
II. Improving function
III. Preventative surgery (i.e., synovectomy)
IV. Improving cosmesis
Options for treatment
Non-surgical
Medication
The advent of effective disease modifying medications has
had a dramatic effect on our ability to control arthropathies.
The monoclonal antibodies have been especially significant.
Patients should be managed in a combined fashion with a
Rheumatologist.
NO SURGERY SHOULD BE PERFORMED UNTIL
MAXIMAL MEDICAL TREATMENT HAS BEEN
FOUND TO BE INEFFECTIVE
Splintage
May be helpful for joint flare ups while increased medication
is taking time to have an effect.
122 S. Hettiaratchy et al.

Hand therapy
Useful to manage symptoms and strengthen the hand within
the context of maximising function. Can assess and recom-
mend devices to assist in ADLs.

Surgical
Lots of different options but broadly start with a predictable
‘winner’; work proximal to distal and always exclude a nerve
compression. Remember that revision procedures are com-
mon. Plan incisions accordingly.

1. Synovectomy
2. Joint fusion
3. Joint replacement
4. Tendon transfers
5. Tendon rebalancing

TRIGGER – never release A1 pulley as this will worsen

ulnar drift. Triggering in arthropathies is due to synovitis!

Risks and Complications

Tissues very friable
Wound healing worse
Bone healing? worse so need to be meticulous about all bone
work
No need to stop steroids and methotrexate
Not clear evidence if anti-TNF must be stopped – arrange
surgery mid/late cycle

Post-operative Management
Depends on procedure.
Ensure adequate support is in place prior to discharge.
Plan surgery carefully, staging as necessary to allow patient to
continue to cope at home.
 Chapter 16. Hand with Inflammatory Arthropathy 123

Aetiology
Multifactoral, possible environmental factors in susceptible
individuals. There is an increased risk in patients with HLA
DR1 and HLA DR4. Hormonal influences are also impor-
tant, during pregnancy disease processes often improve. Flare
ups are common in the post-natal period.

Classifications
Several different systems in use for rheumatoid arthritis:
I. By stage
(a) Stage 1: Proliferative
(b) Stage 2: Destructive
(c) Stage 3: Reparative
II. By number of joints affected
(a) Monoarthropathy
(b) Pauciarthropathy
(c) Polyarthropathy
III. By clinical course
(a) Polycyclic – most common
(b) Explosive onset
(c) Progressive
(d) Monocyclic

Procedures
Arthrodesis
Principles of tendon transfer/reconstruction
Swanson arthroplasty

Controversies
Disease modifying drugs/immunosuppressives/biologics and
surgery – should they be stopped?
Chapter 17
Hypospadias
Ivo Gwanmesia and Matthew Griffiths

Hypospadias results from incomplete closure of the urethral folds

at 12th week and is characterised by a ventral meatus, hooded
foreskin and chordee. It is the most common malformation of the
male genitalia with an incidence of 1 in 300 male births.
It can be classified by the meatal position as glanular, coronal,
distal, penoscrotal, scrotal or perineal. 70% are distal, 10% mid-
penile and 20% the more severe proximal types (Fig. 17.1).

Embryology
3rd week Primitive streak mesenchymal cells migrate
around cloacal membrane to form cloacal folds
that fuse cranially to form the genital tubercle
6th week Cloacal membrane divides into urogenital and
anal membranes
Cloacal folds fuse anteriorly – urethral folds
Cloacal folds fuse posteriorly – anal folds
Genital swellings arise lateral to them – labia/
scrotal swellings
Pulls urethral folds forwards to form urethral groove
Lining of groove is endodermal (urethral plate)

I. Gwanmesia ()
Department of Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 125

DOI 10.1007/978-1-84882-116-3_17,
© Springer-Verlag London Limited 2012
126 I. Gwanmesia and M. Griffiths

Tunica albuginea Glanular

Cavernosal artery Subcoronal
Dorsal vein Distal penile
Skin
Midshaft

Proximal penile

Penoscrotal

Scrotal
Urethra
Corpus cavernosum
Corpus spongiosum
Perineal

Figure 17.1 Classification of hypospadias and penile anatomy

3 months Urethral folds close over plate to form penile

urethra but not into glans
4 months Distal ectodermal cells migrate into glans as a
cord, later to lumenise

Aetiology
Multifactorial
1. Environmental oestrogenic chemicals
2. Androgen hyposensitivity especially with micro penis,
undescended testis + inguinal hernia
3. Genetic father–son 8%. Sibs 14%. But not all identical
twins, so multifactorial

Recognition
Male child with ventrally placed urethral meatus. Otherwise
normal looking child (or adult if delayed presentation).
 Chapter 17. Hypospadias 127

History
General
Name, age, developmental history, PMH, PSH, DH

Specific
Penis – spraying, stream, witnessed erections
Undescended testes
Groin – inguinal hernia
Renal tract – urinary tract infections and failure to thrive
(FTT)
Family history of urogenital problem

AIM: by the end of history you should

1. Have identified the specific issues related to presentation
2. Be aware of family history
3. Have identified any symptoms suggestive of other issues

Examination
General
Normal vs. FTT
Specific
Abdo scars and herniae
Testes
Meatus position
Hooding
Chordee
Depth of urethral groove

AIM: by the end of examination you should

1. Know the position of the meatus
2. Have identified undescended testes and hernia
3. Have identified any previous attempts to correct
128 I. Gwanmesia and M. Griffiths

Investigations – Not Necessary If Distal

Bedside – Urine dipstick
Bloods – FBC U&Es
Specific – Renal tract USS, urethroscopy, voiding cysto-
urethrography

Treatment
Aim to achieve both functional and cosmetic normality
Distal meatal
MAGPI – Duckett (Meatoplasty and glanuloplasty incor-
porated)
TIP – Snodgrass (Tubularised incised plate meatoplasty)
Snodgrass (Journal of Urology 1994)
GA + caudal block, anaesthetises mucosa, less bladder spasm,
lighter GA, fewer opiates. Gent 7 mg/kg.
Horton erection test – GA, tourniquet, 25 F cannula, 0.9%
saline into corpora via glans. Stay suture in glans. Dilate up to 8 F.
Remember to follow curve of urethra with dilator. Mark sub-
coronal circumferential incision. Leave cuff for circumcision.
Incision carries on below native urethra so it does not
retract but rises up with glans once chordee released vertical
shaft incision. Chordee lateral to urethra is released and ure-
thra freed up. Lateral skin flaps raised. Check urethra able to
reach with urethral plate tubed to end of penis. If more length
required will need graft (SnodGraft).
Distal neo-urethra
If ok. Urethral plate incised vertically with bilateral glans inci-
sions to create lateral wall flaps of distal neo-urethra. Dorsal
defect re-epithelises with minimal scarring as.
1. Close urethral plate over catheter as first layer – 7/0
polyglactin.
2. Waterproof fascial layer. Inner layer of prepuce can be
taken as inner skin and fascia or fascia alone. Based later-
ally and dissect off prepuce with sharp scissors.
 Chapter 17. Hypospadias 129

3. Flip over to lateral glans flaps to define terminal meatus.

Glans not fixated to underlying neourethra. Close with
buried 6/0 polyglactin.
4. Close skin with buried 7/0 polyglactin.

Proximal

Bracka – 12 months or at 3 years of age

Bracka does all, does any age, easy to learn, low complication
rate.

Bracka – BJU 1995, 76, Suppl. 3, 31–41

For any severity and for any age
Stage 1 – at 3 years of age
GA, tourniquet, 8F catheter, 7 mg/kg dose of gentamicin,
Horton erection to test
Sub-coronal incision and dissection to distal corpus cavern-
ous to release chordee. Repeat erection test. Glans split and
inner foreskin FTSG or flap to line dorsal aspect of neo-
urethra.
Catheter 5 days, EMLA bath or GA change.
Stage 2–6 months after first stage.
NB: Graft mature and soft – needs to be min 15 mm wide
with extra 5 mm to be de-epithelised to allow double-
breasting.
Prep GA, tourniquet, 8F catheter, dose of gentamicin.
Incision into either side of glans, carried down to form
U-shaped incision 15 mm-wide beneath native meatus.
Graft or flap folded over catheter and closed in two layers
(Ethilon and PDS).
Third layer derived from foreskin and placed over joint as
waterproofing layer.
Circumcision performed as reconstructed foreskin ends up
too tight.
Distally, glans flaps closed over catheter.
Lateral skin de-gloved off penis and then closed over as
fourth layer.
Post-op – Catheter removed after 1/52.
130 I. Gwanmesia and M. Griffiths

Complications
Early
Bleeding
Infection
Catheter blockage
Bladder spasm – less with caudal
Intermediate
Fistulae 3%. Early ones due to obstruction, extravasation,
haematoma, infection, late due to turbulent flow
Late
Stricture 7%. (2% early. Late mostly due to BXO in FTSG
exposed to urine)
Revision 3–5%
Balanitis Xerotica Obliterans – uncommon cause of late stric-
tures – remove all skin graft and replace with buccal mucosa
graft – why not do this in the first place? Because it is very
difficult to get enough buccal mucosa in the young. Lichen
sclerosus (LS) is a chronic, progressive, sclerosing inflamma-
tory dermatosis of unclear etiology. Most reported LS cases
(83%) involve the genitalia. In men, this genital involvement
has traditionally been known as balanitis xerotica obliterans
(BXO). A more accurate term is male genital or penile LS.
Fistulae
Wait for things to settle
Close hole in the urethra
Interpostional fascial flap
Test integrity
NO CATHETER

Follow-Up
Most assessed as normal – 80%
Good urinary function, all forceful stream, 40% spraying
Psyche – 80% confident
83% – straight erections
Chapter 18
Lower Limb Trauma
Shehan Hettiaratchy, Abhilash Jain,
and Jon Simmons

Requires joint and simultaneous orthopaedic and plastic surgi-

cal management to achieve the best outcome. Amputation can
be a good reconstructive option.

Recognition
Treat as a polytrauma using ATLS guidelines. Primary then
secondary survey to identify and manage injuries. Initial
evaluation and treatment may have to occur simultaneously.
External bleeding should be managed with direct pressure.
Beware of high energy injuries (and elderly patients) where
zone of injury may not be immediately apparent (Fig. 18.1).

History
In an emergency situation use AMPLE+.
A: Allergies/airway
M: Medications
P : Previous medical/surgical history. PVD, DM, fitness levels

S. Hettiaratchy ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 131

DOI 10.1007/978-1-84882-116-3_18,
© Springer-Verlag London Limited 2012
132 S. Hettiaratchy et al.

Figure 18.1 Lower limb trauma

L: Last meal
E: Event. What are the exact circumstances and nature of the
trauma. History from first responder gives more detail.
Consider forces
+: Employment, smoking habits, social circumstances
AIM: by the end of history you should
1. Know the exact mechanism of injury (think compartment
syndrome)
2. Have an idea of any adverse patient factors (smoking etc.)
3. Have an idea of patient’s baseline physical activity/social
circumstances

Examination
Look
Identify and manage external bleeding. Identify and docu-
ment all soft tissue, degloving and obvious bony injuries.
Feel and move. Assess by components and document
findings:
Skin – Look for degloving; assess by looseness of skin and
viability by blanching/pinprick. Fluorescein is not practical.
Laser doppler can be useful.
 Chapter 18. Lower Limb Trauma 133

Nerves – Test sensation throughout lower limb especially of the

sole of the foot – if insensate it may be less urgent to salvage.
Outer border of foot (sural n.), dorsum (sup. peroneal n.), 1st
web (deep peroneal n.), inner border (saphenous n.), sole
(medial and lateral plantar from posterior tibial n.).
Bones/joints – Assess any injured joints for gross instability
(within pain limits). XR to assess bony injuries. Views must be
complete (joint above and below): AP and Lat.
Exclude an ischaemic limb – surgical emergency. Muscle
death begins after 4 h of warm ischaemia. Check pulses by
palpation and if not palpable by Doppler compare to an unin-
jured side. Capillary refill is misleading in the toes. If there is
vascular compromise and a non-reduced fracture, reduce the
fracture and re-check. If still pulseless proceed to immediate
exploration. Do not delay theatre for angiography; level of
vascular injury corresponds to fracture site.
Exclude/monitor for a compartment syndrome – surgical
emergency. Even in open injuries. Disproportionate pain is
the biggest clue, pain on passive movement, tenderness
altered sensation. If equivocal, measure all four compartment
pressures. Pressure difference between compartment and
diastolic of less than 30 mmHg is considered appropriate for
decompression.
AIM: by the end of exam you should
1. Have excluded an ischaemic leg and/or compartment syn-
drome or gross contamination (surgical emergencies)
2. Have an idea about the extent of the soft tissue injury
3. Have an assessment of the bony injury and have adequate
imaging of the leg
4. Be ready to photograph, dress and immobilize the limb

Treatment
Immediate treatment
Photograph and then cover the wound with saline soaked
gauze and an adhesive film
Immobilize the limb with a splint
134 S. Hettiaratchy et al.

IV antibiotics co-amoxiclav 1.2 g or clindamycin if allergic to

penicillin
Initial surgical assessment
Done on next trauma list within 24 h of injury unless
ischaemic limb or compartment syndrome or gross contami-
nation – immediate. Senior orthopaedic and plastic surgeon.
Aims: Sampling of wound for microbiology. Surgical assess-
ment of bone and soft tissue. Aggressive debridement.
Perform or plan definitive cover/fixation. It may be possible
to achieve definitive fixation and cover in this initial opera-
tion (e.g., IM nail/local fasciocutaneous flap).
If more complex reconstruction is required then a tempo-
rary external fixator should be put on and the wound(s)
dressed with a VAC.
If the limb is non-salvageable it should not be amputated at
this sitting unless it poses a risk to the patient. Amputation
must be discussed with the patient who should then be given
time to consider it, leading to a better psychological outcome.
Intermediate investigations/operations – prepare patient for
definitive surgery.
If free flap reconstruction is being planned an angiogram
may be required. Consider pre-operative transfusion, filling
and warming. CT may be useful for complex or intra-articular
fractures.
Further debridements necessary for extensive degloving
or contamination. Swabs and samples should be taken each
time. Alter antibiotic therapy on the basis of culture results.
Definitive fixation/reconstruction
This is a joint procedure and the end result should be definitive
fracture fixation and complete soft-tissue coverage. Numerous
options but often involve an Iliziarov/Taylor Spatial Frame
with a free flap. Pin site selection is paramount.
Post-operative care
Free flap observations and care. Warming, IVI, FBC, U + E.
Close liaison with microbiology for advice about continued
 Chapter 18. Lower Limb Trauma 135

antibiotics. DVT prophylaxis is essential. Keep the limb ele-

vated for 5 days and then intermittent lowering to ‘stress’ the
flap and let the venous return improve. Discharge will depend
on mobility and weight bearing status.
Follow-up
Required to monitor wound and fracture healing. Frame
may be required for 3–4 months, longer for transport
procedures.

Outcome
Dependant on injury and treatment
Flap failure 2–4%
Non-union, malunion, delayed union
Osteomyelitis
Amputation
Controversial whether primary amputation or reconstruction
gives better long-term results. Should be decided on a case by
case basis.

Classifications
Gustillo and Anderson
MESS
AO
Byrd and Spicer
Patterson

Controversies
Amputation vs. reconstruction
Muscle flaps vs. fasciocutaneous flaps
The role of angiography
Timing of reconstruction
136 S. Hettiaratchy et al.

Further Reading
Gustillo RB, Anderson, JT. Prevention of infection in the treatment
of one thousand and twenty-five open fractures of long bones:
retrospective and prospective analyses. J Bone Joint Surg. 1976:
453–458.
Byrd HS: Management of open tibial fractures. Plast Reconstr Surg.
1985;76(5):719–30.
Godina M: Early microsurgical reconstruction of complex trauma of
the extremities. Plast Reconstr Surg 1986; 78: 285–92.
Nanchahal J et al: Management of Open Fractures of the Lower
Limb. Royal Society of Medicine Press. 2009. Short Guide - http://
www.bapras.org.uk/downloaddoc.asp?id=141.
Chapter 19
Lump in the Neck
Farida Ali, Ivo Gwanmesia, and Jon Simmons

A primary tumour can usually be identified in all but 0.5–1%.

Patients with positive lymph nodes and an UNKNOWN pri-
mary have a better prognosis.

Recognition
Patients often present to the Head and Neck surgeons first,
but they always require multidisciplinary input (includes sur-
geons (ENT/maxillofacial/plastic), pathologist, radiologist,
radiotherapist, oncologist, speech therapist, psychologist,
clinical nurse specialist and dietician (Fig. 19.1).

History
Age, sex, occupation
General
Cachexia, loss of appetite, weight loss, malaise, pain
Smoker, spices, spirits, poor dentition, drugs (betal nut)

F. Ali ()
Department of Plastic and Reconstructive Surgery,
St George’s Hospital, London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 137

DOI 10.1007/978-1-84882-116-3_19,
© Springer-Verlag London Limited 2012
138 F. Ali et al.

Figure 19.1 Patient with lump in the neck

Previous x-ray therapy (e.g., for tinea capitis)

Comorbidities
Social support network
Specific
Intranasal – bleeding, obstruction (usually present late espe-
cially post-nasal space)
Intraoral – ulcer, lesion, bleeding, pain, trismus
Pharyngo-oesophageal – dysphagia (solids/liquids)
Laryngeal – dysphonia, hoarseness
Ear – masses, hearing change, discharge, bleeding, pain
Salivary glands – swelling, pain
Neck – thyroid, parathyroid mass
Respiratory – cough, haemoptysis, SOB
Upper GIT – dyspepsia, dysphagia, pain
Other, e.g., lymphoma – Other masses elsewhere?
Skin, pigmented/non-pigmented lesions, sun exposure etc. as
for skin cancer, e.g., scalp

Examination
Be systematic
Use a pen torch and tongue depressor for the intraoral
examination (if you do not have one, ASK)
 Chapter 19. Lump in the Neck 139

General
General status of patient (note presence of signs of advanced
CA? – cachexia, anaemia etc.)
Other lymph node basins (lymphoma)
Other systems (respiratory, GI)

Specific
Look
Is there an obvious mass? Single or multiple, midline or
lateral?
Extraoral – lip, external nose, ear, skin, scalp. Look for any
obvious lesions.
Intraoral – mucosa, alveolar ridges, tongue, palate, floor of
mouth, pharyngeal, tonsils – Looking for masses, ulceration,
leukoplakia, blood from Stenson’s duct (opposite upper sec-
ond molar).
Intranasal – using a nasal speculum look for any masses on
both sides.
Salivary gland masses, blood at Stenson’s duct orifice.

Palpation
Neck – clearly demonstrate each level to the examiner.
Involved level can give an indication to potential primary
sites. Identify whether single node or multiple and matted
nodes. With midline masses, identify presence of movement
with swallowing or tongue protrusion.
If there are any suspicious lesions from your inspection,
then examine them.
Intraoral – use gloves and digitally palpate the mucosa,
alveolar ridges, floor of mouth and tongue. Look for blood at
the opening of Stenson’s duct on palpation of the parotid
gland(s).
Aim: By the end of the history and examination, you should
have
1. Narrowed down your likely primary sites (although inves-
tigations are required to rule out synchronous/multiple
system tumours)
140 F. Ali et al.

2. Identified the level and laterality of involved lymph

node(s)
3. Made an assessment of the general status of the patient
including fitness for surgery

Investigations
1. CXR and OPG
2. Further imaging. This should be done BEFORE biopsy for
two reasons. First, it guides biopsy of identified suspicious
areas and secondly, interpretation will not be compromised
by postoperative oedema.
• MRI scan (Head and Neck)
Primary lesion peri tumour oedema on T2 weighted
images. Estimate size, extent, invasion of neighbouring
structures (all required to stage the disease)
• CT Head and Neck
Good for bony lesions/ bony invasion
• PET Scan/PET-CT
More sensitive than CT or MRI
Can be superimposed onto CT to identify whether a mass
on CT and enhancing area on PET scan correspond
3. FNAC: If non-specific, repeat once more. If still inconclu-
sive, then open biopsy (scar placement should allow incor-
poration into neck dissection access incisions).
4. Panendoscopy: Any abnormal site (clinical or radio-
graphic) should be biopsied. IN ADDITION, always biopsy
nasophayrnx, tonsils, piriform fossa, base of tongue and
floor of mouth.

Suspicious Lymph nodes on MRI/CT

>0.5 cm
Central necrosis
Loss of architecture
Extracapsular spread
Multiple or matted nodes
 Chapter 19. Lump in the Neck 141

Treatment
Known primary
Treatment dictated by histopathological diagnosis and a mul-
tidisciplinary discussion of each case. May be non-surgical,
surgical or combined.
Unknown primary
Nodal cytology/histology may guide you somewhat.
Squamous cell carcinoma – more likely head and neck/skin origin
Adenocarcinoma – more likely lung, breast, GI malignancy

Treatment of Likely Primary Sites

Unilateral/ bilateral tonsillectomy – Controversial. Occult
tonsillar carcinoma seen in up to 40% cases (McQuone
et al. 1998).
Radiotherapy to potential sites – Controversial. Likewise,
unilateral or bilateral treatment is also debatable. Suggestion
that bilateral radiotherapy to potential primary sites shows
better disease control, particularly with bilateral lymphade-
nopathy; however, some studies show increase in local control
but no change in overall survival (Mahoney Otolaryngologic
Clinics 2005).

TNM definitions for oral cavity and oropharynx

TX: cannot assess primary tumour
T0: no evidence of primary tumour
Tis: carcinoma in situ
T1: tumour <2 cm
T2: tumour 2–4 cm
T3: tumour >4 cm
T4: tumour invades adjacent structures
N1: single, ipsilateral /unilateral, <3 cm
N2a: single, ipsilateral/unilateral, 3–6 cm
N2b: multiple ipsilateral/unilateral, <6 cm
N2c: contralateral/bilateral, <6 cm
N3: any lymph node, >6 cm
142 F. Ali et al.

MX: distant metastases cannot be assessed

M0: no distant metastases
M1: distant metastases

Treatment of the Neck

This depends on the stage of the disease
N0 neck
Neck dissection not performed for T1 tumours. Neck dissec-
tion is performed for T2, T3 and T4 tumours
N positive neck – Neck dissection is performed for N posi-
tive necks
N1/N2a
Single Modality Treatment
Neck dissection alone or radiotherapy alone (after excision
of node). However, if extracapsular spread or multiple nodes
are confirmed on histology, postoperative radiotherapy is
usually recommended.
N2b/2c/3
Combined Treatment
A combination of neck dissection and radiotherapy is gener-
ally accepted. However, still controversial whether radio-
therapy should be neo-adjuvant or adjuvant.
Chemotherapy. Mixed results reported with chemother-
apy, but usually recommended for inoperable disease or in
the presence of distant metastases.

Surgical Management of the Neck

Known primary – dictates whether selective or modified radi-
cal ND is indicated
Unknown primary – usually indicates modified radical ND
Chapter 20
Complex Wounds:
Pressure Sore
Jon Simmons and Matthew Griffiths

The last thing to consider in pressure sore management is the

wound. Need to optimise all other factors first. Surgery rarely
indicated.

Recognition
Consider pressure areas relative to the individual patient.
Elderly bed-bound patient vs. young patient in a wheelchair.
Approximately 3% of hospitalised patients have a pressure
sore (Fig. 20.1).

Pathophysiology
Capillary arterial circulation will cease with pressures greater
than 32 mmHg, 8–10 mmHg for venous capillary network.
Constant pressure for >2 h produces irreversible changes.
Muscle is more susceptible than skin. Ischial tuberosities are
exposed to 100 mmHg when seated, when supine, occiput,
heel and sacrum are exposed to 50 mmHg. Bacterial growth

J. Simmons ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 143

DOI 10.1007/978-1-84882-116-3_20,
© Springer-Verlag London Limited 2012
144 J. Simmons and M. Griffiths

Figure 20.1 Wound breakdown in a pressure area

also increased in pressure areas due to ischaemia, impaired

lymphatics and impaired immune function. Neurological
injury further decreases local tissue perfusion due to local
tissue oedema. Dilution of sebum concentrations reduces its
anti-staph and anti-strep activity. Shear forces.

History
When and where, how long, getting better/worse, problems,
current dressing management, devices, previous surgery,
changes in circumstances (for instance a patient who has
spent a long time in bed on ITU who has recovered and is
now mobile) and prognosis.
General health
CNS/PNS Level of injury, CVA, MS
CVS Arteriopath, anaemia, BP, cholesterol,
RS COPD, asthmatic (suitability for general
anaesthesia)
GIT Nutrition, stoma, incontinence
GUS Renal function, incontinence
Endo DM, thyroid
MS Skin quality, joint problems, mobility
 Chapter 20. Complex Wounds: Pressure Sore 145

Surgical/medical/medicines history – Previous surgery for

pressure sores, medication, immunosuppression with medi-
cines or illness, smoking.
Social history – Occupation, partner, care package, home
modifications, pressure relieving devices.

AIM: by the end of history you should have

1. Understood the ulcer’s aetiology and history along with
the patient’s likely prognosis
2. Any adverse patient factors (BMI, immobility, immuno-
compromise, infection, smoking)
3. Understood whether any causative or adverse patient fac-
tors can be reversed

Examination
Consider Waterlow Score for ulcer prevention
General – Age, sex, mobility, nutrition, position and posture,
pressure relief (cushions etc.) General health of the patient,
anaemia, cachexia.
Wound and surrounding skin quality – size, edges, base, sur-
face. Areas affected in decreasing frequency; ischium (30%),
sacrum (20%), trochanter (15%) and the heel (10%).
Remember the extent of underlying muscle damage is greater
than that of the overlying skin.
Only now consider staging!
Staging: NPUAP – National Pressure Ulcer Advisory Panel
I: Non-blanchable intact skin
II: Superficial partial skin loss, blistering
III: Full-thickness skin loss and subcutaneous destruction
into muscle
IV: Involvement of bone/joint

AIM: by the end of examination you should

1. Understand the site involved and the aetiology in this par-

ticular individual
146 J. Simmons and M. Griffiths

2. Understand the extent of the soft tissue/bony defect and

be ready to describe the stage of the ulcer
3. Made an assessment of the general health of the patient
and any reversible factors
4. Have understood any previous surgical interventions (with
respect to donor sites already used – some flaps may be
readvanced)

Management: Prevention Is the Key

Patient: Nutrition
Involve dietician – Build up drinks, adequate intake, enteral
or parenteral feeding may be appropriate. Robson et al. dem-
onstrated normal healing if albumin above 20. Consider vita-
min and mineral supplements in the form of Vitamin A and C
(required for normal wound healing), Zinc (epithelialisation
and fibroblast proliferation) and calcium (co-factor for many
enzymes).
Patient/Nursing – Pressure
Dinsdale (Arch Phys Med Rehab 1974) demonstrated the
ability to negate pressure by relieving for 5 min every 2 h.
Pressure when seated is higher than supine and so relief
should be more frequent.
Patient – Continence
Catheterise and consider stoma if large perianal wound.
Patient – Spasticity
Diazepam 10 mg every 8 h
Baclofen 10 mg every 6 h
Dantrolene 25 mg every 12 h
Nursing – different mattresses for increasing risk (based on
Waterlow score)
Foam
Static flotation
Alternating air
Low air loss
Air fluidised, e.g., clinitron
 Chapter 20. Complex Wounds: Pressure Sore 147

Surgery: General Principles

1. Patient selection is of paramount importance – most sores can
be managed non-operatively with pressure relief, patient opti-
misation, manual sharp debridement and careful wound care
2. Excisional debridement of ulcer, bursa and heterotopic
calcification
3. Partial/complete osteotomy/osteoectomy reduce bony
prominence
4. Closure with healthy padded tissue
Debridement
Limited debridement can be performed on the ward to de-
roof the necrotic tissue.
Theatre
Place in position so wound given maximal exposure and
therefore flaps positioned at minimal tension post-op. This
should reduce wound dehiscence post-op. Aggressive exci-
sion of wound – tumour type.
Osteoectomy
Removal of bony prominences required.
Radical excision of bone redistributes pressure to other
areas, causes excessive bleeding and skeletal instability.
Ischial ulcers. Total ischectomies reduce recurrence rate
from 38% to 3% but contralateral ulcers formed in one-third
of patients.
Bilateral ischectomies move pressure to perineum which
can complicate to the formation of urethral fistulas.
Primary closure
Always leaves a subcutaneous space.
SSG
30% success is associated with this technique.
Musculocutaneous flaps
Mathes demonstrated theoretical advantage of muscle flaps.
Excellent blood supply, bulky padding and can be re-advanced
or re-rotated. However muscle is the most sensitive to ischae-
mic injury, may be atrophic in the elderly and spinal patients
or lead to functional disability in ambulatory patients.
148 J. Simmons and M. Griffiths

Fasciocutaneous flaps
Offer adequate blood supply, durable coverage with minimal
potential for a functional deformity and more closely reconstruct
the normal anatomic arrangement over bony prominences.
Limited tissue available for the treatment of large ulcers.

Outcome
Dependant on many factors
Recurrence rates are high
Complications include: haematoma, seroma, infection and
wound dehiscence

Classifications
National Pressure Ulcer Advisory Panel staging system
Waterlow Scoring System

Procedures
Sacral sores – buttock rotation flaps (musculocutaneous or
fasciocutaneous)
Trochanteric sores – TFL, Vastus lateralis, ALT
Ischial sores – hamstrings muscle flap, posterior thigh flap

Controversies
Operative vs. non-operative management
Musculocutaneous vs. fasciocutaneous flaps. Which is
better?
Chapter 21
Abnormal Ear
Ivo Gwanmesia, Matthew Griffiths,
and Jon Simmons

Abnormal ears are either congenital or acquired. Congenital

types may either be prominent ears suitable for correction or
may be more severe and be part of a syndrome and require
reconstruction. Acquired ear deformities are usually second-
ary to trauma.

Recognition
Young patient presenting with parents or adult usually male
following trauma. Young adults may present with prominent
ears where parents have resisted/deferred seeking treatment
for their child (Fig. 21.1).
Embryology
Ear forms between weeks 4 and 8
6 auricular hillocks form around the 1st branchial groove
1–3 form from the 1st arch and form tragus, root and superior
helix
4–6 posteriorly from 2nd arch and form rest of helix, anti-
helix, scapha, antitragus and lobule and triangular fossa

I. Gwanmesia ()
Department of Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 149

DOI 10.1007/978-1-84882-116-3_21,
© Springer-Verlag London Limited 2012
150 I. Gwanmesia et al.

Figure 21.1 Abnormal

ear

History
Prominent ears
Was deformity present at birth?
Are there any hearing problems?
Is the child being teased at school?
Does the child feel that his/her ear is a problem?
Are there any other abnormalities?
Congenital
History similar as above.
More emphasis on hearing status and the presence of
other anomalies if suspicion of congenital cause.
If more severe then relevant paediatric history. Family
history.
Traumatic ears
Previous debridements, replantation or attempts at
reconstruction
 Chapter 21. Abnormal Ear 151

AIM: by the end of history you should have

1. Identified any other conditions which may influence surgi-
cal management
2. Understood the reasons that treatment are sought at this
point in the child’s life – who is driving the process
3. Traumatic – Identified any previous attempts to resolve
the problem

Examination
Prominent ears
Assess upper third – Defined by presence of anti-helical
fold
Assess middle third – Defined by depth of conchal bowl
Assess lower third – Size of lobule
Comment on symmetry – Which side is more projected
Lateral protrusion of helix from head ranges from 17 to
21 mm (normal)

Congenital/traumatic
• Any other congenital anomalies, facial asymmetry
• Quality of surrounding skin
• Previous incisions and skin grafts
• Type of microtia – conchal or lobular
• Size of costal margin (for rib grafting 58–60 cm circumfer-
ence required as a minimum)
• Hairline in relation to projected position (important not to
have hair on the helical rim)
• Extent of defect – what will be required for reconstruction
in terms of partial or complete framework
• Ear problems common in Treacher–Collins (mandibulo-
facial dysostosis), Goldenhar and hemifacial microsomia,
but often sporadic
AIM: by the end of examination you should have
1. Assessed the suitability of the patient for surgery
2. Identified other congenital anomalies that might influence
surgery or timing of surgery
152 I. Gwanmesia et al.

3. Formulated a surgical plan and timeline

4. Identified any factors which might require treatment prior
to definitive surgery, e.g., laser to raise a hairline

Management
Neonates (Ear buddies)
More pliable cartilage, do not sweat, cannot reach ear, splint
for 2/52.
If more than 1/12 splint for 3/52.
Matsuo managed the correction of congenital auricular
deformities in 150 patients using various moulds and tapes to
achieve correction.
Cartilage is uniquely mouldable in the first 6 weeks of life
due to maternal hormones.
Congenital – Microtia
About 90 cases per year/UK sub-specialised field, few sur-
geons doing large numbers.
85% of ear growth done by 3 years of age, but insufficient
costal cartilage until at least 6 years of age.
Ear height continues into the adulthood.
Options
1. Prosthetic reconstruction
(a) Adhesive
(b) Branemark
2. Autologous/alloplastic reconstruction
Medpore implant with local temporoparietal fascial flap
(TPF) and SSG
3. Autologous reconstruction
Costal cartilage with local temporoparietal fascial flap and
SSG
Tanzer 1959 Six stage technique
Brent 1974 Four stage technique – pocket, lobe transposition,
lift ear, tragus
Nagata 1985 Two stage technique – most practiced in the UK
 Chapter 21. Abnormal Ear 153

• Framework constructed using rib held and positioned with

steel sutures and shaped. Depending on the defect a floating
rib is used for the helix and a rib block formed from the
syndesmosis is used to form the remaining structure. Pocket
dissected and framework inserted with tragus premade using
the pedicled transposed lobe. A left over block is banked in
a subcutaneous pocket usually on the abdomen, to be used
in the second stage.
• After a minimum of 6/12. Elevate framework with costal
cartilage in the sulcus. TPF or fascial flap and SSG from
occipital scalp to resurface the sulcus.
Hearing
Inner ear develops from different arches so tends to be pres-
ent. Bone anchored hearing aids (BAHA) work but need to
be positioned sensitively so that local reconstructive options
are not affected.
Traumatic ears
Options
1. Nothing
2. Prosthesis as above
3. Autologous/alloplastic reconstruction as above
4. Replantation. Rarely successful. Small artery, unlikely to
find a suitable vein and may suffer catastrophic fall in Hb
due to leeching
Prominent ears
If very early then may be able to avoid surgery with ‘ear bud-
dies’ when cartilage is mouldable.
The current trend is more for suture based techniques rather
than full degloving of ear, scoring or cartilage excision, accepting a
slightly higher revision rate but much less severe complications.
1. If less severe prominent ear in younger child then consider
degloving of posterior pinna, with or without fascial flap
and then around three scapho-conchal horizontal mattress
of PDS or Ethibond on a round bodied needle to recreate
more normal, rounded anti-helical fold. Then dissect small
154 I. Gwanmesia et al.

pocket in retroauricular area and use similar concho-

mastoid sutures to set and posteriorly rotate the whole pinna.
2. If more severe then may need to consider posterior scor-
ing or classic Chongchet 1963 BJPS cartilage excision and
anterior scoring – rarely necessary.

Miscellaneous
Normal ear characteristics
1. Ear position usually one ear length from lateral orbital rim
2. 6.5–7.5 cm length
3. Width = 55% of length
4. Conchal bowl 1.5 cm deep
5. Top of ear in line with brow
6. Bottom of ear in line with base of columella
Ear anatomy
Need to be able to define all the parts.
Helical rim, scapha, anti-helical fold, concha, superior and
inferior crura, triangular fossa, cymbum concha, cavum con-
cha, tragus, antitragus, lobule, helical root (Fig. 21.2).

Scaphoid fossa

Helix
Triangular fossa

Anti helix Concha

External auditory meatus

Tragus

Anti tragus Lobule

Figure 21.2 Normal ear anatomy

 Chapter 21. Abnormal Ear 155

Tanzer classification of auricular defects

1. Anotia
2. Microtia
(a) Atresia of EAM
(b) Without atresia of the EAM
3. Hypoplasia of the middle third of the auricle
4. Hypoplasia of the superior third of the auricle
(a) Constricted (cup or lop) ear
(b) Cryptotia
(c) Hypoplasia of the entire superior third

McDowell outlined the basic goals – prominent ears

1. Correct all protrusion of the upper third of the ear
2. From the front, helix of both ears should be beyond anti-helix
3. Smooth helix
4. Post-auricular sulcus should not be decreased or distorted
5. Outer helix to mastoid
(a) Top 10–12 mm
(b) Middle 16–18 mm
(c) Lower 20–22 mm
6. Position of the ear should be within 3 mm of each other
Chapter 22
Management of the
Pigmented Lesion
Fiona Harper

Melanoma: Tumour of epidermal melanocytes. Should be

managed in multi-disciplinary team setting: dermatologist,
surgeon, pathologist, oncologist, clinical nurse specialist.
Increasing prevalence in UK. Managed initially by local skin
cancer MDTs (LSMDTs) core services and referred to spe-
cialist skin cancer MDTs (SSMDTs).

Recognition
Elderly patient with Fitzpatrick 1 or 2 presenting with obvious
sun damaged skin. Younger patient with fair skin with history
of excessive sun exposure. Patient with Fitzpatrick 4, 5 or 6
with a lesion on the sole of the foot or subungally (Fig. 22.1).

History
General introduction
2 week rule

F. Harper
Specialist Registrar in Plastic and Reconstructive Surgery,
Pan-Thames Training Scheme,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 157

DOI 10.1007/978-1-84882-116-3_22,
© Springer-Verlag London Limited 2012
158 F. Harper

Figure 22.1 Lymph node melanoma metastasis with unknown pri-

mary

Urgent referral to LSMDT if:

• New mole appearing after onset of puberty with change in
shape/colour/size
• Longstanding mole with change in shape/colour/size
• Any mole with more than three colours, loss of symmetry
• Itching/bleeding
• Persistent skin lesion growing/pigmented/vascular
appearance
General
Age, occupation, hobbies, previous and current sun
exposure
Full medical and drug history
Specific
Duration of lesion
Change in
• Size
• Shape
• Colour
• Itching/bleeding
 Chapter 22. Management of the Pigmented Lesion 159

Risk factors (melanoma)

Moderately increased (8–10×) Atypical mole phenotype
risk Previous melanoma
Organ transplant
Greatly increased risk (>10×) Giant congenital
pigmented hairy naevus
FH x 3 or more cases of
melanoma
Pancreatic carcinoma

AIM: by the end of the history you should know

1. Duration and characteristics of lesion
2. Risk factors for melanoma
3. General medical factors that may influence management

Examination
Look/feel
• Site
• Size
• Elevation
• Description
• Other pigmented lesions
• Regional lymph nodes
• Hepatomegaly

Plus: Complete skin examination including Fitzpatrick

skin type
+/− dermatoscopy
Photography

AIM: by the end of the examination you should know

1. Macroscopic features of the lesion and other lesions
2. Clinical evaluation of the presence of secondary disease
3. General skin quality/evidence of sun exposure
160 F. Harper

Biopsy of Suspected Melanoma

Photograph first
Full thickness, including the whole tumour, 2 mm lateral
margin plus cuff of fat
Incisional biopsy occasionally acceptable (e.g. lentigo maligna)

Subungal melanoma:
Biopsy by surgeons regularly doing so. Important to biopsy
germinal matrix.
Removal of sufficient nail plate + any clinically obvious
tumour.

Investigations
Stage l and ll
Routine investigation not required
NICE guidelines
Patients should be offered sentinel lymph node biopsy
(SLNB) if their tumour is: Stage lB and upwards (<1 mm,
with ulceration or mitoses or >1 mm
Stage lll (Lymph node involvement)
CT head/chest/abdomen/pelvis
Stage lV (Metastic disease)
CT head + consider whole body
Serum LDH

Treatment/Surgical Technique
Of primary tumour
Wide local excision (WLE)
Breslow thickness in situ/lentigo maligna 5 mm
<1 mm 1 cm
1.01–2 mm 1–2 cm
 Chapter 22. Management of the Pigmented Lesion 161

2.01–4 mm 2–3 cm
>4 mm 3 cm

Of lymph node basins

Clinically node –ve SNLB
Performed at same time as WLE
Clinically or FNAC repeat if –ve or US-guided
radiologically core biopsy
suspicious nodes Open biopsy

Confirmed + ve lymph Axillary LND Levels l–lll

node metastases Superficial Inguinal LND
Pelvic LND
Cervical LND – comprehensive

LND should only be performed by SSMDT members who do

AT LEAST 15 LNDs for skin cancer/year

Options for treatment of locoregional recurrence

Single local or Surgery
regional metastasis
Multiple local CO2 laser ablation
metastases

Regional Isolated limb 3 UK centres

chemotherapy infusion
Isolated limb 2 UK centres
perfusion

Electrochemotherapy Novel treatment. Relies on

electroporation using an
intralesional electrode to
damage melanoma cells and
make them more susceptible
to intralesional or systemic
bleomycin
Adjuvant therapy No evidence of a survival
benefit
162 F. Harper

Occult primary melanoma:

May present with solitary metastasis/lymph node/systemic
disease
Prompt referral to SSMDT – thorough examination: skin/
uveal tract/genital/urinary tracts/anorectum
All patients should be staged with CT head/chest/abdo/
pelvis
Treatment should be appropriate to the tumour regardless of
the inability to detect the primary

Risks/Complications

General
Risks of LA
GA: DVT/PE/Chest infection

Specific
Following LND: Damage to nerves/vessels, infection, poor
wound healing wound dehiscence, exposure of vital struc-
tures, seroma, lymhoedema

Post-operative Management

Follow-up rationale Detect recurrence

Detect further primaries
Support/information/education

In situ No follow up
Stage 1A 2–4 visits for 1 year
Stage lB–lllA 5 years
Stage (lllB–lllC + 10 years
Resected stage lV)
Unresectable stage lV Seen according to need
 Chapter 22. Management of the Pigmented Lesion 163

Prevention
Avoid sunburn
Avoid sunbed usage

Papers to Know
Revised UK guidelines for the management of cutaneous
melanoma 2010. British Association of Dermatology.
2009 AJCC Melanoma Staging and Classification
Charles M. Balch, Jeffrey E. Gershenwald, Seng-jaw Soong,
John F. Thompson, Michael B. Atkins, David R. Byrd, Antonio
C. Buzaid, Alistair J. Cochran, Daniel G. Coit, Shouluan Ding,
Alexander M. Eggermont, Keith T. Flaherty, Phyllis A.
Gimotty, John M. Kirkwood, Kelly M. McMasters, Martin C.
Mihm Jr, Donald L. Morton, Merrick I. Ross, Arthur J. Sober
and Vernon K. Sondak Journal of Clinical Oncology.
Veronesi New England Journal of Medicine 1988
• No difference between 1 and 3 cm margins for MM < 2 mm
deep
Balch Annals of Surgery 1995
• 2 cm excision adequate for MM 1–4 mm deep
WHO Lancet 1998
• No benefit from ELND
Morton NEJM 2006 (Multicenter Selective
LymphadenectomyTrial data)
• For MM 1–4 mm SLNB useful for staging and prolongs
disease free interval
• Improved survival for patients undergoing CLND for
micromets
• No increase in local or intransit mets after SLNB
• Support for micromets becoming macro or distant disease
Chapter 23
Aged Face: Facelifting
Shehan Hettiaratchy

The key to success of facial rejuvenation is to refresh the

patient while maintaining facial harmony, i.e., they should
STILL look normal and not Picasso-esque.

Recognition
Middle aged women and less commonly men but increasingly
older and younger patients are presenting (Fig. 23.1).

History
General introduction – Age, occupation, hobbies, smoking,
sun exposure
Specific
• Start with an open question ‘How can I help?’ and let the
patient voice their areas of concern
• How long have they been considering facial rejuvenative
surgery?
• Which areas particularly bother them?

S. Hettiaratchy
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 165

DOI 10.1007/978-1-84882-116-3_23,
© Springer-Verlag London Limited 2012
166 S. Hettiaratchy

Figure 23.1 Patient presenting for facial rejuvenation

• What kind of appearance do they want? Do they want to

look refreshed or significantly younger?
• Have they had any rejuvenative procedures in the past?
• Do they know anyone who has had this type of surgery?
• How much time off do they envisage having, i.e., how
much ‘downtime’ will they accept?
• Who is at home? Where will they convalesce?
• Do they have any specific deadlines/events at which they
must be presentable?
Risk factors
• Smoking
• Medications (aspirin, NSAIDs, herbal medications,
anticoagulants – all increase the risk of bleeding)
 Chapter 23. Aged Face: Facelifting 167

• Bleeding tendencies
• Hypertension
• Previous facial surgery

General
• Full health questionnaire including cardiac/respiratory
history
• Medications and allergies
• Previous surgery and general anaesthesia
• Suggest an anaesthetic assessment if required

AIM: by the end of history you should

1. Have an idea of the problem areas the patient wishes to
address and their expectations
2. Have an idea of how much downtime they are willing to
accept
3. Have assessed their medical fitness for a procedure
4. Have identified any with unrealistic aims – red flags

Examination
Look
This is the part where people get stumped. The typical
changes with aging are brow ptosis, eye changes, midface pto-
sis (with uncovering of the bony skeleton, deepening of the
NLF and jowling with skin bunching up and hanging down
lateral and below the NLF), and neck laxity. Jowling leads to
the face changing from a youthful oval to a more squared
appearance. This can be attractive in a man but makes women
look sad and sour. People talk about the ‘ogee’ which is the
shape the full cheek makes when seen in half profile. This is
lost in aging. The chin can also ptose, adding to the older face
appearing longer and the neck will have developed folds of
loose skin (turkey gobbler neck). In addition there is loss of
cervico-mental angle when seen in profile.
168 S. Hettiaratchy

The best way is to make a quick overall assessment of their

skin, hair and general appearance. Make specific note of any
asymmetries and point these out to the patient.
Next work through the face in areas thinking in terms of
the procedures that can be performed and if the patient
needs them. This should lead to a surgical menu for the
patient that can be used depending on how extensive the
surgery they want is and how rich they are feeling.
General assessment
Assess the skin – is there sun damage, lots of wrinkles
(rhytids) and are they fine or coarse, i.e., does the patient
need some form of resurfacing/fillers/botox?
Look at the hair – is it thin, thick, receding, i.e., can you
hide scars easily in there? Can you move the hairline?
Is their face thin – will they need volume added with fat
transfers? Look particularly at lips, NLF, malars, chin as these
areas can all look good with some gentle augmentation.
Specific
It is somewhat artificial to think of the face in strict thirds.
Think of it as areas to be addressed.
Upper – brow
Midface – eyes, nose, midface comprising cheek, naso-labial
fold and jowl (these will be addressed by midface lifting)
Central/lower – mouth/perioral, chin, neck.

Upper

• Do they have lateral brow ptosis with hooding and heavi-

ness? They may need a browlift (usually endobrow but this
tends to work best in females). Brow position.
• Have they got marked glabellar lines? This would benefit
from botox.

Midface
• Do they need something to be done to their eyes? Do they
need upper blephs? Do they need lower blephs? (See
chapter on blepharoplasties)
 Chapter 23. Aged Face: Facelifting 169

• How much midface ptosis is there? See how much skeletal

show there is (especially along the infraorbital margin),
how deepened the NLF are due to cheek overhang, and
how much jowling they have; all of these can be improved
by midface lifting.
• Nose – should you mention it? Do they need a rhino-
plasty? (see chapter on rhinoplasty) This will not contrib-
ute to making them look younger but may improve the
overall aesthetics of their face. You may not wish to raise
it unless they comment on it.

Central/Lower
• Are their lips thin? Do they need augmentation with fill-
ers/fat transfer/dermal fat graft?
• Do they have perioral rhytids (called bleed lines as lipstick
‘bleeds’ into them)? Do they have marionette lines (verti-
cal lines either side of the mouth)? Would these benefit
from resurfacing or fillers?
• Do they have chin ptosis or a weak chin? Would it benefit
from augmentation/advancing?
• Do they have neck laxity with excess skin? Do they have
platysmal bands (midline divarification of the anterior
edges of the platsyma – can be addressed by lateral platys-
maplasty but may need direct division of the bands to
soften)? Is there loss of the cervico-mental angle? This can
be addressed with submental liposuction and lateral plat-
ysmaplasty which should tighten the neck, give a clean
jawline and redefine the cervio-mental angle.
Finally, make an assessment as to whether they would benefit
from volume addition (e.g., fat transfers). Look particularly
at lips, NLF, malars, chin.
Make sure you check in front and behind the ears for scars
from previous procedures; patients often ‘forget’ that they
have had work before!
B) Feel/move
This is time to employ the ‘magic’ finger to move the soft tis-
sues to get an idea of what surgery can achieve. Try and use
170 S. Hettiaratchy

the same vectors as would occur with the surgical gestures

but explain to the patient that surgery will not do exactly the
same as the finger manipulation. Reproduce the endobrow,
midface lift and neck lift. As well as demonstrating to the
patient what may be achieved, you can assess whether they
will need volume added as well as the lifting procedures.
Finally, check the function of cranial nerves V and VII.
AIM: by the end of exam you should
1. Have an idea of what the patient wants
2. Have an idea of if and how you can deliver it

Investigations
FBC, U&Es, clotting
Photographs

Treatment
Facelift surgery is complicated by lots of different terminol-
ogy so it is important to get back to the basics. The aim of face
lift surgery is to reposition any ptosed soft tissues (e.g., fat
pockets) and tighten skin that has lost elastic recoil.
It is not possible to tighten fat, so facelifts work by tighten-
ing fascia that contains the fat and moves it back to its origi-
nal place.
There are three layers that can be moved to reposition the
soft tissues of the face:

1. Skin
2. SMAS (superficial musculo-aponeurotic system)
3. Periosteum

All facelifts use one, two or all of these layers. The most com-
mon one used is the SMAS that can be tightened in various
ways.
 Chapter 23. Aged Face: Facelifting 171

Skin only
Rarely performed but was the mainstay until 1980s. Possible
indication would be a skin only problem, but most facelifts
now involve some form of SMAS manipulation.
SMAS procedures
SMAS is the modern workhorse of facelifting. Pulling on the
SMAS repositions the malar fat pad, decreases the overhang
on the NLF, corrects jowling and also addresses the neck.
SMAS can either be:
• Left in situ and tightened with sutures (plication)
• Part of the mobile SMAS is excised along an oblique line
and sutured onto the immobile SMAS (SMASectomy)
• SMAS is elevated as a flap and any excess trimmed off
(SMAS flaps)

Periosteal procedures
• These can be very powerful ways of moving the soft tissues
on the bony skeleton. This may be indicated in a redo face-
lift (advantage of a fresh plane) or when trying to correct
lower lid/lateral canthal malposition.
• Various different access options including bicoronal, lower
lid and buccal sulcal.
• Mask lift is a pure periosteal procedure done via a bicoro-
nal approach.
• The downside is the invasiveness of the surgery and the
time to recover.
Composite Rhytidectomy
• Skin and SMAS are dissected as a composite
• Flap is less likely to slough
• Extensive procedure

Neck procedures
Corset platysmaplasty
Submental dissection and platysmaplasty
Plastysma flaps
Liposuction
172 S. Hettiaratchy

Adjuncts to face lifting

Brow-lifting
This is often performed in female patients and addresses not
just the brow but also the forehead and temple. Usually done
endoscopically, but the patient must have a short forehead
(7 cm) and it must not be overly curved.
3 or 5 port techniques are described and there are various
means of fixation.
Advantage of the browlift is that it opens up the eyes espe-
cially laterally.

Fat transfers
Adds volume to the face to regain youthful contours and
fullness.

Fillers
Fill out fine rhytids around the mouth and redefine the ver-
million border.

Resurfacing
Addresses fine rhytids and also causes some tightening. The
available methods are chemical peeling, laser resurfacing and
dermabrasion. Each surgeon will have a preference for a
method and no one method has been shown to be better than
another.

Botulinum toxin type-A

Can be used to deal with glabellar lines, crows’ feet.
Can also be used for contralateral symmetrization for a uni-
lateral marginal mandibular branch palsy.

Post-operative Management
• Sit up post-op for 24 h; sleep at 45°
• Drains (either Penrose or small lantern) reduce bruising
and swelling but not haematomas
• Firm dressing of jelonet/gauze/wool/crepe for 24 h, then no
dressings
 Chapter 23. Aged Face: Facelifting 173

• Remove dressings and wash hair before discharge

• Gentle mobilization but no straining or bending for at
least the first week
• Skin sutures out POD 5; staples (if used) POD 10
• Limited sun exposure for 6 weeks (longer if they have had
resurfacing)
• Review at 6 weeks (wounds), 3 months and final at
6 months
• Downtime before socially presentable (depends on
adjuncts):
– SMAS procedures 3–4 weeks
– Periosteal procedures 6–8 weeks

Risks/Complications
Haematoma
Nerve injury
Wound healing problems, i.e., skin slough, infection
Fixation failure, i.e., pixie ear, altered hairline
Scarring

Outcome
Patients tend to be very pleased. Minor problems often settle.
Wait at least 9 months before revisions/redos.

Terminology
Types of facelift
Composite – SMAS and skin kept as one layer (good for
smokers)
Deep plane – sub SMAS plane
Biplanar – supra and sub-SMAS planes developed and may
be moved in different vectors
Extended – SMAS dissection past zygomaticus major
SMASectomy – excision of part of SMAS
174 S. Hettiaratchy

Volumetric – use of Coleman fat to add volume with minimal

skin incisions

Minimal access techniques

MACS – Minimal Access Cranial Suspension lift; involves
incision in front of and above the ear. Variation on S-lift and
other short scar techniques
Threads – barbed suture to resuspend; no longer advocated

Key names
Mitz & Peyronie, Skoog – described SMAS
Baker/Stuzin – Extended SMAS lift
Krastinova – MASK lift
Bessin/Little/Ramirez – midface lifting
Hamra – composite/deep plane
Marten – MACS
Vasconez – endoscopic browlift
Chapter 24
Nerve Compression
Shehan Hettiaratchy, Abhilash Jain, and Jon Simmons

Think neck down but remember carpal and cubital tunnel are
common, the rest rare.

Recognition
Female, middle aged. May have no obvious visible physical
signs (Fig. 24.1).

History
General intro
Age, occupation, handedness, hobbies
Specific
When did it start?
Did anything trigger it off? Any previous history of neck/
elbow/wrist trauma (may cause traction on the nerve, e.g.,
distal radius fracture or supracondylar humeral fracture, or
nerve compression, e.g., degenerative foraminal stenosis in
the neck).

S. Hettiaratchy ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 175

DOI 10.1007/978-1-84882-116-3_24,
© Springer-Verlag London Limited 2012
176 S. Hettiaratchy et al.

Figure 24.1 Wasting of first dorsal interosseous

Unilateral or bilateral – bilateral suggests neck might be the

source
Specifically what symptoms do they get?
Type Pins and needles/numbness/aching/pain/
burning
Radiation Proximal – into neck?
Distal – into fingers – which ones? Ask
specifically about thumb/index and little
Is the back of the hand affected? (dorsal branch
ulnar nerve – differentiates between cubital
tunnel and Guyon’s canal entrapment)
Is the palm affected? (palmar cutaneous
branch median nerve – if it is affected then
it is likely to be more proximal compression
that carpal tunnel)
Timing Nocturnal
Diurnal – associated with more severe
compression
Triggers Wrist flexed (carpal tunnel) – holding
phone/driving
Pressure on medial elbow (cubital tunnel) –
leaning on a desk
 Chapter 24. Nerve Compression 177

Motor Clumsiness/dropping things – either due to

weakness or proprioceptive impairment
Weak grip – either median or ulnar nerve
Weak wrist/finger extension – radial nerve
(radial tunnel syndrome)
Interventions Splinting at night (carpal tunnel)
Steroid injections – did they work and for
how long
Vascular Only ask if there is a suggestion of
TOCS; symptoms of ischaemia, especially
positional
Activities Affect on work and ADLs
Risk factors
Need to exclude causes of intrinsic nerve damage – DM, neu-
ropathy (ask about other nerves such as feet/vision), neuro-
toxic drugs
Causes of compression – pregnancy, acromegaly, hypothy-
roid, systemic steroids
Predisposing factors – DM, relative ischaemia makes the
nerve more vulnerable to compression

AIM: by the end of history you should

1. Know which nerves are likely to be affected

2. Know severity and duration
3. Know likelihood of reversibility/causative and contribut-
ing factors
4. Have considered likely level

Examination
Look
Signs of wasting:
TOCS/plexopathy check muscle groups of upper limb,
especially biceps (C5,6)
178 S. Hettiaratchy et al.

Median Low – Thenar muscle wasting.

Ulnar Low – Intrinsics (guttering between metacarpals)/
fist web due to adductor pollicis + first dorsal
interosseous wasting.
Radial Radial tunnel unlikely to give wasting; if there
is forearm wasting think of lesion in spiral
groove.

Feel/move
Sensory exam

Test Thumb/index tip (Median)

Palm (PCBMN – unaffected in carpal tunnel
usually)
Little finger (Ulnar)
Dorsum ulnar half (DBUN – preserved in
Guyon’s, affected in cubital tunnel)
First web (Radial)
Motor exam

Test Wrist and finger extension (Radial)

Wrist and finger flexion (Ulnar and Median)
Opposition (Median)
Finger adduction (Ulnar)
Thumb adduction (Ulnar)
Thumb flexion (Median via FPL)
Provocative tests

Test Test Tinel’s on carpal/radial/cubital tunnels

Phalen’s test - Direct pressure on carpal tunnel/
Guyon’s canal
AIM: by the end of exam you should

1. Know which nerves are affected

2. Identify the level of compression
3. Formulate a management strategy
 Chapter 24. Nerve Compression 179

Treatment
Median nerve at wrist (Carpal tunnel)
Carpal tunnel release either open or endoscopic. Non-
operative management for selected patients e.g.,). Mild
symptoms in pregnancy may resolve post-partum.
Median nerve in forearm (Pronator syndrome)
Compression can be under Pronator Terres, FDS arch,
Ligament of Struthers and bicipital aponeurosis. Treat with
decompression.
Ulnar nerve at the wrist (Guyon’s canal)
Release Guyon’s canal through incision along radial border
of FCU.
Ulnar nerve at the elbow (Cubital tunnel syndrome)
Simple decompression vs. medial epicondylectomy vs. ante-
rior transposition in a subcutaneous or submuscular plane.
Radial nerve (Radial tunnel syndrome)
Surgical release using either an anterolateral or posterior approach

Outcome
Established motor weakness may not improve, aim to inter-
vene before this point
1–3% nerve injury depending on procedure
5% delayed healing
<1% ischemia
Pillar pain

Anatomy
Median nerve
Compression at the wrist is in the carpal tunnel.
In the forearm may be under Pronator Terres, FDS arch,
Ligament of Struthers or bicipital aponeurosis.
180 S. Hettiaratchy et al.

Ulna nerve
At the elbow compression is through the cubital tunnel,
Arcade of Struthers, medial intermuscular septum and the 2
heads of FCU.
At the wrist through Guyon’s canal.
Radial nerve
Compression through the radial tunnel may be from the
leash of Henry, Arcade of Frohse or a fibrous band tethering
the radial nerve to the radio-humoral joint.
Anterior Interosseous Nerve
Compression of purely motor branch of median nerve sup-
plying FPL, Pronator Quadratus and FDP to index and
middle. Compression is caused by an aberrant head of FPL
(Ganzer’s muscle), aberrant radial artery or fibrous band in
Pronator Terres or FDS. Results in inability to form an ‘O’
between thumb and index.
Posterior Interosseous nerve
Compression of distal branch of radial nerve in the forearm
results in preserved sensation in superficial radial nerve distri-
bution but weakness in forearm extensors. Causes of compres-
sion are lipoma, tumour, RA involving radial head and trauma
in the form of radial head fracture or elbow dislocation.

Papers
Skoff, Hillel D. M.D.; Sklar, Robin OTR/L CHT. Endoscopic
Median Nerve Decompression: Early Experience. Plastic &
Reconstructive Surgery. 94(5):691–694, October 1994.

Controversies
Endoscopic vs. open approach for carpal tunnel release
Cubital tunnel – simple release vs. epicondylectomy vs. ante-
rior transposition
Simple decompression vs. neurolysis
Chapter 25
Severe Soft Tissue Infection
Jon Simmons, Shehan Hettiaratchy, and Carolyn Hemsley

Must identify infections requiring immediate operative

treatment. Necrotising fasciitis is a surgical emergency and
requires immediate operative treatment.

Recognition
The key question should be: is this necrotising fasciitis or
severe cellulitis?
Necrotising Rapidly progressing (less than 24 h)
fasciitis: Very sick patient (septic, acidotic, coagulopathic)
Patches of skin infarction with viable skin in
between. Elevated Lactate.
Severe Longer history (>24 h)
cellulitis: Patient less sick (raised WCC but not septic/
acidotic/coagulopathic)
Skin red/blistering but not infracted

J. Simmons ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 181

DOI 10.1007/978-1-84882-116-3_25,
© Springer-Verlag London Limited 2012
182 J. Simmons et al.

Figure 25.1 Cellulitis or necrotising fasciitis?

NB: Beware atypical infections, cellulitis refractory to antibi-

otics. If in doubt explore surgically and involve Microbiology
early (Fig. 25.1).

History
General intro
Age, occupation – particularly at risk of unusual organisms –
working with animals/outdoors/water
Health status prior to current illness
Specific
Rate of progression critical
Possible source of infection – minor wounds/injuries
Risk factors
IDDM
Immunoincompetence – immunosuppression/HIV
IVDU
Obesity
Age >60
 Chapter 25. Severe Soft Tissue Infection 183

PVD
NSAID
AIM: by the end of history you should know
1. Does the time course make a necrotising infection likely
2. Does the patient have a predisposing risk factor for
infection
3. Are unusual organisms likely

Examination
Look
Does the patient look sick?
Are they shocked – hypotensive, peripherally shutdown,
oligo/anuric?
Are they pyrexial?
What does the affected tissue look like?
Cellulitis – red, angry, tissues (especially with streptococcus
– erysipelas)
Necrotising fasciitis – skin is dead; non-perfused, infarcted,
necrotic, may smell dead/necrotic
Feel/move
Cellulitis may be hot and tender; necrotising fasciitis may be
tender but may not be hot
Is there subcutaneous crepitus (37% of necrotising fasciitis
has surgical emphysema)?
Move any suspicious joints – possibly septic arthritis
Any subcutaneous collections; cellulitis may result from deep
seated infection/abscess
Needle test areas suspected of infarction if not clearly
demarcated
AIM: by the end of exam
1. Determine if it is necrotising fasciitis or cellulitis
2. Find out how sick the patient is
3. Have a surgical plan – urgency/extent of surgery
184 J. Simmons et al.

Investigations
Imaging
Should not delay surgical management for imaging unless
patient is well and diagnosis uncertain/atypical. XR – 57%
necrotising fasciitis shows air in the soft tissues. Ultrasound
(good to demonstrate collections), CT, MRI if diagnosis
unclear.
Bloods
Baseline FBC (WCC, Hb and neutrophils), clotting (DIC,
coagulopathic), U + E (Renal impairment), lactate and arte-
rial blood gases, inflammatory markers and blood cultures.
Microbiology
Microbiology – get samples before antibiotics. Swab any open
wounds. Any obvious pus send off. Aspirate and send off any
blister fluid – put some in a blood cultures bottle. Take 2 sets
of blood cultures. FNA swab aspirate may be useful in
cellulitis.
Beware – severe cellulitis can make the patient very sick
with sepsis etc. but the clinical and blood picture tend not to
be as deranged as necrotising fasciitis, especially degree of
acidosis.

Treatment
Severe cellulitis requires aggressive non-surgical management.
Necrotising fasciitis requires aggressive surgical management.
Cellulitis
Resuscitation of the patient as can be shocked
High dose antibiotics – empirical initially then directed
Strict elevation of any affected limb
If it involves the hand then splintage in James position (posi-
tion of safety) is needed
If there is any suggestion of a subcutaneous collection this
must be drained. USS may be useful to confirm a collection.
 Chapter 25. Severe Soft Tissue Infection 185

If there is any doubt about the diagnosis then surgery with an

exploration of the tissues and fascial biopsy may be helpful.
Necrotising fasciitis
This is a surgical emergency, resuscitate the patient and
correct coagulopathy.
Surgery – aggressive debridement of all suspicious tissue. Cut
1–2 cm into viable tissue to confirm clear margins. Multiple
specimens for micro (tissue and fluid) and histology – send all
urgently for gram stain and culture.
IV antibiotics – broad spectrum (local micro policy) and
then focussed based on cultures. Example: Ceftriaxone +
clindamycin + gentamicin
Return to theatre within 24 h to check for progression/viabil-
ity of debrided tissue
Patient will need SSG once they no longer have overt infec-
tion and then may require delayed recon after to improve
aesthetics/function.

Outcome
Mortality for necrotising fasciitis is 6–71%.

Pearls
Micro:
Classified by what grows
Type 1 – Polymicrobial; trauma, surgery with risk factors.
May look like cellulitis
Type 2 – Group A streptococcus+/− anaerobe; ?NSAID;
trauma, surgery, IVDU, childbirth
Type 3 – Clostridial – myonecrosis
Coined by Wilson 1962
Mortality 6–71%
Due to toxin production
186 J. Simmons et al.

Group A strep: M type 1–3 – M = surface protein that pre-

vents phagocytosis and increases adherence + exotoxin pro-
duces an inflammatory process which progresses along fascial
planes and causes infraction of skin perforators and hence
skin infarction.
Clindamycin decreases exotoxin production, hence is
often used in conjunction with other bacteriocidal
antibiotics.

Key Evidences
Kotrappa KS, Bansal RS, Amin NM. Necrotizing fasciitis. Am Fam
Phys 1996;53(5):1691–6.
Forbes N, Rankin APN. Necrotizing fasciitis and nonsteroidal anti-
inflammatory drugs: A case series and review of the literature. N Z
Med J 2001;114:3–6.
Urschel JD. Necrotizing soft tissue infections. Postgrad Med J
1999;75:645–9. (Excellent review article)

Controversies
Hyperbaric oxygen treatment
If a diagnosis of necrotising fasciitis is obvious, likely or pos-
sible surgical exploration must be undertaken as an emer-
gency. Beware the ‘cellulitis’ patient deteriorating on broad
spectrum antibiotic treatment who is becoming increasingly
unwell.
Chapter 26
Rhinoplasty
John Henton and Jon Simmons

Refers to open or closed procedures to alter the size or shape

of the nose. It is performed for aesthetic, functional or recon-
structive indications. Beware the man who ‘just doesn’t like’
his nose.

Recognition
Cosmesis is the most common reason for performing rhino-
plasty. Patients may feel their nose is too crooked, large or
protruding. It may be deformed following trauma, or excision
of malignancy. The deformity may also be secondary to con-
genital defects or scar contracture following cleft lip correc-
tion as a child. There may be functional impairment, with the
patient complaining of difficulty breathing through one or
both nostrils. Over 4,000 rhinoplasty procedures were carried
out in the UK by BAAPS members in 2010 (Fig. 26.1).

J. Henton ()
Department of Plastic and Reconstructive Surgery,
Imperial College Healthcare NHS Trust,
London, UK

S. Hettiaratchy et al. (eds.), Plastic Surgery, 187

DOI 10.1007/978-1-84882-116-3_26,
© Springer-Verlag London Limited 2012
188 J. Henton and J. Simmons

Figure 26.1 Pre-operative patient

Anatomy
Soft tissue cover
• Skin – thinner, less sebaceous upper 2/3, thicker more
sebaceous lower 1/3
• Musculoaponeurotic layer
Structural support
Bony/cartilaginous skeleton
• Upper 1/3 – nasal bones, ascending process of maxilla
• Middle 1/3 – upper lateral cartilages, dorsal cartilaginous
septum
• Lower 1/3 – lower lateral (alar) cartilages – lateral, medial
and middle crus
Septum – Quadrangular cartilage, vomer, perpendicular plate
of ethmoid, nasal spine
 Chapter 26. Rhinoplasty 189

Blood supply
• Angular artery, superior labial artery, columellar artery
(branches of facial artery)
• Arterial supply runs in submusculoaponeurotic plane
(superior to perichondrium)
• Venous/lymphatics – subcutaneous plane
• Sensation – Via V1 and V2 branches of trigeminal nerve
Lining – Squamous epithelium in vestibule, changing to cili-
ated columnar respiratory epithelium.
The nasal aesthetic subunits; dorsum, lobule, sidewalls,
alae, columella, soft triangles.

History
General introduction
Age, occupation (do they rely on their sense of smell
for work: chef, wine taster etc.). Reasons for seeking
rhinoplasty, interference with: lifestyle, relationships, self-
confidence.
Nose specific
• What EXACTLY do they not like about their nose?
− Is the procedure for aesthetic, functional (or a combina-
tion of both) reasons?
− Their expectations from rhinoplasty surgery
− Beware patients who cannot specifically point out
which features of their nose they do not like (?body
dysmorphic disorder)
• Any previous nasal surgery?
• Facial/nasal trauma
• Breathing difficulties
• Sense of smell (can be damaged during surgery)
• Epistaxis
• Allergic rhinitis
• Use of nasal decongestants
• Cocaine use – risk of septal necrosis/perforation/poor
results (Slavin PRS 1990)
• Awareness of risks and complications associated with
surgery
190 J. Henton and J. Simmons

Risk factors
• Few absolute contraindications
• Significant past medical history of cardiac, GI or
respiratory problems (this can potentially interfere with
post-op recovery/mobilisation and increase risk of
complications)
• Smoking (despite excellent blood supply to nose)
• Anticoagulants
• Bleeding tendencies

General
Full medical and drug history.
• Must consider co-existing morbidities relative to risks of
procedure (usually a purely cosmetic procedure)
• Autoimmune conditions – e.g., Wegner’s, sarcoid (can
cause saddle nose due to septum collapse)
• Full list of medications such as aspirin, NSAIDs, herbal
medications, anticoagulants
• Any psychological issues (i.e., is patient requesting surgery
for genuine reasons)
• Occupation and sporting hobbies (as this may interfere
with these)
• Any drug allergies
• Smoking

AIM: by the end of history you should

1. Know the patient’s motivation for rhinoplasty
2. Understand exactly what they hope to achieve from
surgery
3. Be aware any co-morbidities which will impact on the pro-
cedure/post-op recovery
4. Know of the need for additional investigations/treatment
of any co-morbidities prior to surgery
5. Have identified if the patient is seeking surgery for appro-
priate reasons (identify patient with body dismorphic
disorder)
 Chapter 26. Rhinoplasty 191

Examination
Look
Whole face
• Divide face into thirds to assess proportions
• Is it really their nose which is an abnormal shape/size – or
other facial features
Nose
Sit opposite patient and at same level. View from front:
• Nose should occupy middle vertical 1/3 of face
• Width (alar base width) should be same as intercanthal distance
• Look for asymmetry or deviation of dorsum
• Assess skin quality and thickness
− Thin skin shows alterations to bony/cartilaginous frame-
work much more obviously than thick skin. Skin drapes
better, but minor imperfections more obvious.
− If skin thick and sebaceous, need to make much more dra-
matic alterations to framework to achieve a visible effect.

View from side

• Radix should be at same level as upper lid eyelashes
• Tip projection – should be same as alar base width
• Nasofrontal angle
• Nasolabial angle – 95–100 degrees in females, 90–95
degrees for men
• Assess dorsum – straight? dorsal hump?
• Supratip/tip deformity
• Columellar show
View nasal base
• Should make equilateral triangle
• Assess septal deviation
Feel/move/measure
Cottle test – for internal nasal valve collapse
In a positive test; lateral traction on cheek opens valve
improving airflow
• Indication for spreader graft.
192 J. Henton and J. Simmons

AIM: by the end of exam you should

1. Have identified any previous unknown pathology which
may require investigation/treatment
2. Understand the problem areas patient wishes to address
3. Have decided on most appropriate technique/combination
of techniques
4. Awareness of patient’s expectations of outcome

Investigations
• ENT for nasoendoscopy + biopsies if any history of cocaine
use/suspicion of intranasal ca
• Routine bloods: FBC, U + Es, Coag
• May also need chest X-ray, ECG etc. depending on
co-morbidities

Clinical Photography
• Anterior, lateral, oblique and basal views
• Important to document pre-operative appearance, both for
planning surgery, any revisions and for medico-legal reasons

Treatment/Surgical Technique
Preparation
GA, shave nasal hairs with small blade, prep with chlor-
hexidine
Mark incision (step or chevron for columella)
LA + Epinephrine infiltration
Topical vasoconstrictor nasal packs
Access: Open or closed approach
Open:
• Incision through narrowest part of columella
• Dissection continues in submusculoaponeurotic plane
to avoid vascular damage
 Chapter 26. Rhinoplasty 193

Closed:
• Intranasal incisions to access desired area
Intranasal incisions
Transcartilaginous: Incision through the structure of the
lower lateral cartilage
Intracartilaginous: Incision placed between the caudal end of
the upper lateral and the cephalic margin of the lower lateral
cartilage
Marginal: Incision courses along the caudal margin of the
lower lateral cartilage
Augmentation/reduction manoeuvres
Tip reshaping with sutures
Onlay graft – Improve tip projection
Umbrella graft – Augments septal tip support
Dorsal hump reduction
Dorsal graft – to raise/support dorsum – e.g., to correct saddle
deformity
Spreader grafts – Holds internal nasal valve open, widens
nasal dorsum
Infracturing – Osteotomy to narrow nose or correct open
roof deformity
Open roof deformity – Flattened appearance of dorsum fol-
lowing dorsal hump reduction

Risks/Complications
General
• DVT/PE/Chest infection
Specific to the nose
• Infection
• Haematoma
• Scarring (columella, open approach)
• Oedema
• Damage to nasal septum
• Altered sensation to nose/upper teeth
• Olfactory changes
194 J. Henton and J. Simmons

Post-operative Management

• Home in evening or next day

• Analgesia, antibiotics +/− steroids
• Avoid any strenuous activity, heavy lifting, sports for mini-
mum of 4 weeks
• Downtime: can be back at sedentary occupation after
2 weeks
• Sutures out at 5 days
• Splint off at 1 week
• Counsel about: duration of oedema – 3 months

Controversies: Open Versus Closed

Rhinoplasty
Open rhinoplasty
• Advantages
− Better visualisation of osteocartilagenous skeleton
− Better access to nasal cartilages for grafts
− Able to make more dramatic alterations to dorsum, tip etc
− Direct access to tissues for haemostasis
• Disadvantages
− Scar across columella
− Delayed healing/prolonged recovery
− Longer duration of swelling

Closed Rhinoplasty
• Advantages
− No external scarring
− Vascular bridges preserved
− Faster recovery
 Chapter 26. Rhinoplasty 195

− Less post-op swelling

− Allows creation of pockets into which grafts can be
placed
• Disadvantages
− Poor visualisation of operative field
− Difficult dissection
Appendix: FRCS Plast
Classification Systems
Contents

• Aesthetic
• Cancer Staging
• Craniofacial
• Congenital
• General
• Hand
• Reconstruction/Flaps
• Trauma
• Incidences
• Other Useful Bits for the Exam

Aesthetic

Baker, Capsule Formation 1975

I – No capsule
II – Palpable
III – Visible
IV – Painful
Heimburg, Tuberous breast, BJPS, 1996;49:339–345
Type 1: Hypoplasia of infero-medial quadrant
Type 2: Hypoplasia of both inferior quadrants
Type 3: Hypoplasia of both lower quadrants and subareolar
skin shortage
Type 4: Severely constricted base
Matarasso Classification of Abdominoplasty
Type 1: Excess fat only – liposuction
Type 2: Mild skin excess, infra-umbilical divarification – mini-
abdominoplasty infra-umbilical plication liposuction

S. Hettiaratchy et al. (eds.), Plastic Surgery, 197

DOI 10.1007/978-1-84882-116-3,
© Springer-Verlag London Limited 2012
198 Appendix: FRCS Plast Classification Systems

Type 3: Moderate skin excess, infra and superior divarifica-

tion – As above
Type 4: Severe skin excess – Standard abdominoplasty with
plication and liposuction
Paysk zones around an expander
Inner zone: Fibrin layer with macrophages
Central zone: Fibroblasts and myofibroblasts
Transitional zone: Loose collagen
Outer zone: Blood vessels and collagen

Regnault classification of ptosis

1st degree: Nipples at or above IMF
2nd degree: Nipples below IMF but above most dependant portion of
the breast
3rd degree: Nipples below the most dependant portion of the breast
• Pseudo-ptosis – where the majority of the breast mound
lies below the IMF but nipple is above or on the IMF. Post
BBR common

Simon classification for gynaecomastia

Stage 1: Slight volume increase no excess skin
Stage 2a: Moderate volume increase without excess skin
Stage 2b: Moderate volume increase with excess skin
Stage 3: Marked volume increase with excess skin

Cancer Staging

Broder’s histological grading of SCC

Grade I: Well differentiated Ratio Diff:Undiff 3:1
Grade II: Mod differentiated Ratio Diff:Undiff 1:1
Grade III: Poorly differentiated Ratio 1:3
Grade IV: Undifferentiated
 Appendix: FRCS Plast Classification Systems 199

TNM classification for cutaneous melanoma

Classification Thickness (mm) Ulceration status/Mitoses
T
Tis NA NA
T1 £1.00 a: Without ulceration and
mitosis < 1/mm2
b: With ulceration or
mitoses ³ 1/mm2
T2 1.01–2.00 a: Without ulceration
b: With ulceration
T3 2.01–4.00 a: Without ulceration
b: With ulceration
T4 >4.00 a: Without ulceration
b: With ulceration
N No. of metastatic nodes Nodal metastatic burden
N0 0 NA
N1 1 a: Micrometastasis*
b: Macrometastasis†
N2 2–3 a: Micrometastasis*
b: Macrometastasis†
c: In-transit metastases/
satellites without
metastatic nodes
N3 4+ metastatic nodes, or
matted nodes, or in-transit
metastases/satellites
with metastatic nodes
M Site Serum LDH
M0 No distant metastases NA
M1a Distant skin, Normal
subcutaneous, or nodal
metastases
M1b Lung metastases Normal
M1c All other visceral Normal
metastases
Any distant metastasis Elevated
200 Appendix: FRCS Plast Classification Systems

AJCC classification 2009

Clinical staging Pathologic staging
T N M T N M
0 Tis N0 M0 0 Tis N0 M0
IA T1a N0 M0 IA T1a N0 M0
IB T1b N0 M0 IB T1b N0 M0
T2a N0 M0 T2a N0 M0
IIA T2b N0 M0 IIA T2b N0 M0
T3a N0 M0 T3a N0 M0
IIB T3b N0 M0 IIB T3b N0 M0
T4a N0 M0 T4a N0 M0
IIC T4b N0 M0 IIC T4b N0 M0
III Any T N > N0 M0 IIIA T1-4a N1a M0
T1-4a N2a M0
IIIB T1-4b N1a M0
T1-4b N2a M0
T1-4a N1b M0
T1-4a N2b M0
T1-4a N2c M0
IIIC T1-4b N1b M0
T1-4b N2b M0
T1-4b N2c M0
Any T N3 M0
IV Any T Any N M1 IV Any T Any N M1

Enneking sarcoma staging

Stage Grade Anatomical location Metastasis
0 Benign (G0) Any None
IA Low (G1) Intra-compartmental (T1) None
IB Low Extra-compartmental (T2) None
IIA High (G2) Intra-compartmental None
IIB High Extra-compartmental None
III Any Any Mets (M1)
 Appendix: FRCS Plast Classification Systems 201

AJCC for sarcoma

Stage Grade Size (cm) Metastasis Relationship to fascia
IA Low <5 None Any
IB Low >5 None Superficial
IIA Low >5 None Deep
IIB High <5 None Any
IIC High >5 None Superficial
III High >5 None Deep
IV Any Any Yes Any

Trojani histological grading system: sarcoma

• Basis of this grading system is based on the following
− Histology
− Mitosis
− Necrosis
− Differentiation
− Stroma
− Number of cells

Tumours of the head and neck

Oral cavity Nasopharynx Hypopharynx Maxillary sinus
(cm)
T1 <2 1 subsite 1 subsite Mucosal only
T2 2–4 >1 subsite >1 subsite not Into bone below
fixed Ohngrens linea
T3 >4 Beyond nasal Into larynx Into bone above
cavity Ohngrens linea
T4 Invades Skull base Into neck soft Invades adjacent
adjacent or CN tissues structures
structures
a
Medial canthus to angle of the mandible
For salivary gland tumours add A or B to the T stage to
signify no local extension or local extension
Nodal classification:
N1: Single ipsilateral <3 cm
N2a: Single ipsilateral 3–6 cm
N2b: Multiple ipsilateral not >6 cm
N2c: Bilateral or contralateral nodes 3–6 cm
N3: Any node >6 cm
202 Appendix: FRCS Plast Classification Systems

TNM staging for head and neck cancer

Stage 1 T1 N0 M0
Stage 2 T2 N0 M0
Stage 3 T3 N0 M0
<T4 N1 M0
Stage 4 T4 N0 M0
Any T N2/3 M0
Any T Any N M1

Classification of neck dissection

• Comprehensive
− Radical
5 levels
IJV, AN, SCM
− Modified radical (functional)
T1 – preserves the AN
T2 – preserves the AN and SCM
T3 – preserves AN, SCM and IJV
− Extended radical
May take parotid, mediastinal nodes or paratracheal nodes
• Selective neck dissection
− Supraomohyoid
Oral cavity tumours
Levels 1,2 and 3
− Anterolateral
Laryngeal and hypopharynx tumours
Levels 2,3 and 4
− Anterior
Thyroid tumours
Levels 2,3 and 4 with tracheo-oesophageal nodes
− Posterior
Posterior scalp
Levels 2,3,4 and 5

WHO classification of salivary gland tumours

1. Adenoma
(a) Pleomorphic
(b) Warthin’s – Adenolymphoma
(c) Oncocytoma
 Appendix: FRCS Plast Classification Systems 203

2. Carcinoma
(a) Muco-epidermoid
(i) Well, inter and poorly differentiated grades.
Well and inter OK
(b) Malignant mixed tumour – arising in PMA
(c) Acinic cell
(d) Adenocarcinoma
(e) Adenoid cystic – Szanto’s grades
(i) Grade 1 – cibrose, no solidity good prognosis
(ii) Grade 2 – tubular, <30% solid
(iii) Grade 3 – solid, poor prognosis
(f) Squamous cell
3. Non-epithelial tumours
4. Malignant lymphomas
5. Secondary tumours
(a) MM
(b) SCC
(c) Breast
(d) Thyroid
6. Unclassified
7. Tumour like
(a) Oncocytosis
(b) Sialadenosis
(c) Cysts
(d) Infection
(e) Granulomatous disease

Craniofacial

Knight and North classification of malar fractures 1961

Type 1: Undisplaced fractures
Type 2: Isolated # of the arch – STABLE AFTER
REDUCTION
Type 3: Unrotated body fracture
Type 4: Medially rotated # of the body
Type 5: Laterally rotated # of the body – STABLE AFTER
REDUCTION
Type 6: Complex
204 Appendix: FRCS Plast Classification Systems

Manson classification of malar fractures – based on CT

findings
Type 1: Low energy fractures – result in little or no displacement.
Often ZF#
Type 2: Medium energy – # of all buttresses, mod displacement,
comminution
Often require intra-oral and eyelid incisions to fix
Type 3: High energy – Frequently occur with Le Fort or panfacial #.
Posterior dislocation of arch and malar eminence. Requires
coronal, eyelid and intra-oral incisions

Angle classification of dental occlusion

• Occlusion defined as the relative position of the upper first
molar. Mesiobuccal cusp should rest in mesiobuccal groove
of mandibular first molar
Class 1: Normal occlusion but other problems e.g., overcrowding
Class 2: Overbite, retrognathism
Class 3: Underbite, prognathism, negative overjet

Le Fort classification of maxillary fractures

LeFort I: Tooth bearing maxilla separated from midface. Fracture
through pterygoid
Plates to piriform aperture through maxilla
LeFort II: Pyramidal fracture
# Extends from frontonasal junction along medial orbital
wall, IO Rim and posteriorly through pterygoid plates
LeFort III: Craniofacial dysjunction .# Extends out through the
lateral orbital wall through the zygoma and high through
the pterygoid plates

Classification of craniofacial anomalies – American Society

of Cleft Lip/Palate
1. Clefts
2. Synostosis
(a) Syndromal
(b) Non-syndromal
3. Hypoplastic conditions
(a) TC
(b) Hemifacial microsomia – OMENS classification
(c) Hemifacial atrophy – Rombergs
 Appendix: FRCS Plast Classification Systems 205

4. Hyperplastic conditions
Fibrous dysplasia – abnormal proliferation of bone form-
ing mesenchyme, maxillary/mandibular mass, osseous
lesions, Albrights including precocious puberty, cafe au
lait, pituitary tumours

Tessier’s classification for hyperteliorism

Type 1: IOD 30–34 mm
Type 2: IOD 35–39 mm
Type 3: IOD 40 mm+

Veau’s classification 1931

1. Incomplete cleft of secondary palate
2. Complete cleft of secondary palate
3. Complete unilateral cleft lip and palate
4. Bilateral cleft lip and palate

Striped Y classification
1. First described by Kernahan and Stark 1958
2. Modified by Millard and Seider 1977
3. Pictorial classification

Craniofacial syndromes
Aperts – 1:160,000
• Bicoronal synostosis – turricephaly/brachycephaly
• Midface hypoplasia
• Beaked nose
• Class 3 occlusion
• CP 20%
• Complex syndactyly
− T1 – Thumb and little finger separate
− T2 – Thumb separate
− T3 – Involves all the hand
Crouzon – 1:15,000 AD
• Bicoronal synostosis – turricephaly/brachycephaly
• Midface hypoplasia
• Exorbitism
• Normal hands
206 Appendix: FRCS Plast Classification Systems

Saethre-Chotzen
• Bicoronal synostosis
• Low hair line
• Ptosis
• Small posterior ears
• Simple syndactyly
Pfeiffer
• Similar appearance to Aperts
• Broad thumbs and toes
Carpenter syndrome – rare
• Various sutures involved
• Pre-axial polydactyly
• Partial syndactyly
Treacher-Collins syndrome
• Chromosome 5 TCOF gene coding for Treacle protein
• AD 1:15,000
• Bilateral features
• Beaked narrowed nose
• Micrognathia
• Confluent 6,7,8 cleft
• Colomboma
• Medial lashes absent
• Malar hypoplasia
• Microtia
• CP
Romberg’s hemifacial atrophy
• Acquired condition
• Usually unilateral
• Sporadic
• Usually starts aged between 5 and late teens
• Do nothing while disease is active
• Results in permanent soft tissue atrophy
− Skin
− Hair
 Appendix: FRCS Plast Classification Systems 207

− Iris
− Forehead
− Cheek
− Skeleton
Goldenhars – OMENS+ classification
• 1 in 5,000
• 90% unilateral
• Ocular, mandibular, ear, facial nerve and normally sporadic
• Goldenhar’s consists of hemifacial microsomia, vertebral
abnormalities and epibulbar dermoids
Prosanski classification of mandibular deformities in HFM/
Goldenhar’s
Group 1: Mild mandibular hypoplasia
Group 2a: Severe hypoplasia with articulating TMJ
Group 2b: Severe without non-articulating TMJ
Group 3: Hypoplasia of mandibular ramus without a TMJ
Craniofacial clefts – Tessier
• Sporadic 1 in 25,000
• Aetiology unclear
− Failure of fusion
− Lack of mesoderm penetration
− Amniotic bands
May occupy any or all layers of the face
Soft tissue defect does not necessarily correspond with the
bony defect
Often have hairline markers
Facial clefts 1–7 (7 most lateral – corner of the mouth)
Cranial clefts 8–14 (8 most lateral – corner of the orbit)
0 Medial craniofacial dysraphia
Associated with encephaloceles and hypertelorism
1 Between incisors then through nasal bone and frontal
process of maxilla
Bifid dome hypertelorism and wide bridge
2 Paranasal
As for cleft 1
208 Appendix: FRCS Plast Classification Systems

3 Oculonasal cleft
Runs through nasal and lacrimal bones into the maxilla
Medial orbit and lacrimal apparatus may be deficient
Coloboma
Lower portion passes through the lateral incisor and canine
4 Oculofacial 1 cleft
More lateral to 3 medial to the IOF
5 Oculofacial 2 cleft
Lateral to IOF
Central coloboma
6 Between maxilla and zygoma
Lateral lower lid coloboma
TC with 7 and 8
7 Between zygoma and temporal bone
May extend medially to the corner of the mouth across the
cheek
8 Outwards from the lateral canthus
9,10,11 Start in supraorbital region associated with 3,4 and 5
12,13,14 Do not involve the orbit
Extensions of 0,1 and 2
30 Median cleft of lower lip and mandible
May extend onto the neck

Congenital

Hand

Swanson classification of upper limb developmental anomalies

Failure of formation
Transverse
Longitudinal – radial, central, intercalated
Failure of differentiation
Soft tissue – syndactyly
Skeletal – Clinodactyly
Duplication
Pre-axial
Post-axial
Central
 Appendix: FRCS Plast Classification Systems 209

Undergrowth
Overgrowth
Amniotic band syndrome/constriction ring syndrome
Generalised conditions
Achondroplasia

Bayne and Klug classification for deficiencies of radius

– 1987
• Usually associated with a Blauth 4 or 5; exception is TAR
• Sporadic, syndromic (VATER, TAR, Cardiac, Fanconi’s,
Holt-Oram)
• Type 4 is most common > Type 1 > Type 3 > Type 2 (Rare)
• ½ bilateral
• 1 in 50,000 (2 times more common than ulna dysplasia)
• R > L (Opposite to ulna dysplasia)
• M > F (M=F in UD)
• If managed surgically manage radius at 6–9/12 and thumb
at 9–18/12
Type 1: Short distal radius – do nothing
Type 2: Hypoplastic radius – can lengthen
Type 3: Partial absence – centralisation
Type 4: Complete absence – centralisation

Ulna dysplasia classification – Bayne

• Use 1 classification for forearm and another for the hand
• BAYNE for forearm and Cole and Manske for the thumb
and first web
• Associated with other musculoskeletal anomalies, scoliosis,
hemimelia not systemic probs
• Reconstruct thumb, correct web space deformity, align wrist
and forearm, stabilise wrist
• Rebalance wrist with tendon transfers
• Usually have good function
Type 1: Hypoplastic ulna
Type 2: Partially absent ulna
Type 3: Absent ulna
Type 4: Humeroradial synostosis
210 Appendix: FRCS Plast Classification Systems

Ulna dysplasia classification – Cole and Manske

• Based on the thumb and first web
• 70% have thumb anomaly
• 30% have syndactyly
Type A: Normal
Type B: Mild first web and thumb deficiency (Narrow)
Type C: Moderate to severe deformity with thumb/index
syndactyly, lack of opposition thumb in palmar plane,
thumb hypoplasia, lack of thumb extensors
Type D: Absent thumb

Upton classification of camptodactyly

• Theories: Abnormal lumbrical insertion, extra or abnormal
FDS slips, abnormal extensor or PIPJ capsular structures
Type 1: Congenital, isolated usually D5 M=F
Type 2: Like type 1 but becomes clinically evident 7–11 years
Type 3: Severe, congenital multiple digits associated with
Trisomy 13–15, short stature syndromes, craniofacial
syndromes
Arthrogryposis

Symbrachydactyly types
Peromelic nubbins
Short finger type telescoping fingers
Cleft hand type ulnar side cleft
Monodactylous single digit

Typical cleft versus atypical cleft (symbrachydactyly) hand

Typical Atypical
Bilateral Unilateral
Feet involved Feet spared
Starts on radial side Starts on ulnar side
Little finger preserved Thumb preserved
+ve Family history −ve Family history
 Appendix: FRCS Plast Classification Systems 211

Adams classification of camptodactyly

Type 1: Flexion contracture of PIPJ
Type 2: Partially fixed
Type 3: Arthrographically fixed
3A – No x-ray changes
3B – With x-ray changes – Wedged shaped (Anvil) P1 head,
divot in the base of P2, subcondylar recess (Drucker’s
space), PIPJ slopes to ulna side
Type 4: More than one digit involved

Stelling classification for polydactyly

• Ulna polydactyly very common 1:300 African Americans
1:3,000 Caucasians
Type 1: No skeletal tissue
Type 2: Skeletal attachment to enlarged or bifid phalynx/metacarpal
Type 3: Complete duplication including a metacarpal

Tetamy classification for polydactyly

Preaxial
Type 1: Bony duplication (Wassel 1–6)
Type 2: Triphalangia
Type 3: Duplication of index finger
Type 4: Synpolydactyly (Syndactyly of D3/D4 fingers + toes +/− polydac-
tyly of same)

Postaxial
Type 1: Fully developed extra ray
Type 2: Rudimentary extra ray

Wassel classification for thumb duplication

• Bilhaut-Cloquet procedure for 1–3
• 4–6 Preserve UCL, ID and preserve Abd PB, shell out
radial thumb, k-wire for 4 weeks
Type 1: Duplicated distal phalynx (BIFID) – least common
Type 2: Duplicated IPJ
Type 3: Duplicated proximal phalynx
Type 4: Duplicated MCPJ – most common
Type 5: Duplicated metacarpal
212 Appendix: FRCS Plast Classification Systems

Type 6: Duplicated CMCJ

Type 7: Tri-phalangia

Blauth classification of thumb hypoplasia

• Types 3B, 4 and 5 best managed with pollicisation; 1-3A
reconstruction of soft tissues
Type 1: Minor hypoplasia
Type 2: Adduction contracture, thenar hypoplasia, normal skeleton
Type 3: Significant hypoplasia, skeletal hypoplasia, intrinsic muscle
hypoplasia
Rudimentary extrinsic tendons
3A: CMCJ OK
3B: CMCJ absent
Type 4: Floating thumb
Type 5: Absence

Weckesser clasp thumb

Type 1: Deficient thumb extension
Type 2: Deficient extension with flexion contracture
Type 3: Thumb hypoplasia
Type 4: Pre-axial polydactyly with deficient extension

Upton classification of macrodactyly

• Index > middle > ring > thumb > little = very very rare
Type 1: Macrodactyly associated with lipofibromatosis of nerve –
median common
Type 2: Associated with NF1
Type 3: Macrodactyly with hyperostosis
Type 4: Macrodactyly with hemi-hypertrophy

Clinodactyly (Cooney)
Simple : bone <45o
Simple/complicated: bone >45o
Complex: soft tissue + bone <45o assoc. with syndactyly
Complex/complicated: soft tissue + bone>45o
 Appendix: FRCS Plast Classification Systems 213

Patterson classification: congenital constriction ring syndrome

• Intrinsic theory – Internal defect in the embryo causing
abnormalities
• Extrinsic theory – Amniotic band compresses or constricts
extremity
Type 1: Band with no distal deficit
Type 2: Band with distal lymphoedema
Type 3: Band with distal acrosyndactyly
Type 4: Distal auto-amputation

Vascular
Schobinger classification of arteriovenous malformations
Stage 1: Blue skin-blush
Stage 2: Mass assoc with bruit and thrill
Stage 3: Mass with ulceration, bleeding and pain
Stage 4: Stage 3 lesion producing heart failure

Waner grading system for capillary malformations

1. Sparce, pale non-confluent
2. Pink non-confluent
3. Discrete ectatic vessels
4. Confluent patch
5. Nodular lesion

Classification of vascular lesions (Mulliken and Glowacki, 82

PRS)
• Haemangioma and vascular malformations in infants and
children: a classification based on endothelial characteristics
• Haemangioma and Vascular Malformations (high and low
flow)
1. Haemangioma
2a. Venous malformation
2b. Arterial malformation
2c. AV malformation
2d Capillary malformation
2e. Lymphatic malformation
214 Appendix: FRCS Plast Classification Systems

Enjolras and Mulliken, 2002 – New Classification

• Vascular tumours vs. vascular malformations

Classification of vascular lesions (Jackson et al., 1993)

Group I Haemangioma
Group II Vascular malformations
A. Low flow – venous
B. High flow – arteriovenous
Group III Lymphatic malformations – lymphatico-venous

Other
Classification of hypospadius
1. Glanular
2. Coronal
3. Subcoronal
4. Distal shaft
5. Mid shaft
6. Proximal shaft
7. Penoscrotal
8. Scrotal
9. Perineal
• Glanular, coronal and subcoronal termed distal and
account for 85%

General

ASA grading of anaesthetic patients

ASA 1: Normal healthy patient
ASA 2: Patient with moderate systemic disease, or minor disease
with operative or anaesthetic risks
ASA 3: Patient with severe systemic disease limiting activity
ASA 4: Severe incapacitating disease, constant threat to life
ASA 5: Moribund, not expected to survive 24 h

Brachial plexus – Mellesi classification

1 – Supraganglionic
2 – Infraganglionic
 Appendix: FRCS Plast Classification Systems 215

3 – Trunk
4 – Cord

Fitzpatrick classification (Photosensitivity) (1988; Arch

Dermatol, 124, 869–71)
Type 1: Pale, white skin, red hair – always burns never tans
Type 2: Fair skin blue eyes – burns easily tans poorly
Type 3: Darker but white – tans after initial burn
Type 4: Light brown skin – burns minimally, tans easily
Type 5: Brown skin – rarely burns, tans darkly
Type 6: Black or very dark – never burns, always dark tanning

House and Brackman grading of facial palsy

Measurement: Superior movement of mid-upper brow and
lateral movement of the oral commissure. 1 point for each
2.5 mm up to a maximum of 10 mm. Points are then added
Grade 1: 8/8
Normal
Grade 2: 7/8
Slight weakness
At rest: normal tone and symmetry
Motion: Asymmetry of mouth, complete eye closure
Grade 3: 5–6/8
Obvious facial asymmetry, spasm
At rest: normal tone and symmetry
Motion: complete eye closure with effort, mouth weakness
Grade 4: 3–4/8
Disfiguring facial asymmetry with obvious weakness
No forehead movement
Incomplete eye closure
Grade 5: 1–2/8
Only slight movement
Grade 6: No facial function

Lymphoedema
Primary lymphoedema
Lymphoedema Milroy’s disease, 10–15% cases, abnormal lymphatic
congenital: development. Familial. LL 3:1 UL. 2/3 both extremities
Hypoplasia or aplasia of SC lymphatics
216 Appendix: FRCS Plast Classification Systems

Lymphoedema 65–80%. 70% due to segmental hypoplasia, other

praecox: causes are aplasia and hyperplastic varicose
lymphatics. Usually incompetent valves lead to
lymphoedema. Presents at puberty Female 4:1 Male.
Usually foot and ankle, 70% unilateral
Lymphoedema Presents after 35 years. Possibly a spectrum of
tarda: praecox where inadequate drainage to meet
demands
Secondary Commonest cause CLND. Filariasis infection, TB,
lymphoedema: neoplasm and trauma

MRC classifications of nerve recovery

M0 – No contraction
M1 – Flicker
M2 – Muscle contraction with active motion with gravity
eliminated
M3 – Full range of motion against gravity
M4 – Full range of motion against gravity with some
resistance
M5 – Full range of motion against gravity with maximum
resistance of that muscle
S0 – No sensibility
S1 – Recovery of deep cutaneous pain
S2 – Return of some superficial cutaneous pain and tactile
sensibility
S3 – 2 point discrimination > 15mm
S3+ – 2 point discrimination 7–15mm
S4 – Normal. 2 point discrimination 3–6mm

Nerve injuries (Seddon 1948)

Neuropraxia Loss of conduction
Axonotemesis Loss of axon continuity may include endo-/
perineurium
Neurotemesis Complete severance

Nerve injuries (Sunderland 1968)

I Loss of conduction
II Loss of axonal continuity: axon only
III Loss of axonal continuity: axon and endoneurium
 Appendix: FRCS Plast Classification Systems 217

IV Loss of axonal continuity: axon, endoneurium and

perineurium
V Loss of axonal continuity: axon, endo-, peri- and epineurium

• Recovery – complete recovery should be observed with

Sunderland I and II i.e. neuropraxia and axonotemesis

Pairolero and Arnold classification of sternal dehiscence

Type 1: 2–3 days post surgical
Serosanguinous discharge, negative cultures
No cellulitis, osteomyelitis or costochondritis
Debride, re-wire cover with ABx
Type 2: 2–3 weeks post surgical
Purulent discharge, cellulitis with positive wound
cultures
Underlying osteomyelitis/costochondritis
Thorough debridement, remove wires, VAC,
vascularised tissue cover
Type 3: 2–3 years post surgical
Chronic discharging sinus
Positive wound culture
Condritis and osteomyelitis
Treat as for a stage 2

Waterlow score for pressure risk

• Score of > 10 indicates a risk of sore, consider special mat-
tress etc…

Categories
Body build Average, below, above
Skin type Healthy, thin, oedematous, broken
Sex and age
Continence
Mobility
Appetite
Special risks Tissue malnutrition
Neurological deficit
Major surgery/trauma
Medication
218 Appendix: FRCS Plast Classification Systems

National Pressure Ulcer Advisory Panel Grading System

Grade 1: Non-blanchable erythema of intact skin
Grade 2: Partial thickness skin loss effecting epidermis and dermis
Grade 3: Full-thickness skin loss down to but not involving deep fascia
Grade 4: Full-thickness injury including underlying fascia, bone
muscle involved

Hand

Boutonniere deformity classification by Nalebuff

Stage 1: Deformity which is passively correctable. Only 10–15° lag in
extension
Full extension of PIPJ may limit DIPJ flexion (tight lateral
bands)
Stage 2: Deformity is passively correctable. Flexion deformity starts
to give a function loss with MCPJ and DIPJ hyperextension
Stage 3: PIPJ cannot be extended passively

Swan neck deformity classification by Nalebuff

Type 1: Deformity with no loss of motion
Type 2: Deformity with loss of motion at different positions in the
MCPJ
Type 3: Deformity with LOM in all MCPJ positions
Type 4: As a type 3 with x-ray changes

Larsens grading of rheumatoid arthritis

0 Normal
1 Osteoporosis, soft tissue swelling
2 Bony erosions, normal architecture maintained
3 Bony erosions, signs of architectural changes
4 Severe joint destruction but joint line is visible
5 Arthritis mutilans with no joint line

Trigger finger classification

Type 1: Pain and nodularity
Type 2: Triggering but self-correctable
Type 3: Triggering correctable manually
Type 4: Locked digit
 Appendix: FRCS Plast Classification Systems 219

Mayfield classification of progressive perilunate instability

• Most common carpal instability occurs between scaphoid
and lunate
Stage 1: Injury to scapholunate interosseous ligament –
scapholunate diastasis
Stage 2: Further injury causing dorsal subluxation of the capitate
relative to lunate
Stage 3: Perilunate dislocation
Stage 4: Dislocation of the lunate from the radiolunate fossa

Classification of thumb deformity on RA – Nalebuff

Group 1 Boutonniere with a flexed MCPJ
Group 2 Flexed MCPJ with metacarpal adduction
Group 3 Z thumb, zig-zag thumb or swan-neck def. CMCJ+IP flexed,
MCPJ hyper-extended
Group 4 Gamekeeper’s thumb

Lispcomb’s classification of Volkmann’s contracture

Mild: No nerve deficit, muscles tight/short – flexor slide
Moderate: No nerve deficit, some functional muscle loss – flexor slide
Severe: Nerve deficit with little functional muscle. Resection,
neurolysis, transfers
V Severe: No motor or sensory activity. Free functional muscle?

Classification of mallet finger deformities (Doyle 1993)

Type 1 : Closed. Loss of tendon continuity +/− small fragment
Type 2 : Laceration of skin and tendon at or proximal to DIPJ
Type 3 : Deep abrasion at DIPJ resulting in loss of continuity
Type 4A : Transepiphyseal in children
Type 4B : Fracture 20–50% of articular surface
Type 4C : Fracture > 50% articular surface and volar subluxation

Leddy and Packer classification of FDP avulsion 1977

Type 1: Tendon avulsion into the palm. No blood supply
Type 2: Tendon avulsion +/− bone fragment caught at PIPJ
Type 3: Bone fragment caught at DIPJ. All vinculae preserved
Type 4: Not originally described. Type 1 injury with bone
fragment destroying annular and cruciate pulleys on its
way to palm
220 Appendix: FRCS Plast Classification Systems

Urbaniak classification of ring avulsions

Type 1: Laceration, vascularity intact
Type 2: Circulation compromised needs revasc, no # or
dislocation
Type 2A: As above only arterial injury
Type 3: Total degloving/with or without #/dislocation

Kay modification of Urbaniak, JHS, 1989

I Circulation adequate, with or without skeletal injury
II Circulation inadequate, with or without skeletal
injury
IIA Arterial circulation inadequate only
IIB Venous circulation inadequate only
III Circulation inadequate, with fracture or joint injury
IIIA Arterial circulation inadequate only
IIIB Venous circulation inadequate only
IV Complete amputation

Kanavel’s 4 cardinal signs

• Fusiform swelling of finger
• Semi-flexed finger position
• Tenderness over flexor sheath
• Pain on passive extension

Weiss and Hastings classification of intra-articular phalangeal

fractures
• Oblique palmar
• Long sagittal
• Dorsal coronal
• Palmar coronal
Kienbock’s disease (Lichtman et al., JHS, 1982)
I No radiological changes – bone scan hot
II Increased density but normal shape; minor radial height loss
IIIA Collapase and sclerosis with carpal disruption. Normal
scaphoid orientation
IIIB Scaphoid rotated
IV Generalized intercarpal arthritis
 Appendix: FRCS Plast Classification Systems 221

Salter Harris
Normal Type I

Type II Type III

Type IV Type V

Type I: Transverse fracture through growth plate

Type II: A fracture through the metaphysic extending through
the growth plate but sparing the epiphysis (Commonest
configuration approx 70%)
Type III: A fracture through the epiphysis and growth plate sparing
the metaphysic
Type IV: A fracture through both the metaphysic, epiphysis and
growth plate (Next commonest)
Type V: A compression fracture of the growth plate

NB: Types VI–IX described but not commonly used

Reconstruction/Flaps

Fasciocutaneous flap classification – Cormack and Lamberty

Type A: Multiple fasciocutaneous perforators at flap base,
orientated along the flap’s long axis
Type B: Single fasciocutaneous perforator with or without the deep
artery
222 Appendix: FRCS Plast Classification Systems

Type C: Multiple perforators reaching the fascia from the deep

artery via the fascial septum – must keep the deep artery
with the flap. RFF
Type D: As for TC with muscle +/− bone

Mathes and Nahai muscle flap classification by Blood Supply

1981
Type 1: 1 pedicle
e.g., TFL
Type 2: 1 Major pedicle with other minor pedicles
e.g., Gracilis
Type 3: 2 dominant pedicles
e.g., RA, Gluteus maximus
Type 4: Many segmental pedicles none of which are able to
completely perfuse
e.g., Sartorius
Type 5: 1 dominant pedicle with minor pedicles able to supply the
entire muscle
e.g., LD

Thatte and Thatte classification of venous flaps

Veno-venous: Unipedicle
Bi-pedicled
Arteriovenous: Arteriovenous shunt
Arterialized venous flow-through flap

FLAPS
(Anatomy, pedicle,
landmarks, dimensions)
Radial forearm
Type C or D
Song, 1982, Clincs in Plastic Surgery
A – Radial artery, type C/D, intermuscular septum between
brachioradialis/FCR distally and PT/brachioradialis
proximally, superficial to FDS, ulnar to superficial branch
of radial nerve
P – 20 cm × 2.5 mm
L – mid-point cubital fossa to radial pulse at wrist
D – upto 10 × 40; 4 × 6 can close V to Y
 Appendix: FRCS Plast Classification Systems 223

Posterior interosseus artery flap

Masquelat, 1987, Ann Chir Main
A – Posterior interosseous A (off common interosseous off
ulnar) emerges beneath supinator 6 cm distal to lat. epicon-
dyle; runs in intramuscular septum between extensor com-
partment 5(EDM) and 6 (ECU)
P – Perforators of PIA; prox. 1/3 0.9–2.7 mm; distal 1/3
0.2–1.2 mm
L – Lateral epicondyle to DRUJ; skin paddle at junction of
proximal and middle 1/3. Pivot point 2 cm prox to DRUJ
D – Close direct if <4 cm in width; otherwise SSG. Rise from
6 cm distal to elbow to 4 cm prox to wrist; subcutaneous bor-
der of ulnar to radial border of radius
“2656” flap- 2 cm prox to DRUJ
6 cm distal to elbow for main perforator
5/6 – between compt 5 and 6

Use proximal pedicle if being used free (much larger). 5% no

communication with AIA

Lateral arm flap

Katsaros, 1984, Ann Plast Surg
A – Posterior collateral radial artery, branch of profunda
brachii. Runs between lat. head of triceps and brachialis.
Radial nerve anterior to it in spiral groove
P – Septal perforators. 4–8 cm long, 1.5–2.5 mm. Venae comi-
tantes 2.5 mm. Nerve – Posterior brachial cutaneous nerve
L – Deltoid insertion to lat. epicondyle. Skin paddle over
distal 1/3 over lateral intermuscular septum
D – 10–14 cm wide (6 cm for direct closure). From midpoint of
humerus to 5 cm distal to lateral epicondyle. Can take bone

Pectoralis major
Type V
Ariyan, 1979, PRS
A – Pectoral branch of thoraco-acromial trunk. Enters mus-
cle deep where line of junction of middle and lateral thirds of
clavicle bisects acromio-xiphisternal line
224 Appendix: FRCS Plast Classification Systems

P – 1. Pec branch of thoraco-acromial trunk; 4 cm long, 2.0

mm wide
2. 1–6th intercostal cutaneous perforators of internal
mammary artery
L – Acromial-xiphis. line bisection with junction middle and lat-
eral one-third of clavicle. Skin paddle either medial or in IMF
D 15 × 20 cm

Fibula
Type C/D
Taylor, 1975, PRS
Hidalgo, 1989, PRS
A – Peroneal artery sends in nutrient branch 16 cm below
fibular head. Skin paddle supplied by cutaneous perforators
in posterior intermuscular septum
P – 4 cm, 0.2 mm. Can be lengthened with periosteal
dissection
L – Skin paddle on line from head of fibula to posterior bor-
der of lat. Malleolus, centred on junction of middle and distal
thirds
D – Bone up to 26 cm
Skin up to 8 × 15 cm

Medial Plantar Artery

Myamato, 1987, PRS
Type B
A – Medial plantar artery, terminal branch of post. tibial
artery; runs between Ab Hall and FDB bellies. Perforators
supply skin paddle on medial edge of central plantar fascia.
P – 12 cm × 1.5 mm
L – Skin paddle on instep along line between head of 1st MT
and midpoint of heel, over Ab Hall muscle. Do not transgress
onto weight bearing areas of the foot.
D – 6 × 12 cm
 Appendix: FRCS Plast Classification Systems 225

Tensor fascia lata

Hill, 1978, PRS
Type I
A – Transverse branch of lateral circumflex femoral artery
from profunda femoris. Divides into 3 and supplies muscle in
thirds. 5–7 musculocutaneous perforators supply skin paddle,
extends to 5 cm above knee.
P – 6 cm × 2.0 mm
L – Axis runs along anterior edge of muscle in line from ASIS
to lateral tibial condyle. Pedicle enters 6–10 cm from ASIS on
the line. Muscle 3 cm wide, 15 cm long.
D – 10 × 20 cm for direct closure, 20 × 40 cm with SSG

Anterolateral thigh
Song, 1984, Br J Plast Surg
Type B/C
A – Perforators from descending branch lateral circumflex
femoral artery. Approx. 80% musculocutaneous, 20% septo-
cutaneous either through vastus lateralis or in septum
between it and rectus femoris. 2–3 main perforators
P – 12 cm × 2.0 mm
L – Axis is line from ASIS to lateral border of patella.
Perforator tends to be in a quadrant 3 cm postero-distal to
the midpoint of this line
D – 10 × 20 cm for direct closure, 15 × 35 cm with SSG

Gracilis
Harii, 1976, PRS
McGraw, 1976, PRS
Type II
A – Terminal branch of medial circumflex femoral artery
from profunda femoris. Enters muscle 10 cm inferior to pubic
tubercle
P – 7 cm × 1.5 mm
L – Axis is 2 cm posterior to line from pubic tubercle to medial
femoral condyle. Main cutaneous perforator at about 10 cm
from pubic tubercle, where the vessel enters the muscle
D – Muscle 6 × 30 cm. Skin 8 × 15 cm
226 Appendix: FRCS Plast Classification Systems

Trauma

Mangled Extremity Severity Score (MESS) (Johansen et al.;

J Trauma; 1984)
Scores of 7+ predictive of amputation
Soft tissue/skeletal injury
Low – very high energy injury. Score 1–4
Limb ischaemia
Reduced pulse with normal perfusion – cool paralysed
numb. Score 1–3. Doubled if
ischaemia time > 6 h
Shock
Systolic BP always > 90 mmHg – persistent hypoten-
sion. Score 0–2
Age
<30, 30–50, 50+. Score 0–2

Classification of open tibial fractures, Gustillo and Anderson;

J Trauma; 1986
Type 1: Wound < 1 cm
Type 2: Wound > 1 cm without extensive soft tissue injury,
flaps and avulsions
Type 3A: Adequate soft tissue cover in a tibial fracture
despite extensive soft-tissue damage or
high-energy trauma
Type 3B: Extensive soft tissue loss with periosteal stripping
and bone exposure. May be heavily contaminated
Type 3C: Open fracture with associated arterial injury
requiring repair

Byrd and Spicer classification of open tibial fractures (PRS;

1985)
Type 1: Low energy spiral/oblique fracture clean <2 cm wound
Type 2: Moderate energy, comminuted or displaced fracture >2 cm
laceration, muscle contusion but no non-viable muscle
Type 3: High energy – extensive soft tissue, skin and muscle loss
Type 4: Extreme energy resulting in degloving, crush or vascular injury
 Appendix: FRCS Plast Classification Systems 227

Incidences

Hypospadia 1/300 2,000 lb/per annum UK

Positional 1/300
plagiocephaly
Cleft lip/palate 1/600–700 1,000 lb/per annum UK
Syndactyly 1/1,000–3,000
Submucosal cleft 1/1,000
palate
Neurofibromatosis 1/3,000
Hemifacial 1/5,000
microsomy
Anotia 1/6,000 UK, 1/4,000 Japan, 1/1,000 Native
American
Constriction Ring 1/15,000
Syndrome
Crouzon 1/15–25,000
Poland 1/25,000
Facial cleft 1/25,000
Treacher-Collins 1/25–50,000
Craniosynostosis 1/25,000
Gorlins 1/60–150,000
Aperts 1/160,000
Exstrophy 1/60,000
Xeroderma 1/million
pigmentosum
BCC 650/100,000
SCC 150/100,000
MM 6–10/100,000
Sarcoma 25/100,000

Other Useful Bits for Exams

Aeitiology of synostosis
• Virchow suggested a primary sutural abnormality
• McCarthy a dural abnormality
• Moss an abnormality in the skull base
• Recently FGFR abnormalities have been discovered in
some synostosis
228 Appendix: FRCS Plast Classification Systems

Diagnostic criteria for RA (American College of Rheuma-

tology)
Morning stiffness
Arthritis of 3 or more joint areas
Arthritis of hand joints
Symmetric arthritis

The above should be present for 6 weeks

Rheumatoid nodules
RHF +ve
X-Ray changes
• 4 or more indicate RA
• Operate proximal to distal with the exception of the PIPJ
boutonniere where PIPJ function effects MCPJ

DVT
Risk groups
Low Minor surgery <30 min. Any age. No risk factors
Major surgery >30 min. Age <40. No other
risk factors
Minor trauma or medical illness
Moderate Major surgery. Age ?40 or other risk factors
Major medical illness: heart/lung disease, CA,
inflammatory bowel disease
Major trauma/burns
Minor surgery, trauma, medical illness in pt. with
previous DVT, PE or thrombophilia
High Major orthopaedic surgery or # pelvis, hip, lower limb
Major abdo/pelvic surgery for ca
Major surgery, trauma, medical illness in pt with DVT,
PE or thrombophilia
Lower limb paralysis (e.g., stroke, paraplegia)
Major lower limb amputation

DVT/Thromboembolism risk factors

Patient Disease
Age Trauma or surgery, esp. pelvis, hip, lower limb
Obesity Malignancy, esp. pelvic, abdominal metastatic
Immobility Heart failure
 Appendix: FRCS Plast Classification Systems 229

Patient Disease
Pregnancy/ Recent M I
puerperium
High dose Lower limb paralysis
oestrogen therapy
Prev. DVT/PE Infection
Thrombophilia Inflammatory bowel disease
Nephrotic syndrome
Polycythaemia
Paraproteinaemia
Paroxysmal nocturnal haemoglobinuria
Behcet’s disease
Homocystinaemia

High risk 1. Graduated elastic anti-embolism stockings

(e.g., Kendal T.E.D.) plus
2. Low molecular weight heparin (contact hospital
pharmacy for available products and dose)
or
Adjusted dose warfarin (INR 2–3)
3. Consider intermittent pneumatic compression
Moderate risk 1. Graduated elastic anti-embolism stockings
(e.g., Kendal T.E.D.)
and/or
2. Low molecular weight heparin (contact hospital
pharmacy for available products and dose)
Low risk 1. Early mobilisation

Foetal wound healing

• Less inflammation
• More collagen type 3
• Epithelialisation more rapid
• Angiogenesis is reduced
• Collagen deposition rapid, not excessive and organised
• In first trimester may be scarless i.e. regenerative
230 Appendix: FRCS Plast Classification Systems

First and second set phenomenon – Gibson and Medawar

rejection
• Reaction to allograft such as skin on first exposure
− 1–3 days graft takes as per usual
− 4–7 days infiltration with leucocytes and thrombi with
punctate haemorrhages evident
− 7–9 days blood flow ceases and graft undergoes
necrosis
• Second set phenomenon occurs if host is exposed to allo-
genic material from the same source again
− Immediate hyperacute rejection
− Graft does not undergo any revascularisation
• Graft destruction is by both
− Direct destruction mediated by the cellular system
CD4/8 T-cells
− Indirect mediated by humoral system. Stimulated B
lymphocytes produce an antibody which binds with the
antigen and stimulates the destruction via complement
• HLAs A B and DR are most important mediators of tissue
rejection (Class 1 and 2)

Features of raised ICP

• Tense fontanelles
• Irratibility
• Seizures
• Papilloedema
• Psychomotor retardation
Glasgow Coma Scale 3–15
1 2 3 4 5 6
Eyes Does not Opens eyes in Opens eyes Opens eyes N/A N/A
open eyes response to in response spontaneously
painful stimuli to voice
Verbal Makes no Incomprehensible Utters Confused, Oriented, N/A
sounds sounds inappropriate disoriented converses
words normally
Motor Makes no Extension to Abnormal Flexion/ Localizes Obeys commands
movements painful stimuli flexion to withdrawal to painful
decerebrate painful painful stimuli stimuli
response stimuli
decorticate
response
Appendix: FRCS Plast Classification Systems
231
232 Appendix: FRCS Plast Classification Systems

Huger’s zones of blood supply – Anterior abdominal wall

1979
Zone 1: Mid abdomen supplied by deep epigastric arcade
Zone 2: Lower abdomen supplied by epigastric arcade and external
iliac. Superficial to the fascia is provided by SIEA and
SEPA, both from the femoral
Zone 3: Lateral abdomen and flanks. Blood supply from the
intercostals, subcostal and lumbar arteries. Intercostals
enter the abdomen between transverses and internal
oblique and anastamose with SEA and DIEA

Infection preventing SSG taking

• 105 organisms per gram

Nerve types
• Group A
− Alpha – Motor and proprioceptive
− Beta – Pressure and proprioceptive
− Gamma – Motor to muscle spindles
− Delta – Touch, pain and temperature
• Group B – Myelinated pre-ganglionic autonomic nerves
• Group C – Myelinated post-ganglionic autonomic nerves

Radiological changes in OA
• Joint space narrowing
• Sclerosis of the bones
• Bone cysts
• Spurs, osteophytes, exostoses

Scoring systems for Inhalational Injury

• Many tried
• Aim to predict outcome
• Based on PaO2/FiO2 ratio, chest x-ray, peek inspiratory
pressures and bronchoscopy
• Brown and Warden
• Kansella
 Appendix: FRCS Plast Classification Systems 233

Suture material
• Absorbable
− Catgut
Submucosal sheep intestine
Strength lost at 10 days lasts a month
− Polyglycolic acid – Dexon
Hydrolysed
Loses strength at 21 days and absorbed at 90
− Polyglactin 910 – Vicryl
Loses strength at 21 days and absorbed at 90
Synthetic braided suture
− Polyglecaprone 25 – Monocryl
Loses strength at 21 days and absorbed at 90
− Polydioxanone – PDS
Loses strength at 3 months and absorbed at 6 months
• Non-absorbable
− Silk
− Polyamide – Nylon
− Polypropylene – Prolene
− Stainless steel

UV light wavelengths
• UVA: 320–400 nm
• UVB: 280–320 nm
• UVC: 200–280 nm
Index

A bleeding tendencies, 167

Abdominoplasty botulinum toxin type-A, 172
abdominal herniae, 2 brow-lifting, 172
abdominal surgery, 2 cardiac/respiratory history, 167
cosmetic patients, 1 central/lower face examination, 169
full medical and drug history, 3–4 clinical findings, 165, 166
laboratory investigations, 5 composite rhytidectomy, 171
patient’s weight, 1 cranial nerves V and VII, 170
physical examination, 4–5 fat transfers, 172
post-operative management, 7 fillers, 172
pre-operative candidate, 1, 2 hobbies, 166
psychological effects, 2 hypertension, 167
risk factors, 3 jowling, 167
risks and complications, 2, 6 medications, 166, 167
treatment/surgical technique, 5–6 midface examination, 168–169
Abductor Pollicis Brevis, 111 minimal access techniques, 174
Abnormal ear neck procedures, 171
anatomy, 154 NLF, 167, 168
clinical findings, 149, 150 occupation, 166
management, 152–153 patient age, 166
McDowell’s basic goals, prominent periosteal procedures, 170, 171
ears, 155 post-operative management,
normal ear characteristics, 154 172–173
patient history, 150–151 ptosed soft tissues, 170
physical examination, 151–152 resurfacing, 172
Tanzer classification, auricular rhytids, 168
defects, 154–155 risks/complications, 173
Acinic cell, 203 skin, 170, 171
Adenocarcinoma, 203 SMAS, 170, 171
Adenolymphoma, 202 smoking, 165, 166
Aged face, facelifting sun exposure, 166
allergies, 167 surgical gestures, 170
anaesthetic assessment, 167 treatment outcome, 173

S. Hettiaratchy et al. (eds.), Plastic Surgery, 235

DOI 10.1007/978-1-84882-116-3,
© Springer-Verlag London Limited 2012
236 Index

Aged face, facelifting (cont.) axillae, 20

types, 173–174 back-up donor, 21
upper face examination, 168 BRCA1/BRAC2, 18
Anotia, 154 clinical findings, 17, 18
Apert syndrome, 77 DIEP/TRAM donor site, 21
Arterial malformation, 213 family history, 18
AV malformation, 213 laboratory investigations, 22
Axonotemesis, 216 latissimus dorsi donor site, 21
patient history, 18–20
B post-op adjuvant therapy, 18
Balanitis xerotica obliterans post-operative management, 24
(BXO), 130 pre-op therapy, 18
Bicoronal synostosis, 205, 206 risk factors, 18–19
Blepharoplasty risks/complications, 23–24
aesthetic lid surgery, 10 SGAP/IGAP donor site, 21
clinical findings, 9, 10 standing/sitting up examination, 20
diplopia and epiphora, 10 surgical management, 18
family history, 10 TMG donor site, 21
full medical and drug history, 11 treatment/surgical technique,
general medical conditions, 9 22–23
glaucoma, 10 Breast reduction
laboratory investigations, 14 clinical findings, 25, 26
lids, anatomy, 16 family history, 26
physical examination, 11–13 full medical and drug history,
post-operative management, 15 26–27
pre-existing eye disease, 10 intertrigo/maceration, 26
ptosis, 10 laboratory investigations, 29
risk factors, 10–11 personal history, 26
risks and complications, 10, 11, 15 physical examination, 27–29
soreness/redness, 10 post-operative management, 31
treatment/surgical technique, 14 psychological effects, 26
Bone anchored hearing aids risk factors, 26–27
(BAHA), 153 risks/complications, 30–31
Brachial plexus treatment/surgical technique,
Erbs’ palsy, 236 29–30
external carotid branches, 237 wearing bra at night, 26
IX, 236 Burns
Klumke’s palsy, 236 accidental injuries, 49
Mellesi classification, 214–215 airway, 49
obstetric palsy, 235 ANY concerns, 50
RXT, 237 breathing, 50
Brachioradialis, 112 burn depth assessment, 51
Brachycephaly, 76 chemical type, 48
Breast reconstruction clinical findings, 47–48
abnormal lumps, 20 clinical outcomes, 55
aesthetic exam, 20–21 concomitant injuries, 49
 Index 237

contact type, 48 complications, 61

delayed excision, 53 Furlow’s double opposing
dressings, 54–55 Z-plasty, 60
early excision, 53 intravelar veloplasty, 61
electrical type, 48 laboratory investigations, 59
escharotomy, 52–53 Millard technique, 60
fascial excision, 53 non-surgical treatment, 59
fasciotomy, 53 patient history, 57–58
flame type, 48 patient management, 61
fluid resuscitation, 51–52 physical examination, 58–59
GCS/AVPU/pupillary reaction, 50 secondary rhinoplasty, 61–63
IV access and fluids, 50 surgical treatment, 59
non-accidental injuries, 49 Veau-Wardill-Kilner
scalds type, 48 technique, 61
self-inflicted injuries, 49 velopharyngeal dysfunction,
skin cover, 54 63–64
tangential excision, 53 vomerine flaps, 61
TBSA, 50, 51 Von Langenbeck technique, 60
tracheostomy, 52 Complex wounds, pressure sore
Burns contracture anatomy, 148
breast, 43 bacterial growth, 143–144
burn history, 42 capillary arterial circulation, 143
clinical findings, 41, 42 classifications, 148
facial scars, 42 clinical findings, 143, 144
joints, 43 ischial sores, 148
laboratory investigations, 45 ischial tuberosities, 143
local flaps, 45 management, 146
neck, 42 neurological injury, 144
perioral and periorbital scars, 42 patient history, 144–145
physical examination, 43–45 physical examination, 145–146
physiotherapy, 45 sacral sores, 148
pressure therapy, 45 surgical treatment, 147–148
resurfacing, 46 treatment outcome, 148
splint, 45 trochanteric sores, 148
tissue expansion, 45 Condylar fractures, 102
Congenital constriction ring
C syndrome, 213
Camptodactyly Congenital hand
Adams classification, 211 aetiology, 71
Upton classification, 210 Bayne–radial/ulnar dysplasia, 72
Capillary malformation, 213 Blauth thumb hypoplasia, 71
Carpal tunnel, 179 botox, 69
Carpenter syndrome, 78, 206 clasped thumb, 70
Cleft lip and palate cleft hand, 69
clinical findings, 57, 58 clinical findings, 65, 66
clinical outcomes, 63 clinodactyly, 69, 70
238 Index

Congenital hand (cont.) dermofasciectomy, 84

first web release, 70 fasciectomy, 84
IFSSH Swanson classification, 71 fasciotomy, 83
laboratory investigations, 68 laboratory investigations, 83
longitudinal deficiencies, 69 non-surgical treatment, 83
patient history, 65–67 pathophysiology, 86
physical examination, 67–68 patient history, 79–81
physiotherapy, 69 physical examination, 81–82
radial longitudinal deficiency, 71 PIPJ management, 84
risks and complications, 71 post-operative management, 85
surgical general timing, 69 risks/complications, 85
syndactyly, 69, 70, 72 skoog, 84
thumb duplication, 71
thumb hypoplasia, 70 E
treatment principles, 69 Electromyography, 90
trigger thumb, 70 Electroneurography, 90
Craniosynostosis Enophthalmos, 97
apert syndrome, 77 Epiphora, 10
brachycephaly, 76 Escharotomy, 52–53
calvarial remodelling, 77 Extensor Pollicis Longus, 112
Carpenter syndrome, 78
clinical findings, 73, 74 F
Crouzon syndrome, 77 Facial palsy
laboratory investigations, 75 aetiologic investigations, 89–90
lambdoidal plagiocephaly, 77 direct nerve repair/
non-surgical treatment, 75 transposition, 91
patient history, 73 electromyography, 90
Pfeiffer syndrome, 78 electroneurography, 90
physical examination, 74 facial weakness, 87, 88
plagiocephaly, 76 free muscle transfer, 91
Saetre-Chotzen syndrome, 77–78 maximal stimulation test, 90
scaphocephaly, 76 medical treatment, 90
trigonocephaly, 75–76 nerve excitability test, 90
Crouzon syndrome, 77 patient history, 87–88
CSF otorrhoea, 98 physical examination, 88–89
CSF rhinorrhoea, 98 regional muscle transposition, 91
Cubital tunnel syndrome, 179 static facial support, 91
topographic investigations, 90
D watchful waiting treatment, 90
Dermofasciectomy, 84 Fasciectomy, 84
Diplopia, 10 Fasciocutaneous flaps, 147, 148
Dupuytrens disease Fasciotomy, 53, 83
anatomy, 85–86 FRCS plast classification systems
bruner, 84 Adams classification,
clinical findings, 79, 80 camptodactyly, 211
clinical outcome, 85 aeitiology of synostosis, 228
 Index 239

AJCC classification 2009, 200 Huger’s zones of blood

Angle classification, dental supply, 232
occlusion, 204 hypospadius, 214
Aperts – 1:160000, 205 Kanavel’s four cardinal
ASA grading, anaesthetic signs, 240
patients, 214 Kay modification, Urbaniak
Bayne and Klug classification, JHS, 220
radius deficiencies, 209 Knight and North classification,
Blauth classification, thumb malar fractures, 203
hypoplasia, 212 Larsen’s grading, rheumatoid
Boutonierre deformity arthritis, 218
classification, Nalebuff, 218 Le Fort classification, maxillary
brachial plexus (see Brachial plexus) fractures, 204
Broder’s histological grading, Leddy and Packer classification,
SCC, 198 FDP avulsion, 220
Byrd and Spicer classification, Liscombs classification,
open tibial fractures, 227 Volkmann’s contracture,
Carpenter syndrome, 206 219
craniofacial anomalies, American lymphoedema, 215–216
Society of Cleft Lip/ Mallet finger deformities,
Palate, 204–205 Doyle, 219
Craniofacial clefts, Mangled Extremity Severity
Tessier, 207–208 Score, 226
Crouzon – 1:15000 AD, 205 Manson classification, malar
diagnostic criteria, RA, 228 fractures, 204
DIEP/TRAM zones, 228–229 Matarasso classification,
DVT risk groups, 229–230 abdominoplasty, 197
Enjolras and Mulliken Mathes and Nahai muscle
classification, 214 flap classification, blood
Enneking sarcoma staging, 200 supply, 226
Fasciocutaneous flap Mayfield classification,
classification, Cormack and progressive perilunate
Lamberty, 222 instability, 219
first and second set phenomenon, melanoma types, 199
Gibson and Medawar, 230 MRC classifications, nerve
Fitzpatrick classification, recovery, 216
photosensitivity, 215 National Pressure Ulcer
Foetal wound healing, 230 Advisory Panel Grading
Glasgow Coma Scale 3–15, 231 System, 218
Goldenhars, OMENS+ neck dissection, 202
classification, 207 nerve entrapment, 232–235
head and neck tumours, 201 nerve injuries, Seddon, 216
Herndon classification, nerve injuries, Sunderland,
neuroma, 206 216–217
House and Brackman grading, open tibial fractures, Gustillo and
facial palsy, 215 Anderson classification, 226
240 Index

FRCS plast classification systems Trojani histological grading

(cont.) system, 201
Pairolero and Arnold classifica- Ulna dysplasia classification,
tion, sternal dehiscence, 217 Bayne, 209
Patterson classification, Ulna dysplasia classification, Cole
congenital constriction ring and Manske, 210
syndrome, 213 Upton classification,
Paysk zones, 198 camptodactyly, 210
Pfeiffer, 206 Upton classification,
Prosanski classification, mandibu- macrodactyly, 212
lar deformities, 207 Urbaniak classification, ring
Radiological changes, OA, 232 avulsions, 220
raised ICP, 230 UV light, 220
Regnault classification, vascular lesions, Mulliken and
ptosis, 198 Glowacki, 213
Romberg’s hemifacial atrophy, Veau’s classification, 205
206–207 Waner grading system, capillary
Saethre-Chotzen, 206 malformations, 199
Salter Harris, 221 Wassel classification, thumb
sarcoma, AJCC, 200 duplication, 211–212
Schobinger classification, arterio- Waterlow score, pressure risk, 217
venous malformations, 213 Weckesser clasp thumb, 212
scoring systems, inhalational Weiss and Hastings classification,
injury, 232 intra-articular phalangeal
Simon classification, gynaecomastia, fractures, 220
198 WHO classification, salivary
Stelling classification, polydactyly, gland tumours, 202–203
211
striped Y classification, 205 G
suture material, 233 Guyon’s canal, 179, 180
Swan neck deformity classifica- Gynaecomastia
tion, Nalebuff, 218 clinical findings, 103, 104
Swanson classification, upper limb laboratory examination, 106
developmental anomalies, 208 medical and drug history, 105
Tessier’s classification, patient’s age, 104
hyperteliorism, 205 physical examination, 105–106
Tetamy classification, post-operative management, 107
polydactyly, 211 risk factors, 104–105
Thatte and Thatte classification, risks/complications, 107
venous flaps, 222 treatment, 106–107
thromboembolism risk
factors, 229 H
thumb deformity on RA, 219 Haemangioma, 213
TNM classification, cutaneous Haematoma
melanoma, 199 gynaecomastia, 107
Treacher–Collins syndrome, 206 maxillofacial trauma, 98
Trigger finger classification, 219 rhinoplasty, 193
 Index 241

Hand with inflammatory arthropathy Lichen sclerosus (LS), 130

aetiology, 123 Lower limb trauma
Belcher shuffle, 119 amputation vs. reconstruction, 136
classifications, 123 anatomy, 135
clinical findings, 117, 118 classifications, 135
elbow examination, 119 clinical findings, 131, 132
hand therapy, 122 definitive fixation/
neck examination, 119 reconstruction, 134
non-surgical treatment, 121 immediate treatment, 133–134
patient history, 117–119 initial surgical assessment, 134
post-operative management, 122 intermediate investigations/
risks and complications, 122 operations, 134
shoulder examination, 119 muscle flaps vs. fasciocutaneous
surgical treatment, 122 flaps, 136
thumb and fingers patient history, 131–132
examination, 120 physical examination, 132–133
treatment procedures, 123 post-operative care, 134–135
trigger, 122 reconstruction timing, 136
wrist examination, 119–120 role of angiography, 136
Hand with nerve palsy treatment outcome, 135
clinical examination, 109, 110 treatment procedures, 135
clinical outcome, 115 Lump in neck
patient history, 109–110 adenocarcinoma, 141
physical examination, 110–112 chemotherapy, 142
post-operative management, 114 clinical findings, 137, 138
risks and complications, 114 histopathological diagnosis, 141
treatment, 112–114 laboratory investigations, 140
Hypoplasia, 154–155 N positive neck, 142
Hypospadias neck dissection, 142
aetiology, 126 nodal cytology/histology, 141
classification, 125, 126 patient history, 137–138
clinical findings, 126 physical examination, 138–140
complications, 130 radiotherapy, 141, 142
distal meatal treatment, squamous cell carcinoma, 141
128–129 surgical management, 142
embryology, 125–126 TNM definitions, oral cavity and
laboratory investigations, 128 oropharynx, 141–142
patient history, 127 unilateral/ bilateral
physical examination, 127 tonsillectomy, 141
proximal treatment, 129 Lymph node melanoma metastasis,
157, 158
I Lymphatic malformations, 214
Intraoral lacerations, 98
M
L Malar fractures
Lambdoidal plagiocephaly, 77 Knight and North classification, 204
Le Fort fractures, 98, 99 Manson classification, 201
242 Index

Malignant lymphomas, 203 parotid duct laceration, 100

Mangled Extremity Severity Score primary survey, 96–97
(MESS), 226 secondary survey, 97
Mastoid ecchymosis, 98 sensation, 95
Mastopexy smoking history, 94
aesthetic breast surgery, 34 soft tissue injuries, 100
bra size, 34 soft tissues re-suspension and
clinical findings, 33, 34 reconstruction, 102
family history, 34 tetanus, 100
full medical and drug history, 35–36 upper third, 94
grooving, 34 X-rays, 100
intertrigo/maceration, 34 Mesiobuccal cusp, 204
laboratory investigations, 38 Microtia, 152, 154
personal history, 34 Millard technique, 60
physical examination, 36–37 Minimal access cranial suspension
post-operative management, 40 (MACS), 174
psychological effects, 34 Muco-epidermoid carcinoma, 203
risk factors, 35 Musculocutaneous flaps, 147, 148
treatment/surgical technique, 38–39
Maxillofacial fractures, 101 N
Maxillofacial trauma National Pressure Ulcer Advisory
alcohol intake, 94 Panel (NPUAP), 145, 148, 218
allergies/medications, 94 Nerve compression
bone grafting, 101 age, occupation, handedness, and
broad-spectrum antibiotic cover, hobbies, 175
100 anatomy, 180
clinical findings, 93, 94 clinical findings, 175, 176
condylar fractures of mandible, 102 compression causes, 177
consciousness loss, 94 intrinsic nerve damage causes, 177
CT scan, 100 neck/elbow/wrist trauma
ears, 98 history, 175
face, 97 physical examination, 177–179
facial lacerations, 95 predisposing factors, 177
facial nerve injury, 100 symptoms, 176–177
injury mechanism, 94 treatment and outcome, 179
intraoral, 98 Nerve entrapment
lacrimal duct, 100 anterior interosseous
lower third, 95 syndrome, 233
maxillofacial fractures, 101 carpal tunnel causes, wrist, 232
middle third, 95 cubital tunnel syndrome, 233
neck pain, 94 Guyons canal, 233
neurological examination, 98–99 posterior interosseous
nose, 98 syndrome, 233
orbits, 97 pronator syndrome, elbow, 232
palpation, 98 radial tunnel syndrome, 233
 Index 243

Neuropraxia, 216 R
Neurotemesis, 216 Radial tunnel syndrome, 179
Non-epithelial tumours, 203 Radial/posterior interosseous nerve
NPUAP. See National Pressure (PIN), 112, 114
Ulcer Advisory Panel Relative afferent pupillary defect
(RAPD), 99
O Rheumatoid arthritis
Oncocytoma, 202 hand with inflammatory
Open tibial fractures arthropathy, 118, 123
Byrd and Spicer Larsen’s grading, 218
classification, 227 Rhinoplasty
Gustillo and Anderson blood supply, 189
classification, 226 bony/cartilaginous skeleton, 188
Orbital dystopia, 97 clinical findings, 187, 188
Osteomyelitis, 135 clinical photography, 192
closed rhinoplasty, 195
P laboratory investigations, 192
Palate haematoma, 98 open rhinoplasty, 195–195
Parotid duct laceration, 100 patient history, 189–190
Periorbital ecchymosis, 97 physical examination, 191–192
Pfeiffer syndrome, 78 post-operative management, 194
Pigmented lesion management risks/complications, 193
clinical findings, 157, 158 septum, 188
laboratory investigations, 160 soft tissue cover, 188
locoregional recurrence squamous epithelium, 189
treatment, 161 treatment/surgical technique,
melanoma biopsy, 160 192–193
occult primary melanoma, 162
of lymph node basins, 161 S
of primary tumour, 160–161 Saetre-Chotzen syndrome, 77–78
patient history, 157–159 Scaphocephaly, 76
physical examination, 159 Sentinel lymph node biopsy
post-operative management, 162 (SLNB), 160
prevention, 163 Septal haematoma, 98
risks/complications, 162 Sero-negative arthropathies, 118
PIN. See Radial/posterior Severe soft tissue infection
interosseous nerve clindamycin, 188
Plagiocephaly, 76 clostridial myonecrosis, 187
Pleomorphic adenoma, 202 group A streptococcus, 187, 188
Polydactyly hyperbaric oxygen treatment, 188
Stelling classification, 211 laboratory investigations, 186
Tetamy classification, 207 mortality, 187
Pronator syndrome, 179 necrotising fasciitis, 183, 184
Psoriasis, 118 patient history, 184–185
Ptotic breasts. See Mastopexy physical examination, 185
244 Index

Severe soft tissue infection (cont.) Upton classification

polymicrobial trauma, 187 camptodactyly, 210
severe cellulitis, 183, 184 macrodactyly, 212
treatment, 186–187
Subconjunctival haemorrhage, 97 V
Superficial musculo-aponeurotic Vascular lesions classification
system (SMAS), 170, 171 Jackson, 214
Szanto’s grades, 203 Mulliken and Glowacki,
199–200
T Vascular malformations,
TOCS/plexopathy, 177 199–200
Total body surface area (TBSA), Veau-Wardill-Kilner technique, 61
50, 51 Venous malformation, 213
Tracheostomy, 52 Von Langenbeck technique, 60
Trigonocephaly, 75–76
W
U Wartenberg’s sign, ulnar nerve, 111
Ulna dysplasia classification
Bayne, 210 Z
Cole and Manske, 210 Zygomatic fractures, 98