Main Plastic and reconstructive surgery : approaches and techniques

Plastic and reconstructive surgery : approaches and techniques

, , , , ,
0 / 0
How much do you like this book?
What’s the quality of the file?
Download the book for quality assessment
What’s the quality of the downloaded files?
"Contemporary guide to the fundamental approach and techniques of plastic surgery"--Provided by publisher.
Abstract: Plastic and reconstructive surgery continues to evolve as new techniques open up new possibilities for the surgeon. In this groundbreaking textbook, contemporary approaches are explained and demonstrated to allow trainee and experienced surgeons alike to understand and assimilate best practice. Read more...
ISBN 10:
ISBN 13:
PDF, 273.56 MB
Download (pdf, 273.56 MB)

You may be interested in Powered by Rec2Me


Most frequently terms


You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you've read. Whether you've loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them.
Plastic and reconstructive surgery

Plastic and reconstructive
Approaches and techniques
Chief Editor
Ross D. Farhadieh
BSc(Med)Hons, MBBS, MD, EBOPRASF, FRACS(Plast), FRCS(Plast)
Panthea Plastic Surgery Clinics
Sydney and Canberra, Australia
Australian National University
Canberra, Australia

Neil W. Bulstrode
BSc(Med)Hons, MBBS, MD, FRCS(Plast)
Clinical Lead Plastic Surgery
Great Ormond Street Hospital
London, UK

Sabrina Cugno
Assistant Professor
McGill University
Department of Plastic Surgery
Montreal Children’s Hospital
Montreal, Canada

This edition first published 2015 © 2015 by John Wiley & Sons, Ltd.
Text illustrations for Chapter 41: © Elizabeth Hall-Findlay, unless stated otherwise. Chapters 67 and 71 remain © Tim Marten and
are published with non‐exclusive rights.
Registered Office
John Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK
Editorial Offices
9600 Garsington Road, Oxford, OX4 2DQ, UK
The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK
111 River Street, Hoboken, NJ 07030‐5774, USA
For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the
copyright material in this book please see our website at‐blackwell
The right of the author to be identified as the author of this work has been asserted in accordance with the UK Copyright, Designs and
Patents Act 1988.
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any
means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents
Act 1988, without the prior permission of the publisher.
Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names
used in this book are trade names, service marks, trademarks or registered trademarks of their respecti; ve owners. The publisher is not
associated with any product or vendor mentioned in this book. It is sold on the understanding that the publisher is not engaged in
rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional
should be sought.
The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and
should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by health science practitioners for
any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness
of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a
particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of
information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided
in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or
indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an
organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the
author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further,
readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written
and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the
author shall be liable for any damages arising herefrom.
Library of Congress Cataloging‐in‐Publication Data
Plastic and reconstructive surgery (Farhadieh)
Plastic and reconstructive surgery : approaches and techniques / [edited by] Ross D. Farhadieh, Neil Bulstrode, Sabrina Cugno.
  p. ; cm.
Includes index.
Summary: “Contemporary guide to the fundamental approaches and techniques of plastic surgery”–Provided by publisher.
ISBN 978-1-118-65542-9 (hardback)
I. Farhadieh, Ross D., editor. II. Bulstrode, Neil, editor. III. Cugno, Sabrina, editor. IV. Title.
[DNLM: 1. Reconstructive Surgical Procedures–methods–Atlases. WO 517]
Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in
electronic books.
Cover images: Courtesy of the editors, apart from ‘two bullets amongst surgical instruments’ iStock photo 10272617, © LockieCurrie.
Set in 9.5/12pt Minion by SPi Publisher Services, Pondicherry, India




Contributors, viii
Foreword, xv
Dedication, xvi

13 Radiation therapy and soft tissue response, 144

Gurdip Kaur Azad and Carie Corner

14 Burns: acute care and reconstruction, 153

Peter Dziewulski

Preface, xvii
About the companion website, xviii

Part I: Basic science and principles
1 Wound healing and scar formation, 3

Simon R. Myers and Ali M. Ghanem

2 Basic skin flaps and blood supply, 12

Edwin J. Morrison and Wayne A.J. Morrison

3 Biomaterials and structural fat grafting, 22

Naghmeh Naderi, Behzad Ardehali and Afshin Mosahebi

4 Local anaesthetics, 34

Yasamin Ziabari

5 Lasers, 44

Se-Hwang Liew

6 Tissue expansion, 51

Dariush Nikkhah, Lara Yildirimer and Neil W. Bulstrode

7 Tissue engineering, 62

Lara Yildirimer and Alexander Seifalian

Part III: Paediatric plastic surgery and
congenital disorders
15 Congenital melanocytic naevi, 183

Sabrina Cugno, Veronica Kinsler and Neil W. Bulstrode

16 Vascular anomalies, 192

Sabrina Cugno, Alex Barnacle, John Harper
and Neil W. Bulstrode

17 Cleft lip, 204

Marc C. Swan and David M. Fisher

18 Cleft palate and velopharyngeal dysfunction, 219

Sabrina Cugno and Brian C. Sommerlad

19 Congenital ear anomalies, 238

Sabrina Cugno and Neil W. Bulstrode

20 Craniofacial clefts, 255

Irene M.J. Mathijssen and Sarah L. Versnel

21 Craniosynostosis, 264

Aina V.H. Greig and David J. Dunaway

22 Orthognathic surgery, 279

Tim Lloyd, Ravinder Pabla, Sujata Sharma and Nigel Hunt

Part II: Integument

23 Facial reanimation, 295

Jonathan I. Leckenby and Adriaan O. Grobbelaar

8 Skin structure, 79

Anthony Barker

9 Melanoma, 88

Carlo Riccardo Rossi and Antonio Sommariva

10 Non‐melanoma skin cancers, 100

Michael Findlay and Mina S. Ally

11 Atypical skin lesions, 115

Michael Findlay and Michael A. Henderson

12 Allotransplantation, 130

Maria Siemionow and Fatih Zor

Part IV: Head and neck reconstruction
24 Head and neck malignancy: staging

and neck dissections, 309
Andrew N. Morritt, Marlene S. See and Navid Jallali

25 Oral tongue reconstruction, 318

Stuart Archibald, Michael Gupta and Achilleas Thoma

26 Mandibular reconstruction, 330

Christopher Glenn Wallace, Chung‐Kan Tsao
and Fu‐Chan Wei


vi   Contents

27 Maxillary reconstruction, 338

45 Pressure sores, 597

28 Pharyngeal reconstruction, 349

46 Lower limb reconstruction, 607

Achilleas Thoma, Michael Gupta and Stuart Archibald
Ross D. Farhadieh and Wayne A.J. Morrison

29 Skull base reconstruction, 362

Ross D. Farhadieh and Wayne A.J. Morrison

30 Cheek reconstruction, 366

Adam C. Gascoigne and Stephen Flood
James K. Chan, Matthew D. Gardiner, Michael Pearse and
Jagdeep Nanchahal

47 Lymphoedema, 628

Kelvin Ramsey and Peter Mortimer

Adam C. Gascoigne and Ross D. Farhadieh

31 Lip reconstruction, 377

Marlene S. See, Andrew N. Morritt and Navid Jallali

32 Nasal reconstruction, 390

Jean‐Brice Duron and Marc Revol

33 Eyelid reconstruction, 407

Konal Saha and Naresh Joshi

34 Ear reconstruction, 416

Françoise Firmin and Neil W. Bulstrode

35 Scalp and calvarial reconstruction, 427

Christopher Glenn Wallace and Fu‐Chan Wei

36 Facial trauma, 437

David David

Part VII: Upper limb
48 Hand examination and investigations, 645

J. Henk Coert, Peter Hoogvliet and Willem D. Rinkel

49 Congenital hand differences, 660

Bran Sivakumar, Jonathan Adamthwaite and Paul Smith

50 Finger tip injuries, 688

Donald Sammut and Robert Pearl

51 Flexor tendon injuries, 707

Sarah Tucker and Georgina Williams

52 Extensor tendon injuries, 722

Gregory McCarten

53 Tendon transfers, 733

Adam C. Gascoigne and Stephen Flood

Part V: Breast
37 Anatomy and physiology of the breast, 479

Giovanni Bistoni and Jian Farhadi

38 Breast augmentation, 486

Ross D. Farhadieh and Jian Farhadi

39 Breast reconstruction, 499

Phillip Blondeel, Maria Athanasiadou and
Andreas Tromaropoulos

40 Gynaecomastia and tuberous breast, 519

Afshin Mosahebi and Amir Sadri

41 Mastopexy and breast reduction, 530

Elizabeth J. Hall‐Findlay

Part VI: Trunk and lower limb
42 Chest wall reconstruction, 551

Mazyar Kanani and Martin J. Elliott
Simon Withey and Robert Pearl

43 Abdominal wall reconstruction, 564

William A. Townley and Stefan O.P. Hofer

44 Genitourinary and perineal reconstruction, 575

Niri S. Niranjan
Paige Fox, Paul Mittermiller and Gordon K. Lee
Kathryn Evans and Imran Mushtaq

54 Amputations, replantation and thumb

reconstruction, 752
Gráinne Bourke

55 Compartment syndrome in the extremities, 769

Steven E.R. Hovius and Tim H.J. Nijhuis

56 Nerve injury, repair and reconstruction, 777

Renata V. Weber, Andrew Yee, Michael M. Bottros
and Susan E. Mackinnon

57 Brachial plexus injuries and reanimation, 797

Kirsty U. Boyd, Kristen M. Davidge and
Susan E. Mackinnon

58 Nerve compressions, 813

Kristen M. Davidge and Susan E. Mackinnon

59 Dupuytren disease, 838

Paul M.N. Werker

60 Fractures and dislocations in the hand, 850

Barbara Jemec and Nicola Burr

61 Osteoarthritis and prosthetic joints in the hand, 861

Adam C. Watts and Ian A. Trail

62 Wrist pathology, 878

Owen L. Ala, T. Shane Johnson and L. Scott Levin

63 Rheumatoid arthritis of the hand and wrist, 890

Rebecca Ayers and Mark Pickford

Contents   vii

64 Lesions of the hand, 904

Richard D. Lawson, David A. Stewart and
Michael A. Tonkin

73 Genioplasty, 1047

Nicholas Lee, Deepak Komath and Tim Lloyd

74 Blepharoptosis, 1063

Alan A. McNab

Part VIII: Aesthetic surgery
65 Facial anatomy and ageing, 923

Chin‐Ho Wong and Bryan C. Mendelson

66 Non‐operative facial rejuvenation, 940

75 Liposuction and liposculpture, 1075

Darryl J. Hodgkinson

76 Abdominoplasty and body contouring, 1083

Alexander Stoff and Dirk F. Richter

Jean Carruthers and Alastair Carruthers

67 Forehead lift, 948

Part IX: Military, simulation training
and exams

68 Upper eyelid rejuvenation, 967

77 Simulation learning in plastic surgery, 1107

69 Lower eyelid–cheek junction rejuvenation, 976

78 Military plastic surgery, 1121

70 Facelift, 992

79 Plastic surgery fellowship and board exams, 1129

Timothy J. Marten and Dino Elyassnia
Adil Ceydeli, Tong C. Duong and Robert S. Flowers
Sam T. Hamra

Bryan C. Mendelson and Ross D. Farhadieh

71 Neck lift, 1004

Ali M. Ghanem and Simon R. Myers

Robert M.T. Staruch and Shehan Hettiaratchy
Robert Pearl, Youssef Tahiri, Sabrina Cugno
and Ross D. Farhadieh

Timothy J. Marten and Dino Elyassnia

72 Rhinoplasty, 1032

David Stepnick, Catherine Weng and Bahman Guyuron

Index, 1135


Jonathan Adamthwaite

Giovanni Bistoni

Department of Plastic Surgery
Great Ormond Street Hospital
London, UK

Plastic Surgery Unit
Hospital de la Ribera
Spain and Department of General Surgery ‘P. Valdoni’
Policlinico Umberto I
University of Rome ‘Sapienza’, Rome, Italy

Owen L. Ala
Department of Orthopaedic Surgery
Hospital of the University of Pennsylvania
Philadelphia, PA, USA

Mina S. Ally
Stanford University
Stanford, CA, USA,

Stuart Archibald
Division of Otolaryngology-Head and Neck Surgery and
Division of Plastic Surgery
Department of Surgery
McMaster University
Hamilton, Canada

Behzad Ardehali
Department of Plastic Surgery
West Hertfordshire Hospital NHS Trust
Watford, UK

Maria Athanasiadou
Department of Plastic
Reconstructive and Aesthetic Surgery
Department of Plastic Surgery
University Hospital Gent, Gent, Belgium

Rebecca Ayers
Department of Plastic Surgery
Queen Victoria Hospital
East Grinstead, UK

Gurdip Kaur Azad
Mount Vernon Cancer Centre
Northwood, UK

Anthony Barker
NSW Rotation Plastic Surgery Registrar
Sydney, Australia

Alex Barnacle
Department of Radiology
Great Ormond Street Hospital for Children
London, UK


Phillip Blondeel
Department of Plastic
Reconstructive and Aesthetic Surgery
Department of Plastic Surgery
University Hospital Gent, Gent, Belgium

Michael M. Bottros
Department of Surgery
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
St Louis, MO, USA

Gráinne Bourke
Department of Plastic and Reconstructive Surgery
Leeds Teaching Hospitals
Leeds, UK

Kirsty U. Boyd
Division of Plastic Surgery
The Ottawa Hospital/Ottawa University
Ottawa, ON, Canada

Neil W. Bulstrode
Department of Plastic Surgery
Great Ormond Street Hospital for Children
London, UK

Nicola Burr
Department of Plastic Surgery
The Royal Free Hospital
London, UK

J. Henk Coert
Department of Plastic
Reconstructive and Hand Surgery
Erasmus University Medical Center
Rotterdam, The Netherlands

Carie Corner
Mount Vernon Cancer Centre
Northwood, UK

Contributors   ix

Alastair Carruthers

Dino Elyassnia

Department of Dermatology and Skin Science
University of British Columbia
Vancouver, BC, Canada

Marten Clinic of Plastic Surgery
San Francisco

Jean Carruthers

Kathryn Evans

Department of Ophthalmology and Visual Sciences
University of British Columbia
Vancouver, BC, Canada

Adil Ceydeli
Plastic Surgery Institute & Spa
Lynn Haven, FL, USA

James K. Chan
Kennedy Institute of Rheumatology
Nuffield Department of Orthopaedics
Rheumatology and Musculoskeletal Sciences
University of Oxford, UK

Sabrina Cugno
Department of Plastic and Reconstructive Surgery
Montreal Children’s Hospital
Montreal, Quebec, Canada

David David
The Australian Craniofacial Unit
Adelaide, Australia

Kristen M. Davidge
Division of Plastic and Reconstructive Surgery
University of Toronto
Toronto, ON, Canada

David J. Dunaway
Department of Craniofacial Surgery
Great Ormond Street Hospital
London, UK

Tong C. Duong
Plastic Surgery Institute & Spa
Lynn Haven

Jean‐Brice Duron
Department of Plastic Surgery
Hôpital Saint‐Louis
Paris, France

Peter Dziewulski
St Andrews Centre for Plastic Surgery and Burns
Essex, UK

Martin J. Elliott
Cardiothoracic Unit
Great Ormond Street Hospital
London, UK

Department of Urology
Great Ormond Street Hospital for Children
Great Ormond Street
London, UK

Jian Farhadi
Department of Plastic & Reconstructive Surgery
St Thomas’ Hospital
London, UK

Ross D. Farhadieh
Panthea Plastic Surgery Clinics
Sydney and Canberra Australia
Australian National University
Canberra, Australia

Michael Findlay
Department of Surgery
Stanford University
Stanford, CA, USA,
Division of Cancer Surgery
The Peter MacCallum Cancer Center
East Melbourne, Australia
The University of Melbourne Department of Surgery
Melbourne, Australia

Françoise Firmin
Clinique Georges Bizet
Paris, France

David M. Fisher
Department of Paediatric Plastic Surgery
The Hospital for Sick Children
Toronto, Ontario, Canada

Stephen Flood
Department of Plastic and Reconstructive Surgery
Austin Health
Heidelberg, Australia

Robert S. Flowers
Flowers Clinic
Hawaii, USA

Paige Fox
Department of Plastic and Reconstruction Surgery
Department of Surgery
Stanford University School of Medicine
Stanford University
Stanford, CA, USA

x   Contributors

Matthew D. Gardiner

Darryl J. Hodgkinson

Kennedy Institute of Rheumatology
Nuffield Department of Orthopaedics
Rheumatology and Musculoskeletal Sciences
University of Oxford, UK

The Cosmetic and Restorative Surgery Clinic
Double Bay
NSW, Australia

Adam C. Gascoigne

Stefan O.P. Hofer

Department of Anatomy and Neuroscience
University of Melbourne

Department of Surgery and Department of Surgical Oncology
Princess Margaret Hospital
University Health Network​
Toronto, ON, Canada

Ali M. Ghanem

Peter Hoogvliet

Department of Plastic Surgery
Barts and the London School of Medicine and Dentistry
London, UK

Aina V.H. Greig
Department of Plastic Surgery
St Thomas’ Hospital
London, UK

Adriaan O. Grobbelaar
Department of Plastic Surgery
The Royal Free Hospital
London, UK

Michael Gupta
Division of Otolaryngology-Head and Neck Surgery and
Division of Plastic Surgery
Department of Surgery
McMaster University
Hamilton, Canada

Bahman Guyuron
Department of Plastic Surgery
University Hospitals Case Medical Center
Cleveland, OH, USA

Elizabeth J. Hall‐Findlay
The Banff Plastic Surgery Centre
Alberta, Canada

Sam T. Hamra
Department of Plastic Surgery
University of Texas Southwestern Medical Center
Dallas, TX, USA

John Harper
Department of Dermatology
Great Ormond Street Hospital for Children
London, UK

Department of Rehabilitation Medicine
Erasmus University Medical Center
The Netherlands

Steven E.R. Hovius
Department of Plastic and Reconstructive Surgery
Erasmus MC University Medical Center
The Netherlands

Nigel Hunt
Craniofacial & Development Sciences
UCL Eastman Dental Institute
London, UK

Se-Hwang Liew
Department of Plastic Surgery
Alder Hey Children’s Hospital
Liverpool, UK

Navid Jallali
Department of Plastic Surgery
Charing Cross Hospital
London, UK

Barbara Jemec
Department of Plastic Surgery
The Royal Free Hospital
London, UK

T. Shane Johnson
Department of Orthopaedic Surgery
Hospital of the University of Pennsylvania
Philadelphia, PA, USA

Naresh Joshi

Division of Cancer Surgery
The Peter MacCallum Cancer Center
East Melbourne, Australia

Chelsea and Westminster Hospital
Cromwell Hospital
London and Imperial College School of Medicine
London, UK

Shehan Hettiaratchy

Mazyar Kanani

Michael A. Henderson

Academic Department of Military Surgery and Trauma
Royal Centre for Defence Medicine
Birmingham, UK

Cardiothoracic Unit
Great Ormond Street Hospital
London, UK

Contributors   xi

Veronica Kinsler

Irene M.J. Mathijssen

Department of Pediatric Dermatology
Great Ormond Street Hospital for Children NHS Trust
London, UK

Department of Plastic, Reconstructive Surgery
and Hand Surgery
Erasmus MC
University Medical Center Rotterdam
The Netherlands

Deepak Komath
Department of Oral and Maxillofacial Surgery
University College Hospital
London, UK

Richard D. Lawson
Department of Hand Surgery & Peripheral Nerve Surgery
Sydney Medical School
University of Sydney
Royal North Shore Hospital
St Leonards, Australia

Gregory McCarten
Department of Plastic, Reconstructive and Hand Surgery
The Canberra Hospital
Canberra, Australia

Alan A. McNab
Orbital Plastic and Lacrimal Clinic
Royal Victorian Eye and Ear Hospital
Melbourne, Australia

Jonathan I. Leckenby

Bryan C. Mendelson

Department of Plastic Surgery
The Royal Free Hospital
London, UK
Department of Molecular and Cell Biology
Harvard University
Cambridge, MA, USA

Paul Mittermiller

The Centre for Facial Plastic Surgery
Toorak, Victoria, Australia

Department of Plastic and Reconstruction Surgery
Department of Surgery
Stanford University School of Medicine, Stanford University
Stanford, CA, USA

Gordon K. Lee
Department of Plastic and Reconstruction Surgery
Department of Surgery
Stanford University School of Medicine
Stanford University
Stanford, CA, USA

Edwin J. Morrison

Nicholas Lee

Wayne A.J. Morrison

Department of Oral and Maxillofacial Surgery
Sheffield Teaching Hospitals
Sheffield, UK

O’Brien Institute and Department of Surgery
University of Melbourne
Victoria, Australia

L. Scott Levin
Department of Orthopaedic Surgery
Hospital of the University of Pennsylvania
Philadelphia, PA, USA

Tim Lloyd
Department of Oral and Maxillofacial Surgery
University College Hospital
London, UK

O’Brien Institute and Department of Surgery
University of Melbourne
Victoria, Australia

Andrew N. Morritt
Department of Plastic Surgery
Charing Cross Hospital
London, UK

Peter Mortimer
Department of Dermatological Medicine
St George’s Healthcare NHS Trust
London, UK

Susan E. Mackinnon
Department of Surgery
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
St Louis, MO, USA

Afshin Mosahebi

Timothy J. Marten

Imran Mushtaq

Marten Clinic of Plastic Surgery
San Francisco

Department of Urology
Great Ormond Street Hospital for Children
Great Ormond Street
London, UK

Department of Plastic Surgery
Royal Free Hospital
London, UK

xii   Contributors

Simon R. Myers

Marc Revol

Department of Plastic Surgery
Barts and the London School of Medicine and Dentistry
London, UK

Department of Plastic Surgery
Hôpital Saint‐Louis
Paris, France

Naghmeh Naderi

Dirk F. Richter

Welsh Centre of Burns and Plastic Surgery
Swansea, UK

Department of Plastic and Reconstructive Surgery
Wesseling, Germany

Jagdeep Nanchahal

Willem D. Rinkel

Kennedy Institute of Rheumatology
Nuffield Department of Orthopaedics
Rheumatology and Musculoskeletal Sciences
University of Oxford, UK

Tim H.J. Nijhuis
Department of Plastic and Reconstructive Surgery
Erasmus MC University Medical Center
The Netherlands

Dariush Nikkhah
Department of Plastic Surgery
Queen Victoria Hospital
East Grinstead, UK

Niri S. Niranjan
Department of Plastic & Reconstructive Surgery
St Andrews Centre
Broomfield Hospital
Chelmsford, UK

Ravinder Pabla
Department of Oral and Maxillofacial Surgery
University College Hospital
London, UK

Robert Pearl
Department of Plastic Surgery
Queen Victoria Hospital
East Grinstead, UK

Michael Pearse
Department of Orthopaedics
St Mary’s Major Trauma Centre
Imperial College Healthcare NHS Trust
London UK

Mark Pickford
Department of Plastic Surgery
Queen Victoria Hospital
East Grinstead, UK

Kelvin Ramsey
Department of Plastic & Reconstructive Surgery
The Royal Marsden NHS Foundation Trust
London, UK

Department of Plastic
Reconstructive and Hand Surgery
Erasmus University Medical Center
The Netherlands

Carlo Riccardo Rossi
Melanoma and Sarcoma Unit
Veneto Institute of Oncology IOV
Padova, Italy

Amir Sadri
Department of Plastic Surgery
Royal Free Hospital
London, UK

Konal Saha
Consultant Ophthalmologist and Oculoplastic Surgeon
London and Manchester, UK

Donald Sammut
Hand Surgeon
Circle Bath Hospital
Bath, UK

Marlene S. See
Department of Plastic Surgery
Charing Cross Hospital
London, UK

Alexander Seifalian
Centre for Nanotechnology & Regenerative Medicine
UCL Division of Surgery & Interventional Science
University College London
London, UK

Sujata Sharma
The Eastman Dental Hospital
London, UK

Maria Siemionow
Department of Orthopaedics
University of Illinois at Chicago
Chicago, IL, USA

Bran Sivakumar
Department of Plastic Surgery
Great Ormond Street Hospital
London, UK

Contributors   xiii

Paul Smith

William A. Townley

Department of Plastic Surgery
Great Ormond Street Hospital
London, UK

Guy’s and St. Thomas’ NHS Foundation Trust
London, UK

Antonio Sommariva
Melanoma and Sarcoma Unit
Veneto Institute of Oncology IOV
Padova, Italy

Brian C. Sommerlad
Department of Plastic Surgery
Great Ormond Street Hospital for Children NHS Trust
London, UK

Robert M.T. Staruch

Ian A. Trail
Centre for Hand and Upper Limb Surgery
Wrightington Hospital
Wigan, UK

Andreas Tromaropoulos
Department of Plastic, Reconstructive and Aesthetic Surgery
Department of Plastic Surgery
University Hospital Gent
Gent, Belgium

Chung‐Kan Tsao

Academic Department of Military Surgery and Trauma
Royal Centre for Defence Medicine
Birmingham, UK

Department of Plastic and Reconstructive Surgery
Chang Gung Memorial Hospital
Chang Gung University and Medical College
Taipei, Taiwan

David Stepnick

Sarah Tucker

Department of Plastic Surgery
University Hospitals Case Medical Center

David A. Stewart
Department of Hand Surgery & Peripheral Nerve Surgery
Sydney Medical School, University of Sydney
Royal North Shore Hospital
St Leonards, Australia

Alexander Stoff
Practice for Plastic and Reconstructive Surgery
PAN Clinic, Cologne

Marc C. Swan
Department of Paediatric Plastic Surgery
The Hospital for Sick Children
Toronto, Ontario, Canada

Youssef Tahiri
Department of Plastic Surgery
Riley Hospital for Children
Indianapolis, IN, USA

Achilleas Thoma
Division of Otolaryngology-Head and Neck Surgery and
Division of Plastic Surgery
Department of Surgery
McMaster University
Hamilton, Canada

Michael A. Tonkin
Department of Hand Surgery & Peripheral Nerve Surgery
Sydney Medical School, University of Sydney
Royal North Shore Hospital
St Leonards, Australia

Department of Plastic Surgery, John Radcliffe Hospital
Oxford, UK

Sarah L. Versnel
Department of Plastic, Reconstructive Surgery
and Hand Surgery
Erasmus MC
University Medical Center Rotterdam
Rotterdam, The Netherlands

Christopher Glenn Wallace
Department of Plastic and Reconstructive Surgery
Chang Gung Memorial Hospital
Chang Gung University and Medical College
Taipei, Taiwan

Adam C. Watts
Centre for Hand and Upper Limb Surgery
Wrightington Hospital
Wigan, UK

Renata V. Weber
Department of Surgery
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
St Louis, MO, USA

Fu‐Chan Wei
Department of Plastic and Reconstructive Surgery
Chang Gung Memorial Hospital
Chang Gung University and Medical College
Taipei, Taiwan

Catherine Weng
Department of Plastic Surgery
University Hospitals Case Medical Center
Cleveland, OH, USA

xiv   Contributors

Paul M.N. Werker

Andrew Yee

Department of Plastic Surgery
University Medical Centre Groningen
Groningen, The Netherlands

Department of Surgery
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
St Louis, MO, USA

Georgina Williams
Department of Plastic Surgery
John Radcliffe Hospital
Oxford, UK

Simon Withey

Lara Yildirimer
Centre for Nanotechnology & Regenerative Medicine
UCL Division of Surgery & Interventional Science
University College London
London, UK

Consultant Plastic Surgeon
Department of Plastic Surgery
Royal Free Hospital
London, UK

Yasamin Ziabari

Chin‐Ho Wong

Fatih Zor

W. Aesthetic Plastic Surgery
Mt Elizabeth Novena Specialist Center

The Central London School of Anaesthesia
Royal Free Hospital
London, UK

Department of Plastic and Reconstructive Surgery
Gulhane Military Medical Academy
Ankara, Turkey


Plastic surgery is a unique specialty, defined by concept rather
than anatomical area. As such, it has grown enormously over
the last 70 years and continues to evolve with changes in technology, improved understanding of anatomy and patient-­
centred outcomes. This progression leads to a vast and ever
increasing array of new techniques and options for reconstruction, benefiting both our patients and the many other
medical and surgical specialties that consult the plastic surgeon. With many tools at their disposal and the wide array of
clinical maladies that they treat, the plastic surgeon has
evolved into a problem solver. This synergy between plastic
surgery and other surgical specialties has enabled these other
specialties to utilize the problem-solving skills of the plastic
surgeon to expand their therapeutic spectrum and tackle
increasingly more difficult problems. However, to be an effective problem solver it is incumbent on the plastic surgeon to be
familiar with the latest developments of our broad and expanding field. This highlights the necessity of a single-volume text
that is comprehensive and practical, covering the full spectrum of plastic surgery and presenting the current state of the
art of our specialty. This is exactly what the editors of Plastic
and reconstructive surgery: Approaches and techniques set out
to achieve in producing this excellent textbook.
It is truly an international effort at all levels, as the editors,
from Australia (Ross D. Farhadieh), the UK (Neil W. Bulstrode)
and Canada (Sabrina Cugno), have joined forces to recruit over
130 international contributors and produce a resource of over
1100 pages that provides a well-organized and thorough, yet
succinct, text of the essentials of current plastic surgery. The
editors are all highly qualified and accomplished young plastic
surgeons, and they have been able to provide a global perspective of our specialty. Many of the contributors are worldrenowned experts; however, there is also a new generation of
young rising stars whose contributions are equally good,
providing a new, fresh and contemporary feel.

Each chapter is clearly organized and provides an overview of
the principles and the most recently described basic science
essentials, as well as clinical applications and techniques, and
pertinent bibliography for additional reading. The critical core
information is provided for each topic, providing an excellent
synopsis and reference for the student and practitioner.
Although aimed primarily at the trainee, I believe that it will
also serve as an excellent and quick reference for the seasoned
practising surgeon faced with complex problems requiring
reconstruction throughout the body. It will also be an especially
useful resource for senior plastic surgery trainees preparing to
take their Board and Fellowship exams. The final chapter,
dealing specifically with the certification process and fellowship
exams, is interesting, and provides useful information and different perspectives of the qualifying processes in the British,
European, Australian and North American systems.
It has been an honour and pleasure for me to have been asked
to contribute the Foreword to this new textbook, which very
nicely fulfills one of the traditions of surgery of passing down
knowledge from one generation of problem solvers to the next.
The new generation is likely to face even more complex ­problems
and, using the latest techniques, solve them more elegantly than
we can now. But the principles in plastic surgery never change,
and this textbook provides the intrinsic fundamentals that all
trainees must know, even as the field is ever expanding.
I congratulate the editors for their Herculean effort in recruiting
an international cast of distinguished surgeons and thank the
authors for flawlessly summarizing the huge avalanche of new
information that has graced our specialty; finally, I thank the
publishers, Wiley Blackwell, for producing this timely, impressive and comprehensive plastic surgery compendium.
Julian J. Pribaz
Professor of Surgery
Harvard Medical School



To inspirational mentors and dedicated apprentices everywhere.



During my plastic surgery training there appeared to be a
plethora of summary and broad-stroke single-volume plastic
surgery textbooks, all of which lacked adequate detail.
Conversely I would encounter multivolume behemoths, detailed
reference texts that always seemed leaden and difficult to digest.
In my experience neither of these options fully addressed the
needs of a trainee surgeon, or for that matter a more senior surgeon. Thus was born, on a long flight from Sydney to London,
the notion of compiling a single-volume textbook that seeks to
achieve the perfect balance of detail and palatability. To that
end, in compiling this textbook we approached some of the
world’s leading authorities in the various fields of plastic surgery. This was with the belief that not only could readers benefit
from such experts’ enormous experience, but they could also
gain practical insights from the ability of such experts to sift
through the ever increasing volume of literature and distil what
is relevant and applicable to everyday practice.
My co-conspirators in this endeavour, Mr Neil Bulstrode
from Great Ormond Street and Dr Sabrina Cugno from
Montreal Children’s Hospital, had the perfect blend of enthusiasm and sense of humour to see this work through. I am grateful to them for their advice, time, effort and, most importantly,
their friendship, all of which made this compendium possible. I
also wish to thank all of our colleagues who took time out of
their busy lives to make this volume possible. It has been an
extraordinary experience for all of us to collaborate on this
project. Our special thanks go to Professor Julian Pribaz for

being kind enough to review the volume and write the Foreword.
We also wish to thank Wiley Blackwell for their continued
support for this project.
On a personal note I wish to thank my mother Tadjvar, my
brother Arash and wife Yassi for enduring me during the last 2
years, and for their unwavering support. My parents have been
my guiding light in demonstrating the importance of a strong
work ethic and integrity. I also wish to thank Messrs Neil
Bulstrode and Adriaan Grobbelaar for the extraordinary
fellowship opportunities and friendship they have afforded me.
I am very grateful to Messrs Ash Mosahebi and Jian Farhadi,
who kindly accommodated me in their operating theatres and
taught me a great deal about the art of plastic surgery. In
Melbourne I wish to extend my sincere thanks to Mr Bryan
Mendelson, who during my visits showed immense patience
and generosity in teaching me the philosophy and techniques of
facial aesthetic surgery. My gratitude also goes to Mr Stephen
Flood, who illustrated by example a sensible approach to plastic
surgery and kindness in mentorship; this continues to serve as
an aspiration. As a plastic surgeon I am most indebted to
Professor Wayne Morrison, who has curiosity, humility, dedication to teaching and generosity of will and spirit, tempered with
a crisp sense of humour, in equal inspirational measure. It was
truly an honour and a privilege to serve as his registrar.
Rostam D. Farhadieh
January 2015


About the companion website

This book is accompanied by a companion website:
The website includes:
• Powerpoints of all figures from the book for downloading


Part I

Basic science and principles

Chapter 1

Wound healing and scar formation
Simon R. Myers and Ali M. Ghanem
Department of Plastic Surgery, Barts and the London School of Medicine and Dentistry, London, UK

Type I – Classical cutaneous wound
A wound, in the context of skin, is a breach in the barrier that
distinguishes an organism from its environment. The process
through which the organism works in order to address this
breach is ‘wound healing’ which, because of the important role
the skin plays in the survival of the organism, is quite literally
vital, and conserved through evolution. In the normal course of
events, a lower species accepts tissue loss and heals a wound by
exposure, licking, picking and, at the molecular level, scarring.
The single most important impact on wound healing in humans
is the early closure of wounds, by apposition with sutures in
incisional wounds, and skin replacement in excisional wounds.
Humans can deny significant skin and composite tissue loss by
a ‘like for like’ replacement in the specialty of plastic and
reconstructive surgery, and here we can boast a form of
‘supranormal wound healing’.1

Wound healing classifications
There are many ways to classify wound healing. In simple terms,
we can consider:
• four phases – coagulation, inflammation, fibroplasia and
• four types – fetal, adult, acute and chronic;
• four ages – young, plateau, regressing, atrophic; and
• two systems of healing – epidermal and dermal.
We can also classify wound healing in terms of clinical features
and their wound management.

Phases of wound healing
Wound healing can be considered a process of four sequential
but overlapping phases by which the body closes a breach in
tissue continuity. There are many ways to define such a complex

process. Key to understanding the standard classification of the
process is a consideration of: the timing, the cellular activation
or influx and the chemical mediators.2
This immediate response to cutaneous injury involves two
­cascades: the clotting cascade, with the formation of platelet clot
which adheres to the collagen exposed following endothelial
disruption; and the complement cascade and complement‐
mediated vasodilatation. Histamine (released by mast cell
degranulation) and kinins contribute to vasodilatation and
increased vascular permeability. The first cells involved then are
platelets and mast cells, and the first mediators histamine,
kinins, platelet‐derived growth factor (PDGF) and transforming growth factor beta (TGF‐β). The increasing interest in
platelet‐rich plasma (PRP) clinically in regenerative medicine is
based on these early cascades.
Between the time of injury and around 4 days post injury, the
clinical signs of inflammation develop. Classically these are
redness, swelling, pain and loss of function. These result
from inflammatory mediators and the capillary leak into the
extracellular space that they coordinate. The next inflammatory
cell type to arrive at the wound is the macrophage, followed by
neutrophils and then lymphocytes. Keratinocytes in the wound
edge and follicle remnants migrate and proliferate, and fibroblasts are chemo‐attracted, and become activated.
From day 4, and for 2–4 weeks, the wound bed becomes vascularized, and type III collagen is laid down by fibroblasts to
replace any dermal loss. In the absence of epidermal cover, this
appears clinically as granulation tissue. Closed wounds become
red and raised for a while. Hydrated glycosaminoglycans form a
ground substance for the collagen fibrils. This phase is characterized by fibroblast proliferation, but also by keratinocyte

Plastic and Reconstructive Surgery: Approaches and Techniques, First Edition. Edited by Ross D. Farhadieh, Neil W. Bulstrode and Sabrina Cugno.
© 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.


4    Basic science and principles

From a few weeks to 18 months or more, the wound goes
through a long phase of remodeling. Fibroblasts mature into
myofibroblasts to contract the wound. Type III collagen is gradually replaced by type I collagen. Disorganized collagen becomes
Repair versus regeneration
There are significant differences between the wound healing
seen in fetal life and that seen in postnatal life. So‐called scarless healing occurs for a period in the fetus, however this is not
absolute but dependent on gestational age and wound size.3 In
late fetal life scarring does occur, and before this point in time,
a large enough wound will still result in scarring. In postnatal
life, scarring is the inevitable and permanent consequence of
wounding beyond the epidermal basement membrane. An
adult lower vertebrate such as a salamander can regenerate an
amputated limb but will not aspire to climb Mount Everest or
graduate from Oxford! Although regenerative medicine
attempts to harness the same plasticity seen in lower vertebrate
regeneration, what is generally achieved is only ‘partial regeneration’, and not replacement of like with like. The ongoing
concern in work to manipulate adult/somatic stem cells to
achieve true regeneration is around a loss of control and the
risk of carcinogenesis.

Acute versus chronic wound healing
Acute wound healing is hard to distinguish absolutely from
chronic wound healing, and the processes at a cell and molecular level may be similar.4 Chronic wound healing occurs when
healing takes longer than might be anticipated in a fit, healthy
person, and is often associated with comorbidity. Such wounds
seem to become stuck in the inflammatory or proliferative/
fibroplastic phases. Local wound management can only usefully
begin following an assessment and optimization of systemic
comorbid conditions.

Epithelial/epidermal versus mesenchymal/
dermal wound healing
The epidermis provides the ultimate barrier between the body
and environment. The main cell type is the keratinocyte.
Regeneration occurs from a population of follicle stem cells.5
The dermis provides the structural support to the epidermis and
other related adnexae. The main dermal cell type is the fibroblast.
As in embryogenesis, there is ongoing ‘cross‐talk’ between the
epidermis and dermis in somatic cutaneous wound healing, the
epidermal element of which has been relatively underplayed.
Even less consideration has been given to the contribution of
subcutaneous fat to cross‐talk.

Wound healing and scarring
In many ways, wound healing and scarring are inseparable – the
one leads to the other at some level and over time. When does a
wound become a scar? That will probably depend at a molecular
level on very early wounding and wound management events.
Although a scar is the inevitable and permanent consequence of
postnatal wounding beyond the basement membrane and a compromise between regeneration and repair, at a clinical level, its
significance is largely patient related and subjective. This can now
be captured clinically by the Patient and Observer Scar Assessment
Scale (POSAS), which draws patients into their own management.6
Most patients would perceive a wound as a scar from the time
that the wound is no longer open, and often that equates to the
absence of exudate and any requirement for dressing care.
Clinically, even a normotrophic scar will go through a natural progression to maturity. When young, it will be active. Most young
scars exhibit features of hypertrophy. Most scars then go through a
plateau period of relatively little clinical change in the absence of
treatment. Most scars then go through a period of regression
of inflammatory signs and symptoms, and eventually settle to a
mature state. Some scars, after many months or years, and sometimes because of treatment, become very thin, pale and atrophic.
When then does a normotrophic scar become a pathological
scar? A normotrophic scar results from uneventful primary
healing, but there is wide variation with age, site and skin type,
and a period of hypertrophy is not unusual. Hypertrophic
­scarring is classically seen in paediatric burn wounds that have
struggled to heal.7 The scar becomes red, raised, painful and itchy
around 2–3 months following wound closure, particularly in
wounds that have taken more than three weeks to heal. The scar
settles over 18 months to 2 years, but often incompletely.
Hypertrophic scars occur particularly in extreme Fitzpatrick skin
types. Presumably, there is a bell curve distribution within the
population, where those at the extreme end of hypertrophic scarring could be termed pathological. Although a keloid scar shares
many of the features of a hypertrophic scar, and may represent an
extreme example of the same, it is defined by extension beyond
the confines of the injury, by almost inevitable progression
beyond 2 years, seldom regressing; by being refractory to most
treatments and recurring within 4–6 months of cessation of most
treatments; and by behaving pathologically like a benign tumour.
Understanding such an extreme phenotype may prove key to the
effective management of more normotrophic scarring.

Epidermal wound healing
Adult epidermal stem cell biology is relatively well understood.
Keratinocyte stem cells reside primarily in the bulge region of
the hair follicle and, by asymmetric division, populate the
interfollicular basement membrane with transit amplifying
cells.8 These divide a number of times to provide the differentiating cells of the stratifying epidermis. A huge array of small

Wound healing and scar formation    5

peptides are involved in coordinating the response to epidermal
wounding by autocrine, paracrine and juxtacrine signaling.9 In
a human model of epidermal healing, a number of phases of
keratinocyte activity are suggested, as shown in Figure 1.1.10
Acute activation
Almost immediately following wounding, the epidermis expresses
interleukin 1β (IL‐1β) and interleukin 6 (IL‐6) and the dermis
TGF‐β1, committing transit amplifying cells to mitosis. Although
TGB‐β1 is antiproliferative, it is pro‐migratory to keratinocytes.11
Early activation
Towards 24 h following wounding, keratinocyte proliferation
and migration are clear. Epidermal expression of TGF‐α and
IL‐6 is accompanied by dermal fibroblast keratinocyte growth
factor (KGF) and IL‐6 expression. A paracrine loop of epidermal
IL‐1β induction of the potent keratinocyte mitogen KGF from
dermal fibroblasts seems likely.12 TGF‐α both is a keratinocyte
mitogen and induces the migratory K6/K16 keratinocyte cyto-

skeletal phenotype in the suprabasal compartment.13 It may also
recruit nearby follicles by juxtacrine signalling.14
Over weeks, homeostasis is restored, with relatively late activation
of the bulge to restore the transit amplifying population.

Dermal wound healing
Wound healing studies have concentrated far more on the
dermis than epidermis, and particularly on macrophage production of TGF‐β isoforms. This multifunctional growth factor
appears to play a key role in dermal healing and scarring.15
Although the TGF‐β1 isoform promotes scarring, the TGF‐β3
isoform appears to have the opposite effect.16 Juvista (Avotermin)
was developed to improve the quality of normotrophic scarring,
but failed in a European phase 3 clinical trial.17 TGF‐β, however,
remains a key pharmaceutical target.

Interleukin-1 beta mRNA

Interleukin-6 mRNA


Relative OD

Relative OD






12 24
Time (h)



TGF-alpha mRNA

12 24
Time (h)



TGF-beta1 mRNA




Relative OD

Relative OD













12 24
Time (h)






TGF-alpha mRNA expression in roof,
edge and base

12 24
Time (h)






and growth factor gene expression in
human suction blister wound healing.
TGF, transforming growth factor; KGF,
keratinocyte growth factor; relative OD,
relative optical density.

Relative OD

Figure 1.1 Temporo‐spatial cytokine

Intergrated band
beta actin band
OD × 100 (%)







Time post-wounding (h)




12 24
Time (h)

6    Basic science and principles

A preoccupation with one growth factor, albeit a powerful,
multifunctional factor with isoforms of different action, and for
each a dose‐dependent heterogeneity of responses, is arguably
to ignore the complexity of wound healing cascades. There are
many factors at play, often pleiotropic, and there is significant
redundancy – so that many factors can contribute to the same
outcome (i.e. rapid closure by scar). The growth factor that has
shown most promise when delivered alone is PDGF.18
The dermis is far more than an extracellular matrix populated
by fibroblasts. It hosts a vascular network (arterial, venous and lymphatic) and a neural network, and supports the follicle and other
adnexal stem cell niches. It must also, it seems, interact with the
subcutaneous fat. One approach to tissue engineering to provide for
wound tissue loss is to synthesize an appropriate nanotechnology
scaffold for key cellular elements to populate and develop. This can
be biofunctionalized by incorporating a latent growth factor.19
Wounds can be classified based on clinical management and
outcome as shown in Table 1.1.

‘Normal’/primary incisional wound
healing (type Ia)
Incisional wound healing occurs following surgical access, or
‘incisional’ or lacerating trauma.20 In the former, the wound will
begin sterile, and in the latter some degree of contamination is
usual. In neither instance is there significant tissue loss. Classically,
in modern medical practice, these wounds are formally closed,

although the timing of that closure will vary, affecting the quality
of the healing processes and the scar that results.
Early closure (type Iai)
If an incisional wound is closed directly, the healing will tend to
be optimal. Elective surgical wounds are closed at the end of the
procedure performed under sterile conditions. Traumatic lacerating wounds will generally be cleaned and closed the same day,
and before significant bacterial colonization occurs. A relatively
arbitrary time limit to early closure has evolved in practice of
48 h from injury. Beyond this, it is considered likely that colonization may be significant enough to deleteriously affect healing,
and as a consequence the quality of scarring, which may become
Late closure (type Iaii)
If a type Ia wound is sutured after 48 h, wound colonization may
result in infection, dehiscence and delayed healing.
Counterintuitively, according to current dogma if the wound is
left open until day 4 or 5, as in ‘delayed primary closure’, satisfactory results can be achieved at a stage when the inflammatory
response has become established – although a recent Cochrane
review found no evidence for this.21
No closure (type Iaiii)
An incisional wound beyond the epidermal basement m
­ embrane
that is left unclosed will gape and behave much like a deep excisional wound, healing by classical ‘secondary intent’.22 The time

Table 1.1 A revised wound classification based on clinical management and outcome

Type I: Classical

Wound ± intervention

Character of healing

(a) ‘Normal’/primary incisional – incisional,
no tissue loss

(i) Closed early (<48 h)

Low risk of infection
Minimal line scar
Increased risk infection
Increased risk chronicity
More significant scar
Healing by granulation (similar to type Ibii), but in
absence of tissue loss)
High risk of chronicity
Rapid re‐epithelialization (<10 days)
Minimal clinical scar
Slow/absent re‐epithelialization
High risk of infection and chronicity
Closure by scar

(ii) Closed late (>48 h)

(iii) Unclosed

‘Normal’/secondary excisional – tangential
tissue loss, no replacement

(i) Above mid‐dermis
(ii) Below mid‐dermis

Type II: Neoclassical
(a) ‘Supranormal’ by skin replacement

(b) ‘Supranormal’ with apparent
acceptance of tissue loss

(i) Early split‐ or full‐thickness skin grafting of
type Ibii)
(ii) Biotechnological skin replacements (Cuono
technique, in vitro composite grafts)
(i) Type Ibi treated with cultured keratinocyte
allografts or vapour‐permeable membrane
(ii) Chronic full‐thickness wound treated with
cultured keratinocyte allografts or vapour‐
permeable membrane

Present gold standards
Cosmetic and functional problems remain
Donor defect
Ideally autologous and with viable cellular elements
Opportunity to improve on types Ibii and IIai
Follicle recruitment by activated extended follicle
Simulation of an acute wound environment

Wound healing and scar formation    7

to healing will be slow, because closure will rely on wound base
contraction and edge re‐epithelialization. As a consequence, the
quality of the scar will tend to ‘pathological’.

‘Normal’/secondary excisional wound
healing (type Ib)
Where surgery requires skin excision, or cutaneous trauma is
tangential (e.g. burn injury or friction loss) and the tissue loss is
not replaced, then the time to healing and the scar quality
will depend on the depth of the loss. Re‐epithelialization and
restoration of barrier function from adnexal remnants will be
slower, the deeper the injury.
Above mid‐dermis (type Ibi)
Tangential tissue loss above the mid‐dermis leaves a partial‐
thickness wound that will heal in around one week under ideal
circumstances, and result in a ‘controllable’ scar – as in the
surgical split‐thickness skin graft donor site. If a traumatic
tangential injury clearly reaches the mid‐dermis acutely (i.e. a
mid‐dermal burn injury), then optimal wound management
is key to prevent extension of the tissue loss to type Ibii. In
extreme Fitzpatrick types, even these type Ibi wounds can scar
Below mid‐dermis (type Ibii)
Tangential tissue loss below the mid‐dermis leaves a partial‐
thickness wound that will take three weeks or more to heal, and
as a consequence will be more liable to chronicity and significant
scarring.7 It is at this depth, or beyond, that intervention is
considered. A full‐thickness defect can only re‐epithelialize
from the wound edge, and will otherwise close substantially by
scar contraction of the base.

Abnormal wound healing
Systemic and local factors may reduce the quality of the skin
and/or affect wound healing adversely. These are important to
recognize and optimize.
Systemic factors
Systemic factors may be congenital or acquired. There are a
handful of congenital conditions that affect the processes of
healing, and in some instances the clinical quality of the skin
and healing. A range of defects in collagen synthesis is seen in
Ehlers–Danlos syndrome, and healing is poor.23 The skin is
­vulnerable, and healing slow in epidermolysis bullosa, where for
example, in the junctional variant, laminin 5 is deficient in the
epidermal basement membrane zone.24 The autosomal recessive
premature ageing condition progeria manifests many features of
normal ‘acquired’ ageing.25

With age, the changes in healing processes are fairly global,
resulting in a delay in wound closure and a reduction in wound
strength. How much these changes are the result of increasing
comorbidities associated with age, rather than age itself, is not
entirely clear. Other acquired systemic factors include: nutrition, drugs, diabetes and smoking. Vitamin C deficiency is the
classical example of a nutritional factor involved in wound
healing. Although scurvy is not likely with Western diets,
vitamin C is an essential cofactor for collagen synthesis. Vitamin
A deficiency is also rare in the developed world, but vitamin A
can reverse steroid‐induced collagenase activity. Zinc is important to many enzyme systems, and deficiency can be seen in
large burn injury. In those same injuries, albumin can plummet
to around 10 g/L, and although this will delay healing, closure
can be achieved.
Obesity is epidemic now in the Western world, and associated
with many comorbidities and wound complications following
surgery.26 Plastic surgery reconstructions following bariatric
surgery are challenging. Large blood vessels will have developed
to support the tissue volume, and these may contribute to
postoperative bleeding complications. Despite these hypertrophic vessels, tissue perfusion may be poor, and the tissue
lymphoedematous and critically colonized. Furthermore, closure
after such excisional surgery is by definition under tension, so
that infection and dehiscence are more common.
Anti‐inflammatory systemic glucocorticoids, non‐steroidal
anti‐inflammatory drugs and chemotherapy drugs globally
­suppress the cellular responses to wounding. Chemotherapeutic
angiogenesis inhibitors, such as bevacizumab, a vascular
endothelial growth factor‐neutralizing antibody fragment used
in colonic cancer, cannot be prescribed six weeks before or after
surgery to limit the wound healing risks.27
Diabetes mellitus may affect healing in a variety of complex
ways, particularly in the lower limbs. Patients with diabetes
are susceptible to atherosclerosis in larger vessels, and tissue
oxygen delivery is further reduced by the stiffness of the red
blood cells, and the higher oxygen affinity of glycosylated
haemoglobin.28 These effects are compounded by any neuropathy, and impaired cellular immunity, phagocytosis and
bacterial killing.
Smoking may affect wound healing in both immediate and
longer term ways.29 Nicotine causes sympathetic vasoconstriction, and carbon monoxide shifts the oxygen dissociation curve
to the left. Long‐term smoking accelerates atherosclerotic
changes. Smoking appears to be a particular problem in surgery
to superficial soft tissue planes, where wide skin undermining
with the sacrifice of multiple perforators, and closure under
tension are combined, as in abdominoplasty surgery.
Local factors
One of the most controllable local factors for incisional wounds
is surgical technique and the handling of tissue. Tissue handling
within the specialty can be observed, par excellence, under the
microscope during a microvascular anastomosis, where poor

8    Basic science and principles

handling results in anastamotic thrombosis.30 Local factors
often reflect systemic comorbidities, so that poor blood supply
and oxygen delivery, and even critical bacterial colonization are
more often than not a local manifestation of a systemic factor.
Conversely, the radiotherapy that results in local thromboendarteritis obliterans and causes healing problems over time may
also have systemic effects.31 In terms of recurrence, radiotherapy
is the most effective treatment for keloid scars, damping down
the ‘overhealing’ provided it follows extralesional excision
directly.32 Breaches in the skin are inevitably colonized by
commensals. With time and increasing bacterial number, the
body mounts an inflammatory response, and the colonization is
termed critical. Critical colonization is not anticipated until
around 48 h as a rule of thumb. Once 105 organisms are present
per gram of tissue, the wound may be considered infected.
Chronicity and some level of colonization go hand in hand.
Bacterial biofilms are prevalent in chronic wounds, including
anaerobic organisms not isolated by standard culture systems, and
this is an area of particular current interest in such wounds33 –
and also of course in subcutaneous/cavity wounding and
scarring (e.g. breast capsular contracture).34


There is a sense that the skin is constantly subclinically injured
to some degree by sheer forces, and indeed even the force of
gravity.35 This may drive the baseline turnover of the skin. The
effects of physico‐mechanical forces on cell behavior, termed
mechanotransduction, are becoming increasingly recognized
and understood in wound healing.36 In 1861, Karl Langer
observed that the skin exhibits intrinsic tension,37 and Langer’s
lines, defined by the direction in which circular excisional
wounds will elongate to ellipses by anatomic site, are used today
to orientate excisional surgery. Tensegrity describes the way in
which mechanical forces regulate biological systems via perturbations in structural architecture; disruption of tensional
integrity triggers cellular pathways that restore mechanical
homeostasis.38 Cells also actively generate intracellular tension,
cell traction forces, as they interact with their environment
during, for example, migration.39 A cell‐centric view of
­mechanotransduction is, however, inadequate. Conformational
changes in the extracellular matrix by mechanical forces can
reveal cryptic binding sites and expose growth factors. Non‐
structural, extracellular, matricellular proteins (e.g. connective
tissue growth factor) are increasingly implicated in the regulation
of healing and scar formation.40 Mechanosensing in the skin is a
feature not just of fibroblasts but also of keratinocytes and
nociceptors. It is quite possible that physical cues during wound
healing direct, in part, stem cell fate within that niche.
Any therapeutic effects of silicone gels, pressure garments
and linear taping may work through mechanical offloading and
mechanotransduction pathways. The use of Botox A to control
tension across healing facial scars and improve scar quality is an
interesting new approach.41 Vacuum‐assisted closure has
become a common approach to complex wound management,

and although poorly understood, must rely to a large extent on

Type II – Neoclassical cutaneous
wound healing

‘Supranormal’ healing by skin replacement
(type IIa)
Classically, intervention to close a wound was sometimes considered ‘tertiary’ wound healing. The great variety of techniques
now available suggest a more structured classification.
Early split‐thickness or full‐thickness skin
grafting of type Ibii (type IIai)
Those tangential traumatic or excisional wounds that are
unlikely to heal in a reasonable timescale and are therefore
likely to scar are most commonly closed with split‐thickness
skin autograft. Where the wound is full thickness, the environment optimal and the defect limited in size, a full‐thickness
autograft will provide a superior reconstruction. Of course,
any number of local and distant skin and fasciocutaneous
flaps are considered for defects that have resulted in an
ungraftable bed, and this category of skin replacement feeds
into other classifications of flap reconstruction. Skin and fasciocutaneous free flaps are increasingly being used to close
defects in hostile comorbid conditions (e.g. in ‘vasculoplastics’
Biotechnological skin replacements (type IIaii)
In recent years, products, often xenograft in nature, have been
developed to provide the quality of a full‐thickness graft reconstruction from a split‐thickness skin graft donor site. ‘Dermal
regeneration templates’, such as Integra, engraft to provide a
‘neodermis’ to support a thin autograft in two operative stages.43
A single‐stage Integra system has been available following the
success of single‐stage Matriderm grafting.44 Included here also
is the system developed by Cuono and colleagues that combines
allograft dermis with autologous cultured keratinocytes in the
closure of full‐thickness burn excision beds.45 Cultured keratinocyte technology represents one of the most established forms
of somatic stem cell therapy, and sits most coherently within
plastic and reconstructive surgery.

‘Supranormal’ healing with apparent
acceptance of tissue loss (type IIb)
When tangential tissue loss is accepted and no apparent
attempt is made to replace like with like to the level of loss,
then there are still interventions that seem to present some
clinical advantage. George Winter presented his understanding
of tangential wound healing in a porcine partial‐thickness

Wound healing and scar formation    9

excisional model that included both edge and base contributions to restoration of epidermal barrier function, and
introduced the world to the concept of ‘moist wound healing’.
This spawned a massive industry in moist wound healing
dressing systems, initially vapour‐permeable membranes.46
Although this transformed the ‘dry’ wound management of
the time, it has not proven a panacea, and far more sophisticated biological systems have evolved since (see below). The
clinical evidence base for these, however, has been slow to
evolve on a cost basis, and so marketplaces have yet to develop
around economy of scale.
Type Ibi treated with cultured keratinocyte
allograft or biological dressing (type IIbi)
Cultured keratinocyte allografts have been used for decades to
accelerate partial‐thickness wound healing.47 Although they
do not survive transplantation long term,48 they present a
­temporary and coordinated ‘growth factor factory’. It may also
be that they provide a juxtacrine mechanism for ‘discontinuous
follicle recruitment’ by bridging adnexal remnants separated
by tangential partial‐thickness wounding.10 Biobrane is a
­conforming bilayer of porcine collagen and nylon.49 It is at least
haemostatic and adheres to a clean partial‐thickness wound
until shed when the epidermal barrier has been restored. The
evidence for its efficacy and detail of any mechanism has never
been established, but a role for the limitation of colonization of
adherence seems likely.
Chronic full‐thickness wound treated with
cultured keratinocyte allograft or biological
dressing (type IIbii)
Chronic full‐thickness wounds are a huge financial burden
to any healthcare system, and generally associated with
comorbidity.50 Any comorbid condition should be optimized
in the first instance. There then may be some further benefit
from cell‐based therapy or biological dressings. Both cultured
keratinocyte allografts and autografts have been used to treat
such wounds.51 It is suggested that even with poor clinical
autograft take, a more acute healing picture is seen, at least
clinically – healing is ‘kick‐started’. The wound bed can be
modulated with, for example, hyaluronic acid, an important
component of the embryonic extracellular matrix, to improve
clinical take, perhaps by supporting a niche‐like stem cell

craniofacial traumatic wounds with the same intent many
decades ago.54 It has been suggested that any effect on healing
and scarring results not from the grafted fat directly, much of
which is lost, but from stimulation of a local mesenchymal stem
cell response. The current controversy is around the method of
enrichment of autologous fat to provide safe augmentation long
term, and the resolution of this will run parallel with resolution
of controversy around any effect on healing and scarring. A
recent randomized controlled study in normal human volunteers demonstrated that enrichment of autologous fat with cultured autologous adipose‐derived stem cells was significantly
more effective, in graft survival terms, than a more standard

Lower limb lymphovenous disease is a recognized cause of
recurrent cellulitis and chronic wound healing. There is a newly
recognized patient base in the morbid obese and postbariatric
population, and with the evolution of supra‐microsurgical techniques, the promise of new therapies (e.g. lymphovenous anastomosis and lymph node transplantation).56

Modern genomic and proteomic techniques allow us to define
the processes that control tissue volume and its nature in
healing at a molecular level – broadly: migration, proliferation,
differentiation and apoptosis. Those techniques require very
little material from biopsy, and we should expect to see more
evidence from controlled longitudinal human studies available
to support our understanding of the different types of healing.
The sheer complexity of the pathways and interactions within
countless networks will require a systiomics, or systems
biology, approach, calling on applied mathematics and computer modelling. Resources to support controlled human
studies of wound healing and interventions are limited in part
by a perception that the area is mundane. There are, however,
many gaps in our basic understanding of what are quite
fundamental processes. Cell‐based therapies are expensive, but
will continue to offer the most rationale wound management
solutions until our understanding is more complete.
Longitudinal cost–benefit analyses of novel therapies remain
few and far between.

There has been a huge recent interest in fat grafting, not only for
augmentation including following subcision of indented scars
and scar‐related fat atrophy, but also to improve healing and the
quality of the overlying scar.53 It is fascinating to reflect that Sir
Harold Gillies may have used whole‐fat grafts in acute closure of

1 Myers S. Keratinocyte growth and differentiation in cutaneous
wound healing and cultured keratinocyte grafting. PhD thesis,
University of London, 1999.
2 Masters in Burn Care. Queen Mary University, London.

10    Basic science and principles

3 Longaker MT, Whitby DJ, Adzick NS, et al. Studies in fetal wound
healing, VI. Second and early third trimester fetal wounds demonstrate rapid collagen deposition without scar formation. Journal of
Pediatric Surgery 1990;25:63–68; discussion 68–69.
4 Monaco JL, Lawrence WT. Acute wound healing an overview.
Clinics in Plastic Surgery 2003;30:1–12. Review.
5 Lavker RM, Sun TT, Oshima H, et al. Hair follicle stem cells. Journal
of Investigative Dermatology Symposium Proceedings 2003;8:28–38.
6 Nicholas RS, Falvey H, Lemonas P, et al. Patient‐related keloid scar
assessment and outcome measures. Plastic Reconstructive Surgery
7 Deitch EA, Wheelahan TM, Rose MP, Clothier J, Cotter J.
Hypertrophic burn scars: analysis of variables. Journal of Trauma
8 Bickenbach JR. Isolation, characterization, and culture of epithelial
stem cells. Methods in Molecular Biology 2005;289:97–102.
9 Navsaria HA, Myers SR, Leigh IM, McKay IA. Culturing skin in
vitro for wound therapy. Trends in Biotechnology 1995;13:91–100.
10 Myers SR, Leigh IM, Navsaria H. Epidermal repair results from
activation of follicular and epidermal progenitor keratinocytes
mediated by a growth factor cascade. Wound Repair and
Regeneration 2007;15:693–701.
11 Jeong HW, Kim IS. TGF‐β1 enhances βig‐h3‐mediated keratinocyte cell migration through the α3β1 integrin and PI3K. Journal of
Cellular Biochemistry 2004;92:770–780.
12 Angel P, Szabowski A. Function of AP‐1 target genes in mesenchymal‐epithelial cross‐talk in skin. Biochemical Pharmacology
2002;64:949–956. Review.
13 Jiang CK, Magnaldo T, Ohtsuki M, Freedberg IM, Bernerd F,
Blumenberg M. Epidermal growth factor and transforming growth
factor alpha specifically induce the activation‐ and hyperproliferative‐associated keratins 6 and 16. Proceedings of the National
Academy of Sciences of the USA 1993;90:6786–6790.
14 Owen MR, Sherratt JA, Myers SR. How far can a juxtacrine signal
travel? Proceedings of the Royal Society B: Biological Sciences
15 O’Kane S, Ferguson MW. Transforming growth factor beta s and
wound healing. International Journal of Biochemistry and Cell
Biology 1997;29:63–78. Review.
16 Occleston NL, Laverty HG, O’Kane S, Ferguson MW. Prevention
and reduction of scarring in the skin by transforming growth factor
beta 3 (TGFbeta3): from laboratory discovery to clinical pharmaceutical. Journal of Biomaterials Science. Polymer Edition
2008;19:1047–1063. Review.
17 Renovo. Juvista EU Phase 3 trial results. 2011. http://www.renovo.
com/en/news/juvista‐eu‐phase‐3‐trial‐results (accessed 23 June
18 Steed DL. Clinical evaluation of recombinant human platelet‐
derived growth factor for the treatment of lower extremity ulcers.
Plastic and Reconstructive Surgery 2006;117(Suppl.):143S–149S;
discussion 150S–151S. Review.
19 Lim EH, Sardinha JP, Myers S, Stevens M. Latent transforming
growth factor‐beta1 functionalised electrospun scaffolds promote
human cartilage differentiation: Towards an engineered cartilage
construct. Archives of Plastic Surgery 2013;40:676–686.
20 Singer AJ, Clark RAF. Cutaneous wound healing. New England
Journal of Medicine 1999;341:738–746.

21 Eliya‐Masamba MC, Banda GW. Primary closure versus delayed
closure for non bite traumatic wounds within 24 hours post injury.
Cochrane Database of Systematic Reviews 2013;10:CD008574.
22 Ward PD, London N, Collar R. Role of secondary intention healing.
Facial Plastic Surgery 2013;29:346–350.
23 Whitaker IS, Rozen WM, Cairns SA, Howes J, Pope FM, Hamish
Laing J. Molecular genetic and clinical review of Ehlers‐Danlos
Type VIIA: implications for management by the plastic surgeon in
a multidisciplinary setting. Journal of Plastic, Reconstructive &
Aesthetic Surgery 2009;62:589–594.
24 Fine JD. Inherited epidermolysis bullosa: past, present, and future.
Annals of the New York Academy of Sciences 2010;1194:213–222.
25 Rosengardten Y, McKenna T, Grochová D, Eriksson M. Stem cell
depletion in Hutchinson‐Gilford progeria syndrome. Aging Cell
26 Albino FP, Koltz PF, Gusenoff JA. A comparative analysis and
systematic review of the wound‐healing milieu: implications for
body contouring after massive weight loss. Plastic and Reconstructive
Surgery 2009;124:1675–1682.
27 Lemmens L, Claes V, Uzzell M. Managing patients with metastatic
colorectal cancer on bevacizumab. British Journal of Nursing
28 Tsourdi E, Barthel A, Rietzsch H, Reichel A, Bornstein SR.
Current aspects in the pathophysiology and treatment of chronic
wounds in diabetes mellitus. BioMed Research International
29 Sørensen LT. Wound healing and infection in surgery: the pathophysiological impact of smoking, smoking cessation, and nicotine
replacement therapy: a systematic review. Annals of Surgery
30 Ramachandran S, Ghanem AM, Myers SR. Assessment of microsurgery competency‐where are we now? Microsurgery 2013;33:
31 Hubenak JR, Zhang Q, Branch CD, Kronowitz SJ. Mechanisms of
injury to normal tissue after radiotherapy: a review. Plastic and
Reconstructive Surgery 2014;133:49e–56e.
32 Ogawa R, Huang C, Akaishi S, et al. Analysis of surgical treatments
for earlobe keloids: analysis of 174 lesions in 145 patients. Plastic
and Reconstructive Surgery 2013;132:818e–825e.
33 Bertesteanu S, Triaridis S, Stankovic M, Lazar V, Chifiriuc MC,
Vlad M, Grigore R. Polymicrobial wound infections:
Pathophysiology and current therapeutic approaches. International
Journal of Pharmaceutics 2014;463:119–126.
34 Tamboto H, Vickery K, Deva AK. Subclinical (biofilm) infection
causes capsular contracture in a porcine model following augmentation mammaplasty. Plastic and Reconstructive Surgery 2010;
35 Farahani RM, DiPietro LA. Microgravity and the implications for
wound healing. International Wound Journal 2008;5:552–561.
36 Wong VW, Akaishi S, Longaker MT, Gurtner GC. Pushing back:
wound mechanotransduction in repair and regeneration. Journal of
Investigative Dermatology 2011;131:2186–2196.
37 [No authors listed]. On the anatomy and physiology of the skin:
conclusions by Professor K. Langer. British Journal of Plastic Surgery
38 Ingber DE. Tensegrity I. Cell structure and hierarchical systems
biology. Journal of Cell Science 2003;116:1157–1173. Review.
39 Wang JH, Lin JS. Cell traction force and measurement methods.
Biomechanics and Modeling in Mechanobiology 2007;6:361–371.

Wound healing and scar formation    11

40 Eckes B, Nischt R, Krieg T. Cell‐matrix interactions in dermal
repair and scarring. Fibrogenesis and Tissue Repair 2010;3:4.
41 Ziade M, Domergue S, Batifol D, et al. Use of botulinum toxin type
A to improve treatment of facial wounds: a prospective randomised
study. Journal of Plastic, Reconstructive & Aesthetic Surgery
42 Kim CY, Kim YH. Supermicrosurgical reconstruction of large
defects on ischemic extremities using supercharging techniques on
latissimus dorsi perforator flaps. Plastic and Reconstructive Surgery
43 Loss M, Wedler V, Künzi W, Meuli‐Simmen C, Meyer VE. Artificial
skin, split‐thickness autograft and cultured autologous keratinocytes combined to treat a severe burn injury of 93% of TBSA. Burns
44 Haslik W, Kamolz LP, Nathschläger G, Andel H, Meissl G, Frey M.
First experiences with the collagen‐elastin matrix Matriderm as a
dermal substitute in severe burn injuries of the hand. Burns
45 Cuono CB, Langdon R, Birchall N, Barttelbort S, McGuire J.
Composite autologous‐allogenic skin replacement: Development
and clinical application. Plastic and Reconstructive Surgery
46 Winter GD. Epidermal regeneration studied in the domestic pig. In:
HI Maibach, DT Rovee (eds), Epidermal Regeneration, pp. 71–112.
Chicago: Year Book Publishing; 1972.
47 Phillips TJ, Gilchrest BA. Cultured epidermal allografts as biological
wound dressings. Progress in Clinical and Biological Research

48 Griffiths M, Ojeh N, Livingstone R, Price R, Navsaria H. Survival of
Apligraf in acute human wounds. Tissue Engineering 2004;10:
49 Yang JY, Tsai YC, Noordhoff MS. Clinical comparison of
commercially available Biobrane preparations. Burns 1989;15:
50 Harding KG, Morris HL, Patel GK. Healing chronic wounds. British
Medical Journal 2002;324:160.
51 Phillips TJ, Gilchrest BA. Cultured epidermal grafts in the
treatment of leg ulcers. Advanced Dermatology 1990;5:33–48;
discussion 49.
52 Myers SR, Partha VN, Soranzo C, Price RD, Navsaria HA.
Hyalomatrix: a temporary epidermal barrier, hyaluronan delivery,
and neodermis induction system for keratinocyte stem cell therapy.
Tissue Engineering 2007;13:2733–2741.
53 Mojallal A, Lequeux C, Shipkov C, et al. Improvement of skin
quality after fat grafting: clinical observation and an animal study.
Plastic and Reconstructive Surgery 2009;124:765–774.
54 Gillies HD, Millard DR. The Principles and Art of Plastic Surgery.
Boston, MA: Little, Brown, & Company; 1957.
55 Kølle SF, Fischer‐Nielsen A, Mathiasen AB, et al. Enrichment of
autologous fat grafts with ex‐vivo expanded adipose tissue‐derived
stem cells for graft survival: a randomised placebo‐controlled trial.
Lancet 2013;382(9898):1113–1120.
56 Koshima I, Narushima M, Yamamoto Y, Mihara M, Iida T. Recent
advancement on surgical treatments for lymphedema. Annals of
Vascular Disease 2012;5:409–415.

Chapter 2

Basic skin flaps and blood supply
Edwin J. Morrison and Wayne A.J. Morrison
O’Brien Institute and Department of Surgery, University of Melbourne, Melbourne, Victoria, Australia

Flap surgery is the commonest procedure in plastic surgery and
is the essence of the discipline. Critical to its success is an
understanding of the soft tissues’ blood supply and its compliance
and mobility. As all flaps ‘rob Peter to pay Paul’ it is also about
conceptualizing the secondary defect and minimizing its consequences. The art and craft of plastic surgery necessarily requires
an aesthetic sense and experience.

For almost a century Manchot1 and Salmon’s2 detailed studies of
the skin’s vascular design were overlooked by clinicians. With
limited understanding and the simplistic belief that the skin’s
blood supply was based on a random distribution in the
horizontal plane, local flap surgery was unpredictable and its
progress curtailed by an adherence to dogmatic rules such as
length‐to‐width ratios and the superiority of proximal over distally
based flaps. A generation of surgeons failed to appreciate the
simple observation that circumferentially incising large skin
lesions in the process of their elevation and removal did not
compromise their circulation. The explanation, of course, was
that their blood supply was derived from the depths and not
horizontally. Surgeons no doubt were aware of the circulation
from below but the reality was that sufficient numbers of these
vessels had to be divided to permit the flaps to transpose or
rotate, and ultimately it was the base fed by the horizontal input
that was the critical lifeline. Not until it was shown that flaps
could be completely islanded and still live was it possible to
move flaps based on these deep vessels. In 1970, Milton elegantly highlighted the fallacy of the length‐to‐breadth ratio
using pig studies to demonstrate the existence of arterialized
zones of the integument that would survive over extreme lengths
even if completely islanded, provided they retained their arterial
source at their base.3 These exciting findings breathed life back
into the clinical study of the soft tissue’s blood supply. True to

the adage that history is written by the victors, the blind
acceptance of random patterns proposed by Harold Gillies4 was
derived in part from the neglect of the publications of the
Dutchman Johannes Esser (1917), Gillies’ plastic surgery
counterpart for the German army in World War I.5 Instead of
the complex tube pedicle, Esser performed one‐stage ‘arterialized
biological island flaps’ based on the palpable arteries of the
head and neck region. He clearly recognized the fundamental
concepts of the flap’s axial blood supply.
The first clinical application of the new ‘axial pattern’ concept
was the groin flap, based on the superficial circumflex iliac
branch of the femoral artery.6 The wide arc of rotation of this
very long and narrow‐based flap of like tissue expanded the
single‐stage reconstructive options for the regional wounds
previously manageable only by multistage transfers requiring
protracted immobilization and hospitalization.
What had been anecdotally reported in the early literature and
had been empirically adopted in practice, the Indian forehead
flap for nasal reconstruction and the epigastric flap in the lower
abdomen, now made sense.7 The former flap unwittingly captured the supratrochlear/supraorbital vessels and the latter the
superficial epigastrics.
With this new awareness, omentum, although not skin, was
quickly recognized for its application as an arterialized flap by
virtue of it wearing its blood supply on the outside of its surface.
The vasculature could be pruned to critical arterial pedicles and
tunnelled from the abdominal cavity to cover far‐flung defects
and then skin grafted.
Other fundamental concepts of skin blood supply were soon
elucidated, such as the myocutaneous flap, where the skin
relied for its blood supply on vessels perforating through the
underlying muscle. Providing the muscle was raised on its
blood supply, the overlying skin would survive even when
completely islanded. As muscles typically are vascularized
often by a single source at their origin, the muscle pedicle
added even further length to the arc of flap rotation. The
­gracilis8 and latissimus dorsi myocutaneous flap,9 reinventing
the earlier findings of Tansini,10 were the first to be described

Plastic and Reconstructive Surgery: Approaches and Techniques, First Edition. Edited by Ross D. Farhadieh, Neil W. Bulstrode and Sabrina Cugno.
© 2015 John Wiley & Sons, Ltd. Published 2015 by John Wiley & Sons, Ltd.


Basic skin flaps and blood supply    13

and widely adopted. Muscle flaps without skin followed and
the anatomical articulation of their vascular basis further
expanded the options for one‐stage locoregional reconstructions (Figure 2.1).11
Fasciocutaneous flaps recognized for the first time that a
significant contribution to skin blood supply was in the plane of
the fascia and provided this fascia was included within the flap,
large areas of previously unreliably vascularized skin would
survive.12 This particularly applied to the lower limb. Initially
they were designed on the assumption their vascularity was in
the plane of the fascia and in the limbs flaps were based proximally to capture its source. It was soon clear that much of this
fasciocutaneous blood supply derived from perforating branches
of named deep vessels emerging vertically between septofascial
muscle planes from deep axial vessels, and furthermore these
zones could be completely islanded from their proximal
connections. Mathes and Nahai have classified fascia and
fasciocutaneous flaps into three types: type A, direct cutaneous
pedicle; type B, septocutaneous pedicle and type C, musculocutaneous pedicle.11
This led to the unifying concept of angiosome blood supply,
where the tissue is considered as a three‐dimensional territory
or somite structure, akin to vertebrate embryological
development, where not only skin but whole mesenchymal
somites including skin, muscle and bone have a vascular zone.13
This was supported by meticulous cadaver studies and expanded
the earlier work of Manchot and Salmon.
Concurrent with this explosion in the understanding of the
skin’s blood supply, advances were being made in microvascular surgical techniques and instrumentation, initially by the
neurosurgeons,14 but quickly adopted for plastic surgery. These
techniques had immediate applications for replantation, but
the possibility of transplanting toes and territories of skin
by anastomosing specific vessels was now opportune. The
Type I

Type II

first such flap was an omental transfer to the scalp.15 Skin
flaps soon followed.16–18

Current understanding of the blood
supply to skin
Flap surgery involves the transfer of tissue with its vascularity
preserved. This requires an understanding of the physiology
and anatomy of the integument’s blood supply.
Physiology of the skin’s blood supply
The blood supply (12.8 mL/100 g/min) to the skin greatly
exceeds its metabolic needs because of its homeostatic role in
thermoregulation. Perfusion of the skin’s capillary beds is
regulated by both local and systemic neurohumoral mechanisms.
These act on precapillary sphincters and arteriovenous anastomoses, influencing the filling and emptying of the dermal
plexuses and in turn not just the circulation of the skin and
subcutaneous tissue, but also insensible heat loss and venous
return to the heart.
Immediately after elevation of a skin flap, perfusion is transiently reduced by transection of blood vessels, inflammation, a
hyperadrenergic state (associated with sympathectomy) and
possible reperfusion injury. With no pharmacological means to
reliably manipulate these effects at the capillary level, unless the
design and execution of a flap includes an adequate circulation
to overcome this ischaemic phase the flap may fail.
Anatomy of the skin’s blood supply
The circulation of the skin and its underlying structures consists
of a three‐dimensional continuous vascular network.
Conceptually this can be broken into horizontal and vertical
components. Running parallel with the skin, and constituting

Type IV
Type V
Type III

Gluteus maximus
Tensor fascia lata



Latirsimus dorsi

Figure 2.1 Mathes and Nahai classification.
Patterns of vascular anatomy: type I, one
vascular pedicle; type II, dominant
pedicle(s) and minor pedicle(s); type III,
two dominant pedicles; type IV, segmental
vascular pedicles; type V, one dominant
pedicle and secondary segmental pedicles.
Source: Mathes and Nahai, 1981.11
Reproduced with permission of Lippincott
Williams & Wilkins.

14    Basic science and principles

the horizontal component of the skin’s blood supply are the
numerous vascular plexuses (Figure 2.2a). Most important of
these are the subdermal plexus and the deeper suprafascial
plexus. Where no deep fascia exists, an equivalent structure
such as the panniculus carnosus (e.g. platysma, palmaris brevis
and the dartos muscles in humans) serves a similar purpose.
These are the vascular bases of (random) cutaneous and fasciocutaneous flaps (Table 2.1).
Vessels arising vertically from their source arteries either
directly supply the skin, or indirectly supply the skin after
nourishing deeper structures such as muscle and bone. These
are known as ‘perforators’ and they arise from the deep named
vessels, along their axial course, with highest density over the
less mobile soft tissue that is adherent to underying septa. This
is particularly evident in the limbs. Perforators anastomose
initially with the prefascial plexus before continuing on to the
subdermal plexus and are the vascular pedicles on which islands
of skin and other soft tissue components may be based
(Figure 2.2b). It follows that separate islands of skin and fascia,
each based on a separate perforator but ultimately deriving from
a common arterial axial vessel, can be raised on this common
axis. This permits complex reconstructions with multiple
independently oriented flaps.
The blood supply of the skin and its underlying structures can
also be divided into vascular territories, or angiosomes.13 Each
territory is connected to its adjacent territory by bidirectional
arterioles, the direction being interchangeable and determined
by the relative pressure in each territory. The angiosome is the
vascular basis for composite flaps.

Drainage of the skin is by a reciprocal three‐dimensional
venous network of avalvular bidirectional veins with a dominant
subdermal component. This in turn drains into large‐calibre
subcutaneous veins or venae comitantes that run with perforators.
Superficial lymphatics follow subcutaneous veins and deeper
lymphatics follow arteries.
Venous flaps are generally transferred as free microvascular
flaps, where the flap is elevated superficially with only the
venous system, thereby obtaining a thin flap and reducing
morbidity.19 The flap is arterialized through its veins by
anastomosing them to an artery in varying configurations, the
tissue being nourished by retrograde perfusion. Understandably,
their reliability is inconsistent.

Indications for flaps
Skin defects should ideally be repaired by replacement of what is
missing and generally this will include fat as well as skin. In
many cases the local laxity of skin will allow direct closure and
conversion of the deformity to a linear scar. Sometimes, however, although the wound can be technically closed directly this
may create a dish deformity with dog‐ears at either end. Removal
of these dog‐ears only aggravates the underlying problem of
missing tissue. Here, well‐designed local flaps from redundant
areas can redistribute the tension so as to preserve available
tissue and restore normal contour.
Defects that cannot be closed directly will need grafting or
replacement with flaps. Skin grafts take by engaging with the



Hypodermis Panniculus



Figure 2.2 (a, b) Illustration showing subdermal plexus and suprafascial plexus. Also perforators.

Direct cutaneous
artery and vein

Basic skin flaps and blood supply    15

Table 2.1 Classification of flaps based on movement and blood supply
(a) Local skin flaps
In‐continuity – rare
Islanded (e.g. V–Y)
In‐continuity (e.g. rhomboid,
bilobed, Z‐plasty)
Islanded (e.g. propeller)
Rotation (e.g. scalp)
(b) Regional (locoregional) flaps
Cutaneous (e.g. groin flap,
forehead, rhinoplasty, Abbe
lip flap)
Neurovascular island flaps
(e.g. digits)
(c) Distant flaps
Two‐stage pedicle (e.g. cross
finger, groin to hand
Multistaged ‘waltzed’ pedicle
(e.g. tube pedicle)
(d) Free flaps
(e) Prelamination and
(f) Allotransplantation –
Opportunistic free flap allograft in
patient simultaneously requiring
organ transplant (e.g. abdominal
wall with bowel transplant)
(g) Tissue engineering –
Although prefabricated and
prelaminated flaps were the early
prototypes of tissue engineered
flaps, cell‐seeded artificial scaffolds
and/or adipogenic matrices are
being investigated

Blood supply

Random – intact skin base
Random – subcutaneous base
Perforator base
Random – intact skin base
Perforator base
Random; arterialized

Subcutaneous arterialized

Arterial pedicle
Septo(myo)fascial perforators
Neurovascular A–V pedicles

Random; arterialized

Arterial – microvascular anastomosis
Venous blood supply


vasculature of the underlying bed. They are inappropriate in
avascular circumstances (exposed bone, tendon, fracture sites,
irradiated tissue and mobile beds) and here flaps are required as
they possess an independent blood supply. Grafts often contract
and may be a poor colour match; where the underlying fatty
tissue is missing, they may result in contour defects and adherence to deeper tissues. Apart from burns and extensive injuries
where large areas of skin are required it is generally accepted,
particularly with the wide range of flap options available, that
skin grafts are inferior to flaps and are rarely first choice. Other
exceptions include the dorsum of the hand and foot, where thin
skin is required. Few flaps meet these needs. Full‐thickness skin
grafts have an important place on the face, where the tissues are
thin with little subcutaneous fat (eyelids, inner canthus,

proximal nose and sometimes nasal tip). Flaps from regions
adjacent to these sites are invariably too thick.
Elsewhere, flaps are indicated. Small defects are closed by
local flaps from the immediate area and find their greatest
expression in the head and neck region, particularly in
association with skin cancer resection. Flaps may be in‐continuity
(transposition, rotation) or islanded (advancement), and their
execution defines the quality of the plastic surgeon. Because of
their near‐perfect tissue match the well‐executed local flap may
be difficult to spot. Larger defects will require locoregional flaps
from a distance and are most likely transposed on their narrow
base to maximize their reach (arc of rotation). Because their
skin texture, colour and thickness may not match that of the
original defect they may require subsequent revisional surgery.
Such distant flaps may be fasciocutaneous, myocutaneous or
muscle flaps with skin grafts. Composites of tissue may be
included – muscle or tendon, fascia or bone – allowing
functional reconstruction of complex defects. Their vascular
basis will be on the vascular pedicle alone or together with their
associated skin, muscle or fascial carrier respectively. Usually
the secondary defect will be directly closable.
For very large skin grafts or complex defects where a specialized tissue is needed, such as functional muscle or bone,
innervated or hair‐bearing skin, free flaps are indicated. These
are based on a vascular pedicle and require microvascular
anastomosis. Prefabricated (arterialized zone of specialized skin
created by the implantation of a vascular pedicle so as to render
it transferable as a free flap suitable to match a specific defect)
and prelaminated flaps (the neovascularization of composite
tissue around a vascular pedicle for subsequent transfer) are
more sophisticated free flap indications. Tubed pedicle flaps are
now rare but still find applications where there is an absence of
recipient vessels at the defect site (Figure 2.3).

Design and application of flaps
Two concurrent considerations are critical to the successful
planning of local flaps: (1) blood supply and (2) availability of
adjacent mobile tissue (laxity).
Flap design and blood supply
The first consideration in designing a skin flap is to determine
whether it will be viable. The vascular limitations on a flap’s
dimensions are not completely understood, though the principles to follow are helpful. Some flaps in some sites seem more
predictable than others, despite the principles, and confidence
in local flap surgery comes with trial and error, and ultimately
experience with what works and what does not.
The simplest skin flaps are based on the subdermal plexus,
the richness of which varies around the body (Figure 2.4). Vague
length‐to‐breadth ratios govern the size of these so‐called
random flaps, with the only certainty being that a flap whose
length equals its width will be viable anywhere on the body.

16    Basic science and principles

Figure 2.3 Tubed pedicle flaps are largely historic. This patient with osteomyelitis in his leg underwent a tubed pedicle flap from the abdomen using the

hand as a carrier. Source: Dr Edwin J. Morrison. Reproduced with permission.

Anatomic and
vascular base

Vascular base


Anatomic base


Vascular base


Figure 2.4 (a) Random flap; (b) axial flap; (c) musculocutaenous flap.

Source: Dr Edwin J. Morrison, Department of Surgery, University of
Melbourne. Reproduced with permission.

Because of the markedly increased vascularity of the face,
such flaps can tolerate significantly higher length‐to‐breadth
The area of conventional flaps can be increased by capture of
an additional vascular component. Axial flaps, which have a
known arterial pedicle coursing along their axis in the superficial
plane (e.g. groin flap, forehead flap), may be further enlarged in
a random fashion, or by incorporating some of the skin supplied
by the next cutaneous perforator in the adjacent angiosome.20, 21
Skin flaps elevated with the deep fascia and therefore with the
suprafascial plexus intact create a fasciocutaneous flap, which
can also be elevated with significantly higher length‐to‐breadth
dimensions. Musculocutaneous flaps are yet another variant.
Length‐to‐breadth ratios of random flaps and the volume of
tissue in axial flaps can also be increased by harnessing the delay
phenomenon. Although its mechanism is incompletely understood, vascular delay is a well‐established surgical technique
capable of improving the vascularity and reliability of a flap
prior to its definitive elevation and inset.22 It involves the
strategic division of the flap’s blood supply so as to deliver a
sublethal ischaemic insult. This is postulated to cause vessel
dilatation, ischaemic preconditioning and neovascularization. It
may also be beneficial in routine flap surgery on high‐risk
patients who are obese, smokers or who have undergone
previous irradiation.
Flaps incorporating the horizontal component of the integument’s blood supply are usefully classified as flaps in‐continuity.
For similarly obvious reasons, flaps that are circumferentially
incised through dermis or deep fascia (or its equivalent) are
island flaps whose vascular supply is through perforators
(Figure 2.5).
Apart from the native vascularity, caution needs to be taken
when flaps are folded to repair complex defects or pass over
convex surfaces. Similarly, tight closure when flaps are too small
and failure to recognize previous scars in the region may compromise vascularity. Haematoma is perhaps the greatest enemy
of local flaps, because of increased tension and the inflammatory
toxicity of the underlying blood clot over time.

Basic skin flaps and blood supply    17

Random/random cutaneous
Pattern skin flaps

Axial/arterial pattern skin flaps

Dermal-subdermal plexus

Direct cutaneous a. & v.

Perforating aa.

Segmental a.

1. Peninsular Axial Pattern Flap


1. Random Cutaneous Flap
2. Island Axial Pattern Flap

2. Myocutaneous Random Flap

3. Free Flap

Figure 2.5 In‐continuity versus island flaps. Source: Daniel & Kerrigan, Principles and Physiology of Skin Flap Surgery. In: McCarthy, Plastic Surgery.

Elsevier, 1990. Reproduced with permission.

Flap design and movement
Having determined that flap tissue is available and that it will be
viable, the next question is how it can be moved to cover the
defect. Flaps move by way of transposition, rotation or advancement though in reality their movement usually involves some
combination of all of these and is often aided by initial partial
direct closure of the defect itself.
The first principle of local flap design is to pinch up the skin
immediately adjacent to the defect and serially march around its
perimeter until the zone of maximally lax skin is detected. It is
from this tissue that the flap will be elevated. Because the tissue
is lax, it follows that the secondary defect should close directly.

Flaps in‐continuity

Most local flaps are totally elevated from their bed but retain a
critical skin base for their vascularity. This especially pertains to
transposition and rotation flaps.

Transposition flaps

Lax tissue immediately adjacent to the defect is elevated and transposed, sometimes across intact skin bridges. This creates a secondary
defect that is usually closable directly because of the laxity.
The rhomboid flap is a particularly useful example of such a
flap.24 It is commonly used in skin cancer surgery and the principles can be applied to all transpositions. The anticipated defect is
conceived in the form of a rhomboid (unequal parallelogram). A
diagonal across the rhomboid is extended the same distance as
the length of an adjacent side of the defect into the zone of laxity
(a through b to c). A diagonal across the rhomboid is extended
the same distance as the length of an adjacent side of the defect

into the zone of laxity (ac = ce). A line is then directed backwards
from the limit of this point (e) parallel with the side of the defect
(ef). The flap thus outlined is elevated and transposed into the
defect. Preoperatively if point (f) is estimated to be able to
approximate to point (c) then the secondary defect will close (see
Figure 30.4a). Selecting the shorter diagonal generally facilitates
flap closure because the flap requires less angulation. In some
situations the adjacent tissue has not enough laxity to permit closure of the secondary defect and a second flap from the more lax
tissue adjacent to this defect will close the tertiary defect (bilobed
flap). When flaps are used to cover exposed bone or other non‐
graftable defects, transposition flaps must be used even if the
adjacent zone will not permit direct closure, and here skin grafts
are used for the secondary defect (Figure 2.6)
The other common application of the transposition flap is in
association with the Z‐plasty, a fundamental design concept in
plastic surgery (Figure 2.7). Z‐Plasties are used to release
(lengthen) tight or webbed scars, redirect scars into a more
favourable alignment and, in combination with linear access
incisions, to prevent secondary linear contracture (e.g.
Dupuytren disease). The traditional Z‐plasty design involves an
axial incision along the course of the scar. A back‐cut extends
from one end of the linear incision into the adjacent tissue at 60°
for the same length as the axial incision. A second back‐cut the
same length is now made on the opposite side of the line, commencing at the other end of the line and directed to the first.
This creates an equal‐limbed Z incision with its diagonal in the
axis of the original scar and flaps at 60°. By interdigitating
(transposing) the two flaps created by the design across the midline, the diagonal will now change at right angles to the original

18    Basic science and principles










Figure 2.6 The rhomboid flap design, execution and outcome for a temple defect. Note the pinch test and the attempt to position the secondary scar in the

natural crease lines of the forehead. Source: Grabb & Smith, 1991.23 Reproduced with permission of Lippincott, Williams & Wilkins.

axis. This way the scar is partially redirected and, provided the
planning is accurate, it should ideally fall within an existing
crease line. It is estimated that with a 60° angle transposition the
original length of the scar axis will increase by 75% (angle proportional to change in length).
To achieve maximum correction of tight scars it is essential
to completely remove the entire underlying scar so that the
­contracture is fully released. Often it is unrealistic to close 60°

flaps, and smaller angles are required at the expense of lesser
lengthening. In fact, when there is not much contracture, the flaps
are used to redirect scars rather than increasing length, which is
undesirable as it will simply create large redundant dog‐ears.
As with all flaps, tissue is borrowed from one place to give to
another. Z‐Plasties lengthen at the expense of reduction in
width. They are n