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GRABB AND SMITH'S
GRABB AND SMITH'S
PLASTIC SURGERY
PLASTIC SURGERY
Seventh Edition
Seventh Edition
GRABB AND SMITH'S
GRABB AND SMITH'S
PLASTIC SURGERY
PLASTIC SURGERY

Editor-in-Chief

Charles H. Thorne, MD Associate Professor of Plastic Surgery NYU Medical Center New York, New
Charles H. Thorne, MD
Associate Professor of Plastic Surgery
NYU Medical Center
New York, New York

Editors

Kevin C. Chung, MD, MS Charles B. G. de Nancrede Professor of Surgery Section of
Kevin C. Chung, MD, MS
Charles B. G. de Nancrede Professor of Surgery
Section of Plastic Surgery, Department of Surgery
Professor of Orthopaedic Surgery
Assistant Dean for Faculty Affairs
Associate Director of Global REACH
University of Michigan Medical School
Ann Arbor, Michigan
Arun K. Gosain, MD Division Head, Plastic Surgery Ann & Robert H. Lurie Children's Hospital
Arun K. Gosain, MD
Division Head, Plastic Surgery
Ann & Robert H. Lurie Children's Hospital of Chicago
Professor of Plastic Surgery
Northwestern University Feinberg School of Medicine
Chicago, Illinois
Geoffrey C. Gurtner, MD Professor, Department of Surgery Stanford University School of Medicine Stanford, California
Geoffrey C. Gurtner, MD
Professor, Department of Surgery
Stanford University School of Medicine
Stanford, California
Seventh Edition
Seventh Edition
Babak J. Mehrara, MD Associate Attending, Department of Surgery Memorial Sloan-Kettering Cancer Center Associate
Babak J. Mehrara, MD
Associate Attending, Department of Surgery
Memorial Sloan-Kettering Cancer Center
Associate Professor of Surgery
Weill Cornell University Medical Center
New York, New York
J. Peter Rubin, MD
J. Peter Rubin, MD

UPMC Endowed Professor and Chair, Department of Plastic Surgery Professor of Bioengineering Director, Life After Weight Loss Body Contouring Program University of Pittsburgh and UPMC Pittsburgh, Pennsylvania

University of Pittsburgh and UPMC Pittsburgh, Pennsylvania ScoH l. Spear, MD Professor, Department of Plastic Surgery
ScoH l. Spear, MD Professor, Department of Plastic Surgery Georgetown University Medical Center Washington, District
ScoH l. Spear, MD
Professor, Department of Plastic Surgery
Georgetown University Medical Center
Washington, District of Columbia
•
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10 9 8 7 6 5 4 3 2 1 Library of Congress Cataloging-in-Publication Data
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Library of Congress Cataloging-in-Publication Data
Grabb and Smith's plastic surgery.- Seventh edition I editor-in-chief, Charles H. Thome; editors,
Kevin C. Chung, Arun Gosain, Geoffrey C. Gurtner, Babak Joseph Mehrara, J. Peter Rubin, Scott
L. Spear.
p.;cm. Plastic surgery Preceded by Grabb and Smith's plastic surgery I editor-in-chief, Charles H. Thorne
p.;cm.
Plastic surgery
Preceded by Grabb and Smith's plastic surgery I editor-in-chief, Charles H. Thorne
[et al.] ;
editors Robert W. Beasley
[et al.]. 6th ed. 2007.
Includes bibliographical rekrences and index.
ISBN 978-1-4511-0955-9
I. Thorne, Charles, 1952- editor of compilation. II. Chung, Kevin C., editor of compilation. III.
Gosain, Arun, editor of compilation. IV. Guntner, Geoffrey C., editor of compilation. V. Mehrara,
Babak Joseph, editor of compilation. VI. Title: Plastic surgery.
[DNLM: 1. Reconstructive Surgical Procedures. 2. Cosmetic Techniques. 3. Surgery, Plastic.

W0600]

RD118

617.9'5-dc23 2. Cosmetic Techniques. 3. Surgery, Plastic. W0600] RD118 2013017779 Care has been taken to confirm the

2013017779

Care has been taken to confirm the accuracy of the information presented and to describe
Care has been taken to confirm the accuracy of the information presented and to describe
generally accepted practices. However, the authors, editors, and publisher are not responsible for
errors or omissions or for any consequences from application of the information in this book and
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of the contents of the publication. Application of the information in a particular situation remains
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The authors, editors, and publisher have exerted every effort to ensure that drug selection
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To our patients who have inspired, humbled, frustrated, and taught us, and without whom this
To our patients who have inspired, humbled, frustrated,
and taught us, and without whom this book
would have no reason to exist.
--Charles H. Thorne, MD
--Charles H. Thorne, MD
David M. Adelman, MD, PhD Assistant Profeuor Department of Plastic Surgery The University of Texas
David M. Adelman, MD, PhD
Assistant Profeuor
Department of Plastic Surgery
The University of Texas MD Anderson Cancer Center
Houston, 'Thxas
Jamil Ahmad, MD
Staff Plastic Surgeon
The Plastic Surgery Clinic
Mississauga, Ontario
AIS. Aly, MD

Profeuor Ae&thet.ic & Plastic Surgery Institute Univeraity of California Irvine Orange, California

Katerina Anuli, MD, MRCS CliDical Fellow Department of Plastic and Reconstructive Surgery Guy's and StThomas'
Katerina Anuli, MD, MRCS
CliDical Fellow
Department of Plastic and Reconstructive Surgery
Guy's and StThomas' NHS Trust
London, United KiDgdom
Mark W. Ashtan, MD
Head, Rb::oD.Structive Plastic Surgery
Royal Melbourne Hospital
Victoria, Australia
Christapher E. Allinger, MD Profe.ooor, Department ofPlastic Surgery Georgetown University Washington, District of
Christapher E. Allinger, MD
Profe.ooor, Department ofPlastic Surgery
Georgetown University
Washington, District of Columbia
Kocli Azari, MD
Associate Professor
Department of Orthopaedic Surgery and Division of
Plastic Surgery
David Geffen School of Medicine at UCLA
Los Angeles, California
Sl8phen B. Baker, MD, DDS

Profe.ooor and Program Director Department of Plastic Surgery Georgetown University Hospibll Washington, District of Columbia Co-Director Craniofacial Anomalies Program INOVA Fairfax Hospital for Children Falls Church, Vuginia

Karim Bakri, MD Chief Resident Division of Plastic S~y Mayo Clinic Rochester, Minnesota
Karim Bakri, MD
Chief Resident
Division of Plastic S~y
Mayo Clinic
Rochester, Minnesota
Division of Plastic S~y Mayo Clinic Rochester, Minnesota Scott P. Bartlett, MD ProkNo;Dep~mt~S~ery Perelman School
Division of Plastic S~y Mayo Clinic Rochester, Minnesota Scott P. Bartlett, MD ProkNo;Dep~mt~S~ery Perelman School
Scott P. Bartlett, MD ProkNo;Dep~mt~S~ery Perelman School of Medicine at the University of Pennsylvania Chief,
Scott P. Bartlett, MD
ProkNo;Dep~mt~S~ery
Perelman School of Medicine at the University of Pennsylvania
Chief, Division ofPlastic Surgery
Children's Hospital of Philadelphia
Philadelphia, PeMsylvaoia
Fritz E. Bart.n, Jr., MD ProkNo; Plastic Surgery Univeraity of Texas Soutlrwestun Medical Center Dallas,
Fritz E. Bart.n, Jr., MD
ProkNo; Plastic Surgery
Univeraity of Texas Soutlrwestun Medical Center
Dallas, Texas
Nichalas Bastidas, MD
Attmding Physician
North Shore-Uj Health System
New York, New York
Bruce S. Iauer, MD CliDical Professor of Surgery, Plastic Surgery University ~Chicago,Pritzker School ~Medicine
Bruce S. Iauer, MD
CliDical Professor of Surgery, Plastic Surgery
University ~Chicago,Pritzker School ~Medicine
Chicago, Dlinois
Chief, Division ofPlastic and ~tructive Surgery
North Shore University Health System
Highland Park, Illinois
Michael S. leckenstein, MD
Alabama Breast Surgery Center
Binninglwn, Alabama
Keith M. Blechman, MD
Chief R.esidmt
Institute for Reconstructive Plastic Surgery
New York University School of Medicine
New York, New York
George C. Bahle Ill, DDS
Implant & Proslhodontic Associates
Oklahoma City, Oklahoma
James P. Bradley, MD
ProkNo; Sarnat Chair
Division of Plastic Surgery
University of California, Los Angeles
Los Angeles, California
Gerald lrandacher, MD
Associate Professor
Depattment ~Plasticand Reconstructive Surgery
Johns Hopkins University School ~Medicine
Baltimore, Maryland
Danald W. luck II, MD
Division of Plastic & R«onstructive Surgery
Nortlrwestun University
Chicago, Dlinois
Contributing Authors Vll Louis P. Bucky, MD Daniel J. Ceradini, MD Clinical Professor Department of
Contributing Authors
Vll
Louis P. Bucky, MD
Daniel J. Ceradini, MD
Clinical Professor
Department of Surgery
University of Pennsylvania School of Medicine
Chief of Plastic Surgery
Pennsylvania Hospital
Philadelphia, Pennsylvania
Assistant Professor
Department of Plastic Surgery
New York University School of Medicine
Chief of Plastic Surgery
Manhattan Veterans Administration Hospital
New York, New York
Due T. Bui, MD
Beniamin Chang, MD
Associate Professor of Surgery
Department of Surgery
Director, Reconstructive Breast Surgery
Division of Plastic and Reconstructive Surgery
Stony Brook School of Medicine
Stony Brook, New York
Renee M. Burke, MD
Associate Professor of Clinical Surgery
Division of Plastic Surgery
The Perelman School of Medicine at the University
of Pennsylvania
Attending Surgeon
Division of Plastic Surgery
The Children's Hospital of Philadelphia
Philadelphia, Pennsylvania
Plastic Surgeon
Department of Surgery
Good Shepherd Hospital
Barrington, Illinois
Plastic Surgeon
Chicago Aesthetic Surgery Institute
Rosemont, lllinois
James Chang, MD
Professor, Departments of Surgery (Plastic Surgery)
& Orthopaedic Surgery
Stanford University Medical Center
Chief, Division of Plastic & Reconstructive Surgery
Stanford University Medical Center
Palo Alto, California
Mary C. Burns, OTR/1., CHT
Johnny T. Chang, MD, MSME
Assistant Professor
Department of Surgery
Southern Illinois University School of Medicine
Certified Hand Therapist
Division of Plastic Surgery
Southern Dlinois University School of Medicine Hand Therapy Center
Springfield, Illinois
Division of Plastic Surgery
Brown Medical School
Providence, Rhode Island
David W. Chang, MD
Chartes E. Butler, MD
Professor, Department of Plastic Surgery
M.D. Anderson Cancer Center
Houston, Texas
Professor with Tenure
Department of Plastic Surgery
The University of Texas MD Anderson Cancer Center
Houston, Texas
Harvey Chim, MBBS
Chief Resident, Plastic Surgery
Case School of Medicine
Cleveland, Ohio
Dominick Cannavo, MD
New York, New York
Manhew S.S. Choi, MD
Joseph N. Carey, MD
Assistant Professor
Division of Plastic Surgery
University of Southern California
Chief, Plastic Surgery
LAC + USC Medical Center
Los Angeles, California
Associate Professor of Plastic Surgery
Department of Plastic and Reconstructive Surgery
Hanyang University College of Medicine
Seoul, South Korea
Chief, Department of Plastic and Reconstructive Surgery
Hanyang University Guri Hospital
Guri, Gyunggi-do, South Korea
J. Guilherme Christiano, MD
Brian T. Carlsen, MD
Assistant Professor
Division of Plastic Surgery, Division of Hand Surgery
Mayo Clinic
Rochester, Minnesota
Assistant Professor
Division of Plastic Surgery
University of Rochester
Rochester, New York
Kevin C. Chung, MD, MS
Grant W. Cartson, MD
Professor of Surgery
Emory University
Wadley R. Glenn Professor of Surgery, Chief of the Division of
Plastic Surgery
Emory University Hospital
Atlanta, Georgia
Charles B. G. de Nancrede Professor of Surgery
Section of Plastic Surgery, Department of Surgery
Professor of Orthopaedic Surgery
Assistant Dean for Faculty Affairs
Associate Director of Global REACH
University of Michigan Medical School
Ann Arbor, Michigan
vw Contributing Authors Mark W. Clemens, MD MaHhias B. Donelan, MD ~s~tantPro~sor Department of Plastic
vw
Contributing Authors
Mark W. Clemens, MD
MaHhias B. Donelan, MD
~s~tantPro~sor
Department of Plastic Surgery
MD Anderson Cancer Center
Houston, Texas
Mark A. Codner, MD
~s~tantPro~sor
Department of Plastic Surgery
Emory University
Atlanta, Georgia
Chief, Plastic Surgery
Department of Surgery
Shriners Hospitals for Children-Boston
~sociate Clinical Professor of Surgery
Harvard Combined Plastic Surgery Residency
Training Program
Harvard Medical School
Boston, Massachusetts
Susan E. Downey, MD
Stephen H. Colbert, MD
~s~tantPro~sor
Department of Surgery
University of Missouri
Head, Hand & Microsurgery
Division of Plastic Surgery
University of Missouri Health Care
Columbia, Missouri
~sociate Clinical Professor
Department of Surgery (Plastic)
I<eck University of Southern California School of Medicine
Los Angeles, California
Gregory A. Dumanian, MD
Damon S. Cooney, MD, PhD
Professor of Surgery
Division of Plastic: Surgery
Chief of Plastic: Surgery
Northwestern Feinberg School of Medicine
Chicago, lllinois
~s~tant Professor of Plastic and Reconstructive Surgery
Johns Hopkins University School of Medicine
Baltimore, Maryland
Anthony Echo, MD
Peter G. Cordeiro, MD
Chief, Plastic & Reconstructive Surgery
Memorial Sloan-Kettering Cancer Center
New York, New York
dinical Instructor
Division of Plastic Surgery
Stanford University Medical Center
Palo Alto, California
Cherry L. Estilo, DMD
Russell J. CorleH, MD
Jack Brockhoff Reconstructive Plastic Surgery
Research Unit
Department of Anatomy and Cell Biology
University of Melbourne
Melbourne, Australia
Associate Attending
Department of Surgery
Memorial Sloan-Kettering Cancer Center
Assistant Attending
Department of Surgery
New York Presbyterian Hospital/Cornell
New York, New York
Catherine M. Curtin, MD Staff Physician Department of Surgery Palo Alto Veterans Hospital ~mtant Professor
Catherine M. Curtin, MD
Staff Physician
Department of Surgery
Palo Alto Veterans Hospital
~mtant Professor
Division of Plastic Surgery
Stanford University
Palo Alto, California
Daniel Alexander Del Vecchio, MD, MBA
~sociate Clinical Staff
Department of Surgery
Massachusetts General Hospital
Boston, Massachusetts
Christopher A. Derderian, MD
~mtant Professor
Department of Plastic Surgery
UT Southwestern Medical Center
Pediatric and Craniofacial Surgery
Children's Medical Center
Dallas, Texas
Joseph J. Disa, MD
Attending Physician
Department of Surgery
Memorial Sloan-Kettering Cancer Center
Pro~sor of Surgery
Department of Surgery
Wiell Cornell College of Medicine
New York, New York
Derek Flekher, MD Resident, Plastic Surgery University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania
Derek Flekher, MD
Resident, Plastic Surgery
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania
Robert D. Galiano, MD Assistant Professor Department of Surgery, Division of Plastic Surgery Northwestern University
Robert D. Galiano, MD
Assistant Professor
Department of Surgery, Division of Plastic Surgery
Northwestern University Feinberg School of Medicine
Chicago, lllinois
Mary K. Gingrass, MD Assistant Clinical Professor Department of Plastic Surgery Vanderbilt University School of
Mary K. Gingrass, MD
Assistant Clinical Professor
Department of Plastic Surgery
Vanderbilt University School of Medicine
Nashville, Tennessee
Chad R. Gordon, DO Assistant Professor Johns Hopkins University School of Medicine dinical Director, Face
Chad R. Gordon, DO
Assistant Professor
Johns Hopkins University School of Medicine
dinical Director, Face Transplant Program
The Johns Hopkins Hospital
Baltimore, Maryland
Arun K. Gosain, MD Division Head, Plastic Surgery Ann & Robert H. Lurie Children's Hospital
Arun K. Gosain, MD
Division Head, Plastic Surgery
Ann & Robert H. Lurie Children's Hospital of Chicago
Professor of Plastic: Surgery
Northwestern University Feinberg School of Medicine
Chicago, lllinois
Contributing Authors lX Nikolaus Gravenstein, MD Scott L Hansen, MD The Jerome H. Modell, MD
Contributing Authors
lX
Nikolaus Gravenstein, MD
Scott L Hansen, MD
The Jerome H. Modell, MD Professor of Anesthesiology
Professor of Neurosurgery
Professor of Periodontology
University of Florida College of Medicine
Gainesville, Florida
Assistant Professor
Department of Surgery
University of California, San Francisco
San Francisco, California
Maximilian W.B. Harhnannsgruber, MD
Lorelei J. Grunwaldt, MD
Assistant Professor of Surgery
Department of Plastic Surgery
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania
Attending Anesthesiologist
Anesthesia Associates of Park Avenue
New York, New York
Geoffrey C. Gurtner, MD

Professor Department of Surgery Stanford University School of Medicine Stanford, California

Nicholas T. Haddock, MD Assistant Professor Department of Plastic Surgery University of Texas Southwestern Medical
Nicholas T. Haddock, MD
Assistant Professor
Department of Plastic Surgery
University of Texas Southwestern Medical Center
Dallas, Texas
J. Joris Hage, MD, PhD
Chief, Department of Plastic and Reconstructive Surgery
Netherlands Cancer Institute-Antoni van Leeuwenhoek Hospital
Amsterdam, The Netherlands
Elizabeth J. Hall-Findlay, MD
Plastic Surgeon
Mineral Springs Hospital
Banff Alberta, Canada
Eric G. Halvorson, MD
Assistant Professor of Surgery
Residency Program Director
Director of Microsurgery
Division of Plastic & Reconstructive Surgery
University of North Carolina
Chapel Hill, North Carolina
Warren C. Hammert, MD
Associate Professor
Department of Orthopaedic Surgery
Associate Professor
Department of Surgery
Division of Plastic Surgery
University of Rochester Medical Center
Rochester, New York
Dennis C. Hammond, MD
Partners in Plastic Surgery of West Michigan
Associate Program Director
Plastic and Reconstructive Surgery
Grand Rapids Medical Education Partners
Grand Rapids, Michigan
Matthew M. Hanasono, MD
Associate Professor
Department of Plastic Surgery
The University of Texas MD Anderson Cancer Center
Houston, Texas
Robert J. Havlik, MD J.J. Harbaugh Jr. Professor of Surgery and Chief Division of Plastic
Robert J. Havlik, MD
J.J. Harbaugh Jr. Professor of Surgery and Chief
Division of Plastic Surgery
Indiana University
Director, Cleft and Craniofacial Surgery
Riley Hospital for Children
Indiana University School of Medicine
Indianapolis, Indiana
Larry H. Hollier, Jr. MD Professor, Division of Plastic Surgery Residency Program Director Baylor College
Larry H. Hollier, Jr. MD
Professor, Division of Plastic Surgery
Residency Program Director
Baylor College of Medicine
Houston, Texas
Richard A. Hopper, MD, MS Associate Professor Department of Surgery University of Washington Chief, Division
Richard A. Hopper, MD, MS
Associate Professor
Department of Surgery
University of Washington
Chief, Division of Plastic Surgery
Seattle Children's Hospital
Seattle, Washington
Erik A. Hoy, MD, MBA
Erik A. Hoy, MD, MBA

Attending Physician, Plastic Surgery UHS Binghamton, New York

Physician, Plastic Surgery UHS Binghamton, New York Joseph P. Hunstad, MD Associate Consulting Professor
Joseph P. Hunstad, MD Associate Consulting Professor Division of Plastic Surgery University of North Carolina
Joseph P. Hunstad, MD
Associate Consulting Professor
Division of Plastic Surgery
University of North Carolina
Section Head, Department of Plastic Surgery
Carolinas Medical Center University Hospital
Charlotte, North Carolina
Joseph M. Huryn, DDS Chief, Dental Service Department of Surgery Memorial Sloan-Kettering Cancer Center Professor
Joseph M. Huryn, DDS
Chief, Dental Service
Department of Surgery
Memorial Sloan-Kettering Cancer Center
Professor of Surgery (Oral and Maxillofacial Surgery)
Department of Surgery
Weill Medical College of Cornell University
New York, New York
JeHrey E. Janis, MD Associate Professor and Program Director Department of Plastic Surgery University of
JeHrey E. Janis, MD
Associate Professor and Program Director
Department of Plastic Surgery
University of Texas Southwestern Medical Center
Chief of Plastic Surgery
Parkland Health and Hospital System
Dallas, Texas

X

Contributing Authors
Contributing Authors
Suhail K. Kanchwala, MD Assistant Professor of Surgery Department of Plastic Surgery Hospital of the
Suhail K. Kanchwala, MD
Assistant Professor of Surgery
Department of Plastic Surgery
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
Michael A.C. Kane, MD Associate Attending Physician Department of Plastic Surgery Manhattan Eye, Ear &:
Michael A.C. Kane, MD
Associate Attending Physician
Department of Plastic Surgery
Manhattan Eye, Ear &: 1broat Hospital
New York, New York
Nolan S. KarJt, MD Associate Professor Department of Plastic Surgery New York University School of
Nolan S. KarJt, MD
Associate Professor
Department of Plastic Surgery
New York University School of Medicine
Chief, Plastic Surgical Service
Department of Plastic Surgery
Tisch Hospital, NYU Langone Medical Center
New York, New York
Annen K. Kasabian, MD System Chief Department of Plastic Surgery North Shore-UJ Health System New
Annen K. Kasabian, MD
System Chief
Department of Plastic Surgery
North Shore-UJ Health System
New Hyde Park, New York
Henry K. Kawamoto, MD, DDS Clinical Professor Division of Plastic Surgery University of California at
Henry K. Kawamoto, MD, DDS
Clinical Professor
Division of Plastic Surgery
University of California at Los Angeles
Los Angeles, California
Patrick Kelley, MD Medical Director, Craniofacial Center Children's Hospital of Austin Austin, Texas
Patrick Kelley, MD
Medical Director, Craniofacial Center
Children's Hospital of Austin
Austin, Texas
Timothy W. King, MD, PhD Assistant Professor Departments of Surgery and Pediatrics University of Wisconsin
Timothy W. King, MD, PhD
Assistant Professor
Departments of Surgery and Pediatrics
University of Wisconsin School of Medicine and Public Health
Plastic Surgery Section Chief
Department of Surgery
William S. Middleton Memorial Veterans Hospital
Madison, Wisconsin
MaHhew B. Klein, MD Assistant Professor Department of Plastic Surgery University of Washington Associate Director
MaHhew B. Klein, MD
Assistant Professor
Department of Plastic Surgery
University of Washington
Associate Director
University of Washington Burn Center
Harborview Medical Center
Seattle, Washington
James Knaetgen Ill, MD Private Practice Fresno, California
James Knaetgen Ill, MD
Private Practice
Fresno, California
MaHhew E. Kaepplinger, DO Assistant Professor Department of Orthopaedic Surgery University of Texas-Houston Health
MaHhew E. Kaepplinger, DO
Assistant Professor
Department of Orthopaedic Surgery
University of Texas-Houston Health Science Center
Attending Physician, Division of Hand and Upper Extremity Surgery
Houston, Texas
Emil J. Kahan, MD Resident Physician Aesthetic and Plastic Surgery Institute University of California, Irvine
Emil J. Kahan, MD
Resident Physician
Aesthetic and Plastic Surgery Institute
University of California, Irvine
Orange, California
John C. Kashy, MD
Resident Physician
Division of Plastic Surgery
Michael E. Debakey Department of Surgery
Baylor College of Medicine
Houston, Texas
Wee Lean Lam, MBChB, M Phil
Consultant Plastic Surgeon
Department of Plastic, Reconstructive and Hand Surgery
Royal Hospital for Sick Children
Edinburgh, United Kingdom
StJohn's Hospital at Howden
Livingston, United Kingdom
Angela Sang Landfair, MD
Chief Resident, Plastic Surgery
Section of Plastic Surgery at Magee Women's Hospital
Department of Plastic Surgery
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania
Patrick Lang, MD
Resident, Division of Plastic and Reconstructive Surgery
University of California, San Francisco
San Francisco, California
Howard N. Langstein, MD
Professor of Surgery
Department of Surgery, Division of Plastic Surgery
University of Rochester School of Medicine
Rochester, New York
W. P. Andrew Lee, MD
Professor and Chairman
Department of Plastic and Reconstructive Surgery
Johns Hopkins University School of Medicine
Baltimore, Maryland
Gordan K. Lee, MD
Assistant Professor
Department of Surgery
Residency Program Director
Division of Plastic Surgery
Stanford University School of Medicine
Stanford, California
Valerie Lemoine, MD, MPH
Assistant Professor of Plastic Surgery
Department of Surgery
Division of Plastic Surgery
Senior Associate Consultant
Department of Surgery
Division of Plastic Surgery
Mayo Clinic
Rochester, Minnesota
Ashley K. Lentz, MD
Assistant Professor of Surgery
University of Florida
Gainesville, Florida
Salvatore C. Lettieri, MD Assistant Professor of Plastic Surgery Rochester, Minnesota Consultant, Department of Surgery
Salvatore C. Lettieri, MD
Assistant Professor of Plastic Surgery
Rochester, Minnesota
Consultant, Department of Surgery
Division of Plastic Surgery
Mayo Clinic
Rochester, Minnesota
Benjamin Levi, MD
House Officer
Department of Surgery
Division of Plastic and Reconstructive Surgery
University of Michigan
Ann Arbor, Michigan
Steven M. Levine, MD
Clinical Instructor
Institute of Reconstructive Plastic Surgery
New York University Langone Medical Center
New York, New York
Jamie P. Levine, MD
Associate Professor, Plastic Surgery
Chief of Microsurgery, Plastic Surgery
NYU Langone Medical Center
Chief of Plastic Surgery
Bellevue Hospital
New York, New York
Eric C. Liao, MD, PhD
Assistant Professor of Surgery
Massachusetts General Hospital, Harvard Medical School
Principal Investigator
Center for Regenerative Medicine
Harvard Stem Cell Institute
Boston, Massachusetts
Paul K. Um, MD, FACS
Assistant Professor
Department of Surgery
University of Minnesota Medical School
Minneapolis, Minnesota
Plastic Surgeon
Center for Craniofacial Services
Gillette Children's Specialty Healthcare
St. Paul, Minnesota
Michael A. Loffredo, MD
Private Practice
Cape and Islands Plastic Surgery
Hyannis, Massachusetts
z. Paul Lorenc, MD
Attending
Plastic Surgery
North Shore/Ilj Lenox Hill Hospital
Lorenc Aesthetic Plastic Surgery Center
New York, New York
David W. Low, MD
Professor of Surgery
Division of Plastic Surgery
Perelman School of Medicine at the University of Pennsylvania
Philadelphia, Pennsylvania
Contributing Authors Xl Susan E. MacKinnon, MD Professor and Chief Division of Plastic and Reconstructive
Contributing Authors
Xl
Susan E. MacKinnon, MD
Professor and Chief
Division of Plastic and Reconstructive Surgery
Washington University School of Medicine
Surgeon and Chief
Department of Surgery, Division of Plastic and
Reconstructive Surgery
Barnes-jewish Hospital
Saint Louis, Missouri
Evan Matros, MD, MMSC
Assistant Surgeon
Department of Surgery
Memorial Sloan-Kettering Cancer Center
Associate Professor
Department of Surgery
Weill Cornell Medical School
New York, New York
Joseph G. McCarthy, MD
Lawrence D. Bell Professor of Plastic Surgery &: Helen Kimmel
Professor of Reconstructive Plastic Surgery
Department of Plastic Surgery
New York University School of Medicine
Chair, Department of Plastic Surgery
New York University Langone Medical Center
New York, New York
Babak J. Mehrara, MD Associate Attending, Surgery Memorial Sloan-Kettering Cancer Center Associate Professor, Surgery
Babak J. Mehrara, MD
Associate Attending, Surgery
Memorial Sloan-Kettering Cancer Center
Associate Professor, Surgery
Weill Cornell University Medical Center
New York, New York
Frederick J. Menick, MD Private Practice Tucson, Arizona Scott A. Mitchell, MD Assistant Professor Department
Frederick J. Menick, MD
Private Practice
Tucson, Arizona
Scott A. Mitchell, MD
Assistant Professor
Department of Orthopaedic Surgery
University of California, Los Angeles
Santa Monica, California
Steven L. Moran, MD Professor, Plastic Surgery and Orthopaedics Chair of Plastic Surgery Mayo Clinic
Steven L. Moran, MD
Professor, Plastic Surgery and Orthopaedics
Chair of Plastic Surgery
Mayo Clinic
Rochester, Minnesota
Maurice Y. Nahabedian, MD Professor, Department of Plastic Surgery Georgetown University Washington, District of
Maurice Y. Nahabedian, MD
Professor, Department of Plastic Surgery
Georgetown University
Washington, District of Columbia
James D. Namnoum, MD
James D. Namnoum, MD

Assistant Clinical Professor Department of Plastic Surgery Emory University Partner Atlanta Plastic Surgery Atlanta, Georgia

Clinical Professor Department of Plastic Surgery Emory University Partner Atlanta Plastic Surgery Atlanta, Georgia
Xl1 Contributing Authors Kate W. Nellans, MD, MPH lvona Percec, MD, PhD Hand Fellow Department
Xl1
Contributing Authors
Kate W. Nellans, MD, MPH
lvona Percec, MD, PhD
Hand Fellow
Department of Surgery
Division of Plastic Surgery
University of Michigan School of Medicine
Ann Arbor, Michigan
Assistant Professor
Division of Plastic Surgery
Perelman School of Medicine at the University of Pennsylvania
Philadelphia, Pennsylvania
Linda G. Phillips, MD
David T. Netscher, MD
Qinical Professor
Department of Orthopaedic Surgery and
Division of Plastic Surgery
Baylor College of Medicine
Chief, Plastic Surgery
VA Medical Center
Chief, Hand Surgery
St. Luke's Episcopal Hospital
Chief, Hand Surgery
Department of Orthopaedic Surgery and
Division of Plastic Surgery
Baylor College of Medicine
Houston, Texas
Truman G. Blocker Distinguished Professor
Chief, Division of Plastic Surgery
UTMB Galveston
Galveston, Texas
Beniamin Z. Phillips, MD, MPH
Chief Resident, Department of Plastic Surgery
The Warren Alpert Medical School of Brown University
Providence, Rhode Island
Karen L Powers, MD
Assistant Professor
Department of Surgery, Division of Plastic Surgery
University of Texas Medical Branch
Galveston, Texas
Michael W. Neumeister, MD
Julian J. Pribaz, MD
Proressor & Chairman
Division of Plastic Surgery
Southern Winois University School of Medicine
The Elvin G. Zook Endowed Chair
Springfield, Illinois
Professor of Surgery, Department of Surgery
Harvard Medical School
Boston, Massachusetts
Adrian M. Przybyla, MD
Bianca M. B. Ohana, MD
Plastic Surgery Private Clinic
Salt Lake City, Utah
Aesthetic Surgery Fellow
Marina Plastic Surgery Associates
Marina del Rey, California
Leo R. Otake, MD, PhD Clinical Instructor Department of Surgery, Division of Plastic Surgery Stanford
Leo R. Otake, MD, PhD
Clinical Instructor
Department of Surgery, Division of Plastic Surgery
Stanford University School of Medicine
Palo Alto, California
Assistant Clinical Professor
Department of Surgery, Section of Plastic Surgery
Yale University School of Medicine
New Haven, Connecticut
David M. Otterbum, MD Assistant Proressor of Surgery (Plastic Surgery) Weill Cornell Medical College Assistant
David M. Otterbum, MD
Assistant Proressor of Surgery (Plastic Surgery)
Weill Cornell Medical College
Assistant Attending Surgeon
NewYork-Presbyterian Hospital
New York, New York
Nima P. Patel, MD Private Practice New York, New York Attending Surgeon and Chief of
Nima P. Patel, MD
Private Practice
New York, New York
Attending Surgeon and Chief of Microvascular Surgery
Department of Surgery
Maimonides Medical Center
Brooklyn, New York
William C. Pederson, MD Adjunct Professor Department of Surgery University of Texas Health Science Center
William C. Pederson, MD
Adjunct Professor
Department of Surgery
University of Texas Health Science Center at San Antonio
Fellowship Director
Hand Surgery Fellowship
The Hand Center of San Antonio
San Antonio, Texas
Mark E. Puhaindran, MBBS, MRCS
Mark E. Puhaindran, MBBS, MRCS

Consultant, Department of Hand and Reconstructive Microsurgery National University Hospital Singapore

Remus Repta, MD Plastic and Reconstructive Surgery Advanced Aesthetic Associates Scottsdale, Arizona
Remus Repta, MD
Plastic and Reconstructive Surgery
Advanced Aesthetic Associates
Scottsdale, Arizona
Gary F. Rogers, MD Division Chief, Plastic and Reconstructive Surgery Children's National Medical Center
Gary F. Rogers, MD
Division Chief, Plastic and Reconstructive Surgery
Children's National Medical Center
Washington, DC
Rod J. Rohrich, MD
Professor and Chairman
Crystal Charity Ball Distinguished Chair in Plastic Surgery
Betty and Warren Woodward Chair in Plastic and Reconstructive Surgery
Distinguished Teaching Professor
Department of Plastic Surgery
UT Southwestern Medical Center
Dallas, Texas
Harvey M. Rosen, MD, DMD Associate Professor, Surgery University of Pennsylvania School of Medicine Philadelphia,
Harvey M. Rosen, MD, DMD
Associate Professor, Surgery
University of Pennsylvania School of Medicine
Philadelphia, Pennsylvania
Stephen Alex Rottgers, MD
Integrated Plastic Surgery Resident
Department of Plastic and Reconstructive Surgery
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania
J. Peter Rubin, MD UPMC Endowed Professor and Chair, Department of Plastic Surgery Professor of
J. Peter Rubin, MD
UPMC Endowed Professor and Chair, Department of Plastic Surgery
Professor of Bioengineering
Director, Life After Weight Loss Body Contouring Program
University of Pittsburgh School of Medicine and UPMC
Pittsburgh, Pennsylvania
Pierre B. Saadeh, MD
Residency Program Director
Department of Plastic Surgery
New York University School of Medicine
New York, New York
Justin M. Sacks, MD
Assistant Professor
Department of Plastic and Reconstructive Surgery
Johns Hopkins School of Medicine
Baltimore, Maryland
Jhanny A. Salamon, MD
Private Practice
Coral Gables, Florida
Renatv Saltz, MD
Saltz Plastic Surgery and Spa Vitoria
Salt Lake City and Park City, Utah
Douglas M. Sommer, MD
Associate Professor, Plastic Surgery
University of Texas Southwestern Medical School
Dallas, Texas
Hani Sbitany, MD
Assistant Professor of Surgery
Division of Plastic and Reconstructive Surgery
University of California, San Francisco
Attending Physician
Department of Surgery
San Francisco General Hospital
San Francisco, California
Sandeep Jacob Sebastin, MCh (Piast)

Consultant, Department of Hand & Reconstructive Microsurgery National University Hospital Singapore

Kenneth C. Shestak, MD Professor of Plastic Surgery Department of Plastic Surgery University of Pittsburgh
Kenneth C. Shestak, MD
Professor of Plastic Surgery
Department of Plastic Surgery
University of Pittsburgh School of Medicine
Chief of Plastic Surgery Magee Women's Hospital
Pittsburgh, Pennsylvania
Jaimie T. Shores, MD
Assistant Professor
Department of Plastic and Reconstructive Surgery
Johns Hopkins University School of Medicine
Baltimore, Maryland
Scott L Spear, MD
Professor, Department of Plastic Surgery
Georgetown University Hospital
Washington, District of Columbia
Contributing Authors Xlll W. Grant Stevens, MD Clinical Professor of Surgery Department of Plastic Surgery
Contributing Authors
Xlll
W. Grant Stevens, MD
Clinical Professor of Surgery
Department of Plastic Surgery
Keck School of Medicine of USC
Los Angeles, California
Medical Director
USC - Marina del Rey Aesthetic Surgery Fellowship
University of Southern California
Marina del Rey, California
Patrick K. Sullivan, MD Associate Professor, Plastic Surgery Brown University School of Medicine Division Chief,
Patrick K. Sullivan, MD
Associate Professor, Plastic Surgery
Brown University School of Medicine
Division Chief, Aesthetic Surgery
Providence, Rhode Island
GeoHrey lan Taylor, AO, MD Professor, Anatomy and Neuroscience University of Melbourne Senior Consultant,
GeoHrey lan Taylor, AO, MD
Professor, Anatomy and Neuroscience
University of Melbourne
Senior Consultant, Reconstructive Plastic Surgery
Royal Melbourne Hospital
Victoria, Australia
Steven Alan Teitelbaum, MD Assistant Clinical Professor Plastic Surgery David Geffen School of Medicine at
Steven Alan Teitelbaum, MD
Assistant Clinical Professor
Plastic Surgery
David Geffen School of Medicine at UCLA
Los Angeles, California
Julia K. Terzis, MD, PhD Adjunct Professor Department of Plastic Surgery New York University Medical
Julia K. Terzis, MD, PhD
Adjunct Professor
Department of Plastic Surgery
New York University Medical Center
Clinical Professor
Department of Surgery, Division of Plastic and
Reconstructive Surgery
New York-Presbyterian Hospital, The University of
Columbia & Cornell
New York, New York
Aliso C. Thorne, MD Professor of Clinical Anesthesia Memorial Sloan-Kettering Cancer Center New York, New
Aliso C. Thorne, MD
Professor of Clinical Anesthesia
Memorial Sloan-Kettering Cancer Center
New York, New York
Paul H. Tran, MD Instructor in Plastic Surgery Division of Plastic Surgery, Department of Surgery
Paul H. Tran, MD
Instructor in Plastic Surgery
Division of Plastic Surgery, Department of Surgery
Mayo Clinic
Rochester, Minnesota
Robin H. Unger, MD Private Practice New York, New York Assistant Clinical Professor Mount Sinai
Robin H. Unger, MD
Private Practice
New York, New York
Assistant Clinical Professor
Mount Sinai Hospital
New York, New York
Walter P. Unger, MD., FRCP(C), FACP Clinical Professor (Dermatology) Mount Sinai School of Medicine New
Walter P. Unger, MD., FRCP(C), FACP
Clinical Professor (Dermatology)
Mount Sinai School of Medicine
New York
XIV Contributing Authors Allen L Van Beek, MD Adjunct Professor Department of Surgery University Minnesota
XIV
Contributing Authors
Allen L Van Beek, MD
Adjunct Professor
Department of Surgery
University Minnesota School of Medicine
Minneapolis, Minnesota
Andrea E. Van Pelt, MD
Clinical Assistant Professor
Surgery/Plastic and Reconstructive Surgery
Michigan State University
Attending Physician
Plastic and Reconstructive Surgery
Grand Rapids Medical Education Partners
Grand Rapids, Michigan
Stephen M. Warren, MD
Associate Professor of Plastic Surgery
Department of Plastic Surgery
New York University Langone Medical Center
New York, New York
Fu-Chan Wei, MD
Professor, Department of Plastic Surgery
Chang Gung University and Medical College
Taoyuan, Taiwan
Carlos K. Wesley, MD Private Practice New York, New York Bradon J. Wilhelmi, MD Professor
Carlos K. Wesley, MD
Private Practice
New York, New York
Bradon J. Wilhelmi, MD
Professor and Chief
Division of Plastic Surgery
University of Louisville
Louisville, Kentucky
Victor W. Wong, MD
Chief Resident in Surgery
Department of Surgery
Oregon Health Sciences University
Portland, Oregon
Michael J. Yaremchuk, MD

Professor of Surgery Harvard Medical School Chief of Craniofacial Surgery Surgery Massachusetts General Hospital Boston, Massachusetts

Surgery Harvard Medical School Chief of Craniofacial Surgery Surgery Massachusetts General Hospital Boston, Massachusetts
Given the availability of information and images from the Internet, is a hard-boun~ single-volume, old-fashione~
Given the availability of information and images from the
Internet, is a hard-boun~ single-volume, old-fashione~ com·
p.tehensive textbook of plastic surgery an anachronism? Having
spent three years on this book, I am afraid to confront the
answer to that question. What I do know is that there is noth-
ing like taking a .real book to bed-well, almost nothing. I .feU
asleep .reading Grabb and Smith when I was a medical student
and a surgery resident and a craniofacial.feUow and as a young
attending and I will be damned if current students, trainees, and
young practitioners will not have that opportunity. I am kid-
ding, of course. My motivation for editiDg this tome for the third
and final time was less altruistic. I derive immense satisfaction
from having a familiarity with the entire body ofplastic surgical
knowledge and hav.ing read every word herein three times has
hope.fully provided that. I have been known to say to the reai·
dents, only half in jest, that I will retire when one ofthem knows
more than I do. If there is anything more fun than learning. I
would appreciatx: someone telling me what it is
soon.
A comprehensive,. single-volume textbook of plastic surgery
will hopefully accomplish the following: (1) define the spec-
trum that is plastic surgery; (2) provide a convenient source
of information for day-to-day studying; (3) ddiver an attrac-
tive introduction to the interested or uninitiated reader; and
(4) serve as the best single source for board exam preparation.
serve as the best single source for board exam preparation. The book is intended for medical
The book is intended for medical professionals and train- ees at aU levels: practicing plastic
The book is intended for medical professionals and train-
ees at aU levels: practicing plastic surgeons, surgeons in related
fields such as ophthalmology, otolaryngology, oral surgery,
orthopaedics and general surgery, surgery residents in all sub-
specialties, medical students, physician's assistants, nurses,
and nurse practitioners.
How is the seventh edition different from the sixth edition?
First, the new edition is in color. Secon~ SS of the 99 chapters
are entirely new with new authors. The remaining chapters
have been rewritten and are almost aU substantively different
from their predecessors. A new section on Body Contouring
has been added. The Transplantation chapter has been
updated to reflect the extraordinary recent advances in that
field. The Hand section is entirely new with a new editor, new
chapters, and new authors. Other changes such as consolida-
tion of chapters and changes in the sections are admittedly
more modest.
I would like to thank the coeditors (who designed the sec·
tions, chose the authors, and edited the text), the authors (who
put up with ruthless editing so that the book would remain a
single volume), Lippincott Williams & Wilkins, Jenny Koleth,
and Sarah Granlund for their contributions.
Charles H. Thorne, MD
Charles H. Thorne, MD

:XV

Preface XV
Preface
XV
PART 1: PRINCIPLES, TECHNIQUES, AND BASIC SCIENCE
PART 1:
PRINCIPLES, TECHNIQUES, AND BASIC SCIENCE
1 Techniques and Principles in Plastic Surgery • • . • • . • 1
1
Techniques and Principles in Plastic Surgery • • . • • . • 1
C'JJarks H. Thorne
2
Wound Healing: Normal and Abnormal ••.••.••.
13
Geoffrey C. Gurtner and Victor W. Wong
3
Wound Care •.••.•
•.••.••
•.••.••.
20
Donald W. Buck and Robert D. Galiano
4
The Blood Supply of the Skin and Skin Flaps. • . • • . 29
Geoffrey Ian Taylor. Russell J. Corlett.
and Mark W. Ashton
5
Muscle Flaps and their Blood Supply. • . • • . • • . • • . 43
Jamie P. Levine
6
Transplantation Biology and Applications to
••
Plastic Surgery •
•••
•••
•••.
.56
Damon S. Coo~ Justin M. Sacks, Gerald
Brandacher. and W. P. Andrew Lee
7
Implant Materials . •
• . • • . • • . •
• . • • . • • . • • .
64
Timothy W. King
8
Principles of Microsurgery••.••.•
•.••.••.••.
70
C'JJarks E. Butler and David M. Adelman
9
Principles and Techniques of Peripheral Nerve
Repair, Grafts, and Transfers ••.•
•.••.••.••.
n
Susan E. Mackinnon and Stephen H. Colbert
10
Tissue Expansion
87
Ashley K. Lentz and Bruce S. Bauer
11
Principles of Office Sedation for Cosmetic Surgery • . 94
Maximilian W. B. Hartmannsgruber.
Dominick Cannavo, and Nikolaus Gravenstein
12
Local
• . • • . • •
• • . • • . • • 100
Alisa C. Thome
PART2:
SKIN AND SOFT nSSUE
13 Dermatology for Plastic Surgeons I-skin care and Benign Dermatologic Conditions •.••.••.•• lOS Renata
13
Dermatology for Plastic Surgeons I-skin care
and Benign Dermatologic Conditions •.••.••.•• lOS
Renata Salt%and Bwnca M. B. Ohana
14
Dermatology for Plastic Surgeons U-Cutaneous
Malignancies • . • • . •
• . • • . • •
• • .
• • . • •
115
Daniel J. Ceradini and kith M. Blechman
15
Thennal, Chemical, and Electrical Injuries . • • . • • 127
Matthew B. Klein
16
Principles of Bum Reconstruction
••.••.••
142
Matthw B. Donelan and Eric C. Lwo
17
Radiation and Radiation Injuries
••.••.••
155
James Knoetgen III and Salvatore C. Lettieri
155 James Knoetgen III and Salvatore C. Lettieri 18 Lasers In Plastic Surgery • 163 David
18 Lasers In Plastic Surgery • 163 David W. Low and Ivona Percec PART3: CONGINrrAL
18
Lasers In Plastic Surgery
163
David W. Low and Ivona Percec
PART3:
CONGINrrAL ANOMAUES AND PEDIATRIC
PlASTIC SURGERY
19
Oeft Lip and Palate: Embryology, Principles,
and Treatment• •.••.• • •.••.• • •
173
RichardA. Hopper
20
Congenital Melanocytic Nevi
.
.
• .
• • .
• .
.
• .
.
• .
.
200
Harvey Chim and Arun K. Gosain
21
Vascular Anomalies .••.•
•.••.•
206
Harvey Chim and Arun K. Gosain
22
Single-Suture Craniosynostosis and Deformational
Plagiocephaly.•
•.••.•
•.••.•
221
Gary F. Rogers and Stephen M. Warren
23
Craniosynostosis Syndromes • .
.
• .
• • .
• .
.
• .
.
• .
.
232
Scott P. Bartlett and Christopher A. Derderian
24 Craniofacial Microsomia and Principles
of Craniofacial Distraction .•
•.••.•
241
Joseph G. McCarthy
25 Orthognathic Surgery
252
Stephen B. Baker
26
Craniofacial Oefts and Hypertelorbitism .
• .
.
• .
.
266
]ames P. Bradley and Henry K. Kawamoto
27
Ear Reconstruction
283
Charles H. Thorne
28
Miscellaneous Craniofacial Conditions: Fibrous
Dysplasia, Moebius Syndrome, Romberg
Syndrome, Treacher Collins Syndrome,
Dermoid Cyst, and Neurofibromatosis •
295
Robert J. Havlik
PART 4: HEAD AND NECK 29 Soft-Tissue and Skeletal Injuries of the Face • 311
PART 4:
HEAD AND NECK
29 Soft-Tissue and Skeletal Injuries of the Face
311
Larry H. Hollier Jr., Patrick Kelley. and John C. Koshy
30 Head and Ned: Cancer and Salivary
Gland Tumors.
.
.
• .
• • .
• .
.
• .
.
• .
• • .
• .
.
• .
.
• .
.
327
David M. Otterbum and Pierre B. Saadeh
31
Reconstruction of the Scalp, Calvarium,
and Forehead.•
•.••.•
•.••.•
342
J.Guilherme C'JJristiano, Nicholas Bastidas, and
Howard N. Langstein
32 Reconstruction of the Eyelids, Correction
of Ptosis, and Canthoplasty . • .
.
• .
• • .
• .
.
• .
.
• .
.
352
Nicholas T. Haddock
33 Nasal Reconstruction
361
Jlrederick J. Menick

Contents

xvii

34 Reconstruction of Acquired Lip Deformities • . • 372 Evan Matros andJulian]. Prib~ 35
34
Reconstruction of Acquired Lip Deformities • . •
372
Evan Matros andJulian]. Prib~
35
Reconstruction of the Cheeks • . •
• .
• • .
• • .
• .
.
384
Babak ]. Mehrara
36
Facial Paralysis
• . • • . • • . • .
.
• .
• • .
• • .
• .
.
399
Julia K. Tmis and K4terina Anesti
37
Mandible Reconstruction
• .
• • .
• .
.
• .
• • .
• • .
• .
.
410
joseph]. Disa and Evan Matros
38
Craniofacial and Maxillofacial Prosthetics • • . •
420
George C. Bohle III. Cherry L. Estilo. and
Joseph M. Huryn
39
Reconstruction of the Maxilla and Skull Base . •
430
Eric G. Halvorson. DueT. Bui. and
Peter G. Cordeiro
40
and
Reconstruction of the Oral Cavity, Pharynx,
• . • • . • • . • .
.
• .
• • .
• • .
• .
.
443
Matthew M. Hanasono
PART5: AESTHmC SURGERY 41 Skin Resurfacing . • • . • • . • •
PART5:
AESTHmC SURGERY
41
Skin Resurfacing . •
• . • • . • •
• . • • . •
451
Fritz E. Barton
42
Dermal and Soft-Tissue Fillers: Principles,
Materials, and Techniques
458
Z. Paul Lorenc
43
Botulinum Toxin .•
•.••.••.•
•.••.••.•
464
Michael A.C. Kane
44 Fat Grafting in Plastic
• . • • . •
473
Louis P. Bucky, Ivana Percec, and
Daniel Del Alexander Vecchio
45 Forehead and Brow Rejuvenation
• . • • . • • . •
480
Betifamin Z. Phillips, Erick A. Ho:>~ojohnny T. Chang.
]bonny A. Salomon, and Patrick K. Sullivan
46
• . • • . • •
• . • • . •
487
Mark A. Codner and Renee M. Burke
47
Facelift. • . • • . •
• .
• • .
• • .
.
.
.
.
.
.
• .
• .
• .
.
501
Charles H. Thorne
48
• . • • . • •
• . • • . •
512
Jeffrey E. Janis, ]amil Ahmad, and Rod]. Rohrich
49 Otoplasty.••.•
•.••.••.•
•.••.••.•
530
Charles H. Thorne
50 Facial Skeletal Augmentation with Implants • . •
537
Michael]. Yaremchuk and Chad R. Gordon
51
Osseous Genioplasty . • . • • . • • . •
• . • • . • • . •
544
Harvey M. Rosen
52
Hair Transplantation.•.••.••
•.••.•
549
Carlos K. Wesley, Robin H. Unger,
and Walter P. Unger
PART6: 53 Augmentation Mammaplasty: Principles, Techniques, Implant Choices, and Complications . 565 Steven Alan
PART6:
53
Augmentation Mammaplasty: Principles,
Techniques, Implant Choices, and Complications . 565
Steven Alan Teitelbaum
54
Mastopexy and Mastopexy/Augmentation ••.•
582
W. Grant Stevens, Andrea E. Van Pelt,
and Adrian M. Przybyla
55 Breast Reduction: Inverted-t Technique .••.••.•• 593 Scott L. Spear 56 Vertical Reduction Mammaplasty •
55 Breast Reduction: Inverted-t Technique .••.••.•• 593
Scott L. Spear
56 Vertical Reduction Mammaplasty •
• . • • . • • . • • 603
Elizabeth]. Hali-Findlt!:y
57
Gynecomastia . • • . •
• . • • . • • . •
• . • • . • • . • • 615
Nolan S. Karp
58 Breast Cancer: Current Trends in Screening,
Patient Evaluation, and Treatment
•.••.••.••
620
Grant W. Carlson
59 Breast Reconstruction: Prosthetic Teclmiques •.•• 625
Joseph]. Disa and Nima P. Patel
60 Latissimus Dorsi Flap Breast Reconstruction. • . • • 636
Dennis C. Hammond and Michael A. Loffredo
61 Breast Reconstruction: Tram Flap Techniques •.•• 643
fames D. Namnoum
62 Breast Reconstruction: Free Flap Techniques. • . • • 649
Maurice Y. Nahabedian
63 Nipple Reconstruction.•.••.••.•
•.••.••.••
662
MichaelS. Beckenstein
64 Congenital Anomalies of the Breast: Tuberous
Breasts, Poland's Syndrome, and Asymmetry••.•• 668
Kenneth C. Shestak, Stephen Alex Rottgers,
Lorelei]. Grunwaldt, Derek Fletcher,
and Angela Song Landfair
PART7: BODY CONTOURING 65 Liposuction • • . • • . • • . •
PART7:
BODY CONTOURING
65
Liposuction • • . • • . •
• . • • . • • . •
• . • • . • • . • • 679
Mary K. Gingrass
66
Abdominoplasty and Belt Lipectomy.
• . •
• . •
• . •
• 688
AI S. Aly and Emil]. Kohan
67
Lower Body Lift and
Thighplasty •
• . • • .
• • . • •
696
Joseph P. Hunstad and Remus Repta
68
Brachioplasty and Upper Trunk Contouring • • . • • 707
Susan E. Downey
69
Principles of Plastic Surgery After Massive
Weight
Loss.
• .
• • .
• .
.
• .
• • .
• • .
• .
.
• .
• • .
• • .
• •
713
]. Peter Rubin
PART8: HAND 70 Functional Anatomy and Principles of Upper Extremity Surgery •.••.• •.••.••.••
PART8:
HAND
70 Functional Anatomy and Principles
of Upper Extremity Surgery •.••.•
•.••.••.••
721
Kate W. Nellans and Kevin C. Chung
71 Anesthesia Techniques
727
Warren C. Hammert
72 Treatment of Hand lnfections ••.•
•.••.••.••
731
Benjamin Chang and Suhail K. Kanchwala
73 Soft Tissue Reconstruction of the Upper Extremity 737
St:ott L. Hansen, Patrick Lang, and Hani Sbitany
74
Management of Nerve Injuries and Compressive
Neuropathies of the Upper Extremity • • • • • • • • • • 750
St:ott A. Mitchell and Kodi Azari
75
Management
of Hand Fractures . •
• . • • . • • . • • 758
Matthew S.S. Choi andJames Chang
76 Management of Wrist Fractures .•
•.••.••.••
767
Sandeep Jacob Sebastm and Kevin C. Chung
xvi.ii Contentr 77 Flexor Tendon Repair , , , , , , •• , •
xvi.ii
Contentr
77
Flexor Tendon Repair , , , , , , •• , • , , • , •• , •• , • • 784
Brat/on]. Wilhelmi
78
Extensor Tendon
Surgery
•• , •• , • , , • , •• , •• , • • 792
Marft
E.
Puhairulran
79
Tenoaynovitis Disorders of the Upper Extn:mity
.
.
799
Mary
C.
Bums
and
Michael
W.
Neumeister
80 Principles of Tendon Transfers
.
.
.
.
.
.
.
.
.
.
• • . • •
807
Doug/a$
M.
Sam~Mr
81 Ligament Injuries of the Hand and
817
Karim Baltri,
Brian
T.
Carlsen,
and
Steven L.
Moran
82
Management of Mutilating Injuries of the
Upper
Extremity
833
]aimie
T.
Shores and W:
P.
Andrew
Lee
83
Replantation Strategies of the Hand
and Upper Extrenlity.
.
.
.
.
.
.
.
• .
• .
.
• .
• • . • • • • •
839
Sandup
ftUob
~bastinand
Kevin
C.
Chung
84
Thumb Reconstruction
•.••.••
, •• , • •
8S4
Wee Leon
Lam
and Fu-Chan Wei
85
Dupuytren's Disease
•.••.••.•
•.••.••
, ••
863
Catherine
M.
Curtin
16
Hand Tumors
868
Benjamin Levi
and
Kevin
C.
Chung
17
Management of Vasoconstriction
878
Paul K.
Lim
and
Alkn L.
Van Beelt.
II
Management of the
Burned
Hand
.
.
.
.
.
.
.
.
.
.
885
William
C.
Pederson
19
Common Congenital
Hand
Anomalies
.
• • .
• • .
• .
890
Robert
f.
Havlik
90 Targeted Muscle Reinnervation and Upper Limb Amputation 900 Gregory A. Dunumian 91 Rheumatoid 908
90 Targeted Muscle Reinnervation and Upper
Limb Amputation
900
Gregory A. Dunumian
91 Rheumatoid
908
David
T. Nmcher and
Matthew
E. Koepp/inger
92 Chest Wall Reconstruction
921
Joseph
N. Carey,
Leo R.
Otake, Anthony Echo,
and
Gordon
K. Lee
93 Abdonlinal Wall Reconstruction •.••.•
,,.,,.,,
933
Gregory A. Dunumian
9"
Lower
Extremity
• • . • . • • • • •
941
Armen
K.
Kasabian
and
Nolan S. Karp
95
Foot and Ankle Reconstruction
.
.
• • .
• .
.
• .
.
• .
.
955
Christopher E. Attinger
and
Mark
W:
Clemens
96
Reconstruction of the Perineum.•.••.•
,
.
• .
.
971
Paul H.
Tran and Valerie
I
emaine
97
Lymphedema: Diagnosis and Treatment
980
Steven M. Levine, David
W.
Chang.
and
Babak ].
Mehrara
91
Preasure Sores
989
Karen
L.
Powers and Linda
G.
Phillips
99
Reconstruction of the Penis
,
.
.
998
]. ]oris Hage
Illde:r; ••••••••••••••••••••••••••••••••••••••••••••
1003
• PRINCIPLES, TECHNIQUES, AND BASIC SCIENCE CHAPTER 1 • TECHNIQUES AND PRINCIPLES IN PLASTIC SURGERY
PRINCIPLES, TECHNIQUES, AND BASIC SCIENCE
CHAPTER 1 •
TECHNIQUES AND PRINCIPLES
IN PLASTIC SURGERY
CHARLES H. '!HORNE
Plastic surgery is the single most diverse specialty in the medical field, dealing with problems
Plastic surgery is the single most diverse specialty in the
medical field, dealing with problems from the top of the
head to the tip of the toes and with patients ranging in
age from the newborn to nonagenarian. Plastic surgeons are
the ultimate specialists but are also the modem day general
practitioners, unrestricted by organ system, disease process,
or patient age. Without an organ system of its own plastic
surgery is based on principles rather than specific proce-
dures in a defined anatomic location. Because of this free-
dom, whole subspecialties can be added to the field when
new ideas, procedures, and techniques are developed. Since
the previous edition less than a decade ago plastic surgery
has enlarged significandy, adding, for example, vascularized
composite allotransplantation (Chapter 06), fat grafting to
the breast (Chapter 44), and a variety of perforator flaps to
its armamentarium.
What is plastic surgery? No adequate definition exists.
What is the common denominator between craniofacial
surgery and hand surgery and between pressure sore sur-
gery and cosmetic surgery? McCarthy from NYU defines
it as the "problem-solving specialty." A grandiose defi-
nition from a plastic surgery states: "Plastic surgery is
surgery of the skin and its contents." The phrase, plastic
surgery, is derived from the Greek "Plastikos," meaning
to mold or to shape. While many plastic surgical pro-
cedures deal with reshaping, the majority do not, mak-
ing even the title of the specialty somewhat misleading.
No wonder the public has difficulty understanding what
plastic surgery is!
No specialty receives the attention from the lay press that
plastic surgery receives. At the same time, no specialty is less
well understood. Although the public equates plastic surgery
with cosmetic surgery, the roots of plastic surgery lie in its
reconstructive heritage. Cosmetic surgery, an important com-
ponent of plastic surgery, is but one piece of the plastic surgi-
cal puzzle.
Plastic surgery consists of reconstructive surgery and
cosmetic surgery but the boundary between the two, like
the boundary of plastic surgery itself, is difficult to draw.
The more one studies the specialty, the more the distinction
between cosmetic surgery and reconstructive surgery disap-
pears. Even if one asks, as an insurance company does, about
the functional importance of a particular procedure, the
answer often hinges on the realization that the function of the
fac:e is to look like a W:e (i.e., function = appearance). A cleft
lip is repaired so the child wiD look, and therefore hopefully
function, like other children. A common procedure such as a
breast reduction is enormously complex when one considers
the issues of appearance, self-image, sexuality, and woman-
hood, and defies categorization as simply cosmetic or neces-
sarily reconstructive.
This chapter outlines basic plastic surgery principles and techniques that deal with the skin. Cross-references
This chapter outlines basic plastic surgery principles
and techniques that deal with the skin. Cross-references
to specific chapters providing additional information are
provided. Subsequent chapters in the first section will dis-
cuss other concepts and tools that allow plastic surgeons to
tackle complex problems. Almost all wounds and all pro-
cedures involve the skin, even if it is only an incision, and
therefore the cutaneous techniques described in this chapter
are applicable to virtually every procedure performed by
every specialty in surgery.
OBTAINING A FINE-LINE SCAR
OBTAINING A FINE-LINE SCAR
by every specialty in surgery. OBTAINING A FINE-LINE SCAR "Will there be a scar?" Even the

"Will there be a scar?" Even the most intelligent patients ask this preposterous question. When a full-thickness injury oa:urs to the slcin or an incision is made, there is always a scar. The question should be, "Will I have a relatively incon- spicuous, fine-line scar?" The final appearance of a scar is dependent on many fac- tors, including the following: (a) Differences between indi- vidual patients that we do not yet understand and cannot predict; (b) the type of skin and location on the body; (c) the tension on the closure; (d) the direction of the wound; (e) other local and systemic conditions; and, lasdy, (f) surgical technique. The same incision or wound in two different patients will produce scars that differ in quality and aesthetics. Oily or pig- mented skin produces, as a general rule, more unsightly scars (Chapter 2 discusses hypertrophic scars and kdoids). Thin, wrinkled, pale, dry, "WASPy" skin of patients of English or Scotch-Irish descent usually results in less conspicuous scars. Rules are made to be broken, however, and an occasional patient wiU devdop a scar that is not characteristic of his or her skin type. Certain anatomic areas tend to produce unfavorable scars that remain hypertrophic or wide. The shoulder and sternal area are such examples. Conversely, eydid incisions almost always heal with a fine-line scar. Skin loses elasticity with age. Stretched-out skin, combined with changes in the subcutaneous tissue, produces wrinkling, which makes scars less obvious and less prone to widening in older individuals. Children, on the other hand, may heal faster but do not heal "better," in that their scars tend to be red and wide when compared with scars of their grandparents. In addition, as body parts containing scars grow, the scars become proportionately larger. Beware the scar on the scalp of a small childt Just as the recoil of healthy, elastic skin in children may lead to widening of a scar, tension on a closure bodes poorly for the eventual appearance of the scar. The scar associated with a simple elliptical excision of a mole on the back will

eventual appearance of the scar. The scar associated with a simple elliptical excision of a mole
1
1
2 Pan I: Principles, Technique., and Batie Scienc::e likely result in a much less appealing
2
Pan I: Principles, Technique., and Batie Scienc::e
likely result in a much less appealing scar than an incisional
wound. The body knows when it is missing tissue.
The direction of a laceration or excision also determines the
eventual appearance of the scar. The lines of tension in the skin
were first noted by Dupuytren. Langer also described the nonnal
tx:nsion lines, which became known as "Langer lines." Borges
referred to skin lines as '"relcoo:d skin tension lines" (Figure 1.1).
Elective incisions or the excision of lesions are planned
when possible so that the final scars will be parallel to the
relaxed skin tension lines. Maximal contraction occurs when
a scar crosses the lines of minimal tension at a right angle.
Wrinkle lines are generally the same as the relaxed skin ten-
sion lines and lie perpendicular to the long axis ofthe underly-
ing muscles.
Other issues, which are not related to the scar itself but
to perception, detx:rmine if a scar is noticeable. Incisions and
scars can be "hidden" by placing them at the junction of aes-
thetic units (e.g., at the junction of the lip and cheek and along
the nasolabial fold), where the eye expects a change in contour
(Chapter xx).ln contrast, an incision in the midcheek or mid-
chin or tip of the nose wiU always be more conspicuous.
The shape of the wound also affects ultimatx: appearance.
The "trapdoor" scar results from a curvilinear incision or
laceration that, after healing and contracture, appears as a
depressed groove with bulging skin on the inside of the curve.
Attempts at "defatting" the bulging area are never as satisfac·
tory as either the patient or surgeon would like.
Local conditions, such as crush injury of the skin adja-
cent to the wound, also affect the scar. So, too, wiD systemic
conditions such as vascular disease or congenital conditions
affecting elastin and/or wound healing. Nutritional status
can affect wound healing, but usually only in the extreme
of malnutrition or vitamin deficiency. Nutritional status is
overemphasized as a factor in scar formation.
Technique is also overemphasized (by self-serving plas-
tic surgeons) as a factor in determining whether a scar will
be inconspicuous, but it is certainly of some importance.
be inconspicuous, but it is certainly of some importance. FIGUJlE 1.1. RelaxJ:d skin tmsion lines. (Reproduced
FIGUJlE 1.1. RelaxJ:d skin tmsion lines. (Reproduced with pc:.nnis- aion from Ruberg R. L.lD: Smith
FIGUJlE 1.1. RelaxJ:d skin tmsion lines. (Reproduced with pc:.nnis-
aion from Ruberg R. L.lD: Smith DJ, cd. Plastic Surgery, A Ccwe
Cumculum. St. Louis, MO: Mosby, 1994.)
Minimizing damage to the skin edges with atraumatic tech- nique, debridement of necrotic or foreign
Minimizing damage to the skin edges with atraumatic tech-
nique, debridement of necrotic or foreign material, and a ten·
sion-free closure are the first steps in obtaining a fine-line scar.
Ultimately, however, scar formation is unpredictable even
with meticulous technique.
Two technical factors are of definite importance in increas·
ing the likdihood of a "good" scar. First is the placement
of sutures that are not excessively tight and are removed
promptly so disfiguring "railroad tracks" do not occur. In
other words, removing the sutures may be more important
than placing them! Plastic surgeons have been known to mock
other specialists for using heavy-gauge suture for skin clo-
sure, but the choice of sutures is irrelevant if the sutures are
removed soon enough and if they have not been tied so tightly
that they tear through the skin. Sutures on the face can usually
be removed in 3 to S days and on the body in 7 days or less.
Except for wounds over joints, sutures should rarely be left in
for more than 1 week. A subcutaneous layer of closure and
Steri-Strips are usually sufficient to prevent dehiscence.
The second important technical factor that may aflect the
appearance of sc:ars is wound-edge eversion. While there is no
evidence to support this statement, it is the author's clinical
experience that evertl:d wound closures never look worse and
often result in a less conspicuous scar than their non-everted
counterparts. In wounds where the skin is brought precisdy
together, there is a tendency for the scar to widen. In wounds
where the edges are everted, or even hyper-everted in an exag-
gerated fashion, this tendency may be reduced, possibly by
reducing the tension on the closure. In other words, the ideal
wound closure is not perfectly flat, but rather bulges with an
obvious ridge, to allow for eventual spreading of that wound.
Wound-edge eversion always goes away. The surgeon need not
ever worry that a hyper-evertx:d wound will remain that way.
CLOSURE OF SKIN WOUNDS
CLOSURE OF SKIN WOUNDS
While the most common method of closing a wound is with sutures, there is nothing
While the most common method of closing a wound is with
sutures, there is nothing necessarily magic or superior about
sutures. Staples, skin tapes, or wound adhesives are also useful
in certain situations. Regardless of the method used, precise
approximation of the skin edges without tension is essential to
ensure primary healing with minimal scarring.
Wounds that are deeper than skin are closed in layers. The
key is to eliminate dead space, to provide a strong enough clo-
sure to prevent dehiscence while wound healing is occurring,
and to precisely approximate the skin edges without tension.
Not all layers necessarily require separate closure. A closure
over the calf, however, is subject to motion, dependence, and
stretching with walking, requiring a stronger closure than the
scalp, which does not move, is less dependent, and not subject
to tension in daily activities. Placing deep absorbable sutures
is not always desirable. The author tends to use only Nylon
skin sutures without any deeper sutures when approximating
pediatric facial lacerations because of an impression that there
is less inflauunation and erythema and certainly less chance of
suture abscess.
Except for dermal sutures, which are placed with the knot
buried to prevent it from emerging from the skin during the
healing process, sutures should be placed with the knot super-
ficial to the loop of the suture (not buried), so that the tissue
layers can be everted (Figure 1.2A).
Buried dermal sutures provide strength so the external
sutures am be removed early, but do not prevent the scar £rom
spreading over time. There is no technique, even the technique
of eversion desaibed above, that reliably prevents a wound
that has an inc:lination to widen £rom doing so.
Suturing Techniques Techniques for suturing are illustrated in Figure 1.2 and are listed below.
Suturing Techniques
Techniques for suturing are illustrated in Figure 1.2 and are
listed below.

A

D

A D E Chapter 1: Techniqua and Principles in Plastic Suqery 3 B c F H
A D E Chapter 1: Techniqua and Principles in Plastic Suqery 3 B c F H

E

Chapter 1: Techniqua and Principles in Plastic Suqery
Chapter 1: Techniqua and Principles in Plastic Suqery

3

B

E Chapter 1: Techniqua and Principles in Plastic Suqery 3 B c F H FIGURE 1.2.
E Chapter 1: Techniqua and Principles in Plastic Suqery 3 B c F H FIGURE 1.2.
c
c
Chapter 1: Techniqua and Principles in Plastic Suqery 3 B c F H FIGURE 1.2. Types

F

1: Techniqua and Principles in Plastic Suqery 3 B c F H FIGURE 1.2. Types of
1: Techniqua and Principles in Plastic Suqery 3 B c F H FIGURE 1.2. Types of
H
H

FIGURE 1.2. Types of sldn closure. A. Simple inte.rrupted. B. Vertical mattress. C. Horizontal mattress. D. Subcuticular continuoUJ. E. Half- buried horizontal mattress. F. Cont:inuoUJ over-and~ver.G. Staples. H. Skin tapes (skin adhesive pe.rforms a similar function).

Simple Interrupted Suture. The simple interrupted suture is the gold standard and the most commonly
Simple Interrupted Suture. The simple interrupted suture
is the gold standard and the most commonly employed suture.
The needle is introduced into the skin at an angle that allows
it to pass into the deep dermis at a point further removed from
the wound edge. This allows the width of suture at its base in
the dermis to be wider than the epidermal entrance and exit
pGints, giving the suture a triangular appearance when viewed
in cross sectiGn. It also everts the skin edges. Care must be
taken to ensure that the suture is placed at the same depth on
each side Gf the incision or wound, otherwise the edges will
overlap. Sutures are usually placed approximately 5 to 7 mm
apart and 1 to 2 mm from the skin edge, although the location
and size of the needle and caliber of the suture material make
this sGmewhat variable.
Vertical Mattress Suture. Vertical mattress sutures may be used when eversion of the skiD. edges
Vertical Mattress Suture. Vertical mattress sutures may
be used when eversion of the skiD. edges is desired and cannot
be accomplished with simple sutures alone. Vertic:al mattress
sutures tend to leave the most obvious and unsighdy cross-- hatching if not removed early.
sutures tend to leave the most obvious and unsighdy cross--
hatching if not removed early.
Horizontal Mattress Suture. Horizontal mattress sutw:es
have been much maligned but are the author's favorite suture
for reliable skin edge approximation and eversion. They are
particularly advantageous in thick glabrous skin (feet and
hand). In the author's opinion, homontal mattress sutures are
&r superior to their vertical counterparts.
Subcuticular Suture. Subcuticular (or intradermal) sutures
can be interrupted or placed in a running fashion. In a run-
ning subcutaneous closure, the needle is passed horizontally
through the superficial dermis, parallel to the skin surface,
to provide close approximation of the skin edges. Care is
taken to ensure that the sutures are placed at the same level.
Such a technique obviates the need for external skin sutures
and circumvents the possibility of suture marks in the skin.
4 Pan I: Principles, Techniques, and Batie Scienc::e Absorbable or nonabsorbable suture can be used,
4
Pan I: Principles, Techniques, and Batie Scienc::e
Absorbable or nonabsorbable suture can be used, with the lat-
ter to be removed at 1 to 2 weeks after suturing.
Half-Buried Horizontal Mattress Suture. Half-buried
horizontal mattress sutures are used when it is desirable to
have the knots on one side of the suture line with no suture
marks on the other side. For example, when insetting the are-
ola in breast reduction, this method leaves the suture marks
on the dark, pebbly areola instead of on the breast skin.
Continuous Over-and-Over Suture. Continuous over-
and-over sutures, otherwise known as running simple sutures,
can be placed rapidly but depend on the wound edges being
more or less approximated beforehand. A continuous suture
is not nearly as precise as interrupted sutures and the author
almost never uses them on the face. Continuous sutures can
also be placed in a locking fashion to provide hemostasis by
compression of wound edges. They are especially useful in
scalp closures.
Skin Staples. Skin staples are particularly useful as a time- saver for long incisions or
Skin Staples. Skin staples are particularly useful as a time-
saver for long incisions or to position a skin closure or flap
temporarily before suturing. Grasping the wound edges with
forceps to evert the tissue is helpful when placing the staples
to prevent inverted skin edges. Staples must be removed early
to prevent skin marks and are ideal for the hair-bearing scalp.
Skin Tapes. Skin tapes can effectively approximate the
wound edges, although buried sutures are often required in
addition to skin tape to approximate deeper layers, relieve
tension, and prevent inversion of the wound edges. Skin tapes
can also be used after skin sutures are removed to provide
added strength to the closure.
Skin Adhesives. Skin adhesives have been developed and may have a role in wound closure,
Skin Adhesives. Skin adhesives have been developed and
may have a role in wound closure, especially in areas where
there is no tension on the closure, or where strength of clo-
sure has been provided by a layer of buried dermal sutures.
Adhesives, by themselves, however, do not evert the wound
edges. Eversion must be provided by deeper sutures.
wound edges. Eversion must be provided by deeper sutures. Methods of Excision lar, or serial excision.
Methods of Excision lar, or serial excision.
Methods of Excision
lar, or serial excision.

Lesions of the skin can be excised with elliptical, wedge, circu-

of the skin can be excised with elliptical, wedge, circu- Elliptical Excision. Simple elliptical excision is

Elliptical Excision. Simple elliptical excision is the most commonly used technique (Figure 1.3). Elliptical excision of inadequate length may yield "dog-ears,,. which consist of excess skin and subcutaneous fat at the ends of a closure. There are several ways to correct a dog-ear, some of which are

are several ways to correct a dog-ear, some of which are A FIGURE 1.3. Elliptical e:xcision.
are several ways to correct a dog-ear, some of which are A FIGURE 1.3. Elliptical e:xcision.
are several ways to correct a dog-ear, some of which are A FIGURE 1.3. Elliptical e:xcision.
are several ways to correct a dog-ear, some of which are A FIGURE 1.3. Elliptical e:xcision.
A
A
FIGURE 1.3. Elliptical e:xcision. A. If the ellipse is too short, dog-ears (arrows) form at
FIGURE 1.3. Elliptical e:xcision. A. If the ellipse is too short, dog-ears
(arrows) form at the ends of the closed wound. B. Correct method
with length ofellipte at least tluee times the width.
shown in Figure 1.4. Dog-ears are the bane of plastic surgical existence and one must
shown in Figure 1.4. Dog-ears are the bane of plastic surgical
existence and one must be facile with their elimination. Dog·
ears do not disappear on their own.
Wedge Excision. Lesions located at or adjacent to free margins can be excised by wedge
Wedge Excision. Lesions located at or adjacent to free
margins can be excised by wedge excision. In some dderly
patients, one third of the lower lip and one fourth of the upper
lip can be excised with primary closure (Figure 1.5).
Circular Excision. When preservation of skin is desired
(such as the tip of the nose) or the length of the scar must be
kept to a minimum (children), circular excision might be desir-
able. Figure 1.6 shows some closure techniques. Figure 1.6 is
included because these techniques may be of value, as well
r rr r r r r;.!!!. !J--!! £:f -:::.;.-=- A B
r rr r r r r;.!!!. !J--!!
£:f
-:::.;.-=-
A
B
FIGURE 1.4. Three methods of removing a dog-ear caused by making the elliptical excision roo
FIGURE 1.4. Three methods of removing a dog-ear caused by making the elliptical excision roo short. A. Dog-ear excised, making the incision
looger, or converted to a "Y
B. One method of remo'riDg a dog-ear caused by designing an elliptical excision with one side longer than the
other. Converaion to an "L,. e:ffecti.velylengthens the sborll:r side.
Chapter 1: Techniqua and Principles in Plastic Suqery
Chapter 1: Techniqua and Principles in Plastic Suqery

5

Chapter 1: Techniqua and Principles in Plastic Suqery 5 FIGURE 1.5. Wedge excisions of the car,lower
FIGURE 1.5. Wedge excisions of the car,lower eyelid, and lip.
FIGURE 1.5. Wedge excisions of the car,lower eyelid, and lip.
1.5. Wedge excisions of the car,lower eyelid, and lip. B as for historical purposes. Circular defects
1.5. Wedge excisions of the car,lower eyelid, and lip. B as for historical purposes. Circular defects
1.5. Wedge excisions of the car,lower eyelid, and lip. B as for historical purposes. Circular defects
1.5. Wedge excisions of the car,lower eyelid, and lip. B as for historical purposes. Circular defects

B

1.5. Wedge excisions of the car,lower eyelid, and lip. B as for historical purposes. Circular defects
as for historical purposes. Circular defects can also be closed with a purse-string suture that
as for historical purposes. Circular defects can also be closed
with a purse-string suture that causes significant bunching of
the skin. This is allowed to mat:llre for many months and may
result in a shorter scar on, for example, the face of a child.
Serial Excision. Serial excision is the excision of a lesion
in more than one stage. Serial excision and tissue expansion
(Chapter xx) are frequently employed for large lesions such
as congenital nevi. The inherent viscoelastic properties of skin
are used, allowing the skin to "stretch" over time. Serial exci-
sion enables wound closure to be accomplished with a shorter
scar than if the original lesion was elliptically excised in a
B'
single stage.
SKIN GRAFTING
SKIN GRAFTING
Skin grafts are a standard option for closing defects that can- not be closed primarily.
Skin grafts are a standard option for closing defects that can-
not be closed primarily. A skin graft consists of epidermis and
some or all of the dermis. By definition, a graft is something
that is removed from the body, is completely devascularized,
and is replaoed in another location. Grafts of any kind require
vascularization from the bed into which they are placed for
survival. Any tissue that is not completely removed prior to
placement is not a graft.
FIGURE 1.6. Closure of wounds following circ:ular excision. A. Skin graft. B. Sliding triangular subcutaneous
FIGURE 1.6. Closure of wounds following circ:ular excision.
A. Skin graft. B. Sliding triangular subcutaneous pedicle flap• can be
advanced to close the cin:ular defect; the triangular delect i• closed in a
V-Y fashion. C. Tran~positionflaps based on a skin pedicle and rotated
toward each other can abo be !lied. Circular defect~can abo be closed
by other local Saps (Figures 1.10-1.15) or by purse«ring suture.
Skin Graft Types Skin grafts are classified as either split-thickness or .full-thick- ness, depending on
Skin Graft Types
Skin grafts are classified as either split-thickness or .full-thick-
ness, depending on the amount of dermis included. Split-
thickness skin grafts contain varying amounts of dermis,
whereas a .full-thickness skin graft contains the entire dermis
(Figure 1.7}.
All skin grafts contract immediately after removal from the
donor site and again after revascularization in their final loca-
tion. Primary c:ontraction is the immediate recoil of freshly
harvested grafts as a result of the elastin in the dermis. The
more dermis the graft has, the more primary the contraction
that will be experienced. Secondary c:ontraaure, the real nem-
esis, involves contraction of a healed graft and is probably
a result of myofibroblast activity. A full-thickness skin graft
contracts more on initial harvest (primary contraction) but
less on healing (secondary contracture) than a split-thickness
skin graft. The thinner the split-thickness skin graft, the
greater the secondary contracture. Granulating wounds left to
heal secondarily, without any skin grafting, demonstrate the greatest degree of contracture and are most
heal secondarily, without any skin grafting, demonstrate the
greatest degree of contracture and are most prone to hyper-
trophic scarring.
The number of epithelial appendages transferred with a
skin graft depends on the thickness of the dermis present.
The ability of grafted skin to sweat depends on the num-
ber of glands transferred and the sympathetic reinnerva-
tion of these glands from the recipient site. Skin grafts are
reinnervated by ingrowth of nerve fibers from the recipient
bed and from the periphery. Full-thiclrness skin grafts have
the greatest sensory return because of a greater availability
of neurilemmal sheaths. Hair follicles are also transferred
with a full-thickness skin graft. In general, full-thickness skin
grafts demonstrate the hair growth of the donor site whereas
split-thickness skin grafts, especially thin split-thickness skin
grafts, are generally hairless.
Chapter 1: Techniqua and Principles in Plastic Suqery
Chapter 1: Techniqua and Principles in Plastic Suqery

7

Skin graft
Skin graft
FIGURE 1.8. Tie-over bolst:u dr~iDgfor skin graftt;.
FIGURE 1.8. Tie-over bolst:u dr~iDgfor skin graftt;.
Biologic Dressings Skin grafts can also be used as temporary coverage of wounds as biologic
Biologic Dressings
Skin grafts can also be used as temporary coverage of wounds
as biologic dressings. This protects the recipient bed from
desiccation and further trauma until definitive closure can
occur. In large burns where there is insufficient skin to be har-
vested for coverage, skin substitutes can be used (Chapter 18).
Biologic skin substitutes include human allografts (cadaver
skin), amnion, or xenografts (such as pig skin). Allografts
become vascularized (or "take") but are rejected at approxi-
mately 10 days unless the recipient is immunosuppressed
(e.g., has a large burn), in which case rejection takes longer.
Conversely, nnografts are rejected before becoming vascular-
ized. Synthetic skin substitutes such as silicone polymers and
composite membranes can also be applied, and new skin sub-
stitutes are constantly being developed. Human epidermis can
be cultured in vitro to yield sheets of cultured epithelium that
will provide coverage for large wounds. The coverage is frag-
ile as a result of the lack of a supporting dermis.
SKIN FLAPS Unlike a skin graft, a skin flap has its own blood supply. Flaps
SKIN FLAPS
Unlike a skin graft, a skin flap has its own blood supply. Flaps
are usually required for covering recipient beds that have poor
vascularity; covering vital structures; reconstructing the .full
thickness of the eyelids. lips, ears. nose, and cheeks; and pad·
ding body prominences. Flaps are also preferable when it may
be necessary to operate through the wound at a later date to
repair underlying structures. In addition, muscle flaps may
provide a .functional motor unit or a means of controlling
infection in the recipient area. Muscle flaps and microvascular
free flaps are discussed in Chapters xx and xx.
In an experimental study, Mathes et al. compared muscu·
locutaneous flaps with "random" skin flaps to determine the
bacterial clearance and oxygen tension of each (Figure 1.9).
Placement of 10 7 Staphylococcus aureus underneath random
skin flaps in dogs resulted in 100% necrosis of the skin flaps
within 48 hours; the musculocutaneous flaps, however, dem-
onstrated long-term survival. The quantity of viable bacteria
placed in wound cylinders under these flaps demonstrated an
immediate reduction when placed deep to musculocutaneous
flap. Oxygen tension was measured at the distal end of the
random flap and compared with that underneath the muscle
of the distal portion of musculocutaneous flap as well as in its
subcutaneous area. It was found that the oxygen tension in
the distal random flap was significantly less than in the distal
muscular and cutaneous portions of the musculocutaneous flap.
This study has been used to justify transfer of muscle flaps in
infected wounds. It may be that well-vascularized skin flaps
would be equally efficacious as muscle flaps.
Finally, a flap may be chosen because the aesthetic result
will be superior. For example, a nasal defect from a skin can·
cer could be closed with a skin graft, leaving a visible patch.
A local skin flap may require incisions in the adjacent nasal
tissue, but may be aesthetically preferable in the long term.
There is no better tissue to replace nasal tissue than nasal tis·
sue. Replace like with like.
A skin flap consists of skin and subcutaneous tissue that
are transferred from one part of the body to another with a
vascular pedicle or attachment to the body being maintained
for nourishment. Proper planning of a flap is essential to the
success of the operation. All possible sites and orientations for
the flap must be considered so that the most suitable option
is selected.
Derma l-suhdermal ple xus D irect cu taneous artery I. Axial pat tern flap 2.
Derma l-suhdermal
ple xus
D irect cu taneous artery
I. Axial pat tern flap
2. Island axia I pattern fnap
locu tancous
3
Free Ha p
perforator artery
A . RANDOM PATT ERN SKIN F LA P
B.
AXIAL PAT TERN SKIN FLAPS
FIGURE 1.9. "Ol~fashloned"classification of skin flaps. A. Random patwn. B. Axial pattl:rn.

8

Pan I: Principles, Tedmiquet, and Batie Scienc::e
Pan I: Principles, Tedmiquet, and Batie Scienc::e
Planning the flap in reverse is an important principle. A pattern of the defect is
Planning the flap in reverse is an important principle. A
pattern of the defect is transkrred onto a piece of cloth towel-
ing. The steps in the operative procedure are carried out in
reverse order, using this pattern until the donor site is reached.
The flap is designed slightly longer than needed, as some
length will be lost in the rotation process and slight redun-
dancy may avoid kinking of the flap blood supply. The pro·
cess is repeated, being certain each time the base is held in a
fixed position and not allowed to shift with the flap. Measure
twice, c:ut onc:e. It is easier to trim a flap that is slightly long
than to add to one that is too small.
Planning a transposition or rotation flap requires atten-
tion to ensure that the line of greatest tension from the pivot
point to the most distal part of the flap is of sufficient length
(Figures 1.10, 1.11, and 1.12).
Local skin flaps are of two types: flaps that rotate about a
pivot point (rotation, transposition, and interpolation flaps)
(Figures 1.10 and 1.11) and advancement flaps (single-pedicle
advancement, V-Y advancement, Y-V advancement, and
bipedicle advancement flaps) (Figures 1.17 and 1.18).
Flaps Rotating about a Pivot Point Rotation, transposition, and interpolation flaps have in common a
Flaps Rotating about a Pivot Point
Rotation, transposition, and interpolation flaps have in
common a pivot point and an arc through which the flap is
rotated. The radius of this arc is the line of greatest tension of
Defect
Defect
A c B Backcut Burow's. triangle
A
c
B
Backcut
Burow's. triangle
FIGURE 1.10. Rotation flap. The edge ofthe flap is four to five times the length
FIGURE 1.10. Rotation flap. The edge ofthe flap is four to five times
the length ofthe base ofthe defect triangle. A badt-cutor a Biitow tri-
angle c:an be used if the Sap is under e:x:teS6ive tx:nsion. A. Pivot point
and line of greatm tx:mion. B. Back-cut. C. Biitow's tri~UJ3(e.
Pritmary defect Secondary defect A Pivot point B Backcut
Pritmary
defect
Secondary
defect
A Pivot point
B
Backcut
FIGURE 1.11. Transposition flap. (A) The secondary deled: is often closed by a skin gralt.
FIGURE 1.11. Transposition flap. (A) The secondary deled: is often
closed by a skin gralt. (B) A back-cut can be used if the flap is wtde.r
excessive tx:nsion.
, ---- - - ~' ,,.-~ // ', .I ~\"' '/ I ' I ,,
,
----
-
-
~'
,,.-~
//
',
.I
~\"'
'/
I
'
I
,,
/
I
\
I
I
'
'/
I
',
,'
I
\
'I
\
'\:
,'
\
'I
'
: ' ,,
,_J
\
'\
I
,
,.
I
-
,
\
'
:
1/
,'
'\\
',
l
/'
I
\
',,
\ /
/
If
'">.<
/
180 °
,~-- --
'
'
t<
·~t(E
>I

FIGURE 1.12. Importance of the pivot point. A skin flap rotated about a pivot point becomes shortx:r in effective length the farther it is rotated. Planning with a cloth pattern is helpful when designing sucha&ap.

in effective length the farther it is rotated. Planning with a cloth pattern is helpful when
in effective length the farther it is rotated. Planning with a cloth pattern is helpful when
in effective length the farther it is rotated. Planning with a cloth pattern is helpful when
Chapter 1: Techniqua and Principles in Plastic Suqery FIGURE 1.13. Transpos.ition Sap that can be
Chapter 1: Techniqua and Principles in Plastic Suqery
FIGURE 1.13. Transpos.ition Sap that can be used to close de:fea:s on
the anll:rior cheek. A. Small defects can be closed by a s.ingle transpo-
sition cheek flap that follow• the skin lines. B. Large defect~ can be
closed by a double transposition £lap that U!iell a flap of postauricular
skin to close the secondary defect left by the cheek £lap.
that are the same length as the short axis of the rhomboid defect (Figures 1.15
that are the same length as the short axis of the rhomboid
defect (Figures 1.15 and 1.16).
Advancement Flaps All advancement flaps are moved directly forward into a defect without any rotation
Advancement Flaps
All advancement flaps are moved directly forward into
a defect without any rotation or lateral movement•
the flap. The realization that these flaps can be rotated only about the pivot point
the flap. The realization that these flaps can be rotated only
about the pivot point is important in preoperative planning.
The rotation flap is a semicircular flap of skin and subcuta-
neous tissue that rotates about a pivot point into the defect to
be closed (Figure 1.10). The donor site can be closed by a skin
graft or by direct suture of the wound.
A flap that is too tight along its radius can be released by
making a short back<ut from the pivot point along the base of
the flap. Because this back-cut dec.n:ases the blood supply to the
flap, its use requires some degree of caution. With some flaps
it is possible to back<ut only the tissue responsible for the ten-
sion, without reducing the blood supply to the flap. Examples
of this selective cutting are found in the galea aponc:urotica of
the scalp and in areas over the trunk where the fascia within
the thick subcutaneous layer can be divided. The necessity for a
back<ut may be an indication of poor planning. A triangle of
skin (Biirow triangle) can be removed from the area adjacent
to the pivot point of the flap to aid its advancement and rota-
tion (Figure 1.10C). This method is of only modest benefit in
decreasing tension along the radius of the flap.
The transposition flap is a rectangle or square of skin and
subcutaneous tissue that also is rotated about a pivot point
into an immediately adjacent defect (Figure 1.11). This neces-
sitates that the end of the flap adjacent to the defect be des-
ignated to ex:tend beyond it (Figures 1.12 and 1.13). As the
flap is rotated, with the line of greatest tension as the radius
of the rotation arc, the advancing tip of the flap will be suf-
ficiently long. The flap donor site is closed by skin grafting,
direct suture of the wound, or a secondary flap from the most
lax skin at right angles to the primary flap. An example of this
latter technique is the ingenious bilobed flap (Figure 1.14).
The key to a successful bilobed flap is an area of loose skin to
permit direct closure ofthe secondary flap defect. Pinching the
skin between the examiner's fingers helps find the loosest skin,
for example, in the glabellar area and lateral to the eyelids.
The Limberg flap is a type of transposition flap. This
flap, like the bilobed flap and the Z·plasty (discussed below),
depends on the looseness of adjacent skin, which can be
located by pinching various areas of skin between the thumb
and the forefinger. Fortunately, most patients who require
local skin flaps are in the older age group and therefore have
loose skin. A Limberg flap is designed for rhomboid defects
with angles of 60" and 120", but most wounds c:an be made
rhomboid, or imagined as rhomboid, so the principle is appli-
cable to most facial wounds. The flap is designed with sides
cable to most facial wounds. The flap is designed with sides + • z ~ (,/)

+

• z ~ (,/) 1.1-l Vl 0 0 -l
z
~
(,/)
1.1-l
Vl
0
0
-l
FIGURE 1.14. Bilobed flap. After the lesion is excised, the primary flap (P) is traD.sposed
FIGURE 1.14. Bilobed flap. After the lesion is excised, the primary flap (P) is traD.sposed into the initial defea. The secondary flap {S) is then
transpoaed into the defect left after the primary flap has been moved. The primary flap is slightly narrower than the defect caused by excision of
the initial lesion, and the secondary flap is half the diameter of the primary flap. For the bilobed £lap to be successful. the secondary flap must
c:ome from an area of loose skin to that the defect remaining after moving the secondary flap can be closed by approximation of the wound edges.
Three possible choices for the secondary flap (Sl. S2, and S3) are depicted. The surgeon chooses the location of the secondary flap based on the
skin laxity and the location of the eventual scar.

10

Pan I: Principles, Teclmiquet, and Basic Scienc::e
Pan I: Principles, Teclmiquet, and Basic Scienc::e
D D' 0 F • LOOSE SI<IN • F E ~
D
D'
0
F
LOOSE
SI<IN
F
E
~
FIGURE 1.1S. Planning a rhomboid (Limberg) flap. The rhomboid defect must have 60• and 120"
FIGURE 1.1S. Planning a rhomboid (Limberg) flap. The rhomboid defect must have 60• and 120" angle&. The Sap is planned in an area ofloose
skin so that direc:t closure o£ the wound edges is possible. The short diagonal BD (which is the same length as each side) is extended by its own
length to point B. The line BP is drawn parallel to CD and is o£ the same length. After the flap margins have been incised, the flap is traasposed
into the rhomboid de:fect:.
Modifications are the single-pedicle advancement, the V-Y advancement, and the bipedicle advancement flaps. Advancement
Modifications are the single-pedicle advancement, the
V-Y advancement, and the bipedicle advancement flaps.
Advancement flaps are also used in the movement of
expanded skin (Chapter 10).
The single-pedicle advancement flap is a rectangular or
square flap of skin and subcutaneous tissue that is stretched
forward. Advancement is accomplished by taking advantage
of the elasticity of the skin (Figure 1.17A) and by excising
Burow triangles lateral to the flap (Figure 1.17B). These trian-
gular excisions help to equalize the length between the sides of
the flap and adjacent wound margins.
A B C D
A
B
C
D

FIGURE 1.16. Four Limberg flaps are available for any rhomboid defect with 60" and 120• angles. The choice is made based on the location ofthe eventual sc:ar, skin laxity, and blood supply ofthe flap.

eventual sc:ar, skin laxity, and blood supply ofthe flap. The V-Y advancement technique has numerous applica-
eventual sc:ar, skin laxity, and blood supply ofthe flap. The V-Y advancement technique has numerous applica-
eventual sc:ar, skin laxity, and blood supply ofthe flap. The V-Y advancement technique has numerous applica-
The V-Y advancement technique has numerous applica- tions. It is not an advancement in the
The V-Y advancement technique has numerous applica-
tions. It is not an advancement in the same sense as the forward
movement of a skin flap just described. Rather, a V-shaped
incision is made in the skin, after which the skin on each side of
the Vis advanced and the incision is closed as a Y (Figure 1.18).
This V-Y technique can be used to lengthen such structures as
the nasal columella, eliminate minor notches of the lip, and, in
certain instances, close the donor site of a skin flap.
Z-PLASTY Geometric Principle of the Z-Plasty The Z-plasty is an ingenious principle that has numerous
Z-PLASTY
Geometric Principle of the Z-Plasty
The Z-plasty is an ingenious principle that has numerous
applications in plastic surgery (Chapter 18). Z-plasties can be
applied to revise and redirect existing scars or to provide addi-
tional length in the setting of scar contracture. The principle
involves the transposition of two triangular flaps (Figure 1.19).
The limbs of the Z must be equal in length to the central limb,
but can extend at varying angles (from 30° to 90°) depend-
ing on the desired gain in length. The classic Z-plasty has an
angle of 60° (Table 1.1) and provides a 75% theoretical gain
in
length of the central limb by recruiting lateral tissue.
Gain in length is in the direction of the central limb of the
Z
and depends on the angle used and the length of the central
limb. Although the theoretical gain can be determined math-
ematically, the actual gain is based on the mechanical proper-
ties of the skin and is always less.
Planning and Uses of the Z-Plasty
Planning and Uses of the Z-Plasty

The resulting central limb, after flap transposition, will be perpendicular to the original central limb. In scar revi- sion, the .final central limb should lie in the direction of the skin lines and should be selected first. The Z-plasty is then designed. The Z-plasty principle can be used to increase the length of skin in a desired direction. For example. it is useful for release of scar contractures, especially in cases in which the scar crosses a flexion crease. Any number of Z-plasties can be designed in series, especially in cosmetically sensitive areas (such as the face) to break up the appearance of a straight line or to release a contracture. Large Z-plasties, however, do not look good on the face and it is better to use many tiny Z-plasties. Congenital skin webs can also be corrected with

do not look good on the face and it is better to use many tiny Z-plasties.
Chapter 1: Techniqua and Principles in Plastic Suqery 11 0"':1 . i ~ ~.! A
Chapter 1: Techniqua and Principles in Plastic Suqery
11
0"':1
.
i
~
~.!
A
A
c
B
B
FIGURE 1.1,. Classic 60• angle Z.plasty. Inset shows the method of
finding the 60° angle by first drawing a 90° angle, then dividing it in
thirds by sighting. The limbs of the Z must be equal in length to the
central member. A. Design. B. Transposition of flaps. C. Final result.
Note that the central limb has changed the cfuection by 90°.
I
I' I~Jil'.
and universality that Z-plasty has. This technique simply
involves excising the scar in multiple small triangles that are
so situated that they interdigitate (Figure 1.20). Although the
/
I
(~
.
u
W-plasty changes the direction of the linear scar, it would only
be by chance that one of the limbs of the W would lie in the
same direction as the skin lines. Because a W-plasty does not
'
I
y
Pantographic
C
expansion
FIGURE 1.17. Siqle-pedicle advancement flaps. A. Advanc:ei11CDt by
taking advantage of the skin elasticity. B. Advanc:ei11CDt by exciting
Biirow triangles of skin laterally to equalize the length of the flap and
the adjacent wound edge. C. Pantographic expansion. This method is
frequently used after the skin expansion but is risky as the back-cuts
decrease the blood supply.
lengthen a contracted scar line, it is bert to use the Z-plasty for
this purpose.
Both the Z-plasty and the W-plasty have the additional
attribute of breaking up a linear scar into an accordion-like
scar that has some degree of elasticity to it. This change per·
mits the skin to be more mobile in its conttibution to facial
expressions. To their detriment, both techniques more than
double the length of the scar. If the W-plasty is employed,
the triangles must be made very small to avoid worsening the
appearance of the scar.
RECONSTRUCTIVE LADDER
RECONSTRUCTIVE LADDER
Z-plasties. U-shaped or "trapdoor" scars may be improved by breaking up the conttacting line. Circwnferential
Z-plasties. U-shaped or "trapdoor" scars may be improved
by breaking up the conttacting line. Circwnferential scars are
amenable to lengthening using Z-plasties, especially in con-
stricting bands of the extremities. These deformities are best
released one-half at a time because of concern over interrup-
tion of blood supply to the extremity.
Borges described the W-plasty as another method of revis-
ing a scar. It is useful occasionally, but lacks the applicability
scar. It is useful occasionally, but lacks the applicability > FIGURE 1.18. V-Y advancement. It is

>

It is useful occasionally, but lacks the applicability > FIGURE 1.18. V-Y advancement. It is the
FIGURE 1.18. V-Y advancement. It is the skin on each side of the V that
FIGURE 1.18. V-Y advancement. It is the skin on each side of the V
that is actually advanc:ed.
the skin on each side of the V that is actually advanc:ed. The techniques described above

The techniques described above are applicable to cutaneous defects. Plastic surgeons often are consulted regarding clos- ing more complex defects. When analyzing a wound. whether

ing more complex defects. When analyzing a wound. whether TABLE 1.1 Z·PLASTY, ANGLES, AND THEORETICAL GAIN
ing more complex defects. When analyzing a wound. whether TABLE 1.1 Z·PLASTY, ANGLES, AND THEORETICAL GAIN
TABLE 1.1 Z·PLASTY, ANGLES, AND THEORETICAL GAIN
TABLE
1.1
Z·PLASTY, ANGLES, AND THEORETICAL GAIN
• ANGELS OF Z-PLASTY (DEGREES) • nmoRETICAL GAIN IN LENGTH (%) 30-30 25 45-45 50
• ANGELS OF Z-PLASTY
(DEGREES)
• nmoRETICAL GAIN
IN LENGTH (%)
30-30
25
45-45
50
60-60
75
75-75
100
90-.90
120

12

Pan I: Principles, Technique., and Batie Scienc::e
Pan I: Principles, Technique., and Batie Scienc::e
FIGURE 1.20. The W-plasty can also be used to break up a long scar that
FIGURE 1.20. The W-plasty can also be used to break up a long scar
that does not lie in the direction of the skin lines.
FREE TISSUE TRANSFER
FREE TISSUE
TRANSFER
t REGIONAL TISSUE TRANSFER
t
REGIONAL TISSUE
TRANSFER
t LOCAL TISSUE TRANSFER
t
LOCAL TISSUE
TRANSFER
t SKIN GRAFT
t
SKIN GRAFT
t DIRECT TISSUE CLOSURE
t
DIRECT TISSUE CLOSURE
t ALLOW WOUND TO HEAL BY SECONDARY INTENTION FIGURE 1.21. Rtlconstructi.ve ladder demonstrating the fundamental
t
ALLOW WOUND TO HEAL BY SECONDARY
INTENTION
FIGURE 1.21. Rtlconstructi.ve ladder demonstrating the fundamental
principle in planning dosu.re of a de:fect from s.imple to more complex.
planning dosu.re of a de:fect from s.imple to more complex. cutaneous or more complex. the options

cutaneous or more complex. the options for closure are eval- uated beginning with the simplest and progressing up the "reconstructive ladder" to the more complex (Figure 1.21). This progression from primary closure to skin graft, to local flap, to regional flap, and to microvascular free flap pro- vides a framework that can be applied to any reconstructive situation. Application of the simplest option that meets the reconstructive requirements ensures a "lifeboat" should the procedure fail. In many situations, however, a higher "IUJJ8" on the ladder is intentionally chosen. For example, a local flap may be selected over a skin graft for a defect on the nose because it may provide a superior result, or a free flap may be chosen for a breast reconstruction when an attached, pedicled flap would suffice because the blood supply of the former is superior.

because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
because the blood supply of the former is superior. CONCLUSION The application of fundamental principles in
CONCLUSION
CONCLUSION
The application of fundamental principles in the practice of plastic surgery allows the surgeon to
The application of fundamental principles in the practice of
plastic surgery allows the surgeon to approach even the most
complex problem in an organized, systematic fashion. This
chapter presents fundamental principles that can be applied to
any wound closure situation.
Suggested Readings Birch j, Br11J1t1JW:k 1'1. The vuculamation of a free full thickne. WD. graft
Suggested Readings
Birch j, Br11J1t1JW:k 1'1. The vuculamation of a free full thickne. WD. graft a
vital microscopic study. Seimd Pl4.uJSIW8. 1!16.!173:1.
Borges AF. Ekaiue lnci$iom tli1UI Sav Rei!Won. Becton, MA: Little, Brown;

1.!173.

CapLI. j, Cerll.dilli D, Tepper 0, et a!. Skin graft ,-uculariution invobes pre- cisely regulated
CapLI. j, Cerll.dilli D, Tepper 0, et a!. Skin graft ,-uculariution invobes pre-
cisely regulated regreaion ud repLr.cement of endothelial cells through
both angiogenesis and ,-asculogenesis. PltUt Reeo:nstf' S11rg. 2{){)5.
In press.
Con
etlle
JM. ~paport Fr. The vasculamation of akin autogrllfts and homo-
grafts: an experimental study in mtu1. Ann Sftrg. 1956;143:306.
Edgerton MT. The An of SllrgiuJ Tt~dniiJIIII. Baltimore, MD: Williams l!c

Wil.k.ins; 1.!188. EdgertonMT, Hansen FC. Matching facial oolor with split thic:kneoss akin grafts from adjacent areas. Pl4.u R«onstr Sftrg. 1960;25:455. Furnas DW, Fischer GW. The Z-plasty: biomechanics and mathemati~s. Bf' J Pltut Sllrg. 1971;24:144. Krizek 1J, R.obton MC. E•ohuion of quantitati'fe bacteriology in 'Wtl'Wid man- agement. AmJSwrg. 1975;130:579. Mathes S, Alpert B, Chang N. Use of the m11sde flap iD. c:hroni~ Meomy- elitis: experimental and clini~al ~orrelation. Pltut R«arntr S11rg. 1982;

and clini~al ~orrelation. Pltut R«arntr S11rg. 1982; 69:815. Robson MC, Krizek TJ, Heaggars JP. Biology of

69:815.

Robson MC, Krizek TJ, Heaggars JP. Biology of surgi~al infe~tions. In:
Robson MC, Krizek TJ, Heaggars JP. Biology of surgi~al infe~tions. In:

Ra'fitch MM, ed. Owrent Probkrm in Sltrgery. Chica&~~;1973. R11dolph R. Inhibition of myofibroblam by sham skin grafts. Pltut R«arntr S•g. 1979;63:473. Tanner JC, Vudep11t J, Olley JF. The mesh skin graft. Pltut R«O'fllh' Swrg.

The mesh skin graft. Pltut R«O'fllh' Swrg. 1964;34:287. Vogt PM, Andree C, et al. Dry, moist

1964;34:287.

Vogt PM, Andree C, et al. Dry, moist and wet skin wo~md repllir. Ann Pltut
Vogt PM, Andree C, et al. Dry, moist and wet skin wo~md repllir. Ann Pltut
S•g. 1995734:493.
CHAPTER 2 •
CHAPTER 2 •
CHAPTER 2 • WOUND HEALING: NORMAL AND ABNORMAL the myYiad events occurring in wound healing, the

WOUND HEALING: NORMAL AND ABNORMAL

the myYiad events occurring in wound healing, the reader is referred to a nwnber of
the myYiad events occurring in wound healing, the reader is
referred to a nwnber of excellent recent reviews.H However,
given the inherent lag in book publication and the rapid pace
of the field, the reader should refer to Medline (http://www
.ncbi.nlm.nih.gov/entrez/query.fcgi) and search for the
latest reviews in the field of wound healing to obtain the most
up-to-the-minute information.
healing to obtain the most up-to-the-minute information. GEOFFREY C. GURTNER AND VICTOR W. WONG Tim RESPONSE
GEOFFREY C. GURTNER AND VICTOR W. WONG
GEOFFREY C. GURTNER AND VICTOR W. WONG
Tim RESPONSE TO INJURY What is wound healing? Definitions might include the repair or reconstitution
Tim RESPONSE TO INJURY
What is wound healing? Definitions might include the repair
or reconstitution of a defi:ct in an organ or tissue, commonly
the skin. However, it is clear that the process of wounding acti-
vates systemic processes that alter the physiology far beyond
the confines of the defi:ct itself. Inflammatory cascades that
impact nearly every organ system and have potentially dire
consequences for survival are initiated, as illustrated by multi-
system organ failure. Furthermore, recent research implicating
the participation of stem and progenitor cells in the wound
healing process requires a broader perspective than one that
SCAR FORMATION VERSUS TISSUE
REGENERATION
focuses
solely on the defect itself. 1 .Z Wound healing may be
best understood as an organism's global response to injury,
regardless ofwhether the location is in the skin, liver, or heart.
Seen from this perspective, it is certainly not an exaggeration
to regard the response to injury as one of the most complex
physiologic processes occurring during adult life.
The complexity of this process is easily demonstrated in
cutaneous wound healing. During the progression from a
traumatic injury to a stable scar, the intrinsic and extrinsic
dotting system are activated; acute and chronic inflamma-
tory responses occur; neovascularization proceeds through
angiogenesis and vasculogenesis; cells proliferate, divide, and
undergo apoptosis; and extracellular matrix (ECM) is depos-
ited and remodeled. These (as well as other events) occur
simultaneously and also interact and influence each other at
the level of gene transcription and protein translation in a
dynamic and continuous fashion. Further, normally sterile tis-
sues encounter and interact with bacteria and other elements
of the external environment in a way that never occurs except
following injury. Thus, it is not surprising that wound heal-
ing and the response to injury are still poorly understood by
scientists and clinicians alike, except at a purely descriptive
or empiric level. The sheer number of commercially avail·
able products of unproven efficacy is a testament to the lack
of mechanistic understanding regarding this most common
surgical problem.
Most textbook chapters on wound healing are an ency-
clopedic catalog of the phenomenology of wound healing.
They list the multitude of cytokines and growth factors that
are observed during wound healing, usually based on experi-
mental models or in vitro systems that may be prone to arti-
fact. With the increasing sensitivity of new technologies such
as quantitative polymerase chain reaction and microarray, the
list of cytokines, growth factors, chemokines, etc. that appear
during wound healing continues to grow at an alarming rate.
How will we ever make sense of this mountain of data so that
we can intervene and alter the outcome of wound healing/
response to injury? In this chapter, a theoretical framework
with which to classify wound healing will be proposed. The
broad biologic transitions that occur during cutaneous wound
healing (i.e., inflammatory phase, proliferative phase, and
remodeling phase) will be described within this context. A:s:J.
abbreviated list of major "factors" will be provided but not
discussed in detail since it remains unclear which of these fac-
tors are of primary or incidental importance in either func-
tional or abnormal wound healing. Finally, an attempt will
be made to understand abnormal hwnan healing within the
proposed theoretical context. For a more detailed list of
A3 discussed, wound healing is an extremely broad and com-
plex topic covering a variety of responses to injury in a variety
of different organ systems. However, some common features
exist. Generally, wound healing represents the response of an
organism to a physical disruption of a tissue/organ to re-estab-
lish homeostasis of that tissue/organ and stabilize the entire
organism's physiology. There are essentially two processes by
which this re-establishment of homeostasis occurs. The first
is the substitution of a different cellular matrix as a patch to
immediately re-establish both a physical and physiologic conti·
nuity to the injured organ. This is the process ofscar formation.
The second process is a recapitulation of the developmental
processes that initially created the injured organ. By reactivat·
ing developmental pathways, the architecture of the original
organ is re-created. 'This is the process ofregeneration.'
The dynamic balance between scarring and tissue regenera-
tion is unique to different tissues and organs (Figure 2.1). For
example, neural injury is characterized by little regeneration
and much scarring, whereas hepatic and bone injury usually
heals primarily through regeneration. It is important to note,
however, that the liver can respond to injury with scarring as
it does in response to repetitive insults during the progression
of alcoholic cirrhosis. Moreover, the same injury in phyloge-
netically related species can result in very different responses.
Thus, limb amputation in newts results in limb regeneration,
whereas in humans, only scarring can occur.
lt is important to realize that the balance between scar
and regeneration is likely subject to evolutionary pressures
and may, in fact, be functional. Thus, a cutaneous injury in
our prehistoric predecessors disrupted their homeostasis with
respect to thermoregulation, blood loss, and, most impor-
tantly, prevention of invasive infection. ln an era before anti-
biotics and sterility, invasive infection was clearly a threat to
life. & such, a very rapid and dramatic recruitment of inflam·
matory cells and a proliferative/contractile burst of activity
to close the wound as quickly as possible were adaptive. The
more leisurely pace of tissue regeneration was a luxw:y that
could not be afforded. However, in the modem world, these
adaptive responses often lead to the disfigurement and func-
tional disability characteristic of burn scars. What was once
functional has become unwanted, in part because of our abil·
ity to close wounds with sutures, circumventing the need for a
vigorous contractile response following injury.
In the same way that scar formation is not always bad,
tissue regeneration is not always good. Peripheral nerve neu·
romas are dysfunctional and harmful attempts at regeneration
of organ systems that have been damaged. They often result in
disabling conditions that threaten the livelihood of an entire

14

Pan I: Principles, Teclmiquet, and Basic Scienc::e
Pan I: Principles, Teclmiquet, and Basic Scienc::e
Re-establis h ing Tissue Homeostasis i n Resp o nse to Injury Tissue regenerilti()n
Re-establis h ing Tissue
Homeostasis i n
Resp o nse to
Injury
Tissue
regenerilti()n
FIGURE 2.1. The different ways organisms and organ systems respond to injuries. Scar formation refers
FIGURE 2.1. The different ways organisms and organ systems
respond to injuries. Scar formation refers to the patx:hing of a defect
with a different or modified tisrue (i.e., scar). Tissue regeneration
refers to the complete re-creation of the original tissue architecture.
Obviously, mostprocesses involve both, but usually one predominates
and may be the source of undesirable side effects that we would like
to prevent or modify. For c:utaneous wounds, scar formation usually
predominates (e:xa:pt in the unique situation of fetal wound healing}
and is the source of many of the problems plastic: su.rgeons address.
organism. In these cases, scar formation would be preferable. Indeed, the ablative measures used to
organism. In these cases, scar formation would be preferable.
Indeed, the ablative measures used to treat these neuromas are
attl:mpts to prevent further regeneration.
Thus, when analyzing an undesirable or dysfunctional
response to injury in a tissue or organ system, it is useful
to consider a) what the undesirable portion of the response
to injury is and b) whether substitution of a new tissue (scar)
or re-creation of the pre-existing tissue (regeneration) is
responsible for this undesirable effect. It is important to con-
sider the possible adaptive role the dysfunctional process
might have. In the event of a neuroma. the case can be made
that the occasional return of protective or functional sensibil·
ity following a partial nerve injury is more adaptive and has
a survival advantage over the occurrence of complete anes-
thesia in a peripheral nerve territory. Similarly with respect
to fetal wound healing, in the sterile intrauterine environment
the predominance of regenerative pathways may be adaptive,
whereas for the adult organism existing in a microbe-filled
environment, it may not be.
Such an analysis immediately suggests strategies to correct
the undesirable end result in a given tissue or organ. If the
problem is overex:11berant scar formation, then it is likely that
measures to decrease scarring would be helpful. However,
since this balance is dynamic, efforts at accelerating regen-
eration might also be effective. And perhaps even better still
would be the simultaneous decrease in scar formation and
increase in tissue regeneration.
It is clear that the response to injury in different tissues
involves different proportions of scar formation and tis-
sue regeneration. By understanding the differences using the
approach described above, we may be able to begin to under·
stand why different organs and tissues respond to injuries
in very different ways. Just as a corneal ulcer, a myocardial
infarction, and a stage IV decubitus ulcer have different func·
tional implications for the organism, the dynamic balance of
scarring and regeneration will be different in the attempt to
re-establish homeostasis. The failure of either scar formation
or regeneration may lead to similar appearing clinical prob-
lems that have a completely different underlying etiology.
Hopefully, this type of analysis will lead to a more organized
approach to the classification and treatment of injuries in a
variety of different organ systems. Most importantly, it may
suggest strategies for intervention to optimize the response to
injury and prevent the undesirable sequelae of wound healing.
SEMANTICS OF WOUND HEALING
SEMANTICS OF WOUND HEALING
The nomenclature of both scientific and clinical wound healing research is at times imprecise and
The nomenclature of both scientific and clinical wound
healing research is at times imprecise and confusing. For
example, what is the difference between a chronic wound
and a non-healing wound? For purposes of this chapter, sev-
eral terms should be defined. The vast majority of surgical
wounds are incisional wounds that are re-approximated by
sutures or adhesives and in the absence of complications will
heal "primarily" or by "primary intention." Generally such
wounds heal with a scar and do not require special wound care
or the involvement of a specialist in wound healing. This is in
contrast to wounds that are not re·approximated (for any rea-
son) and left "open." The subsequent defect is "filled in" with
granulation tissue and then re-epithelialized. This is referred
to as healing by seconhry intention and generally results in a
delay in the appearance of a healed or "closed" wound. Often
these wounds require special dressings and treatments {to
be discussed in detail in Chapter 3) and have a higher likeli-
hood of progressing to a chronic wound. In the discussion of
normal wound healing that follows, we will be discussing
healing by secondary intention, although the same phases
occur in all wounds.
An acute wound is a wound for which the injury has
occurred within the past 3 to 4 weeks. If the wound persists
beyond 4 to 6 weeks, it is considered a chronic wound, a term
that also includes wounds that have been present for months
or years. "Non-healing, recalcitrant," and "delayed healing"
are terms used interchangeably to describe chronic wounds.
Wounds that are "granulating" represent the formation of
highly vascular granulation tissue during the proliferative
phase of healing (see below).
PHASES OF NORMAL WOUND HEALING
PHASES OF NORMAL WOUND
HEALING
The normal mammalian response to a break in cutaneous integrity occurs in three overlapping but
The normal mammalian response to a break in cutaneous
integrity occurs in three overlapping but biologically distinct
phases (Figure 2.2). Following the initial injury, there is anini-
tial inflammatory phase, the purpose of which is to remove
devitalized tissue and prevent invasive infection. Next, there
is a proliferative phase during which the balance between
scar formation and tissue regenerations occurs. Usually, scar
formation predominates, although in fetal wound healing an
impressive amount of regeneration is possible. Finally, the lon-
gest and least understood phase of wound healing occurs in
the remodeling phase, whose main purpose is to maximize the
strength and structural integrity of the wound.
Inflammatory Phase The inflammatory phase (Figure 2.3) of wound healing begins immediately following tissue injury.
Inflammatory Phase
The inflammatory phase (Figure 2.3) of wound healing begins
immediately following tissue injury. The functional priori-
ties during this phase of wound healing are attainment of
hemostasis, removal of devitalized tissues, and prevention of
colonization and invasive infection by microbial pathogens,
principally bacteria.
Initially, components of the injured tissue, including
fibrillar collagen and tissue factor, act to activate the clot·
ting cascade and prevent ongoing hemorrhage. Disrupted
blood vessels allow circulating elements into the wound
while platelets clump and fonn an aggregate to plug thedisrupted
vessels. During this process, platelets degranulate to release
growth factors such as platelet-derived growth factor (PDGF)
and transfonning growth factor P(TGF-p). The end result of the
coagulation cascade is the conversion of fibrinogen to fibrin and
subsequent polymerization into a mesh. This prcwisional matrix
provides the scaffolding for cell recruitment and attachment
required during the subsequent phases ofwound healing.
Almost immediately, inflammatory cells are recruited to
the wound site. During the initial stages of wound healing.
lnfiommaro"' Proliferative R~modeling Fi brob lasts • EndotheflaI cells • Monocytes/macrophaBes
lnfiommaro"'
Proliferative
R~modeling
Fi brob lasts
• EndotheflaI cells
Monocytes/macrophaBes
J<:er~tinocyt«K
')(
of,. Netrtro phi ls
Platelets
~,,
le
zo
u
1.$
DiliVSPost·iMIUI"/
FIGURE 2.2. The three phases ofwound healing (inftammatory, pro- liferative, and remodeliD3), the timing of
FIGURE 2.2. The three phases ofwound healing (inftammatory, pro-
liferative, and remodeliD3), the timing of these phases in adult cutane-
ous wound healing, and the characteristic cells that are seen in the
healing wound at these time points.
inflammatory cells are attracted by numerous biophysical cues, including activation of the complement cascade, TGF-P
inflammatory cells are attracted by numerous biophysical
cues, including activation of the complement cascade, TGF-P
released by degranulating platelets, and bacterial degradation
products such as lipopolysaccharide? For the first 2 days fol-
lowing wounding, there is an impressive infiltration of neu-
trophils into the fibrin matrix that fills the wound cavity. The
primary role of these cells is to remove dead tissue by phagocy-
tosis and prevent infection by oxygen-dependent and oxygen-
independent killing mechanisms. They also release a variety of
proteases to degrade remaining ECM to prepare the wound for
healing. It is important to realize that although neutrophils play
a role in dec.reasing infection during cutaneous wound healing.
their absence does not appear to prevent the overall progress of
wound healing. 8 However, their prolonged persistence in the
wound has been proposed to be a primary factor in the conver-
sion of acute wounds into non-healing chronic wounds.'
Monocyte/macrophages follow neutrophils into the wound
and appear 48 to 72 hours post-injury. They are recruited to
healing wounds primarily by expression of monocyte che-
moattractant protein 1. Monocyte/maa:ophages are a hetero-
geneous population of cells that critically regulate both early
Inflammatory Phose .r:--"'"'"' ~ . ~-- _r-1 : brin ::;ix ~ ~ Neutrophils • '
Inflammatory Phose
.r:--"'"'"'
~
. ~--
_r-1
: brin ::;ix
~
~ Neutrophils
'
;
Fibroblasts/matrix
,.,;:
~ ~ Neutrophils • ' ; Fibroblasts/matrix ,.,;: FIGURE 2.3. The inflammatory phase of wound healing

FIGURE 2.3. The inflammatory phase of wound healing begins immediatdy following t:i5sue injury and sem:s to achieve hemostasis, remove devitalized tissues, and prevent invasive infection by microbial pathogens.

and prevent invasive infection by microbial pathogens. Chapter 2: Wound Healina: Normal and Abnormal 15 and
and prevent invasive infection by microbial pathogens. Chapter 2: Wound Healina: Normal and Abnormal 15 and
Chapter 2: Wound Healina: Normal and Abnormal
Chapter 2: Wound Healina: Normal and Abnormal

15

and later stages of wound repair.l° Circulating monocytes traffic to wounds and egress into the
and later stages of wound repair.l° Circulating monocytes
traffic to wounds and egress into the tissue to become macro-
phages. By 3 days post-wounding, they are the predominant
cell type in the healing wound. Macrophages phagocytose
debris and bacteria, but are especially critical for the orches-
trated production of the growth factors necessary for the
production ofthe ECM by fibroblasts and the production of new
blood vessels in the healing wound. A partial listing of chemo-
kines, cytokines, and growth.factors presentin the healingwound
is provided in Table 2.1, but the list grows daily. The exact func-
tion of each of these factors is incompletely understood, and the
literature is filled with contradictory data. HOWI:Ver, it is clear
that unlike the neutrophil, the absence of monocyte/macro·
phages has severe consequences for healing wounds. 11
The lymphocyte is the last cell to enter the wound and
enters between days 5 and 7 post-wounding. Its role in wound
healing is not well defined, although it has been suggested that
populations of stimulatory CD4 and inhibitory CD8 cells may
usher in and out the subsequent proliferative phase of wound
healing.U Similarly, the mast cell appears during the later part
of the inflammatory phase, but again its function remains
unclear. Recently, it has become an area of intense research
inquiry because of a correlation between mast cells and some
forms of aberrant scarring.
Given the consistent and precise appearance of different
subsets of inflammatory cells into the wound, it is likely that
soluble factors released in a stereotypic pattern underlie this
phenomenon. The source of these factors, the upstream regu-
lators for their production, and the downstream consequences
of their activity are extraordinarily complex topics and the
subject of intense ongoing research. Again in Table 2.1, a
partial list of growth factors thought to be important during
wound healing is provided. All are targets for the development
of therapeutics to either accelerate wound healing or decrease
scar formation. 5 However, the biologic relevance of any one
factor in isolation remains unclear.
Proliferative Phase The proliferative phase of wound healing is generally accepted to occur from days
Proliferative Phase
The proliferative phase of wound healing is generally accepted
to occur from days 4 to 21 following injury. However, the
phases of wound healing are not exclusive and have features
that overlap. Certain facets of the proliferative phase such as
re-epithelialization probably begin almost immediately fol-
lowing injury. Keratinocytes adjacent to the wound alter their
phenotype in the hours following injury. Regression of the
desmosomal connections between keratinocytes and to the
underlying basement membrane frees cdls and allows them
to migrate laterally. Concurrent with this is the formation
of actin filaments in the cytoplasm of keratinocytes, which
provides them with the locomotion to actively migrate into
the wound. Keratinocytes then move via interactions with
ECM proteins (such as fibronectin, vitronectin, and type I
collagen) via specific integrin mediators as they proceed
between the desiccated eschar and the provisional fibrin
matrix: beneath (Figure 2.4).
The provisional fibrin matrix: is gradually replaced by a new
platform for migration: granulation tissue. Granulation tissue
is largely composed of three cell types that play critical and
independent roles in granulation tissue formation: fibroblasts,
macrophages, and endothelial cells. These cells form ECM
and new blood vessds, which histologically are the ingredients
for granulation tissue. Granulation tissue begins to appear in
human wounds by about day 4 post-injury. Fibroblasts are
the workhorses during this time and produce the ECM that
fills the healing scar and provides a scaffold for keratinocyte
migration. Eventually this matrix: will be the most visible
component of cutaneous scars. Macrophages continue to pro-
duce growth factors such as PDGF and TGF-P1 that induce
fibroblasts to proliferate, migrate, and deposit ECM, as well
as stimulate endothelial cells to form new vessels. During the

16

Pan I: Principles, Tedmiquet, and Batie Scienc::e
Pan I: Principles, Tedmiquet, and Batie Scienc::e
TABLE 2.1 GROWTH FACTORS, CYTOKINES, AND OTHER BIOLOGICALLY ACTIVE MOLECULES IN WOUND HEALING
TABLE 2.1
GROWTH FACTORS, CYTOKINES, AND OTHER BIOLOGICALLY ACTIVE MOLECULES IN WOUND HEALING
• NAMB • ABBRBVIATION • SOURCB • DESCRIYriON Vascular endothelial VEGF Endothelial cells Promotes
NAMB
ABBRBVIATION
SOURCB
DESCRIYriON
Vascular endothelial
VEGF
Endothelial cells
Promotes
angiogenesis
growth factor
Fibroblast growth
FGF-2
factor 2
Macrophages, mast cells,
endothelial cells,
Promotes angiogenesis. Stimulates
endothelial cell migration and growth
T
lymphocytes
Platelet-derived
PDGF
growth factor
Platelets, mac:rophages,
endothelial cells
Keratinocyte growth
KGF
Fibroblasts
factor
Epidermal growth
EGF
Platelets, macrophages
factor
Transforming growth
factor beta
TGF-JJ
Platelets, macrophages,
T and B cells, hepatoc:ytes,
thymocytes, placenta
Tumor necrosis
1NF-a
factor alpha
Mac:rophages, T and B cells,
NKcells
Granulocyte
G-CSF
colony-stimulating
factor
Granulocyte-
GM-CSF
macrophage colony-
stimulating factor
Stromal cells, fibroblasts,
endothelial cells,
lymphocytes
Mac:rophages, stromal cells,
fibroblasts, mdothelial cells,
lymphocytes
Interreron alpha
JFN-a
Macrophages, B and
Promotes epithelialization via
keratinoc:yte and fibroblast migration
and proliferation
Euhances proteoglycan and collagen
synthesis
Recruits mac:rophages and fibroblasts
Controls keratinocyte growth and
maturation
Induces epithelial secretion of other
growth factors
Stimulates collagenase secretion by
fibroblasts to remodel matrix
Promotes angiogenesis
Establishes chemoattractant gradients,
induces adhesion molecule expression,
and promotes proinflammatory
moleatles that stimulate leukocyte
and fibroblast migration
Induces extracellular matrix synthesis
by inhibiting protease activity and
upregulating collagen and proteoglycan
synthesis
Induces collagen synthesis in wounds
Regulates polymorphonuclear neutro-
phil leukocyte (PMN) margination and
cytotoxicity
Stimulates granulocyte proliferation,
survival, maturation, and activation
Induces granulopoiesis
Stimulates granulocyte and macrophage
proliferation, survival, maturation, and
activation
Induces granulopoiesis
Activates mac:rophages. Inhibits
T
cells, fibroblasts,
fibroblast proliferation
epithelial cells
---
Interleukin 1
n.-1
Mac:rophages, keratinoc:ytes, Proinflammatory peptide
endothelial cells,lympbo- Induces chemotaxis of PMNs,
cytes, fibroblasts, osteoblasts
Interleukin 4
n.-4
T cells, basophils, mast cells,
bone marrow stromal cells
Jnterleukin 8
U
-8
Monocytes, neutropbils,
fibroblasts, endothelial cells,
keratinocytes, T cells
EDdothelial nitric
eNOS
EDdothelial cells, neurons
oxide synthase
Inducible nitric
iNOS
oxide synthase
Neutropbils, endothelial
cells
fibroblasts, and keratinocytes
Activates PMNs
Activates fibroblast proliferation
Induces collagen and proteoglycan
synthesis
Activates PMNs and macropbages to
begin chemotaxis
Induces marginatiou and maturation
of keratinocytes
Synthesizes NO in endothelial cells with
multiple downstream effeas
Synthesizes NO by macropbages
and basal keratinocytes, multiple
downstream effects
Chapter
Chapter

2: Wound HealintJ: Normal and Abnormal 17

Proliferat ive Phase Keratinocyte Eschar proliferation/migration ~- Proliferati ng ~ fibroblasts • Macrophages
Proliferat ive Phase
Keratinocyte
Eschar
proliferation/migration
~-
Proliferati ng
~
fibroblasts
Macrophages
~ ---r-
FIGURE 2.4. The proliferative phase of wound hea.Ung oa:urs from days 4 to 21 post-wounding.
FIGURE 2.4. The proliferative phase of wound hea.Ung oa:urs from
days 4 to 21 post-wounding. During this phase, granulation tissue fills
the wound and keratinocytes migra~to restore epithelial continuity.
proliferative phase, the provisional matrix of fibrin is replaced with thinner type m collagen, which
proliferative phase, the provisional matrix of fibrin is replaced
with thinner type m collagen, which will in turn be replaced
by thicker type I collagen during the remodeling phase.
Endothelial cells are a critical component ofgranulation tis-
sue and form new blood vessels through angiogenesis and the
newly described process of vasculogenesis, which involves the
recruitment and assembly of bone marrow-derived progenitor
cells.U Proangiogenic factors that are released by macrophages
include vascular endothelial growth factor, fibroblast growth
factor 2, angiopoietin 1, and thrombospondin. The upstream
activator of gene transcription of these growth factors may be
hypoxia via hypoxia-inducible factor 1a. protein stabilization.
The relative importance of these different vascular growth
factors and the precise timing of their arrival and disappear·
ance are areas of active investigation. However, it is clear that
the formation of new blood vessels and subsequent granula-
tion tissue survival is important for wound healing during the
proliferative phase of wound healing.
One interesting element of the proliferative phase of wound
healing is that at a certain point all of these prooesses need to be
turned off and the .formation of granulation tissue/ECM halted.
It is clear that this is a regulated event because once collagen
matrix has filled in the wound cavity, fibroblasts rapidly dis-
appear and newly formed blood vessels regress, resulting in a
relatively acellular scar under normal conditions. So how do
these processes turn off? It seems likely that these events are
programmed and occur through the gradual self-destruction
of cellular apoptosis. The signals that activate this program
are unknown but must involve environmental factors as well
as molecular signals. Since dysregulation of this process is
believed to underlie the pathophysiology of fibrotic disorders
such as hypertrophic scarring, understanding the signals for
halting the proliferative phase is of obvious importance for
developing new therapeutics for these disabling conditions.
Remodeling Phase The remodeling phase is the longest component of wound healing and in humans
Remodeling Phase
The remodeling phase is the longest component of wound
healing and in humans is thought to last from 21 days up to
1 year. Once the wound has been "filled in" with granulation
tissue and after keratinocyte migration has re-epithelialized
it, the process of wOlmd remodeling occurs. Again, these pro-
cesses overlap and the remodeling phase likely begins with
the programmed regression of blood vessels and granulation
tissue described above. Despite the long duration ofthe remod-
eling phase and the obvious relevance to ultimate appearance, it
is by far the least understood phase of wound healing.
ln humans, remodeling is characterized by the processes of wound contraction and collagen remodeling (Figure
ln humans, remodeling is characterized by the processes of
wound contraction and collagen remodeling (Figure 2.5). The
process of wound contraction is produced by wound myofi-
broblasts, which are fibroblasts with intracellular actin micro-
filaments capable of force generation and matrix contra<non. 1 "
It remains unclear whether the myofibroblast is a separate cell
from the fibroblast or whether all fibroblasts retain the capac·
ity to "trans-differentiate" to myofibroblasts under the right
environmental conditions. Myofibroblasts contact the wound
through specific integrin-mediated cell-matrix interactions
with the dermal environment.
Collagen remodeling is also characteristic of this phase. Type
m collagen is initially laid down by fibroblasts durirJg the prolif-
erative phase, but over the next f<:w weeks to months this will be
replaced by type I collagen. This slow remodeling phase is largcly
mediated by a class of enzymes known as matrix metalloprotein-
ases that are secreted in large part by m.acrophages, fibroblasts,
andendothelialcells.uThe breakingstrengthofthehealingwound
improves slowly duriDg this process, reflecting the turnover in col-
lagen subtypes and increased collagen cross-linking. At 3 weeks,
the beginning of the remodeling phase, wounds have only about
20% of the strength of unwounded skin and will ultimately only
possess 70% to 80% ofthe breaking strength ofunwounded skin
at 1 year.
ABNORMAL RESPONSE TO INJURY AND ABNORMAL WOUND HEALING Just as it is overly simplistic to
ABNORMAL RESPONSE TO INJURY
AND ABNORMAL WOUND HEALING
Just as it is overly simplistic to consider all the different
responses to injury seen in different tissues as simply "wound
healing," it is naive to try to classify all the manifestations
of abnormalities in this process as simply
abnormal
wound
healing." To more accurately classify all the different types of
abnormal wound healing, it is useful to consider the balance
between attempts to replace tissue defects with new. substitute
tissues (scar formation) against the re-creation of the original
tissue in situ (regeneration), as illustrated in Figure 2.1. It is
also hdpful to determine where within the normal phases of
wound healing the problem occurs. The goal is to understand
each abnormal process in terms of dynamic balance and to
propose therapeutic strategies to restore homeostasis on a cel-
lular. tissue, and organ level.
Such a process is not merely a semantic exercise but has
potential therapeutic implications. Thus, although a corneal
ulcer, a peripheral neuroma, and stage IV sacral decubitus
Remodeling Phase
Remodeling Phase
FIGURE l.S. The remodeling plwe of wound healing is the longest plwe and lastt from
FIGURE l.S. The remodeling plwe of wound healing is the longest
plwe and lastt from 21 dayt to 1 year. Remodeling. though poorly
underatood. is charac:tuized by the proce1111ell of wound contrac:tion
and collagen remodeling.

18

Pan I: Principles, Technique., and Batie Scienc::e
Pan I: Principles, Technique., and Batie Scienc::e
ulcer are all examples of abnormal healing, the treatment as guided by an understanding of
ulcer are all examples of abnormal healing, the treatment as
guided by an understanding of the underlying mechanism
will be completely different. Thus, for a corneal ulcer, which
represents a defect in epithelial regeneration, growth factor
therapy would make sense to augment the potential for regen·
eration, whereas it would make less sense for a defect such
as a peripheral neuroma. For a neuroma, treatments aimed
at preventing nerve regeneration would seem to make more
sense. In the following paragraphs, we will attempt to clas·
sify the various types of abnormal wound healing using the
dynamic balance between scar formation and regeneration.
It is hoped that such an analysis might elucidate and clarify
new therapeutic opportunities targeting one component or the
other, as illustrated in Figure 2.1.
Inadequate Regeneration Underlying an Abnormal Response to Injury The classic example of this is found
Inadequate Regeneration Underlying
an Abnormal Response to Injury
The classic example of this is found in central nervous system
injuries that occur following traumatic injury or following tumor
ablation. The response to injury in these cases is usually char-
acterized by virtually no restoration or recovery of functional
neural tisrue. The absence of neural regeneration is compensated
by a normal physiologic process of replacement with scar tis-
rue, but in most cases this process does not appear excessive or
overexuberant. Although efforts to decrease scar formation have
been attempted, it is CUITently thought that these will be ineffec-
tive unless neural regeneration can also be achieved. Thus, cur·
rentlyefforts arefocused on strategies to increase regeneration of
neural tissue to treat this abnonnal response to injury.U' Current
modalities under investigation include the use ofimplanted neu·
ral stem/progenitor cells ortheuse ofdevelopmentalmorphogens
to recapitulate the processes of neural development. Techniques
to decrease neural scar formation might also be useful to provide
a window of opportunity for regeneration to occur, but they are
unlikely to be ruccessful in and of themselves. Other examples
of inadequate regeneration would include bone nonunions and
corneal ulcers.
Inadequate Scar Formation Underlying an Abnormal Response to Injury Many examples of impaired wound healing
Inadequate Scar Formation Underlying
an Abnormal Response to Injury
Many examples of impaired wound healing seen by plastic
surgeons belong in this category. In most cases, these diseases
result from a failure to replace a tissue defect with a substitute
patch of scar (i.e., inadequate scar formation). ln these condi-
tions, stable scar tissue would be sufficient to restore cutane-
ous integrity and eliminate the pathology. Regeneration of the
skin, although perhaps ideal, is not required for an adequate
functional outcome. Examples of these types of conditions
include diabetic foot ulcers, sacral decubiti, and venous sta-
sis ulcers. ln all these cases, restoration of cutaneous integ-
rity would be sufficient, and as such, efforts must be made
to understand and correct the defects in scar formation that
occur in these disease states.
Once the derect in scar formation is understood, therapeu·
tics can be rationally designed to correct these defects. At times,
it is useful to subdivide the scar formation defects further and
examine whether the primary derect occurs in the inflamma-
tory, proliferate, or remodeling phases of wound healing. For
instance, in humans and experimental models, diabetic ulcers
occur because of defects in the inflammatory and prolifera-
tive phases of wound healing. Accordingly, therapeutics are
targeted toward these phases. 17 ln contrast, wounds occurring
because of vitamin C depletion (i.e., scurvy) are due to abnor-
mal collagen cross-linking, which occurs during the remodel-
ing phase of wound healing. Therapeutics should be directed
at this later phase. While in both cases therapeutic efforts are
focused on correcting defects in scar formation (as opposed
to augmenting tissue regeneration), the therapeutic targets
wiD be different.
Excessive Regeneration Underlying an Abnormal Response to Injury These situations are relatively rare. In these
Excessive Regeneration Underlying
an Abnormal Response to Injury
These situations are relatively rare. In these cases, pathways of
tissue regeneration lead to the re-creation of the absent tissue,
but there are functional problems reintegrating the tissue into
the systemic physiology. They often occur in peripheral nerve-
like tissue, such as peripheral nerve regeneration leading to
neuroma. Other examples might include the hyperkeratosis
that occurs in cutaneous psoriasis or granuloma formation
in healing wounds. lt seems plausible that many conditions
we consider "precancerous" are the result of overeXIlberant
attempts at tissue regeneration following minor traumatic
insults. This then leads to disordered and uncontrolled
growth. Clearly, in these situations, scar formation would be
preferable to regeneration because of the risk of loss of growth
control and possible transformation to overt cancer.
In these disease states, therapeutic measures are targeted
toward decreasing cellular proliferation and blocking or
impeding the aberrant regenerative pathways. Irritant strate-
gies to maximize scar formation may also play a role, as when
alcohol is injected into a neuroma. The goal is to limit the
ability of the tissue to activate pathways leading to regenera-
tion. lt is sobering to realize that although much current effort
is focused on maximizing tissue regeneration, there are cir-
cumstances where this already occurs and has proven to be
dysfunctional. lt also illustrates the need to strictly control the
growth and development of tissue generation using emerging
stem and progenitor cell technologies.
Excessive Scar Fonnation Underlying an Abnormal Response to Injury When these conditions affect the skin,
Excessive Scar Fonnation Underlying
an Abnormal Response to Injury
When these conditions affect the skin, they are very commonly
treated by plastic surgeons, but they can occur elsewhere as in
pulmonary fibrosis or cirrhosis. "Excessive" cutaneous scar
formation remains a poorly understood and ubiquitous dis-
ease for which there are few treatment options. Abnormal
scarring is classified as either hypertrophic scarring or keloid
formation. Both are manifestations of overexuberant scarring.
although the upstream etiology is probably different. 11 Keloids
are less common and have a genetic component that limits
them to <6% of the population, primarily the black and Asian
populations. Histologically, keloids are differentiated by the
overgrowth of dense fibrous tissue beyond the borders of the
original wound, with large thick collagen fibers composed of
numerous fibrils closely packed together. Hypertrophic scars
are also characterized by the formation of dense collagen fibers
following injury but, in contrast to keloids, do not extend
beyond the original wound margins. They are more prone to
forming disabling contractures and are a near-universal out-
come following extensive deep bum injury.
The etiology and pathophysiology of both hypertrophic
scarring and keloid formation remain unknown. Many theo·
ries have been proposed to account for the fibroproliferation
observed in hypertrophic scar and keloid formation, includ-
ing mechanical strain, inflammation, bacterial colonization,
and foreign body reaction. Unfortunately, investigation of the
mechanisms underlying these diseases has been hindered by the
absence of animal models that reproduce the characteristics of
human overscarring. Decreasing the process of scar formation
is the prime goal of therapy for both disease states. Modalities
employed include steroid injections, pressure therapy with sili-
cone sheeting, and e:x:temal beam irradiation. However, with
current treatment
modalities, recurrence rates approach 75%. 19
The prolonged secretion ofinflammatory cytokines has been
shown to induce fibrosis in numerous in vitro and animal mod-
els. Thus, researchers have long sought to manipulate the cyto-
kine environment to prevent scar formation. Most recently, a
phase m clinical trial based on the use of recombinant human
TGF-pJ (an antagonist of profibrotic TGF-Pl) to improve scar revision outcomes was tenninated after failing
TGF-pJ (an antagonist of profibrotic TGF-Pl) to improve scar
revision outcomes was tenninated after failing to reach primary
endpoints. Given the known complexity of wound healing, it
should not be surprising that targeting a single cytolcine would
be inadequate to reduce organ-level .fibrosis.
Recent research has also implicated a key role for mechani-
cal force in promoting both hypertrophic scarring and keloid
formation. 20 .2 1 Plastic surgeons have long recognized the
importance of tension during wound healing, and several
current treatments for scarring (e.g., silicone sheeting and
compression garments) may have a "mechanomodulatory"
mechanism of action. Mechanical cues are known to activate
fibroproliferative pathways in skin cells, and the underlying
molecular pathways are only beginning to be uncovered in
vivo. 22 Further, the ability of physical forces to control clini-
cal outcomes is demonstratl:d by the incorporation of nega-
tive pressure wound therapies in modem wound treatment
algorithms.v Future strategies to prevent scar formation may
in fact be aimed at manipulating the mechanical and physical
cues controlling wound repair and fibrosis.
EMERGING CONCEPTS IN WOUND HEALING Human skin must continually adapt and renew during devel- opment
EMERGING CONCEPTS IN
WOUND HEALING
Human skin must continually adapt and renew during devel-
opment and in response to injury and disease. This suggests the
intrinsic ability of the skin to "regenerate." Several stem cell
populations have been identified in the skin and are increas-
ingly studied as potential therapies for wound repair. These
progenitor populations include epidermal stem cells, hair fol-
licle stem cells, and adipose-derived stem cells that have the
capacity to restore almost all skin compartments. 2 .Z 4 .1S Further,
studies in mammalian digit tip regeneration suggest that the
biologic machinery necessary to regrow damaged soft tissues
may already be present in adults in the form of tissue-specific
adult stem cells.u Thus, it is clear that stem cells play a key
role in normal wound healing; the question for researchers
is how to exploit these powerful cell populations to promote
cutaneous repair in disease states.
Another component of the wound environment that has
been largely overlooked is the ECM. As stated earlier, wound
remodeling is the least well understood phase of wound heal-
ing but appears to involve regulation of extracellular enzymes
that control the structural architecture of the ECM. lt has
been shown that the ECM is a dynamic and active component
of the wound that can directly control cell activity, 17 resulting
in a "dynamic reciprocity" between cells and their immediate
environment that maintains skin homeostasis. 28 This concept
underlies the development of tissue engineering strategies to
deliver and re-create the precise biophysical cues that promote
biologic programs conducive to healing. 2
'.3°
The three traditional phases of wound healing were estab-
lished decades ago, and since then, research in wound repair has
continued to build upon these fundamental concepts. However,
as modem research continues to elucidate the complexity of
tissue repair processes, we will undoubtedly need to redefine
what normal wound healing is in terms beyond just inflam-
matory cell trafficking and a handful of cytokines. Traditional
approaches to wound healing will also need to be integrated
with our improved understanding of the molecular pathophysi-
ology of aberrant cutaneous repair. Plastic and reconstructive
surgeons need to be intimat~:lyfamiliar with these evolving con·
cepts to ensure the optimal care of our patients.
CONCLUSIONS
CONCLUSIONS
to ensure the optimal care of our patients. CONCLUSIONS ln this chapter, a theoretical framework has

ln this chapter, a theoretical framework has been proposed with which to understand and classify the normal responses to injury that occur in different tissues and different species.

that occur in different tissues and different species. Chapter 2: Wound HeaJin&: Normal and Abnormal 19
that occur in different tissues and different species. Chapter 2: Wound HeaJin&: Normal and Abnormal 19
Chapter 2: Wound HeaJin&: Normal and Abnormal
Chapter 2: Wound HeaJin&: Normal and Abnormal

19

These responses can be conceptualized as favoring replace- ment of injured tissue with a patch,
These responses can be conceptualized as favoring replace-
ment of injured tissue with a patch, otherwise known as
scar formation, or recapitulating developmental processes to
duplicate the original architecture, otherwise referred to as
regeneration. The dynamic balance between these two pr~
cesses may underlie the myriad abnonnal responses to injury
that occur in human disease states. It is hoped that such a
framework will suggest new therapeutic strategies to correct
imbalances, by either augmenting or suppressing one component
or the other. lhis may provide a basis for accelerated prog·
ress in the care of patients with abnormal or dysfunctional
responses to injury that result in human disease.
References
1. Gurtner GC, Werner S, B.iu.Tandon Y, Lcngiker MT. Wound repair and
regmeratioo
~e. 2008;453:314-321.
2. Cha J, Falanga V. Stem cells in cutaneous wouo.d heiling. Clin Dt:rmtillOI.
2007;25:73-78. 3. Grose R, Werner S. Wouo.d-heiling studies in transgenic and knockout mice. Mol Bioudmo'l.
2007;25:73-78.
3. Grose R, Werner S. Wouo.d-heiling studies in transgenic and knockout
mice. Mol Bioudmo'l. 2004;28:147-166.
4. Singer AJ, Cluk RA. Cutaneous wouo.d healing. N Eng/ J Mtul.
19997341:738-746.
5. Werner S, Grose R Reguhtion of wouo.d healing by growth facton and
cytokines. Phy&iol Rev. 2003;83:835-870.
6. Woolley K, Martin P. Co~ mechanisms of repair: from c!amaged single
cells to wouo.ds in multicellulu ti!ssues. Bi~. 20()0-,.22:911-919.
7. Martin P, LeiboYich SJ.InfWDmatory cells during wouo.d repair: the good,
the bad and the ugly. Tf'mds Otll Bioi. 2005;15:599-607.
8. Simpson DM,
Ron R The neutrophilic leukocyte iD. woUD.d repair: a stlldy
with antineutrophil set~~m.JClin InveJt. 1972;51:2009-2023.
9. Yager DR, Nwomeh BC. The proteolytic emironment of chronic woUD.ds.
WownJ Reptlif' Regen. 1999;7:433-441.
10. Gordon S, Taylor PR. Mono~ and macrophage heterogeneity. Nllt Rev

I,_r10l. 2005;5:953-964.

11. Leibovich SJ, Ross R. The role of the macrophage iD. woUD.d repair. A stlldy
11. Leibovich SJ, Ross R. The role of the macrophage iD. woUD.d repair.
A stlldy with hydroc:ortisone and antimacrophage senun. Am J PtUhol.

1975;78:71-100.

12. Park JE, Barbul A. Understanding the role of im11nme l'l!gll!ation iD. woUD.d healiD.g. AmJs.rg.
12. Park
JE, Barbul A. Understanding the role of im11nme l'l!gll!ation iD. woUD.d
healiD.g. AmJs.rg. 2004;187:11S-16S.
13. Asahara T, MIU'Ohara T, Sulli'fan A, et al. l110lation of putati'fe proeenitDr
endotheliil. cells {or augiogenesis. Science. 1997;275:964-967.
14. Desmouliere A, Ch&ponnier C, Gabbiani G. Tilll!llt repair, contraction, and
the myofibroblast. WownJ kptJir Regm. 2005;13:7-12.
15. Page-McCaw A,
Ewald AJ, Werb z. Matrix metalloproteiu.ases and
the regulation o{ tissue remodelling. Ntll Rev Mol Cell Bioi. 2007;8:

221-233.

Hare! NY, Strittmatter SM. Can regenerating axons recapitll!ate denl- opmenta.l guidance during re<:onry from spinal. cord injury? Ntll Rw Nnl'foui. 2006;7:603-616. Brem H, Tomic:-Cauic M. Cellular and mol~ basis ofwoiiDII healing iD. diabetes. J ClinltuH!'#. 2007;117:1219-1222. Kose O, Waseem A. Keloids and hypertrophic scars: are they two di££erent sides of the same coin? Dt:rmtillOlSllf'g. 2008734:336-3%'. Mustoe TA, Cooter RD, Gold MH, et al. International. clinical rec- ommendations on scar management. Pltut ReeomtT Sl.rg. 2002;110:

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20. Gunner GC, Dauskardt RH, Wong VW, et al. Impro'fiD.g cutmeous scar by controlliug the
20. Gunner GC, Dauskardt RH, Wong VW, et al. Impro'fiD.g cutmeous scar by
controlliug the mechanical eu;riroumet~t:large animal and phase I studies.
A"" s,.g. 2011;254:217.
21. Ogawa R. Keloid and hypertrophic scarriug may result from a mecha-
noreceptor or mechauoseusitin nociceptor disorder. Med Hypotbet~et~.

2008;71:493-500.

22. Wong VW, Rustad KC, Akaishi S, et al. Focal adhesion kinase links mec:hanic:al for(;e
22. Wong VW, Rustad KC, Akaishi S, et al. Focal adhesion kinase links
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2011;18:148-152.

23. Orgill DP, Manders EK, Sumpio BE, et al. The mechanisms o{ action o{ ncuum.
23. Orgill DP, Manders EK, Sumpio BE, et al. The mechanisms o{ action o{
ncuum. usisted closure: more to le.ar:u. S111'gery. 2009;1%':40-51.
2.4. Blanpain C, Fuchs E. Epidetmil. stem cells of the akin. Anllll Rev CtU Dev
Bioi. 2006;22:339-373.
2S. Yang L, Peng R
Uueiling hair follicle stem cells. Sum Cell Rw.

2010;6:658-664.

26. Rillkel'ich Y, LincLut P, Ueo.o H, Lcngaker MT, Weissmann Cerm.-Llyet and lineage-restricted stem/progenitors
26. Rillkel'ich Y, LincLut P, Ueo.o H, Lcngaker MT, Weissmann
Cerm.-Llyet
and lineage-restricted stem/progenitors regenerate the mouse digit tip.
N_,,, 2011;476:409-413.
27. Hynes RO. The extracellular matrix: not just pretty fibrils. Scin!.a.
20097326:1216-1219.
28. Schultz GS, Dal'idson JM. IGnner RS, Bornstein P, Herman IM. Dynamic
reciprocity in the wouo.d microen,-ironment. WoNnd Repllir Regen.

2011;19:134-14ll.

2.9. Glotzbach ]P, Wong VW, Gunner GC, Lcngaket MT. Rqenetative medi- cine. a.,. Pf'obl SNrg.
2.9. Glotzbach ]P, Wong VW, Gunner GC, Lcngaket MT. Rqenetative medi-
cine. a.,. Pf'obl SNrg. 2011;4ll:14ll-212.
30. Metcalle AD, Ferguson MWJ. Bioengineering skin using mech.Wsms ol
regmeration 11J1drepair. BiontlliUriAis. 2007;.28:5100-5113.
CHAPTER 3 •
CHAPTER 3 •
WOUND CARE
WOUND CARE
DONALD W. BUCK AND ROBERT D. GALIANO
DONALD W. BUCK AND ROBERT D. GALIANO
INTRODUCTION addressing these factors, the surgeon will be able to manage most wounds.
INTRODUCTION
addressing these factors, the surgeon will be able to manage
most wounds.
The wound is a microcosm of the patient. While most wounds heal without intervention in
The wound is a microcosm of the patient. While most wounds
heal without intervention in healthy individuals, patients with
systemic diseases or acute illnesses can develop non-healing
wounds that require evaluation by a plastic surgeon. In gen·
eral, the plastic surgeon is consulted to evaluate three types of
wounds: (1) the acute wound where the final appearance may
be the principal concern, (2) the wound in a patient whose
medical status and/or mode of injury predisposes him or her to
wound healing difficulties and the threat of a problem wound,
or (3} the chronic wound refractory to past interventions.
In recent years, significant strides have been made in our
overall understanding of problem wound physiology. This has
led directly to clinical advances that have resulted in better
treatments and overall wound care. With the staggering prev·
alence of chronic wounds and an ever-increasing armamen·
tarium of wound care tools, it is imperative that the plastic
surgeon maintain an updated understanding of wound healing
biology and the principles of wound care. In this chapter we
will focus on the basics of wound care and highlight some of
the recent advances in this dynamic and expanding field.
FUNDAMENTALS
FUNDAMENTALS
All wounds, whether acute or chronic, should be evaluated by a physician to determine their
All wounds, whether acute or chronic, should be evaluated
by a physician to determine their mechanism and to outline
an approach to treatment. Tetanus prophylaxis is adminis·
tered when prior immunity is unknown or the most recent
booster vaccine is over S years old. A thorough history and
physical examination should be performed, with particular
emphasis on any aspect that relates to the wound cause and/
or persistence (e.g., comorbidities, systemic diseases, and
medications}. The term wound encompasses a broad range of
lesions without consideration to etiology, and the list of pos·
sible etiologies is vast. Table 3.1lists some of the major fac-
tors, both systemic and local, that can have profound effects
on wound healing.
Adjunctive diagnostic tests are guided by history and phys·
ical examination of the wound. Some useful studies include
laboratory tests that reflect nutritional status (albumin,
prealbumin, and transferrin levels), the level of physiologic
inflammation (C-reactive protein and erythrocyte sedimen·
tation rate), and the degree of diabetes control (plasma glu-
cose and hemoglobin Ate). In addition, patients should have
a recent complete blood count and basic chemistry panel to
assess for leukocytosis, anemia, and renal disease. Other use·
.fu1 laboratory tools include transcutaneous oxygen pressure
(tcPo 2 ) measurements, toe pressures, neurofilament testing,
and ankle-brachial index (ABI) (Chapter 9S). Results of these
tests may direct the need for procedures such as surgical
revascularization. Wound parameter documentation is also
useful to monitor the progression of wound healing in an
objective manner.
The main fundamentals of wound care are summarized in
Table 3.2. To attain these goals, it is useful to emphasize the
common causative factors that are shared by problem wounds,
as opposed to isolating the differences between diverse types of
wounds. With this more simplistic view, it is possible to link the
majority of problem wounds to a combination of three factors:
age, ischemia (including repeated episodes of ischemia-reper-
.fusion injury}, and bacterial infection. By understanding and
Age and Wound Healing Although most wounds heal without incident in aged patients, there is
Age and Wound Healing
Although most wounds heal without incident in aged
patients, there is a slight, but consistent, decline in wound
healing rates in the elderly. This decline is exacerbated when
ischemia and infection are superimposed. Laboratory studies
reveal a functional decline in aged fibroblasts and endothelial
cells that leads to accelerated senescence, diminished growth
factor production, decreased stress response to hypoxia and
toxins, and a reduction in collagen and matrix production.
Interestingly, aged cells share many of the same molecular
derangements as those seen in diabetic patients and irradiated
wound beds. Obviously age cannot be reversed; however,
it should be considered an important component of wound
pathology and prompt the surgeon to aggressively optimize
appropriate systemic parameters in these patients (nutri·
tion, infection, ischemia, etc.). The use of growth fac:tors or
advanced wound protocols should be considered earlier in
the elderly patient.
Ischemia and Wound Healing The role of hypoxia in wound healing is well established. In
Ischemia and Wound Healing
The role of hypoxia in wound healing is well established.
In fact, local tissue hypoxia is a common charac:teristic of
most chronic wounds. The diffusion of oxygen and nutri-
ents from capillaries to cells is limited to a distance of 60
to 70 pm in a person breathing room air. Therefore, any-
thing that increases tissue diffusion requirements or limits
TABLE 3.1 FACTORS THAT CONTRIBUTE TO WOUND HEALING IMPAIRMENTS
TABLE 3.1
FACTORS THAT CONTRIBUTE TO WOUND
HEALING IMPAIRMENTS
Age Ischemia Repe.tfusion injury Inkction or bacterial bioburden Malnutrition Foreign bodies Diabetes Steroids
Age
Ischemia
Repe.tfusion injury
Inkction or bacterial bioburden
Malnutrition
Foreign bodies
Diabetes
Steroids
Uremia
jaUDdice
Cmcer
GeDetic causes (e.g., Ehlers-DaDlos, Werner syndromes)
Irradiation
Chemotherapy
Tobacco use
Alcohol use
Edema
Pressure
Chapter 3: Wound Care
Chapter 3: Wound Care

21

TABLE 3.2 Bacteria and Wound Healing BASIC FUNDAMENTALS OF WOUND CARE All wounds are contaminated,
TABLE 3.2
Bacteria and Wound Healing
BASIC FUNDAMENTALS OF WOUND CARE
All wounds are contaminated, but excessive numbers of bacte-
ria will interfere with wound healing. A quantitative ailture of
• Optimize ~y~temic::parameters
Nutrition
10' bacteria per gram of tissue is usually diagnosticofinfection.
Glucose control
Smoking cessation
• Debride nonviable tissue
However, this tool is rarely used because kw microbiology lab-
oratories perform the test reliably. Furthermore, the value of
10' is relative and not universally applicable. In fact, more viru-
lent strains of bacteria can establish systemic infections at much
lower densities. The presenc:e of diabetes, ischemia, or other
comorbidities will also lower the threshold needed to estab-
• Reduce wound biobwden
lish a true infeaion to an unknown extent. Likewise, as more
• Optimize blood flow
Warmth
Hydration
Surgical zevascularitation
• Reduce edema
Elevation
Compression
• Use appropriate dressiugs
Moist wound healing
Exudate removal
research on the physiology of bacterial biofilms is introduced, it
is likely that only a fraction of the 1OS bacterial count is actually
necessary to establish a biofilm and create a significant barrier
to wound healing.
An important mechanism by which tissue hypoxia pre-
disposes wounds to infection is by impairing the "oxidative
burst" essential to microorganismal.killing by leukocytes. This
enormously elevated production of oxygen-derived radicals
is a self-regulated process that is important in clearing the
wound off bacteria. Notably. this process of radical produc-
tion, which is normally limited to the early stages of wound
repair. can be aberrantly prolonged in the setting of persis-
tent infection or inflammation (Figure 3.1). This can result
in bystander damage to the body's normal cells and in many
Avoidance of trauma to wound or patient
• Use pharmacologic therapy when necessary
• Close wounds surgically with grafts or flaps as mdicated
available capillary delivery systems will establish a hypoxic environment. For example, oxygen tension in wound
available capillary delivery systems will establish a hypoxic
environment. For example, oxygen tension in wound tissues
is reduced an average of 15 to 20 mm Hg (25 vs. 40 mm
Hg} as a result of the damage to small vessels in periwound
areas. Likewise, the tissue fibrosis commonly encountered in
chronic wounds can create a significant barrier to oxygen dif-
fusion that subsequently produces persistent tissue hypoxia
and further fibrosis.
While hypoxia alone is an important component of
chronic wounds, most problem wounds are characterized by
repeated episodes of ischemia followed by reperfusion. The
detrimental effects of ischemia-reperfusion injury have been
well established in cardiac pathology and organ transplanta-
tion, but are underappreciated in cutaneous wound healing.
Reperfusion injury is particularly important in lower extrem-
ity wounds, where walking and standing can lead to local-
ized ischemia in pressure-bearing areas, or through increased
edema in patients with venous stasis. Pressure relief, through
sitting, rest, and foot elevation, leads to resumption of ade-
quate tissue perfusion and a vicious cycle ensues. Repeated
episodes, sometimes multiple per day, result in gradual cel-
lular damage and a chronic milieu of persistent inflamma-
tion. Similar cycles of ischemia-reperfusion may also occur
in patients with pressure sores as they shift about in bed or
wheelchairs.
Surgical and nonsurgical interventions can be undertaken
to maximize oxygen delivery to tissues. Examples include ele-
vation of edematous extremities, off-loading pressure points,
debridement of necrotic tissue or foreign bodies that act as a
physical barrier to diffusion. pain control that reduces sympa-
thetic constriction of peripheral vasculature associated with
the "fight-or-flight" response, heating that will result in vaso-
dilatation of cutaneous vasculature, and smoking cessation
and hydration that increase oxygen delivery at the cellular
level. Recent research indicates that the benefits of ensuring
adequate oxygen delivery to a wound not only are restricted
to established wounds but may also be useful in preventing
wound complications.
but may also be useful in preventing wound complications. A , ,_ , ,."' pitltilllli>iiW)- B

A

, ,_ , ,."' pitltilllli>iiW)-
,
,_
,
,."'
pitltilllli>iiW)-
A , ,_ , ,."' pitltilllli>iiW)- B FIGURE 3.1. The normal healing milieu. A. Normal response