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Michigan manual of plastic surgery / [edited by] David L. Brown, Gregory H. Borschel, Benjamin Levi.
— Second edition.
p. ; cm.
Manual of plastic surgery
Includes bibliographical references.
ISBN 978-1-4511-8367-2
I. Brown, David L. (David Lawrence), 1968- editor of
compilation. II. Borschel, Gregory H., editor of compilation. III. Levi, Benjamin, editor of compilation. IV. T itle: Manual of plastic surgery.
[DNLM: 1. Reconstructive Surgical Procedures—Outlines. WO 18.2]
RD118
617.9'5—dc23
2013035530

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10 9 8 7 6 5 4 3 2 1
I would like to dedicate this second edition to the amazing students and residents that I am privileged to work
with on a daily basis. They keep me on my toes and stimulate all of us to ask more questions about the world
around us. The work on this manuscript would not have been possible without my family—their love and
support are the most important things in my life. Thank you, Andrea, Matthew, Andrew, Mom, Dad, and
Marcia, and Chad and Jenny.
–D.L.B.

I dedicate this book to the next generation of plastic surgeons. Welcome to a unique and amazing specialty! I
hope this edition becomes your favorite traveling companion—informing, enlightening, stimulating, and
encouraging you during your upcoming journey. Special thanks to my coeditors, and especially the resident
authors—your vitality and dedication made this work possible. I would also like to extend special thanks to
Debaroti Borschel, Anjali, Nikhil, Mom, Dad, Amanda, and David Borschel, Great-Granny Jackie Rankin for
her inspiration, and Debdas and Sandhya Mullick for their support during this edition.
–G.H.B.

I would like to thank my mentors David Brown, Paul Cederna, Steven Buchman, Stewart Wang, and Richard
Gamelli. I also owe appreciation to Ian and Patricia Lanoff, Ivan, Sheri, Israel, and Cindy Levi, and Jordan,
Michael, and Ellen Hornstien. I can never thank my parents Cheryl and Yaish Levi enough as they have
provided me immeasurable support throughout this fun journey of plastic surgery. They have shown me the
importance of education, persistence, and honesty. To my wife Emily: your smile and compassion are
unmatched; you inspire me daily to be excellent and offer the best care to my patients; time with you is never
enough.
–B.L.
About the Editors

David Brown is an Associate Professor of Surgery in the Section of Plastic Surgery at the University of Michigan. He received his
BA at Wittenberg University in Springfield, Ohio; his MD at Vanderbilt University in Nashville, Tennessee; General Surgery training
and Plastic Surgery Fellowship at the University of Michigan in Ann Arbor; and Microvascular Reconstruction Fellowship at St.
Vincent’s Hospital, University of Melbourne, Australia. He continues to repay the debt he was left with from many outstanding
mentors at those fine institutions by passing on the gift of knowledge to students, residents, and others at the University of Michigan.
Gregory Borschel graduated from the Johns Hopkins University School of Medicine and completed a residency and a research
fellowship in Plastic and Reconstructive Surgery at the University of Michigan. He completed a fellowship in Pediatric Plastic and
Reconstructive Surgery at the Hospital for Sick Children in Toronto. He currently practices at the Hospital for Sick Children
(SickKids) and University of Toronto and he investigates nerve regeneration both clinically and in his federally funded research
laboratory. This work has resulted in new strategies to manage nerve injuries in children. His clinical work focuses on pediatric facial
paralysis, nerve injury, hand surgery, and microvascular reconstruction. He is an Associate Professor of Surgery with a cross
appointment in the University of Toronto Institute of Biomaterials and Biomedical Engineering and the SickKids Research Institute
Program in Neuroscience.
Benjamin Levi is a fellow in Burn and Surgical Critical Care at the Massachusetts General Hospital in Boston, Massachusetts.
He received his BS at Washington University in St. Louis, his MD at Northwestern Feinberg School of Medicine, Chicago, Illinois,
and integrated Plastic Surgery Training at the University of Michigan in Ann Arbor, MI. He also completed a two-year basic science
research fellowship in Stem Cell Biology and Tissue Engineering at Stanford University. He will begin as an Assistant Professor in
Plastic Surgery with a focus on Acute and Reconstructive Burn Surgery and run a Basic Science Laboratory with a focus on Burn
Injury and Trauma in 2014. He looks forward to applying the many technical, clinical, and life skills he has learned from the
outstanding colleagues and mentors he has had throughout his training.
Contributors

Shailesh Agarwal, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Oluseyi Aliu, MD, MS


Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Tiffany N.S. Ballard, MD


Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Matthew D. Chetta, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Eric Culbertson, MD
Resident
Section of General Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

William J. Dahl, MD
Clinical Lecturer
Department of Orthopaedic Surgery
University of Michigan
Ann Arbor, Michigan

Rafael J. Diaz-Garcia, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Russell E. Ettinger, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Frank Fang, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Sharifeh Farasat, MD
Resident
Department of Dermatology
University of Michigan
Ann Arbor, Michigan

K. Kelly Gallagher, MD
Resident
Department of Otolaryngology
University of Michigan
Ann Arbor, Michigan

Katherine M. Gast, MD, MS


Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Aviram M. Giladi, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Emily Hu, MD
Attending Surgeon
Private Practice
Lake Oswego, Oregon

Brian P. Kelley, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Anita R. Kulkarni, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Theodore A. Kung, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Benjamin Levi, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan
Kate W. Nellans, MD, MPH
Hand Surgery Fellow
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Adam J. Oppenheimer, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Nicholas H. Osborne, MD, MS


Fellow
Vascular Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Christopher J. Pannucci, MD, MS


Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Kavitha Ranganathan, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Ian C. Sando, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Erika Davis Sears, MD, MS


Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Jennifer Strahle, MD
Resident
Department of Neurosurgery
University of Michigan
Ann Arbor, Michigan

Kristoffer B. Sugg, MD
Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Christian J. Vercler, MD, MA


Clinical Assistant Professor
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Jennifer F. Waljee, MD
Clinical Assistant Professor
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan

Keith G. Wolter, MD, PhD


Assistant Professor
Plastic Surgery
University of Arkansas for Medical Sciences
Little Rock, Arkansas

Shoshana L. Woo, MD, BS


Resident
Section of Plastic Surgery
Department of Surgery
University of Michigan
Ann Arbor, Michigan
Foreword

It is with great pleasure that I write the foreword for the second edition of the Michigan Manual of Plastic Surgery. As a follow-
up to the highly successful inaugural Michigan Manual, I am very excited about the enhancements and additions made by Drs.
David Brown, Gregory Borschel, Benjamin Levi, and Shoshana Woo to the second edition including significantly improved and
updated content, new chapters on hot topics in plastic surgery, and double the number of illustrations and figures compared with the
first edition. The visual learning experience has also been enhanced by the addition of color to the already expertly created
illustrations. The Michigan Manual highlights all of the critical aspects of plastic surgery and has become the go-to reference guide
for medical students, physician assistants, nurses, residents, and medical practitioners from around the world in related fields, as they
provide care for their patients. This compact and yet surprisingly comprehensive text provides exactly what you need to know in
sufficient depth and breadth to be highly valuable. In addition, the manual has been written entirely by residents in plastic surgery and,
as such, has a focus, structure, and approach which is perfectly suited to the people who need to access this information the most. It
doesn’t require reading exhaustively detailed chapters or intense focus to glean the critical information on each topic presented.
Instead, the nicely crafted Michigan Manual has a visually pleasing presentation style with readily accessible information which is
designed to provide “on-time” learning, whether it is the night before an operation, during an outpatient clinic visit, on the hospital
wards, or between cases in the operating room. I am excited about the release of the second edition of the Michigan Manual. I am
sure you will find it an incredibly valuable resource to provide “just-in-time” information as you care for your patients.

Paul S. Cederna, MD, FACS


Chief, Section of Plastic Surgery
Robert Oneal Professor of Plastic Surgery
Professor, Department of Biomedical Engineering
University of Michigan Health System
Preface

We are excited to present the second edition of the Michigan Manual of Plastic Surgery, the world’s only pocket-sized, yet
comprehensive treatise on this vast subject.
As in the first edition, we sought to present the entire scope of contemporary plastic surgery in an easily accessible format. We
have produced this handbook primarily for medical students and surgical residents to facilitate clinical consultations and pre-, intra-,
and postoperative care. The content and format are also an excellent reference for practitioners in the multitude of other fields with
which plastic surgery interacts, who need ready access to basic, practical information. Additionally, we trust that the Michigan
Manual will provide a succinct review for the in-service and written board examinations. To aid in review for such examinations, we
have placed an * in front of material that is commonly tested. Additionally, we have included questions that are commonly asked in
the operating room at the end of each chapter to prepare for each case. We have also included key references for additional reading
on each topic.
This book was written and edited by residents at the University of Michigan. We owe a debt of gratitude to our illustrations
editor, Shoshana Woo, for her work in significantly improving the quality and quantity of figures. Additionally, we wish to thank our
section editors, Jennifer Waljee, Theodore Kung, Kristofer Sugg, Adam Oppenheimer, Anita Kulkarni, Christopher Pannucci,
Kathleen Gallagher, and Rafael Diaz-Garcia, for their contributions.
We hope that you find this handbook helpful in your quest for improving your knowledge base of plastic surgery. We are
delighted to contribute to the education of those dedicated to caring for plastic surgery patients. Never stop learning!

David L. Brown, MD, FACS


Gregory H. Borschel, MD
Benjamin Levi, MD
Contents

About the Editors


Contributors
Foreword
Preface

1 Tissue Injury and Repair


Frank Fang
2 Surgical Techniques and Wound Management
Kavitha Ranganathan

3 Grafts
Erika Davis Sears

4 Flaps
Erika Davis Sears

5 Perforator Flaps
Shoshana Woo
6 Microsurgery, Endoscopic Surgery, and Robotic Surgery
Anita R. Kulkarni
7 Composite Tissue Allotransplantation (CTA)
Shailesh Agarwal • Benjamin Levi
8 Tissue Expansion
Kristoffer B. Sugg
9 Fat Grafting and Adipose-Derived Stem Cells
Benjamin Levi
10 Local Anesthetics
Ian C. Sando

11 Lasers in Plastic Surgery


Sharifeh Farasat

12 Basic Statistics
Christopher J. Pannucci
13 Malignant Skin and Soft Tissue Lesions
Keith G. Wolter
14 Benign Skin Lesions
Shailesh Agarwal
15 Vascular Anomalies, Lymphedema, and Tattoos
Kavitha Ranganathan
16 Squamous Cell Carcinoma of the Head and Neck
K. Kelly Gallagher
17 Neck Masses and Salivary Gland Neoplasms
K. Kelly Gallagher
18 Principles of Head and Neck Reconstruction
Keith G. Wolter
19 Eyelid Reconstruction
Kristoffer B. Sugg
20 Nasal Reconstruction
Frank Fang

21 Lip and Cheek Reconstruction


Theodore A. Kung

22 Congenital Ear and Ear Reconstruction


Kristoffer B. Sugg • Christian J. Vercler
23 Scalp and Calvarial Reconstruction
Christopher Pannucci
24 Facial Paralysis
Kristoffer B. Sugg

25 Cleft Lip
Matthew D. Chetta • Adam J. Oppenheimer

26 Cleft Palate
Adam J. Oppenheimer
27 Craniosynostosis and Craniofacial Syndromes
Russell E. Ettinger
28 Facial Trauma
Katherine M. Gast

29 Orthognathic Surgery
Adam Oppenheimer

30 Rhinoplasty
Theodore A. Kung

31 Evaluation and Surgical Management of Facial Aging


Christian J. Vercler

32 Non-Operative Facial Rejuvenation


Shailesh Agarwal • Eric Culbertson

33 Body Contouring
Aviram M. Giladi

34 Periocular Rejuvenation: Brow Lift and Blepharoplasty


Christian J. Vercler
35 Breast Disease
Tiffany N. S. Ballard • Emily Hu
36 Reduction Mammoplasty, Augmentation Mammoplasty, and Mastopexy
Tiffany N. S. Ballard
37 Breast Reconstruction
Anita R. Kulkarni
38 Hand and Wrist Anatomy and Examination
Aviram M. Giladi
39 Fractures and Dislocations of the Hand and Wrist
Rafael J. Diaz-Garcia
40 Tendon Injuries and Tendonitis
Ian C. Sando
41 Amputation, Replantation, and Fingertip and Nailbed Injuries
Kate W. Nellans
42 Nerve Injuries, Compression Syndromes, and Tendon Transfers
Kristoffer B. Sugg • Rafael J. Diaz-Garcia
43 Rheumatoid Arthritis, Osteoarthritis, and Dupuytren’s Contracture
Rafael J. Diaz-Garcia
44 Hand Tumors
Oluseyi Aliu
45 Congenital Upper Extremity Anomalies
Jennifer F. Waljee

46 Thumb Reconstruction
Jennifer F. Waljee

47 Brachial Plexus Injuries


Jennifer Strahle

48 Hand Infections, Compartment Syndrome, and High-Pressure Injections


William J. Dahl

49 Thoracic and Abdominal Reconstruction


Brian P. Kelley

50 Pressure Sores
Oluseyi Aliu
51 Lower Extremity Reconstruction
Brian P. Kelley
52 Necrotizing Soft Tissue Infections
Nicholas H. Osborne
53 Penile and Vaginal Reconstruction, Gender Surgery
Katherine M. Gast
54 Thermal Injury: Acute Care and Grafting
Christopher J. Pannucci
55 Electrical and Chemical Burns
Christopher J. Pannucci
56 Frostbite, Stevens–Johnson Syndrome, and Toxic Epidermal Necrolysis
Christopher J. Pannucci
57 Burn Reconstruction
Benjamin Levi
58 How to Read an Article for Journal Club
Christopher J. Pannucci
59 Preoperative Cardiopulmonary Risk Stratification and Prophylaxis
Christopher J. Pannucci
Index
Figure Credits

The following figures are reprinted with permission from: Thorne CH, ed. Grabb and Smith’s Plastic Surgery. 6th ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2007.

1-2, 2-1, 2-2, 4-1, 4-2, 4-3A, 19-10, 19-11, 20-5, 20-6, 20-7, 22-2, 22-3, 22-4, 22-5, 25-3, 27-4, 31-1, 31-5, 33-1, 40-1, 40-2, 40-3, 40-4,
53-3, 53-4.

The following figures are reprinted with permission from: Thorne CH, ed. Grabb and Smith’s Plastic Surgery. 7th ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2014.

19-3, 19-4, 19-5, 19-8, 20-1, 20-2, 20-4, 21-1, 21-2, 21–3, 21-4, 21-5, 21-6, 25-1, 27-3A–C, 29-2, 29-3, 29-4, 30-2, 33-2, 33-4, 34-1, 34-
3, 34-4, 35-2, 36-2, 37-6, 38-2, 39-6, 39-7, 41-5, 43-1, 49-2, 50-3, 50-4.
ANATOMY
I. COLLAGEN: Most abundant connective tissue protein in mammals.
A. Twenty types of identified collagen; most abundant types are:
1. *Type I: Skin, tendon, and mature scar have a 4:1 ratio of type I : type III
2. Type II: Cartilage and cornea
3. Type III: Blood vessels and immature scar
4. Type IV: Basement membrane
B. Composed of high concentration of hydroxyproline and hydroxylysine amino acids.

II. SKIN LAYERS AND STRUCTURES (FIG. 1-1 A,B)


A. Epidermis: Derived from ectoderm—stratified, keratinized, and avascular layer
1. Stratum basale (aka germinativum): This layer also contains melanocytes (of neural crest origin) that produce melanin,
which is taken up by the predominant keratinocytes.
2. Stratum spinosum: Desmosomes connect cells and create a shiny appearance.
3. Stratum granulosum: Cytoplasmic granules contribute to keratin formation.
4. Stratum lucidum: Dead cells without nuclei
5. Stratum corneum: Acellular layer of keratin
B. Dermis: Derived from mesoderm
1. Papillary: Loose vascular tissue
2. Reticular: Dense, more vascular layer
3. Contains fibroblasts, adipocytes, macrophages, collagen, and ground substance.
C. Adnexa: Sources of reepithelialization in partial-thickness wounds
1. Hair follicles (ectodermal origin)
a. Ingrowth of epidermis into dermis and subcutaneous tissue.
b. Associated sebaceous glands secrete into the hair follicle.
c. Retained in split-thickness skin grafts.
2. Eccrine sweat glands (ectodermal origin)
a. Coiled structures that secrete via a single duct into the epidermis.
b. Not present in split-thickness skin grafts and can lead to dryness.
3. Apocrine sweat glands (ectodermal origin)
a. In axillary and inguinal regions; secrete into hair follicles.

III. MUSCLE: Derived from paraxial mesoderm; classified as smooth, skeletal, and cardiac muscles. Muscle anatomy should be
understood in this regard.
A. Microscopic: Sarcomere unit—organized myofibrils composed of actin and myosin filaments; bundles of myofibers form
muscle fibers.
B. Macroscopic: Organized groups of muscle fibers for fascicles; bundles of fascicles form muscles.
C. Neuromuscular junction: “Motor end plate” consists of sarcolemmal folds within which acetylcholine receptors reside.

______________
*De note s common in-se rvice e xamination topics
Figure 1-1. Cross section of the skin. A: All skin layers. B: Epidermis. Meissner and Pacinian corpuscles only in glaborous skin.

IV. BONE: Derived from lateral plate mesoderm (except for skull bones derived from neural crest)
A. Cross-sectional anatomy
1. Outer layer: Fibrous periosteum and osteogenic periosteum (these cells participate in fracture repair).
2. Mature compact (cortical) bone: Eighty percent of total bone mass; lamellar structure that is permeated by elaborate
interconnecting vascular canals (Haversian canals).
3. Immature compact (cortical) bone: Woven structure of collagen fibrils that is replaced by mature bone through
remodeling.
4. Trabecular (cancellous) bone: Only 20% of total bone mass, but much greater surface area due to lower density;
bony matrix organized into a matrix (trabeculae) along lines of stress. Develops into compact bone via osteoblasts along
the trabeculae.

V. TENDON: Derived from lateral plate mesoderm


A. Organizational anatomy
1. Collagen is arranged longitudinally into fibrils.
2. Fibrils and fibroblasts are organized into fascicles, which are grouped into tendons.

VI. CARTILAGE: Derived from lateral plate mesoderm, the cartilage consists of extracellular matrix (ECM) composed of
collagen fibers, ground substance, and elastin, and is classified into elastic cartilage, hyaline cartilage, and fibrocartilage,
depending on the proportion of each component.
A. Cross-sectional anatomy
1. Zone 1: Superficial, uncalcified cartilage
2. Zone 2: Intermediate cartilage
3. Zone 3: Deep cartilage (abutting bone)
Figure 1-2. Anatomy of peripheral nerve. Nerves are composed of fascicles, each of which contain multiple nerve fibers (axons).

VII. NERVE: Peripheral nerves have neural crest origin


A. Organizational anatomy (Fig. 1-2)
1. Clusters of cell bodies or ganglia
2. A nerve describes a bundle of axons traveling together peripherally
3. The majority of axons are myelinated and individual axons are enveloped in endoneurium
4. Bundles of axons are called fascicles and are wrapped in perineurium
5. The nerve is covered by epineurium

NORMAL WOUND HEALING


VIII. SKIN AND SUBCUTANEOUS TISSUE
A. Wound healing categories
1. Primary intention
a. Immediate primary closure of a surgical incision *(epithelialization occurs in ~24 hours).
b. Delayed closure of a surgical incision (usually to either allow clearance of infection or resolution of edema) is known
as “delayed primary closure”.
2. Secondary intention
a. Full-thickness wound healing by a combination of wound contraction and migration of fibroblasts and keratinocytes
from the wound periphery.
B. Overview of the phases of wound healing
1. Inflammatory phase (first minutes to first week)
a. Vasoconstriction of vessels for first 10 minutes after injury.
b. Coagulation: *Platelets arrive and degranulate, releasing thromboxane A2 that causes transient
vasoconstriction to facilitate hemostasis with thrombus formation. PDGF and TGFB are also released.
c. Vasodilation and increased permeability: Small vessels dilate in response to prostaglandins to allow white blood
cells (neutrophils, plasma cells, and monocytes) attracted by the leukotrienes, complement, and cytokines (inter-
leukin-1 [IL-1], tumor necrosis factor-α [TNF-α], transforming growth factor-β [TGF-β], and platelet factor 4 [PF4])
to enter.
d. Cellular response
i. Neutrophils
a) Dominant cell type at 24 hours
b) Approach injury site by chemoattractants via circulatory system
c) Undergo magination and diapedsis
d) Migrate through interstitium by chemotaxis to injury site
ii. Macrophages (transformed monocytes) are the dominant cell type at 2 to 3 days, releasing cytokines to attract
fibroblasts
2. Proliferative phase (aka “fibroblastic phase,” ~days 3 to 14)
a. *Fibroblasts are the predominant cell population at 3 to 5 days and transform into myofibroblasts to promote
wound contraction under the influence of platelet-derived growth factor (PDGF) and TGF-β1 released by
macrophages.
b. High rate of collagen synthesis from days 5 to 21.
c. Tensile strength begins at days 4 to 5
d. Fibroblasts form ECM by synthesizing proteoglycan and fibronectin (which is then replaced by collagen).
e. *Keratinocytes migrate into the wound starting with the loss of contact inhibition.
f. *Neovascularization occurs under the influence of vascular endothelial growth factor expression.
3. Remodeling (maturation) phase (~week 3 to 1 year)
a. Collagen replaces proteoglycan/fibronectin and reorganizes creating stronger crosslinks.
b. Equilibrium between collagen breakdown and synthesis by weeks 3 to 5.
c. Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) remodel the collagen matrix.
d. The wound achieves 3% of its original strength at 1 week, 30% original strength at 3 weeks, and 80% original
strength at 2 months and beyond. *Final ratio of type I:type III collagen is 3.5:1.
C. Epithelialization
1. Mobilization: Loss of contact inhibition.
2. Migration: Cells migrate across the wound until meeting cells when the contact inhibition sets in.
3. Mitosis: Cells further back from wound edge proliferate to bridge wound.
4. Differentiation: Reestablishment of epithelial layers from basal layer to stratum corneum after migration ceases.
D. Contraction (happens when full-thickness injury through dermis is present). Fibroblasts transform into myofibroblasts
1. Myofibroblasts are present throughout granulating wound
2. Myofibroblasts appear at day 3 and reach the maximum level at days 10 to 21.
3. Less contraction when more dermis within the wound

IX. PHASES OF MUSCLE HEALING


A. Phases of muscle healing (phases overlap with each other)
1. Destructive phase (days 0 to 7 following injury). Myoblasts join with each other to form myotubes which then fuse to
form new myofibers.
a. Analogous to inflammatory phase of skin healing
b. Inflammatory response with cytokine release
c. Initial neutrophil response followed by macrophages
2. Repair phase (starting at day 3, lasting up to several weeks)
a. Regeneration of disrupted myofibers
b. Production of connective tissue scar
3. Remodeling phase (occurs concomitantly with repair phase)
a. Vascular ingrowth (to feed the upregulated metabolism of regeneration)
b. Regeneration of intramuscular nerves is necessary for functional regeneration
c. Adhesion of myofibers to ECM

X. BONE
A. Bone healing categories
1. Primary (direct) bone healing by surgical fixation
a. Minimal callus formation (bypasses the stage of woven bone formation)
b. Lamellar bone formation parallel to the long axis of the bone
2. Secondary (indirect) bone healing by external splint/cast fixation
a. Typical callus formation, amount of callus correlates with the amount of instability encountered during healing.
b. Immobilization is important to allow for healing.
B. Phases of bone healing
1. Inflammatory phase (from time of fracture and tapering off at when bone formation starts at 7 to 10 days)
a. Initial platelet degranulation and contained hematoma aids in healing.
b. Inflammatory response as detailed in previous section; osteoclasts break down necrotic bone edges, releasing
osteogenic cytokines.
2. Reparative phase (starting during the first week and lasting up to several months)
a. Inflammatory debris is cleared by macrophages.
b. Acid tide—acidic local environment stimulates osteoclasts.
c. Vascular ingrowth from periosteum and endosteum.
d. pH rises at ~day 10 with the presence of increased alkaline phosphatase, leading to the formation of newly woven
bone at the edges.
e. At ~3 weeks callus fills in between the edges (starts a soft callus populated by chondrocytes, which gradually
calcifies into hard callus by endochondral ossification); continued bone formation by osteoblasts leads to bony edge
unification.
3. Remodeling phase (starting after fracture solidly united at 2 to 3 months and continuing for years)
a. Woven bone is slowly replaced by the lamellar bone according to the Wolff law; medullary canal is restored.
b. “Clinical healing” (defined as the state of adequate stability and resolution of pain to allow protected motion) occurs
in most bones by 4 to 6 weeks. Radiographic healing may lag by 6 months.
C. Bone grafting
1. Aspects of healing: An ideal bone graft (autogenous, cancellous) possesses osteoconductive, osteoinductive, and
osteogenetic properties
a. *Osteoconduction—donor bone placed adjacent to the recipient bone will allow ingrowth of capillaries
and osteoprogenitor cells, ultimately resulting in complete incorporation. Acts as a scaffold.
b. *Osteoinduction—active induction of differentiation of osteoblast precursors into bone-forming cells.
Bone morphogenetic proteins: 2, 4, and 7 isotypes have the most significant osteoinductive effects.
c. *Osteogenesis—formation of new bone by virtue of osteogenic precursors present within a graft.

XI. TENDON
A. Two mechanisms of tendon healing categories
1. Intrinsic healing
a. Tendon’s intrinsic capacity to heal (operative repair aims to maximize this type of healing)
b. Mediated by tenocyte/fibroblast population that arises from the tendon and epitenon.
c. Relies on synovial diffusion for nutrition
d. Enhanced by mobilization
2. Extrinsic healing
a. Surrounding soft tissue’s tendency to repair damaged tendon
b. Ingrowth of inflammatory cells and fibroblasts overlying the sheath
c. Immobilization leads to the formation of debilitating adhesions to tendon, limiting range of motion (early mobilization
minimizes adhesions caused by extrinsic healing).
B. Phases of healing
1. Inflammatory phase (within first few days, inflammatory response peaking at 3 days)
a. Tendon defect fills with hematoma, tissue debris, and fluid
b. Both intrinsic cells and cells that have migrated from the periphery bridge the defect
c. Increased phagocytic activity clears necrotic debris
2. Proliferative phase (starting at ~day 5 and lasting up to several weeks)
a. Fibroblasts are the predominant cell type, proliferating from epitenon and endotenon.
b. Collagen initially deposited perpendicular to the tendon axis; at ~4 weeks, the collagen fibers realign to the long axis.
c. Strength of repair begins and increases at ~2 to 3 weeks; synovial sheath is reconstituted at 3 weeks.
d. Vascular ingrowth occurs
3. Remodeling phase (starting at several weeks after injury and lasting up to 1 year after):
a. Collagen fibers continue to realign to the long axis of the tendon
b. Fibers realigned by 8 weeks
C. Tendon grafts
1. Extrasynovial tendon grafts (most commonly include palmaris longus or plantaris)
a. Early cell death and eventual repopulation by fibroblasts and neovascularization.
b. Acts as a conduit for vessel and cell ingrowth
2. Intrasynovial tendon grafts (rare; e.g., Flexor digitorum longus)
a. Cellular viability is thought to be maintained, and healing occurs by the normal mechanisms.
b. Less adhesion formation

XII. CARTILAGE
A. Avascular tissue without intrinsic healing potential
B. Healing initiated by damage to the surrounding tissue (e.g., perichondrium and subchondral bone)
C. Extra-articular cartilage versus intra-articular cartilage healing
1. Extra-articular cartilage (e.g., auricular and nasal) injury
a. Tissue injury response generated by perichondrium with fibroblast influx and scar formation (but not true
regeneration of cartilage).
2. Intra-articular cartilage injury
a. Superficial (without violation of subchondral bone)—no blood-carrying progenitor cells are released, thus no repair
occurs.
b. Full-thickness (through cartilage and into subchondral bone)—allows influx of progenitor cells and formation of
fibrocartilage. Fibrocartilage is less organized, more vascular, less tolerant of mechanical force, and more susceptible
to degradation compared with normal cartilage. Fibrocartilage eventually breaks down, resulting in an arthritic joint.

XIII. NERVE
A. Response to injury
1. Trauma to vasa nervorum and surrounding tissue leads to inflammatory response.
2. If the injury is close to the neuron cell body, the entire neuron may die (e.g., brachial plexus avulsion injuries).
3. Typical injuries to nerves in peripheral locations (e.g., complex forearm laceration) will affect connective tissues
(Schwann cells) and the axon but not the actual neuronal cell body.
4. Wallerian degeneration: Schwann cells will die, and the distal axon degrades. This can extend up to 2 cm proximal to the
injury site.
5. Axon degradation and clearing of debris takes 15 to 30 days and precedes nerve regeneration.
6. Axonal regrowth occurs in response to neurotrophins (e.g., brain-derived neurotrophic factors, ciliary neurotrophic
factor, and nerve growth factor) secreted by target cells (postsynaptic neurons or muscle cells) and by Schwann cells.
7. Macrophages secrete interleukins that induce Schwann cell proliferation.
8. Schwann cells along the distal axonal tract express laminins and adhesion molecules, which help guide the regenerating
axon.
9. Axonal sprouts from the proximal cut end must enter the distal tract to regrow. If disruption of the nerve is severe
and/or scarring is great, the budding axons cannot cross the gap, and regeneration does not occur.
10. Muscles innervated by the injured nerve will atrophy (70% loss at 2 months). Some muscle fibers die at 6 to 12 months
if there is no regeneration of nerve. Motor end plates remain open for approximately 1 year (variable) before fibrosis
develops, making reinnervation of that particular muscle impossible.
11. *Once growth is initiated, axons extend by approximately 1 mm a day
B. *Seddon nerve injury classification
1. Neuropraxia
a. Segmental interruption of myelin sheath leading to local transient block of conduction along a nerve.
b. The anatomy of the nerve is preserved, and no Wallerian degeneration occurs.
c. Recovery is usually rapid (few weeks), but may take several months.
d. Selective demyelination of fibers may occur.
2. Axonotmesis
a. Axonal damage within the nerve. Schwann cell basal lamina (inner endoneurial sheath) is preserved.
b. Wallerian degeneration occurs. Recovery rate is 1 mm/day along the nerve, once healing begins.
c. Fibrillations are present on electromotor testing.
d. Recovery is typically complete eventually (without surgery) if axonal regeneration is able to progress across the
injury zone.
3. Neurotmesis
a. Nerve is transected with destruction of nerve, myelin sheath, and surrounding connective tissue; Wallerian
degeneration occurs.
b. Spontaneous recovery does not occur; surgical repair is needed for the best outcome.
C. Sunderland/Mackinnon nerve injury classification (Table 1-1)
1. First-degree injury
a. Nerve is demyelinated, resulting in a local conduction block.
b. Treatment is nonoperative and recovery is complete within approximately 12 weeks.
2. Second-degree injury
a. Some nerve fibers are disrupted, but the Schwann cell basal lamina remains intact.
b. Wallerian degeneration occurs with second-degree and higher injuries.
c. Tinel’s sign indicates an advancing growth cone.
d. Treatment is nonoperative. Complete recovery is expected in months.
3. Third-degree injury
a. Some areas of Schwann cell basal lamina are disrupted with scarring, while the perineurium remains intact.
b. Incomplete recovery; some nerve fibers do not reinnervate their target.
c. Treatment is usually nonoperative.
4. Fourth-degree injury
a. Loss of continuity of the perineurium.
b. Scar blocks all fiber growth; little or no nerve recovery.
c. Treatment is operative.
5. Fifth-degree injury
a. The nerve is completely transected.
b. The epineurium is disrupted.
c. No recovery is expected without operative management.
6. Sixth-degree injury
a. Combination of any of the previous five levels of injury.

PATHOLOGIC WOUND HEALING


I. WOUND FAILURE (SKIN, SUBCUTANEOUS TISSUE, FASCIA, MUSCLE)
A. Acute wound failure (dehiscence): Postoperative separation of the surgical incision
1. Occurs when the load applied to the wound exceeds the strength of the suture line and provisional matrix.
2. Most commonly happens at 7 to 10 days postoperatively, can happen any time from day 1 to more than 20 days after
surgery.

3. Associated factors
a. Surgeon factors
i. Technical error (most common cause for early fascial dehiscence within several days after abdominal surgery)
ii. Emergency surgery
b. Systemic factors
i. Advanced age
ii. Chronic corticosteroid therapy
iii. Malnutrition
iv. Radiation therapy
v. Chemotherapy
vi. Systemic disease (jaundice, renal failure, and diabetes)
c. Local factors
i. Hematoma
ii. *Seroma (the most common cause of late postoperative skin dehiscence following post-bariatric body
contouring)
iii. Infection
iv. Edema
v. Excessive tension (noncompliance with following activity restrictions)
vi. Elevated intra-abdominal pressure (for abdominal closures)
vii. Previous wound dehiscence
B. Chronic wound failure (nonhealing wounds)
1. Failure to achieve anatomic/functional integrity over 3 months
2. Diabetes, venous stasis, ischemic tissue loss, and pressure sore are common etiologies
3. Underlying osteomyelitis, hidradenitis, or pyoderma gangrenosum
4. Possibility exists for the development of squamous cell carcinoma (aka Marjolin’s ulcer) in the setting of a chronic
wound
5. Associated physiologic derangements
a. Cytokine abnormalities: Increased IL-1, IL-6, TNF-α; decreased epidermal growth factor, PDGF.
b. *Abnormal ECM dynamics: Increased MMPs, decreased TIMPs
6. Associated factors
a. Local factors
i. Infection
ii. Infected foreign body (e.g., orthopedic hardware)
iii. Ischemia (arterial insufficiency or pressure-related)
iv. Venous insufficiency (leads to protein extravasation, edema, and decreased oxygen diffusion)
v. *Radiation therapy leads to vascular fibrosis (relative ischemia) and decreases mitotic potential of
fibroblasts (also consider possibility of osteoradionecrosis of the bone).
b. Systemic factors
i. Hypoxia
ii. Smoking
iii. Diabetes (microvascular and macrovascular diseases leading to local ischemia; glycosylation of hemoglobin
impairs oxygen delivery; impaired neutrophil function; peripheral neuropathy)
iv. Chronic disease
v. Advanced age (shortened inflammatory phase causing decreased strength of healing)
vi. Malnutrition
a) Vitamin C
1) *Collagen cross-linking by hydroxylation of proline and lysine
2) *Lack of vitamin C leads to “scurvy”: Low collagen tensile strength manifests in collagen-
containing tissues (skin, dentition, bone, and blood vessels) as hemorrhage (petechiae and swollen gums),
loss of dentition, and impaired bone healing.
b) *Folate and vitamin B 6 (pyridoxine): DNA synthesis and cellular proliferation
c) *Vitamin E: Strong antioxidant and immune modulator
d) *Zinc: Cofactor for numerous metalloenzymes and proteins; necessary for protein and nucleic acid synthesis.
e) *Assess nutrition with albumin level (normal >3.5 g/dL, 20 day half-life) or pre-albumin level (normal
>17 g/dL, 3 day half-life)
vii. Chemotherapy: Most detrimental agents are doxorubicin, cyclophosphamide, methotrexate,
bischloroethylnitrosourea (BCNU), and nitrogen mustard
viii. Glucocorticoids
a) Inhibit the inflammatory phase and inhibit collagen synthesis of fibroblasts, leading to decreased wound
strength.
b) *Can reverse effect with oral vitamin A to augment epithelialization and fibroblast proliferation
ix. Tamoxifen (dose-dependent effect)
x. *Anemia by itself does not impair wound healing

II. BONE—PATHOLOGIC HEALING


A. Types of bone healing pathology
1. Delayed union: When clinical healing is delayed beyond the usual expected time with radiographic evidence of
inadequate osteocyte activity and deficient callus formation.
2. Nonunion: When there is no evidence of clinical or radiographic healing beyond the usual healing time, often with a
mobile area fibrous scar and interposed tissue in the gap (pseudoarthrosis).
a. Atrophic nonunion: Marked resorption of the bony ends at the fracture site without callus (therapeutic intervention
may involve provision of internal fixation along with an osteoinductive stimulus such as bone graft).
b. Hypertrophic nonunion: Significant callus formation, but no bridging of fracture (usually result of failure to provide
stable fixation).
B. Factors detrimental to bone healing
1. Local factors: Soft tissue crush/loss, soft tissue interposition into fracture gap, open fractures, segmental fractures,
articular fractures, infection, pathologic fractures, extensive soft tissue stripping, inadequate reduction, inadequate
immobilization, rigid fixation with gap, distraction of fracture, and delay in treatment
2. Systemic factors: Anemia, malnutrition, vitamin D deficiency, growth hormone deficiency, diabetes, smoking, NSAIDs,
steroids, and anticoagulants

III. TENDON—PATHOLOGIC HEALING


A. Immobilization after primary tendon repair
1. Extrinsic healing predominates with tendon sheath adhesion formation.
2. Disorganized collagen fibrils and decreased strength of repair.
B. Overuse tendinosis: Painful condition beginning with repetitive microtrauma to tendon; characterized by degenerative
changes in tendon.
1. Aging, inflammatory cytokines, and ischemia are thought to be contributing factors
2. May be seen with or without inflammation of paratenon
C. Postoperative rupture of tendon repairs
1. Attributable to a greater load encountered than the strength of repair (repair is weakest between days 6 and 18, peak
occurrence at day 10).
2. Poor tendon healing due to gapping caused by poor surgical technique
3. *Fluoroquinolones inhibit tenocyte metabolism, reducing cell proliferation and collagen/matrix synthesis and
can lead to spontaneous rupture of tendons.

IV. NERVE—PATHOLOGIC HEALING


A. Neuroma—painful regrowth of nerve in a scarred area of previous injury.
B. Failure of axonal regeneration (potential for axonal regeneration decreases with age)
1. Degeneration of sensory receptors (for sensory nerves)
2. Fibrosis of motor end plates (for motor nerves)
C. Cross-innervation (e.g., facial synkinesis, gustatory sweating [Frey’s syndrome])

NORMAL SCARRING
I. VISIBLE SCAR IS THE NORMAL ENDPOINT FOR ALL FULL-THICKNESS SKIN INJURIES
A. Factors that lead to less conspicuous scars
1. Older age
2. Lighter colored skin
3. Surgical incision as opposed to traumatic laceration
4. Placement of incision or laceration within (parallel to) relaxed skin tension line
5. Minimal tension following closure (e.g., eyelids)
6. Optimal surgical technique (e.g., atraumatic manipulation, skin edge eversion, and removal of suture in 5 to 7 days on
face)

PATHOLOGIC SCARRING
I. HYPERTROPHIC SCAR
A. Definition: An abnormal wound healing endpoint in response to trauma, inflammation, burn, or surgery
1. Raised, erythematous, and often pruritic
2. *Remains within the boundaries of original wound
3. Upregulated fibrogenic cytokines (TGF-β isoforms, PDGF, and insulin-like growth factor 1 [IGF-1]) lead to higher levels
of collagen synthesis
B. Etiology
1. Major factors
a. Amount and depth of trauma (most commonly with burns)
b. Inflammation, infection
c. Prolonged open wound (>21 days, most commonly with burns)
2. Contributing factors
a. Areas of tension
b. Darker skin tone
C. Natural history
1. Becomes apparent at ~6 to 8 weeks after injury
2. Worsens over 6 months
3. May cause contractures at joints
4. May take 1 to 2 years to mature (scar will become less red, less tender, and less pruritic)
5. May regress somewhat without any intervention at all
D. Histologic characteristics (under standard light microscopy, hypertrophic scar and keloid are indistinguishable)
1. Cigar-shaped nodules of blood vessels, fibroblasts, and collagen fibers that are arranged parallel to epidermis and
oriented along tension lines (normal skin: the basket-like woven pattern of collagen fibers)
2. *Presence of α-smooth muscle actin producing myofibroblasts (not present in keloids)
3. Lower ratio of type I:type III collagen (2:1). (Type I:type III collagen ratio is 3.5:1 in normal scars.)
E. Treatment approach
1. Nonoperative
a. Pressure garments
i. Commonly used for hypertrophic burn scars
ii. Induces local tissue hypoxia, reduces fibroblast proliferation and collagen synthesis
iii. Compression of 24 to 30 mmHg to be effective
b. *Silicone sheeting and topical silicone gel
i. Unclear mechanism of action—thought to increase hydration of remodeling scar
ii. Require application of at least 12 hours/day for at least 3 months to be effective
c. Corticosteroid injection
2. Surgical excision
a. Attention to atraumatic technique, excision of inflamed tissue, avoidance of nidus for inflammation (e.g., trapped hair
or unnecessary deep resorbable suture), and tension-free closure.
b. Z-plasty tissue rearrangements to release contractures
c. May require graft or flap reconstruction for coverage
d. Fractional ablative CO2 laser can be helpful adjunct

II. KELOIDS
A. Definition: An abnormal wound healing endpoint in response to trauma, inflammation, burns, or surgery.
1. May start as a raised, erythematous, and pruritic lesion
2. *Evolves into an enlarging mass that extends beyond the original boundaries of the wound.
3. Higher level of collagen synthesis compared with hypertrophic scars due to upregulated fibrogenic cytokines (TGF-β
isoforms, PDGF, and IGF-1) and increased number of receptors for these cytokines within keloidal fibroblasts.
4. *Increased fibroblast proliferation
5. *Absence of myofibroblasts and decreased density of blood vessels in comparison to hypertrophic scars.
6. Decreased expression of MMPs (that degrade ECM)
7. Increased levels of adenosine triphosphate within keloid
B. Etiology
1. Major factors
a. Darker skin tone
b. Genetic predisposition
2. Contributing factors
a. Age (peak just after puberty)
b. Hormones (keloids worsen during puberty and pregnancy; postmenopausal women experience softening and
flattening of keloids)
C. Natural history: Evolves over time without a significant regression or quiescent phase
D. Histologic characteristics (under light microscopy, hypertrophic scar and keloid are indistinguishable)
1. Thick and large collagen fibers haphazardly packed closely together
2. *Much higher ratio of type I:type III collagen (18:1)
E. Treatment approach: Nonoperative and operative interventions are required, and an extremely high rate of recurrence
persists (50% to 80%)
1. Nonoperative
a. Pressure devices (e.g., pressure clip for earlobe)
b. Silicone sheeting and topical silicone gel
c. Corticosteroid injection
d. Radiation therapy
2. Surgical
a. Attention to atraumatic technique, excision of inflamed tissue, avoidance of nidus for inflammation (e.g., trapped hair
or unnecessary deep resorbable suture), and tension-free closure
b. Excision ± skin graft depending on the size of the lesion

III. COLLAGEN SYNTHESIS DISORDERS


A. Ehlers–Danlos syndrome
1. Autosomal dominant transmission
2. Significant joint laxity, thin and friable skin, and severe skin hyperlaxity
3. Extreme risk for wound healing problems (e.g., recurrent ventral hernia)
4. Increased risk of infection (inherently defective immune response)
5. Should be discouraged from pursuing elective and aesthetic surgery
B. Cutis laxa
1. Defective collagen synthesis results in hyperextensible skin
2. Can be autosomal dominant, autosomal recessive, or X-linked
3. Autosomal and X-linked variants have more generalized manifestations: Growth retardation, skeletal dysplasia, facial
dysmorphia, emphysema, cardiovascular involvement, hernias, and hollow viscus diverticula
4. *Not a contraindication to surgery

PEARLS
1. Scars typically widen over time. Some areas, such as the back or the legs, are especially prone to scar widening.
2. Nicotine in any form (smoking, patches) impairs wound healing significantly due to vasoconstrictive effects
3. Macrophages are critical cells in wound healing and initiate the growth factor cascade, fibroblast proliferation, and collagen
formation
4. Prior to considering scar revision, at least 1 year should pass to allow for complete scar remodeling

QUESTIONS YOU WILL BE ASKED


1. What is the difference between wound contraction and wound contracture?
Wound contraction is a part of secondary healing beginning a few days after injury as myofibroblasts contract and reduce the
size of the wound to be epithelialized. Wound contractures occur when bands of collagen are deposited at the site of
hypertrophic scar formation; these are termed “contractures” when they impair functionality (e.g., hands) or range of motion
(e.g., axillae and neck).
2. What is the difference between hypertrophic scar and keloid?
Hypertrophic scar does not extend beyond the borders of the original wound, whereas keloids grow well beyond these borders;
histologically, these two fibroproliferative disorders are different, but they are indistinguishable under standard H&E preparation
on light microscopy. They have much different type I:type III collagen ratios. Hypertrophic scars produce smooth muscle actin
by myofibroblasts, whereas keloids do not.
3. What are the factors that impair wound healing?
Systemic conditions (e.g., diabetes, autoimmune conditions, and medications), ischemia, pressure injury, infection, malignancy,
foreign body, venous insufficiency, irradiation, hypoxia, smoking, advanced age, and malnutrition.
4. What are the types of nerve injury and their expected recovery? Which types require surgical intervention?
See “NORMAL WOUND HEALING” → “NERVE” → Sections B and C.

Recommended Readings
Broughton G, Janis JE, Attinger CE. T he basic science of wound healing. Plast Reconstr Surg. 2006;117(7 Suppl):12S–34S. PMID:16799372.
Garner WL, Rahban SR. Fibroproliferative scars. Clin Plast Surg. 2003;30(1):77–89. PMID: 12636218.
Maggi SP, Lowe JB 3rd, Mackinnon SE. Pathophysiology of nerve injury. Clin Plast Surg. 2003;30(2): 109–126. PMID: 12737347.
INITIAL ASSESSMENT OF WOUNDS
I. EXAMINE ETIOLOGY OF THE WOUND AND ASSESS FACTORS THAT PROVIDE THE FOUNDATION FOR
WOUND HEALING
A. Acute versus chronic (see Fig. 2-1)
1. Origin and duration of wound
a. Traumatic versus atraumatic
i. Zone of injury is larger in high- versus low-impact traumas
ii. Assessment of other associated injuries
b. Timing: Injuries that are closed after 6 to 8 hours of remaining open have increased rate of infection.
c. Extent of contamination
i. Antibiotics are not needed for most wounds unless they demonstrate signs of active infection (e.g., cellulitis in
chronic venous stasis ulcers).
ii. Bite wounds are always contaminated and have a high likelihood of infection.
a) Assume that the contamination is polymicrobial, and always treat with antibiotics that cover Gram-positive and
anaerobic organisms (e.g., ampicillin/sulbactam or amoxicillin/clavulanate, ciprofloxacin + clindamycin if
allergic to penicillin).
b) Bacteria specific to wounds
1) *Human bite wounds are contaminated by Eikenella corrodens S.aureus, Eikenella corrodens
and anaerobes.
2) *Cat bite wounds are also contaminated by Pasteurella multocida
iii. Tetanus prophylaxis (see Table 2-1)
d. Size of wound
i. Extent of exposed tissue: Dermis versus subcutaneous tissue versus fascia versus muscle versus bone
a) >85% chance of osteomyelitis in wounds with exposed bone
2. Assessment of patient local and systemic factors
a. Presence of ischemia–reperfusion injury
b. Hypoxia in the wound bed
c. Bacterial load of the wound
i. Contaminated: Bacteria present without proliferation
ii. Colonized: Bacteria present and proliferating but without causing host response.
iii. Critically colonized: Bacteria present, proliferating, and causing host response, but not enough to overcome host’s
resistance.
iv. Infected: Expanding bacterial counts that have overcome the host’s ability to respond.

II. PHYSICAL EXAM


A. General assessment
1. Overall health of the patient
2. Quality of tissue surrounding the wound

______________
*De note s common in-se rvice e xamination topics
Figure 2-1. T he phases of wound healing.

a. Presence/absence of
i. Radiation-induced chronic skin changes
ii. Edema
iii. Color: Dependent rubor versus erythema
iv. Induration/focal fluid collections
v. Hemorrhage
vi. Foreign bodies
vii. Other wounds in the area
3. Condition of wound bed
a. Location: Evaluate the area for excess pressure or dependent positioning
b. Depth: Evaluate for damage to surrounding structures, including blood vessels, nerves, bone, muscle, and
subcutaneous tissues
c. Characteristics of wound bed
i. Amount of granulation tissue versus fibrinous exudate
ii. Odor

iii. Exposed structures


iv. Foreign bodies
v. Sinus tract/tunnel formation
4. Neurosensory exam
a. Gross sensation based on dermatomes involved
b. Two-point discrimination: Normal two point: <5 mm
c. Vibration sensation
5. Vascular exam
a. The presence of both palpable peripheral pulses and Doppler signals in vascular territories adjacent to the wound
b. Temperature of extremity or digit
c. Skin changes consistent with venous stasis, peripheral arterial disease, and lymphedema

III. LABORATORY/RADIOGRAPHIC TESTING


A. Complete blood count (CBC): Evaluate for elevated white blood cell (WBC) count and anemia
B. Albumin
1. 2.8 to 3.5 g/dL: Mild malnutrition
2. 2.1 to 2.7 g/dL: Moderate malnutrition
3. <2.1 g/dL: Severe malnutrition
C. Erythrocyte sedimentation rate and C-reactive protein: May signal the presence or recurrence of osteomyelitis, but
are nonspecific inflammatory markers that may be elevated in any pro-inflammatory state, so should be interpreted in the
context of the entire clinical picture.
D. Hemoglobin A1C
E. Creatinine
1. Renal failure may predispose patients to chronic wounds and poor wound healing.
2. Calciphylaxis is an important underlying cause of chronic wounds in patients with end-stage renal disease.
F. Plain films: Assess for fractures, orthopedic plates/screws, foreign bodies, and osteomyelitis
G. Computed tomography (CT): Assess for abscesses, chronic sinuses, extent of wound, and involved structures
H. Three-phase technetium bone scan: Radioactive study designed to indicate areas of abnormal bone metabolism or
remodeling.
I. Magnetic resonance imaging (MRI): To evaluate the extent of osteomyelitis, especially if spine is involved
J. Ankle–brachial indices
1. >1.2: Calcified vessels (e.g., diabetes)
2. 0.9 to 1.2: Normal
3. 0.5 to 0.9: Mixed arterial/venous disease
4. <0.5: Critical stenosis, symptomatic claudication
5. <0.2: Ischemia and gangrene
K. Angiography: To evaluate the extent of vascular disease
1. If there is evidence of significant peripheral vascular disease, wounds should not be debrided until revascularization
procedures are complete to optimize wound healing.
a. Exception: Wounds must be debrided regardless of vascular status if there are signs of overt infection (e.g., “wet”
suppurative gangrene).
L. Biopsy/cultures
1. Help target antibiotic regimens and durations.
2. Evaluate for malignancy for atypical or chronic nonhealing wounds.
3. Quantification of bacterial colonies helps in diagnosis and in following progression of treatment.

DEBRIDEMENT
I. SURGICAL, ENZYMATIC (COLLAGENASE), MECHANICAL (VERSAJET, WATERPIK), AND AUTOLYTIC
A. Reduces bioburden by removing inflammatory component of wound, biofilms, fibrinous tissue, which contains cytotoxic
mediators that inhibit wound healing.
1. Promotes wound healing by converting a chronic wound into an acute wound to promote keratinocyte migration.
2. Eradicates biofilm and reduce bioburden in wounds with exposed plates or foreign bodies.
B. Vital structures (e.g., nerve, tendon, bone, and vessels) should not be debrided whenever possible unless gross infection or
ischemia is present.
C. Complete debridement with irrigation and application of appropriate dressing.

DRESSINGS
I. GOALS
A. Protect the wound from the external environment and mechanical forces.
B. Absorb secretions/maintain a clean environment.
C. Promote granulation tissue formation and reepithelialization: Moist environment leads to increased granulation tissue
formation and tissue reepithelialization as compared with dry environment.
D. Optimize patient comfort.

II. TYPE OF DRESSINGS


A. Nonocclusive dressings (e.g., Gauze)
1. Permeable to both gas particles and fluids
2. “Wet to dry” dressing
a. Allowing the gauze to dry prior to removal results in mechanical debridement of the wound during each dressing
change.
b. Removal of the dry gauze also creates a mild pro-inflammatory state, which can inhibit wound healing.
c. Coarse gauze provides greater debridement compared with fine gauze.
3. “Wet to wet” dressing: Used over exposed tendon, bone, and neurovascular structures to minimize desiccation.
B. Semiocclusive dressings (e.g., Tegaderm)
1. Sheet dressings that are impermeable to fluids but allow passage of gas molecules.
2. Usually used to cover graft donor sites to keep area moist.
3. Must be cautious in using on areas of thin/fragile skin.
4. Should not be used in contaminated wounds.
C. Occlusive dressings
1. Hydrogel (e.g., Aquasorb and Hydrosorb)
a. Composed of complex polysaccharides, nonadhesive
b. Use in wounds with mild, superficially exudative regions and in painful wounds.
c. Rehydrate wounds and maintain moisture independent from the moisture that is inherently present in the wound.
d. Can be used in infected wound beds.
2. Hydrocolloids (e.g., Duoderm)
a. Comes in paste, powder, and sheet forms
b. Fully adhesive, minimally absorptive
c. Cannot use in infected wounds
d. Induces autolytic debridement within wound
e. Use in mild, superficially exudative wounds
3. Foam (e.g., Mepilex)
a. Usually composed of nonadhering polyurethane
b. Highly absorptive, but nonhydrating
c. Use in moderately to heavily exudative wounds
4. Alginates (e.g., Algiderm)
a. Derived from seaweed
b. Comes in ribbon/rope forms
c. Can absorb 20× the dry weight of the dressing
d. Use in highly exudative wounds
D. Antimicrobial dressings
1. Silver-coated or -impregnated dressings (e.g., Silverlon)
2. Xeroform: 3% bismuth tribromophenate–impregnated gauze
E. Negative pressure wound therapy
1. “Wound vac” therapy
2. Consists of using a sponge, occlusive dressing, and vacuum
a. Reduces edema
b. Removes exudates from leaky blood vessels/lymphatic channels to improve oxygen diffusion
c. Removes harmful enzymes and inflammatory mediators
3. Most commonly used in
a. Venous stasis ulcers
b. Lymphatic leaks
c. Diabetic wounds
4. *Must not use over
a. Normal skin
b. Infected tissues
c. Tissues harboring malignant cells
d. Inadequately debrided wounds
e. Neurovascular structures

SURGICAL WOUNDS
I. CLASSIFICATION OF SURGICAL WOUNDS
A. Clean (class I): Nontraumatic, no entry into respiratory, gastrointestinal (GI), genitourinary (GU) systems prior to incision,
no break in sterile technique (<2% risk of infection).
B. Clean–contaminated (class II): Nontraumatic, minor breaks in sterile technique, entry into GU, GI, and/or respiratory
tracts, but without significant spillage (<10% risk of infection).
C. Contaminated (class III): Traumatic, may include gross entry and spillage from GI or GU systems, involves grossly
infected tissues/fluid (~20% risk of infection).
D. Dirty (class IV): Traumatic, dirty wound, significant devitalized tissue, fecal matter, foreign bodies, evidence of perforated
viscus, and inflammation (40% risk of infection).

II. GENERAL CONSIDERATIONS WHEN CREATING INCISIONS AND FOR WOUND CLOSURE
A. Type of skin and location on the body
1. Specific areas are prone to scar widening and hypertrophy (e.g., shoulder/sternal areas), whereas others tend to heal
more favorably (e.g., eyelid and dorsum of the hand).
2. Hair-bearing skin: Scalp incisions are typically beveled to allow for hair growth after incision has healed by avoiding
disruption of the hair follicles.
3. Extremity
a. Longitudinal incisions are preferred to avoid crossing joint surfaces to minimize tension and lessen the chance of
mobility-limiting scar contracture.
b. Excisional and incisional biopsies should always be oriented longitudinally in order to prevent later morbidity and
complexity if additional resection and reconstruction is required (e.g., sarcoma).
4. Hand incisions.
a. Mid-axial or volar zigzag (Bruner) incisions are preferred to approach the digit volarly.
b. S-shaped, C-shaped, or curvilinear incisions are preferred to approach the digit dorsally.
B. Direction and length of the incision
1. Langer lines of tension (relaxed skin tension lines): Incisions that are able to be planned should be made parallel
to the relaxed skin tension lines.
C. Surgical technique
1. Minimize damage to skin edges with atraumatic technique
2. Debridement of necrotic or foreign material
3. Tension-free closure
4. Wound edge eversion
5. Placement of suture that should not leave permanent suture marks
6. Prompt removal of sutures
a. Face: 5 to 7 days
b. Hand/foot: 10 to 14 days
c. Trunk/breast: 7 to 10 days

III. TYPES OF CLOSURE


A. Primary closure: Tissues are reapproximated (using sutures, staples, etc.) on initial presentation.
1. Edges must be under minimal tension
2. Wound cannot be infected
a. Bacterial counts of >105 CFU/g of tissue heal very poorly without debridement.
b. β-Hemolytic streptococci can inhibit wound healing at concentrations >103 CFU/g of tissue.
B. Secondary intention closure: Wound heals with time through accumulation of granulation tissue, usually with frequent
dressing changes.
C. Delayed primary closure: Wound initially heals through secondary intention. Once wound bed is clean and under minimal
tension, wound edges can be reapproximated using primary closure techniques.

IV. CLOSURE MATERIALS (SEE TABLE 2-2)


A. Suture
1. Classified as absorbable versus nonabsorbable; monofilament versus braided; synthetic versus natural
a. Absorbable
i. Lose at least 50% of strength in 4 weeks.
ii. Often used in children to avoid suture removal.
b. Non-absorbable: Permanent, body induces a cell-mediated reaction around the suture which eventually
encapsulates the suture.
c. Monofilament versus braided: Braided sutures are easier to work with, but have slightly increased risk of
infection.
d. Synthetic versus natural: Silk and gut are the only natural sutures available, the rest are synthetic.
B. Staples
1. Quick closure
2. Good for hair-bearing regions
3. Use forceps to initiate wound eversion and staple in place
C. Surgical adhesives
1. Cyanoacrylate (Dermabond)
a. Used in conjunction with a proper closure initiated by suture material, which is under minimal tension.

b. Pros: Decreased time for closure, improved cosmetic outcome, possible decreased risk of infection due to decrease
in suture use.
c. Cons: Must have a tension-free closure, must not be used on mucosal surfaces.
D. Surgical tapes. Steristrips: Can be used in conjunction with sutures or alone if the closure is completely tension free.

V. METHODS OF WOUND CLOSURE (SEE FIG. 2-2)


A. Simple interrupted: Needle is placed perpendicular to the skin and drawn into the targeted layers of tissue on one side,
then out through the same layers/levels of tissue on the opposite side, then tied in place.
1. The needle pathway allows the width of the suture at the base to be wider than at the epidermal entrance to allow
eversion of the skin edges.
2. Place sutures 5 to 7 mm apart and 1 to 2 mm from the skin edges to allow for appropriate wound closure.
Figure 2-2. A: Simple interrupted closure. B: Interrupted vertical mattress pattern. C: Interrupted horizontal mattress pattern. D: Running subcuticular (intracuticular)
sutures. E: Half-buried horizontal mattress (applicable in corners). F: Simple running (“ over-and-over”) suture. G: Stapled closure. H: Steristrips (adhesive tape).

B. Vertical/horizontal mattress suture


1. Good for glabrous skin and wounds under tension.
2. Horizontal mattress causes more hypoxia to tissues than vertical mattress.
C. Subcuticular: Avoids marks on the external surface of the incision to result in a more favorable scar; left in place for 2 to 3
weeks if permanent suture is used.
D. Running suture: Best used when wound edges are already somewhat approximated, fast closure. Use locking running
stitch if hemostasis is needed.

PEARLS
1. Antibiotic ointments (e.g., Bacitracin) should only be used for 2 to 3 days as patients can develop hypersensitivity and rash that
may be mistaken for cellulitis/infection if used for prolonged periods of time.
2. Absorbable suture should be used in children whenever possible, or when suture removal is anticipated to be difficult or may
disrupt closure.
3. Wounds should be examined at regular intervals, and wounds that fail to heal or improve over several weeks should be
reassessed for potential barriers to healing such as inappropriate dressings, presence of infection or malignancy, need for
additional debridement, and need for more complex reconstruction (graft or flap coverage).

QUESTIONS YOU WILL BE ASKED


1. Describe the classification of sutures and what factors of a wound/incision affect the choice of suture.
Sutures are classified as absorbable versus nonabsorbable, natural versus synthetic, and braided versus monofilament. The
suture chosen should effectively minimize tension on the closure, promote eversion of the skin edges, and remain in place for the
optimal length of time necessary to maintain a strong and durable closure while minimizing the body’s inflammatory response to
the suture itself to optimize the appearance of the scar.
2. Describe the timing of suture removal for the extremities, face, and trunk. Extremities: 10 to 14 days; face: 5 to 7 days;
trunk/breast: 7 to 10 days.
3. What are the contraindications to wound vac therapy?
Do not use a wound vac over normal skin, infected tissues, tissues harboring malignant cells, inadequately debrided wounds, or
directly on top of neurovascular structures.
4. What dressings are good for highly exudative wounds?
Alginates and foam (e.g., Mepilex) are good for highly exudative wounds.
5. Describe the treatment of animal/human bite wounds.
Bite wounds should be washed out aggressively and thoroughly on presentation given the predisposition of such wounds for
infection. If closure is needed, tissues should be loosely approximated to allow for egress of debris and infected fluid. Antibiotics
that provide coverage against anaerobic and Gram-positive organisms should be prescribed. Patients should be followed closely
to monitor for signs of infection.

Recommended Readings
Leach J. Proper handling of soft tissue in the acute phase. Facial Plast Surg. 2001;17(4):227-238. PMID: 11735055.
Singer AJ, Quinn JV, Hollander JE. T he cyanoacrylate topical skin adhesives. Am J Emerg Med. 2008;26(4):490-496. PMID: 18410821.
Ueno C, Hunt T K, Hopf HW. Using physiology to improve surgical wound outcomes. Plast Reconstruct Surg. 2006;117(7 Suppl):59S-71S. PMID: 16799375.
I. GENERAL INFORMATION
A. Unlike flaps, grafts do not bring independent blood supply to a recipient bed
1. *Autograft: From same individual
2. *Allograft: From another individual of same species (aka homograft/cadaver graft)
3. *Xenograft: From another species (aka heterograft)
B. Skin, dermis, fat, bone, tendon, cartilage, nerve, fascia, or combinations of tissues can be transferred as grafts

II. ANATOMY
A. Skin: Composed of epidermis and dermis
1. Epidermis: 5% of skin thickness
2. Dermis: 95% of skin thickness, contains sebaceous glands
B. Subcutaneous fat: Deep to dermis, contains hair follicles and sweat glands

III. EVALUATION
A. History: Nutritional status, age, comorbid conditions, smoking status, anticipated compliance
B. Physical exam
1. The recipient site should be assessed for potential bacterial load, blood supply, presence of devitalized tissue, and
exposed vital structures.
2. Donor site availability
3. *Perform recipient site tissue culture if history or concern for infection (counts <105 CFU/g tissue for most
pathogens required before grafting).

IV. SKIN GRAFTS


A. Indications
1. Primary closure not feasible
2. Lack of adjacent tissue for coverage (poor quality, insufficient quantity, and inferior aesthetic appearance)
3. Uncertain tumor clearance
4. Patients with significant comorbid conditions who may not tolerate the potential risks or complications of more complex
reconstructive options.
B. Contraindications
1. Infected recipient bed
2. Unreliable vascularization from recipient bed (e.g., history of radiation)
3. Repeated motion or trauma to recipient bed
4. Exposed white/avascular structures (tendon, nerve, bone, and cartilage) in recipient bed; grafts can technically be placed
on paratenon, periosteum, and perichondrium, but typically do not provide durable coverage
5. Anticipated staged reconstruction beneath recipient bed (nerve, tendon reconstruction).
C. Benefits (in comparison with healing by secondary intention): Faster healing, less scar contraction, improved aesthetic
appearance, and less fluid loss

______________
*De note s common in-se rvice e xamination topics

D. Recipient site requirements


1. Wound site preparation critical to success of graft in order to rid the recipient bed of devitalized tissue and
contamination.
a. Viability: Adequate blood supply, no devitalized tissue
b. Hemostasis: Hematoma is the major cause of graft failure
c. Bacterial load: Contamination prevents graft take
2. Patient comorbidities: Systemic diseases/conditions (diabetes, smoking, use of anticoagulants, and nicotine) and local
conditions (prior radiation and venous/ arterial insufficiency) can impair graft survival.
E. Donor site considerations: Skin is best replaced with like skin. Example: A skin graft to cover an eyelid defect requiring a
thin skin graft is best harvested from “like” tissue, such as preauricular or cervical skin, rather than thicker skin harvested
from the inguinal region.
F. General application principles
1. Harvest graft based on the size of defect or slightly larger to account for primary contraction (see below).
2. Graft is secured to skin edges and base of recipient bed with staples, suture (usually chromic or absorbable
monofilament), or skin glue.
3. Recipient site dressing and postoperative care
a. Key to bolster is ability to keep the graft in contact with the donor site (tie over or staple into place).
b. Should provide uniform pressure to prevent seroma, hematoma, and shear.
c. Bolster dressing commonly made of nonadherent layer (Xeroform), covered with cotton balls, secured to wound with
staples or tie over sutures; a vacuum-assisted closure device can also be used depending on the size and location of
the wound, though a nonstick layer (Xeroform (±) Acticoat) should be placed between the vac sponge and graft.
d. Can include additional layer of Acticoat or silver-impregnated gauze if concern for high risk of infection.
e. Bolster not used when graft placed over a transferred muscle flap (e.g., soleus flap for lower extremity defect) due
to undesired compression and need to check flap viability.
f. Elevate and immobilize recipient site if possible.
g. Dressing left undisturbed for 4 to 5 days unless shows signs of infection.
h. After bolster removal, BID to QD Xeroform dressing changes ± antibiotic ointment until healing is complete
(approximately 2 to 3 weeks) to prevent desiccation.
i. Graft is fragile for several weeks and should be protected from shear forces and edema even after initial bolster is
removed.
4. Excess harvested skin may be stored on donor site or at 4°C for several weeks (viability of graft decreases with
time) to use for delayed application.
5. May delay graft application for several days with coverage of muscle flaps to facilitate early monitoring of viability.
G. Split-thickness skin grafts (STSGs) (Table 3-1)
1. Contain epidermis and variable thickness of dermis; thicker grafts contain more donor skin characteristics but
require more optimal recipient site conditions for survival.
2. More robust and available in larger quantity compared with full-thickness skin grafts (FTSGs).
3. Indications: Resurface large wounds, cavities, mucosal defects, muscle flap coverage, flap donor site closure, and
temporary closure of wounds after tumor extirpation pending margin clearance with less donor site morbidity compared
with other reconstructive options.
4. Donor site
a. Location based on patient preference for location of scar, ease of donor site care, anticipated match of donor skin to
recipient site, and availability of sufficient quantity of tissue.
b. Typical sites: Anterolateral thigh, back, abdomen, upper inner arm, and scalp
c. Heals spontaneously by reepithelialization from epidermal appendages in residual dermis.
d. It is possible to reharvest skin at the same site after donor site is healed; back is the best site for reharvesting.
e. Can use tumescence to flatten out area of harvest as well as to decrease blood loss from donor site.
5. Technique
a. Harvest technique options: Free hand knife, drum dermatome, air- or electricity-driven dermatome (most common
method).
b. Most grafts are 12/1,000 to 18/1,000 inches thick (infants, elderly, and immunocompromised patients may have thin
skin, thus should consider patient and recipient site needs when choosing thickness).
c. Mineral oil is applied to donor site to prepare for harvest
d. Meshed versus sheet grafts
i. Meshed grafts
a) Increase surface area of graft while decreasing harvest area
b) Improve contour of grafts over irregular surfaces
c) Allow for drainage of exudate and blood
d) Increase secondary contraction (may be desired in some locations, but should be avoided over joints and face);
1.5:1 meshing is most commonly used to allow egress of fluid or blood
ii. Sheet (unmeshed) grafts:
a) Provide superior aesthetic benefit
b) Used in face and hands
c) May need pie crusting (small holes) depending on graft size to allow egress of fluid or blood
iii. The larger the meshing, the worse the aesthetic outcome, though interstices will fill in over time
iv. Even if you mesh the graft, it is better if you do not spread it out widely to decrease contraction and to improve
aesthetic outcome
6. Donor site care
a. Options: Occlusive dressings (e.g., Duoderm), semiocclusive dressings (e.g., Tegaderm), and semiopen dressings
(e.g., Xeroform and Mepilex)
b. *Semiocclusive dressings encourage faster reepithelialization, least painful, nearly maintenance free, and
keep wound moist.
c. Semiopen dressings reliable but require daily drying.
d. Watch for infection that can convert a donor site wound from partial- to full-thickness injury.
H. FTSGs (Table 3-1)
1. *Contain epidermis and dermis in entirety and therefore undergo more primary contraction but less
secondary contraction than STSGs.
2. Indications: Limited to small, uncontaminated and well-vascularized wounds, generally preferred in cosmetic or
functionally sensitive sites (e.g., joints, hands, and face); preferable when color match, thickness, and resistance to
contraction are important qualities.
3. Require better vascularized recipient bed due to thickness of graft.
4. Donor site selection
a. Should be inconspicuous and easily closed primarily.
b. Texture, thickness, pigmentation, and presence/absence of hair are important in selection.
c. Common harvest sites: Preauricular, supraclavicular, forehead sites for head and neck recipient sites; groin, lower
abdomen, and medial forearm for hand recipient sites.
5. Technique
a. Recipient site preparation is same as with STSG application (see above).
b. Harvest of FTSGs usually done in ellipse shape to facilitate primary closure of donor site.
c. Aggressive defatting of donor skin critical to improve initial survival.
d. Recipient site: Bolster dressing applied as in STSG (see above)
6. Tissue expansion of lower abdomen or groin prior to FTSGs can be used to allow for primary closure of larger graft
harvest.
I. Skin graft survival and healing
1. *Imbibition (first 24 to 48 hours): Plasma imbibition (diffusion) responsible for skin graft survival until angiogenesis
occurs → thinner grafts more likely to survive.
2. *Inosculation (48 to 72 hours): Process of capillaries joining between skin graft and recipient bed.
3. Revascularization (4 to 7 days): Ingrowth of capillaries into graft
4. Primary contraction
a. Occurs at the time of graft harvest/application
b. Due to elastin fibers in dermis
c. Greater in FTSGs (>40%) compared with STSGs (<20%)
5. Secondary contraction
a. Occurs after graft take
b. During healing phase of graft over 6 to 18 months
c. Greater in STSGs
d. Dermal components of FTSGs suppress myofibroblast activities responsible for secondary contraction
6. Regeneration of dermal appendages
a. More likely to regenerate in thicker grafts
b. Sweating assumes characteristics of recipient site when glands are reinnervated
c. Sebaceous glands retain characteristics of donor site
7. Reinnervation
a. Begins 2 to 4 weeks after grafting
b. Process takes several months to years
c. Assumes characteristics of recipient site
d. Reinnervation incomplete and some degree of decreased sensation will persist
e. STSGs regain sensation quicker, but FTSGs regain more complete innervation.
f. Pain returns first, then touch, then temperature.
8. Hair growth: Assumes characteristics of donor site, but only has potential to return after FTSGs.
9. Pigmentation
a. More predictable in FTSGs
b. Permanent hyperpigmentation may result from early sun exposure before full maturation.
10. Growth potential: STSGs have limited ability to grow in pediatric patients, FTSGs have potential to grow.
J. Skin graft complications
1. Graft failure (due to hematoma, seroma, infection, poor graft fixation, and smoking)
2. Pigment changes (donor and recipient sites), scar contraction, hypertrophic scarring, and graft instability

V. BONE GRAFTS
A. Classifications
1. By composition (Table 3-2)
a. Cortical: Composed of nonporous; lamellar bone; primarily used for support of major bony defects; more
osteogenesis.
b. *Cancellous
i. Composed of porous, trabecular bone
ii. Used to stimulate healing/bony ingrowth
iii. Bridge smaller defects, increase bulk
iv. Offers little structural support, easily remodeled
v. More osteoinductive and osteoconductive (see below) and more quickly revascularized than cortical
bone graft
c. Corticocancellous: Theoretically provides benefits of both
2. By vascular supply
a. Nonvascularized: Provides scaffolding and template for vascular and cellular ingrowth; ingrowth eventually resorbs
and replaces graft (creeping substitution or osteoconduction).
b. Pedicled vascularized: Bone graft transferred on vascular pedicle.
c. Free vascularized: Transfer of large segment of bone, promotes healing at recipient site, retains epiphyseal growth.
3. By origin
a. Autograft: Maximal healing potential, increased surgical time, no risk of viral transmission
b. Allograft
i. From cadaveric sources
ii. Readily available, avoids donor site morbidity, increased time for incorporation due to immunogenicity
iii. Freeze-dried allografts have higher availability, lower immunogenicity, and lower risk of disease transfer
compared with fresh-frozen allografts
c. Bone graft substitutes: All have minimal structural integrity (e.g., bone morphogenic protein [BMP])
B. Indications
1. Promote and enhance healing: Delayed union, nonunion, osteotomies, or other sites of poor healing potential
2. Bridge bony defects: Fill cortical defects (comminuted fractures and tumor excision), provide continuity
3. Fill cavities: In cases of cyst, tumor, or sequestrum removal
4. Arthrodesis: Replacement of native joint with bone graft
5. Provide structural support to implanted devices
C. Donor sites: Selection depends on quantity, type, vascularity of bone desired, donor site morbidity, and patient
characteristics
1. Ilium: Large quantity cancellous and corticocancellous bone; inner or both tables of iliac crest available for harvest with
additional cancellous bone available by curettage; vascularized graft based on deep circumflex iliac artery can be used
a. Use osteotome to lift cartilage cap superior to anterior, superior iliac spine coming from lateral aspect of iliac rim.
b. Advantages: Little aesthetic deficit, limited use of cortical bone in patients <10 years old due to incomplete
ossification.
c. Disadvantage: Donor site pain
2. Cranium (along the origin of temporalis muscle if possible where calvarium thickest): Large quantity of cortical bone
(outer table used in adults; both inner and outer tables used in children due to osteogenic potential of dura)
a. Advantages: Low graft resorption, low donor morbidity, and good aesthetic result.
b. Disadvantages: Brittleness, larger bone grafts require formal craniotomy.
3. Ribs (11th and 12th): Cortical bone that is more porous and malleable than graft from other sources.
a. Advantages: Malleable, can split in half
b. Disadvantages: Difficult fixation due to porosity
4. Fibula: Pedicled or free graft based on peroneal artery and venae comitantes; bridges defects in long bones. Important
to leave cuff of fibula proximal proximally and distally.
a. Advantages: Good graft length, long pedicle, and little functional deficit
b. Disadvantages: Limited size
5. Other sites: Distal radius, proximal ulna for cortical and cancellous bone
D. Harvesting and recipient site preparation tips
1. Minimize time between harvest and placement
2. Graft should be kept wrapped in blood-soaked sponges
3. Use copious irrigation during sawing and drilling to reduce mechanical and thermal damage to bone.
4. Bone edges at recipient site should be freshened to bleeding edges to ensure potential for revascularization of graft.
E. Graft survival and healing
1. *Osteoconduction: Scaffold or template function that graft provides to allow ingrowth of capillaries, osteoprogenitor
cells, and matrix components from host tissue. (Example: Non vascularized bone graft)
2. *Osteoinduction: Growth factors (BMPs) present within graft recruit host stem cells to form bone-
producing cells (osteoblasts). (Example: Cancellous bone)
3. *Osteogenesis: Production of new bone by cells in graft that survive transplantation. (Example: Vascularized bone
graft)
4. Costochondral bone grafts retain ability to grow and may grow excessively.

VI. CARTILAGE GRAFTS


A. Classifications
1. By matrix characteristics
a. Hyaline cartilage: Trachea, larynx, nasal septum, nasal ala, and ribs; offers support through rigidity
b. Elastic cartilage: External ear, external auditory meatus, eustachian tube, and epiglottis; more malleable, elastic,
more resistant to repeated bending than hyaline cartilage
c. Fibrocartilage: Pubic symphysis, intervertebral disks, ligamentous and tendinous insertions; resists tensile and
compressive forces; lacks flexibility
2. By source
a. Autogenous: Primary and preferred source
b. Homologous (cadaveric): Produces relatively small immune response (chondrocytes surrounded by nonreactive
extracellular matrix); freeze-dried/preserved cartilage reduces further inflammation/disease transfer; more absorption
compared with autogenous cartilage
B. Indications
1. Structural support and augmentation: Ear reconstruction, eyelid and tracheal support
2. Contour deformity: Correction of nasal deformity (e.g., saddle nose) and inverted nipples, alternative to bone graft in
facial contour deformities
3. Joint repair and resurfacing: Spacer in temporomandibular joint (TMJ) repair, fill defects in articular cartilage
C. Donor sites
1. Ear (concha): Elastic cartilage source, possesses natural curvature, used for eyelid support and nipple reconstruction,
TMJ, and orbital floor repair
a. Advantages: Easily accessible, abundant
b. Disadvantages: Curvature not always desirable
2. Nasal septum: Straight, rigid, hyaline cartilage source, used for nasal or lower eyelid reconstruction
a. Advantages: Easily accessible
b. Disadvantages: Limited availability, overresection results in saddle-nose deformity
3. Costal cartilage: Abundant source of hyaline cartilage, used for reconstructions requiring large amount of cartilage
(total auricular reconstruction, tracheal reconstruction)
a. Advantages: Large quantity graft material, reliable, and distant recipient site allows two-team harvest approach
b. Disadvantages: Tend to warp with time, donor site morbidity (pneumothorax and pain)
D. Graft survival and healing
1. Chondrocytes and extracellular matrix survive and maintain cartilage characteristics
2. Survives by osmosis from well-vascularized recipient site (avascular)
3. Limited inflammatory reaction with little graft resorption (<20% in autografts)
4. Requires coverage to prevent desiccation and infection
5. Scoring allows graft to be shaped (bending away from scored side)
6. Symmetric carving, K-wire stabilization, harvest without perichondrium, making central rather than peripheral cuts, and
waiting at least 30 minutes after carving before placement at recipient site can be employed to decrease warping

VII. FAT GRAFTS (SEE CHAPTER 9)

VIII. COMPOSITE GRAFTS


A. Composed of two or more tissue components (e.g., skin or mucosa with cartilage, skin with fat, and full-thickness
eyelid)
B. Indications
1. Nasal ala: Prevent alar collapse
2. Nasal sidewall: Prevent nasal valve obstruction
3. Nasal tip: Provide structural integrity
4. Ear (anterior helical root): Repair substantial auricular defects, restoration of ear structure for glasses or hearing aid
placement
5. Eyelid: Prevent ectropion and lid contraction from loss of tarsal plate
C. Donor sites: Septal cartilage, auricular cartilage, and costal cartilage
D. Graft survival and healing
1. Survival occurs via imbibition, inosculation, then revascularization
2. Initial survival dependent on revascularization solely from wound edges; thus no portion of the graft should be >1 cm
from wound edges
3. Metabolic demand of graft limits size that will survive to 1.0 to 1.5 cm width
4. More prone to graft loss than other graft types

PEARLS
1. Dermal side of skin graft can be distinguished from epidermal surface by its shiny appearance (graft placed shiny side [dermis]
down)
2. Donor scars for harvesting of FTSGs should be oriented parallel to relaxed skin tension lines (RSTLs)
3. Harvest of FTSGs from volar wrist should never be performed due to social stigma of wrist scar
4. Patients should be warned that composite grafts often initially appear cyanotic

QUESTIONS YOU WILL BE ASKED


1. Name the stages and timing of skin graft healing?
Imbibition (first 24 to 48 hours), inosculation (48 to 72 hours), and revascularization (4 to 7 days).
2. After skin grafting, does the donor or recipient site determine characteristics of hair growth, sweating, and sensibility?
Hair growth assumes characteristics of the donor site, but only has potential to return after FTSG, sweating assumes
characteristics of recipient site when glands are reinnervated, and sensibility is incomplete and assumes characteristics of
recipient site.
3. What is the difference between primary and secondary contraction and which type of skin graft is primarily affected by each?
Primary contraction occurs immediately at the time of graft harvest/application due to elastic fibers in dermis, greater in FTSGs;
secondary contraction occurs during healing phase of graft over 6 to 18 months, greater in STSGs.
4. Draw the layers of skin from epidermis to subcutaneous fat.
See Figure 1-1

Recommended Readings
Coleman SR. Facial augmentation with structural fat grafting. Clin Plast Surg. 2006;33(4):567–577. PMID: 17085224.
Hallock GG, Morris SF. Skin grafts and local flaps. Plast Reconstr Surg. 2011;127(1):5e-22e. PMID: 21200192.
I. ANATOMY
A. Definitions
1. Flap: Segment of tissue that is transferred with its own blood supply (in contrast to graft, which is revascularized from
recipient bed).
2. Pedicle: Base of flap that contains blood supply.
3. Pedicled flap: Remains attached to native vascular supply
4. Free flap: Fully detached from vascular supply and reconnected to recipient vessels using microvascular technique.
B. Flap classification
1. Blood supply
a. Random pattern flap: Raised without regard to any named blood supply, relying on blood flow through subdermal
plexus (Fig. 4-1).
b. Axial flaps: Raised on dominant (named) arterial supply running along its long axis.
c. Perforator flap: Blood supply from perforator from dominant feeding vessel.
d. Reverse flow flaps: Dominant supply is divided, flap left to survive on intact distally based vessels that form
connections to another blood supply system.
2. Location
a. Local flap: Shares side with the defect
b. Regional flap: In same region of the body as the defect, but does not share defect margin.
c. Distant flap: Not in the region of the defect, located in a different part of the body
3. Method of transfer
a. Advancement
b. Transposition
c. Rotation
d. Interpolation
e. Jumping
f. Free

Figure 4-1. Random pattern skin flap.


______________
*De note s common in-se rvice e xamination topics

4. Tissue composition
a. Cutaneous flap
b. Fascia/fasciocutaneous flap
c. Muscle/musculocutaneous flap
d. Osseous/osteocutaneous/osteomusculocutaneous flap
e. Omental flap
C. Angiosomes
1. Definition: Composite unit of skin and deeper structures between skin and bone supplied by a source vessel.
2. Entire surface area of body composed of angiosomes.
3. Majority of flaps cover more than two angiosomes.
4. Neighboring angiosomes can be linked by true arterial anastomoses or by choke vessels (reduced caliber anastomoses)
that dilate under certain circumstances, such as flap delay (see below).
5. Connections between angiosomes explain how flaps can support more than one angiosome area under certain
conditions.

II. FLAP SELECTION


A. Reconstructive goals
1. Restore form and function to the defect
2. Minimize donor site morbidity
B. Reconstructive ladder (Fig. 4-2)
1. Systematic approach to facilitate decision-making for reconstruction of defects.
2. Least complicated technique chosen to address needs of the defect and reconstructive goals.
3. Ladder progresses from simple to complex options
a. Healing by secondary intention
b. Primary closure
c. Skin graft
d. Local flap
Figure 4-2. Reconstructive ladder.

e. Regional flap
f. Distant flap
g. Free flap
C. Reconstructive elevator
1. Often best solution is not simplest
2. Option is chosen that will give patient best aesthetic and functional result, often requiring a “jump” in the ladder (e.g.,
free flap may be the best first choice if superior result is unmatched by other options, even if simpler option can also be
used).
3. In reality, this is the method in which flap selection is typically done.
D. Flap selection considerations
1. Goals of intervention
2. Shape, contour, and structural needs of reconstruction
3. Location of the defect
4. Size of the defect
5. Exposed and underlying structures
6. Viability of surrounding tissue (e.g., previous radiation, vascular disease, tissue necrosis)
7. Available donor sites
8. Effect on donor site: Morbidity, secondary defect, distortion of nearby structures (especially important in face)
9. Pedicle length and caliber
10. Technical demand
11. Patient expectations
12. Patient comorbidities
13. Anticipated risk for complications (infection, would healing complications, etc.)
14. Cost of care

III. CUTANEOUS FLAPS


A. Indications
1. Reconstruction of the local defect with similar, adjacent tissue
2. Need for full-thickness skin coverage of relatively less vascularized tissue (e.g., coverage of bone, tendon without
periosteum/paratenon intact) for which skin graft is insufficient
B. Blood supply: Dependent on blood supply from fascial plexus (unless random pattern)
1. Direct cutaneous (axial) arteries
2. Septocutaneous arteries
3. Musculocutaneous arteries
4. Random pattern flaps
a. Designed on random vascular supply from subdermal plexus
b. *Size limited to length-to-width ratio ~2:1 in lower extremity and up to 4:1 in head and neck.
c. Ischemia expected when the recommended length-to-width ratio dimensions exceeded without flap delay.
d. Most (but not all) small local cutaneous flaps based on random blood supply
C. Method of transfer: Advancement, pivotal, or hinge
1. Advancement flaps: Moved by sliding or stretching flap toward the defect in one direction, requires skin laxity
a. Single-pedicle advancement flap (Fig. 4-3A)
i. Raised as square or rectangle
ii. Undermined and advanced to fill defect sharing border with flap
iii. Bürow’s triangles made at base to facilitate advancement and closure (helps correct length discrepancy between
skin surrounding wound and skin of flap margin)
b. Bipedicle advancement flap
i. Incision parallel to the defect
ii. Flap undermined and advanced
iii. Useful for longitudinal defects of extremities
Figure 4-3. A: Single pedicled advancement flap with Bürow’s triangles. B: V–Y advancement flap. C: Rotation advancement flap. D: Rhomboid flap.

c. Island advancement flap


i. Pedicle of island flap not connected with surrounding skin, supplied only by connection with subcutaneous tissue
(or artery/vein)
ii. Transferred by advancement or pivot (see below)
iii. Geometry of cutaneous portion depends on the defect
d. V–Y advancement flap (Fig. 4-3B)
i. Can be designed as advancement (where skin at base is not divided) or island flap (where skin at base of flap is
divided)
ii. Flap raised in V shape and advanced to fill the defect
iii. Closed in Y to close the donor defect
iv. Flap may be modified to a Y–V variation
v. Useful on face and fingertips to fill defects (island design) or can be used to release contracture (advancement
design)
2. Pivotal flaps: Moves around fixed point at base of pedicle
a. Rotation flap: Pivotal flap with curvilinear configuration (Fig. 4-3C)
i. Flap raised in semicircle immediately adjacent to the defect.
ii. Height of the defect = ½ to 1 times radius of flap curvature
iii. Standing cutaneous deformity may occur at base (depending on shape of the defect), requiring removal.
iv. Back cut at base of flap shifts pivot point to reduce tension of closure
v. Bürow’s triangle at secondary defect margin may help to facilitate closure. (corrects length discrepancy between
flap margin and surrounding skin edge)
vi. Flap design with length of incision ˜4 times width of the defect typically does not require Bürow’s triangle to
equalize length.
vii. Also uses some advancement or stretch of flap to correct length discrepancy between lengths of closure of flap
margin and skin edge (often called rotation advancement flap).
viii. Undermining base of flap and pivot point facilitates advancement and limits standing cutaneous deformity.
ix. Flap should be inferiorly based on face to facilitate lymphatic and venous drainage.
x. Useful for scalp defects and sacral pressure sores (among other defects)
b. Transposition flap: Pivotal flap with linear configuration
i. Rhomboid (Limberg) flap (Fig. 4-3D)
a) Defect made into rhombic shape (equilateral parallelogram) with 60 and 120 degree angles.
b) First side of flap is a short diagonal of rhombus extended at an equal length.
c) Second side of flap is a line parallel to and same length as nearest limb of flap.
d) Four flaps can be designed around sides of the defect, flap design chosen with best skin mobility and scar
placement.
ii. Dufourmentel flap
a) Variation of rhomboid flap
b) Used for rhomboid-like defects with angles other than classic 60 and 120 degrees.
c) First side of flap is same length of defect, drawn at angle halfway between a line extending from a short
diagonal and a line extending from the side of the defect.
d) Second side of flap is parallel to long diagonal of the defect same length as the defect.
iii. Bilobed flap
a) Transposition of two flaps with common base
b) *Two flaps raised 45 to 50 degrees apart next to the defect (total arc of movement should be
limited to 90 to 100 degrees)
c) First flap fills the primary defect, second flap fills donor site of first flap, and second flap donor site closed
primarily.
d) Useful for nasal defects where site of the defect (nasal tip) does not have laxity for primary closure, but donor
site of second flap (nasal dorsum) has sufficient laxity for closure.
iv. Z-plasty (Fig. 4-4A)
a) Transposition of two adjacent and opposing triangular flaps
b) Used to lengthen scar contractures, change scar direction, break up scar, release epicanthal folds or
constricting bands.
c) Moves lateral tissue inward from both directions in order to increase tissue length longitudinally (Table 4-1) at
the expense of width.
d) Classic design: Central segment with limbs oriented at 60 degrees (although can be 30 to 90 degrees); three
lines are equal in length; central segment oriented along the direction of the desired lengthening (e.g., in the
same direction as scar to be released).
Figure 4-4. A: T he standard Z-plasty. B: Percent length gained with the Z-plasty. C: Multiple Z-plasties.

e) Increasing angle of limbs increases percent gain in length along the central limb (Fig. 4-3B).
f) Multiple Z-plasties can be designed in series (Fig. 4-4C)
v. Interpolation flap
a) Skin paddle transposed into the nearby defect over or under a skin bridge.
b) Base of flap is not contiguous with the defect in initial procedure.
c) Flap is divided from base in secondary procedure and inset fully into the defect.
vi. Island transposition flap
a) Single-stage version of interpolation flap
b) Transferred by pivoting or advancement (see above)
vii. Other design configurations
a) Rectangular-shaped transposition flap
b) Parabola-shaped transposition flap
c) Triangular-shaped note flap
1) Closure of small (<2 cm) circular defect with triangular-shaped transposition flap
2) Tangent is drawn from any side of the circular defect 1.5 times length of diameter of the defect (parallel
to relaxed skin tension lines)
3) Second side of flap same length as defect, drawn at 50 or 60 degree angle to first incision
4) Distal tip of flap is trimmed
3. Hinge flaps
a. Flap elevated in subcutaneous plane
b. Pedicle base is on one border of the defect
c. Flap is turned over into the defect like a book
d. Flap elevated with or without skin
i. Design with skin used in full-thickness defects that require internal lining (nasal reconstruction)
ii. Designs without skin require skin graft or second flap coverage

IV. FASCIAL FLAPS


A. Skin elevated with underlying deep fascia (fasciocutaneous flap) or fascia is elevated alone (fascial flap).
B. Indications
1. Need for thin, pliable coverage when bulk of muscle flap not desired.
2. Cases where secondary procedures anticipated under flap; fascial flaps easier to elevate during reoperative procedures.
3. Better gliding surface for coverage of exposed tendons.
C. Blood supply/Mathes and Nahai classification (Fig. 4-5)
1. Type A: Direct cutaneous perforator; pedicle courses beneath deep fascia on its way to skin (e.g., temporoparietal
fascia flap, groin flap).
2. Type B: Septocutaneous perforator; pedicle travels within intermuscular septa (e.g., radial forearm flap)
3. Type C: Musculocutaneous perforator; pedicle based on musculocutaneous perforators that travel through muscle
to supply deep fascia and overlying skin (e.g., anterolateral thigh flap)
Figure 4-5. Mathes and Nahai classification of fasciocutaneous flaps. Type A: direct cutaneous perforator; Type B: septocutaneous perforator; Type C:
musculocutaneous perforator.

D. Flap design
1. Flaps include deep fascia, incorporating rich vascular fascial plexus that reach the skin via direct or indirect perforators.
2. Type A and B pedicles are relatively constant in location; Type C pedicles have more variability in location
3. Pedicle can be lengthened by tracing perforators back to source vessel.
4. Fascia-only flaps advantageous because donor site can be closed primarily; fasciocutaneous flaps may or may not
require skin graft to close donor site.
E. Workhorse fasciocutaneous flaps (Table 4-2)

V. MUSCLE FLAPS
A. Muscle can be transferred alone (muscle flap) or with overlying skin (musculocutaneous flap)
B. Indications
1. Muscle flaps are useful when a bulkier reconstruction is needed.
2. Eradication of dead space
3. Need for tissue with robust blood supply due to risk of infection or poor perfusion.
4. Restoration of motor function (functional muscle transfer)
C. Blood supply/Mathes and Nahai classification (Fig. 4-6)
1. Type I: Single vascular pedicle (e.g., gastrocnemius, tensor fascia lata)
2. Type II: Single dominant pedicle and one or more minor pedicles; flap cannot survive on minor pedicles alone; most
common type of muscle in body (e.g., soleus, gracilis, rectus femoris, biceps femoris)
3. Type III: Two dominant pedicles; flap can survive on either pedicle alone (e.g., rectus abdominis, gluteus maximus)
4. Type IV: Segmental pedicles; multiple pedicles enter along course of muscle, each supplies a portion of the flap; least
reliable type (e.g., sartorius, tibialis anterior)
5. Type V: One dominant pedicle and secondary segmental pedicles; flap can survive on segmental pedicles alone (e.g.,
latissimus dorsi, pectoralis major)
D. Flap design
1. Skin island is designed to include skin perforators arising from the source artery.
2. Musculocutaneous perforators typically located near entry of dominant pedicle into hilum of the muscle.
3. All or part of muscle can be used as a flap.
Figure 4-6. Mathes and Nahai classification of musculocutaneous flaps. (From Berger RA, Weiss AC, eds. Hand Surgery. Philadelphia, PA: Lippincott Williams &
Wilkins; 2004.)

4. May also include bone, motor nerve, or sensory nerve in transfer (depending on donor muscle).
5. Functional muscle is sacrificed, thus donor morbidity must be considered when selecting flap.
E. Workhorse musculocutaneous flaps (Table 4-3)

VI. FLAP MODIFICATIONS


A. Flap delay
1. Staged technique to augment flap circulation and improve flap survival.
2. Flap is partially elevated and entirely elevated, or selected pedicles are divided into one or more procedures; flap is
brought back to in situ position in staged procedure before definitive flap elevation and transfer.
3. Allows harvest of larger flap because areas farthest from blood supply (random-supply component) have improved
perfusion following delay.
4. Time between delay and definitive procedure is usually 2 weeks.
5. Delay used with flap locations or designs at high risk for compromised blood supply.
6. Physiology of improved perfusion with delay
a. Decrease in sympathetic tone from transection of sympathetic fibers.
b. *Dilation of previously closed choke vessels increases the area of tissue supplied by the dominant
pedicle.
c. Relative tissue ischemia stimulates angiogenesis, increasing flap vascularity before transfer.
B. Crane principle
1. Pedicled flap used to lift, transport, and deposit subcutaneous tissue to recipient bed.
2. Flap is raised and transferred to recipient bed.

3. After 10 to 21 days, new blood vessels have grown in the recipient bed which will support a skin graft. In the next stage,
the top layer (superficial one-half to three-fourths) is raised and returned to original donor site.
4. Viable subcutaneous tissue is left behind and can be covered with skin graft.
5. Provides coverage to local or regional area without significant donor site morbidity.
C. Flap prefabrication
1. Introduction of new vascular pedicle into tissue
2. Indication: When desired donor tissue has required qualities but does not have reliable axial blood supply.
3. Two-stage process
a. Stage 1: Transfer of a new vascular pedicle into an area of tissue that will be used to reconstruct defect (pedicle
wrapped in Gore-Tex or silicone sheet to prevent scarring around pedicle).
b. Stage 2: The flap, based on new vasculature, can be raised after approximately 6 to 8 weeks (transferred as pedicle
flap or free tissue transfer).
4. Rarely used because of the availability of many alternative flap options.
5. Can be performed with tissue expansion; introduced pedicle is placed beneath donor tissue and above tissue expander;
Doppler flow is monitored during expansion.
6. Flap delay helps to hasten neovascularization.
7. Venous congestion is a common complication (may be lessened with flap delay).
D. Prelamination
1. Introduction of additional tissue layers into flap prior to transfer to create multilayer composite flap; allows tissue to have
time to mature before transfer.
2. Indication: Allows custom-made flaps for specialized areas of the body with 3D structure (e.g., central face, penis).
3. Two-stage process
a. Stage 1: Modify donor flap by introducing additional tissue layer into vascularized tissue before transfer to recipient
site (e.g., introduce cartilage and/or skin grafts to forehead flap before transfer to the defect).
b. Stage 2: Raise flap en bloc as composite flap and transfer to recipient site after approximately 2 to 4 weeks (shorter
maturation time than prefabrication because vascular supply is not altered).
E. Supercharging
1. Enhancing blood supply of a pedicled flap by performing microvascular anastomosis to a secondary pedicle of the flap.
2. Example: Transverse rectus abdominis musculocutaneous flap with classic superior epigastric artery pedicle that also
has deep inferior epigastric artery anastomosed to vessels in the axilla, neck, or chest to enhance blood supply.
F. Free tissue transfer
G. Perforator flaps: Perforating vessel(s) dissected down to deeper vessels, leaving intervening tissue intact and not included
in flap to produce thinner flaps and reduce donor site morbidity.
H. Composite flaps
1. Angiosome principle provides basis for transfer of composite flaps that contain combinations of multiple tissue types
(e.g., skin, muscle, bone, nerve, and/ or tendon).
2. Tissues supplied by single source artery can be transferred together.
3. Useful when reconstruction of multiple tissue components is needed.
4. Vascularized bone flaps
a. Blood supply classification (Serafin)
i. Direct (endosteal) circulation
ii. Indirect (periosteal) circulation
b. Commonly transferred bones and vascular pedicle
i. Radius: Radial artery
ii. Fibula: Peroneal artery
iii. Scapula: Circumflex scapular or thoracodorsal artery
iv. Iliac crest: Deep circumflex iliac artery
c. Toe transfer
i. Great toe: First dorsal metatarsal artery
ii. Second toe: First dorsal metatarsal artery
5. Innervated flaps
a. Motor nerve and/or sensory nerves are preserved or coapted to appropriate nerve near the recipient site.
b. Common functional muscle flap transfers and motor nerve
i. Gracilis with obturator nerve
ii. Latissimus with thoracodorsal nerve
iii. Serratus with long thoracic nerve
iv. Pectoralis minor with medial and lateral pectoral nerves
c. Common sensory flaps and sensory nerves
i. Lateral arm flap with posterior brachial cutaneous nerve
ii. Radial forearm flap with medial and/or lateral antebrachial cutaneous nerves
iii. Dorsalis pedis flap with deep peroneal nerve and/or superficial peroneal nerve
I. Chimeric versus conjoined (Siamese) flap
1. Chimeric flap: Has multiple territories, each with independent vascular supply (perforators or named branches), but
territories are NOT connected except by connection to common source vessel.
2. Conjoined flap: Has multiple territories, each with independent vascular supply, but territories remain connected.
J. Tissue expansion

VII. POSTOPERATIVE MANAGEMENT


A. Flap monitoring
1. Evidence of arterial or venous insufficiency in immediate post-op period requires immediate exploration
2. *Clinical evaluation: Gold standard method of flap assessment
a. Temperature: Should be body temperature
b. Color: Should be pink
c. Capillary refill: Should be approximately 2 seconds
d. Bleeding: Upon introduction of fine-gauge needle, bright-red bleeding should be present
e. Firmness: Should be soft, with some appreciable turgor
3. Additional methods of flap monitoring
a. Doppler (implanted or external)
b. Fluorescein dye
c. Pulse oximetry, pH, or temperature sensors
4. Signs of arterial insufficiency
a. Cool temperature
b. White color
c. Slow capillary refill >2 seconds
d. Slow or absent pinpoint bleeding
e. Low turgor
5. Signs of venous insufficiency
a. Increased temperature
b. Blue to purple color
c. Brisk capillary refill <2 seconds
d. Brisk pinpoint bleeding, dark in color
e. Increased turgor, tense, swollen
f. If congested, unwrap, release sutures and consider leech therapy (patient must be on quinolone or third generation
cephalosporin against Aeromonas)
B. Risk factors for flap vascular compromise
1. Tight dressings and/or splints
2. Tight sutures
3. Patient position or motion that puts pressure on flap
4. Hematoma (increases tissue pressure and interferes with perfusion)
5. Kinking of flap, pedicle, or both (may be influenced by flap design, pedicle length, interpositional vein graft length)
6. Cool ambient room temperature
7. Poor surgical technique
8. Systemic patient factors: Use of vasoconstrictive pharmaceutical agents (vasopressors, nicotine, caffeine, etc.),
hypovolemia, anemia, inadequate blood pressure

QUESTIONS YOU WILL BE ASKED


1. What is the most common (Mathes and Nahai) type of muscle flap in the body?
Type II
2. What is the physiology behind improved perfusion after flap delay?
Flap perfusion is increased through (1) decrease in sympathetic tone from transection of sympathetic fibers, (2) dilation of
previously closed choke vessels which increases the area of tissue supplied by dominant pedicle, and (3) relative tissue ischemia
stimulates angiogenesis, increasing flap vascularity before transfer.
3. What is the theoretical gain in length along the central limb of a Z-plasty with 60 degree angle?
75% gain in length
4. What is the pedicle to your flap?
Table 4.3
5. What is difference bertween a type II and type V flap?
Type II flap has secondary pedicle that cannot support the flap alone. Type V flap can be transfered on the secondary pedicles
which are segmental.

THINGS TO DRAW
1. Z-plasty before and after
2. Cross section through lower extremity
Recommended Readings
Ghali S, Butler PE, T epper OM, Gurtner GC. Vascular delay revisited. Plast Reconstr Surg. 2007;119(6):1735–1744. PMID: 17440348.
Hallock GG, Morris SF. Skin grafts and local flaps. Plast Reconstr Surg. 2011;127(1):5e–22e. PMID: 21200192.
T aylor GI. T he angiosomes of the body and their supply to perforator flaps. Clin Plast Surg. 2003;30(3):331–342, v. PMID: 12916590.
Taylor GI, Palmer JH. T he vascular territories (angiosomes) of the body: experimental study and clinical applications. Br J Plast Surg. 1987;40(2):113–141. PMID:
3567445.
I. HISTORICAL PERSPECTIVE
A. Perforator flap era began in 1989—Koshima and Soeda described an inferior epigastric artery skin flap without the
rectus abdominis muscle for reconstruction of floor-of-mouth and groin defects.

II. WHAT IS A “PERFORATOR”?


A. In Latin, per means “through” and forare means “to pierce or bore”.
B. Describes a blood vessel that branches off a major named vessel (or source vessel), supplying a particular tissue
territory, or angiosome.
C. *Mathes and Nahai tripartite system of fasciocutaneous flaps: Based on three major types of perforators (see
Chapter 4—Fig. 4-4)
1. Type A (direct cutaneous vessel)
2. Type B (septocutaneous vessel)
3. Type C (musculocutaneous vessel)
D. “Direct” versus “indirect” perforators
1. Direct perforators course from the source vessel to the skin without first supplying any other deep structure.
Examples: An axial vessel, a direct cutaneous vessel (Mathes and Nahai Type A), or a septocutaneous vessel (Mathes
and Nahai Type B).
2. Indirect perforators first pass through an intermediary structure before ultimately reaching the subdermal plexus.
Example: A muscle or musculocutaneous perforator (Mathes and Nahai Type C), in which the source vessel to the skin
passes through and arises from the underlying muscle.
E. Branching patterns of musculocutaneous perforators
1. Type 1 perforators pass almost directly from deep fascia to subdermal plexus without branching.
2. Type 2 perforators branch in the adipose tissue just before reaching the subdermal plexus, with branches then running
parallel to the flap surface (e.g., lateral femoral circumflex artery (LCFA)-tfl, tensor fascia lata, deep inferior epigastric
artery (DIEP)).
3. Type 3 perforators follow deep fascia for an indeterminate distance before eventually proceeding into subcutaneous
tissues (e.g., LCFA-vastus lateralis or ALT flap).

III. WHAT IS A “PERFORATOR FLAP”?


A. A perforator flap generally refers to tissue that receives its blood supply via a “perforator”.
B. Not always a cutaneous flap—can eliminate the cutaneous component to create an adiposal or adipofascial flap.
C. Terminology is historically controversial, with multiple terms used.
D. Some surgeons believe that the muscle perforator flap is the only “true” perforator flap because of the additional time and
effort required to dissect the perforator out from between muscle fibers, and intramuscular dissections are technically more
difficult.

______________
*De note s common in-se rvice e xamination topics

IV. CURRENT STANDARDIZED NOMENCLATURE


A. Perforator flaps are described according to the main artery of origin (e.g., LCFAP for lateral circumflex femoral
artery perforator).
B. Suffix “AP” (Artery Perforator) signifies a true musculocutaneous perforator flap.
C. Suffix “-s” is added if the flap is harvested based on direct septal or fasciocutaneous vessels.
D. When multiple flaps are based on musculocutaneous perforators from the same source artery, the muscular origin of the
vessel is abbreviated and italicized to indicate the anatomical origin of the flap (e.g., LCFAP-vl for vastus lateralis [VL]).
E. When flaps are based on source arteries that have numbered segmental origins, such as the posterior intercostal arteries, the
corresponding vessel number is added after the flap abbreviation (e.g., PIAP-8 for eighth posterior intercostal artery
perforator flap).
F. Examples (common name → current nomenclature)
1. Deep inferior epigastric perforator flap → DIEP flap
2. Thoracodorsal artery perforator → TAP
3. Anteriolateral thigh flap → ALT flap
4. Superior gluteal artery perforator flap → SGAP flap

V. *PROPOSED ADVANTAGES OF PERFORATOR FLAPS


A. Reduced donor site morbidity.
B. Reduced postoperative pain.
C. Faster recovery, shorter hospital stay.
D. Less difficult to tailor or thin the flap for covering or filling defects.
E. Longer pedicle than with the parent musculocutaneous flap.

VI. TECHNICAL POINTS


A. Can increase length of pedicle by dissecting perforator back to its origin.
B. Should deliberately preserve a subcutaneous or other large perforator vein during the harvest for supercharging venous
outflow in case there is venous congestion.
C. The need for preoperative studies is dependent on the surgeon. Can identify perforators preoperatively by color duplex
ultrasound, computerized tomography (CT) angiogram, or handheld audible Doppler.

VII. WORKHORSE PERFORATOR FLAPS (TABLE 5-1)


A. Deep inferior epigastric artery perforator (DIEAP) flap—known more commonly as DIEP flap.
1. Indications: Primarily breast reconstruction
2. Anatomy
a. Pedicle length 7.5 to 20.5 cm, diameter 3.3 ± 0.4 mm.
b. Deep inferior epigastric artery (DIEA).
i. Typically divides into two main branches
a) Lateral branch gives rise to lateral row of perforators
1) Usually dominant over medial branch.
2) Has shorter intramuscular course.
3) Gives off more perforators.
b) Medial branch gives rise to medial row of perforators and an umbilical branch.
1) Usually 5 ± 2 perforators can be found concentrated in periumbilical region, which is necessary if zone IV
is used.
ii. Usually accompanied by two venae comitantes.
c. Superficial inferior epigastric venous system
i. Responsible for most of the flap’s venous drainage.
ii. Superficial inferior epigastric vein (SIEV) is larger than the deep inferior epigastric vein (DIEV).
3. Surgical technique
a. Flap harvesting
i. Use standard abdominoplasty markings (Fig. 5-1), extending laterally to anterior superior iliac spines (ASIS).
Figure 5-1. Standard markings for the transverse rectus abdominis musculocutaneous flap or DIEP flap markings at our institution.

ii. Search for superficial inferior epigastric artery (SIEA) and SIEV first
a) If SIEA is of sufficient caliber, dissection is carried down to origin at common femoral artery (CFA) to harvest
the SIEA flap.
1) Decreased donor site morbidity.
2) Only zones I and II are reliably perfused.
b) If only SIEV is present, this can be used as a backup for additional venous drainage if congestion occurs after
DIEV anastomosis.
iii. Can raise the flap on more than one perforator from the same perforator row by performing atraumatic
longitudinal separation of rectus muscle fibers.
iv. Take care to preserve segmental intercostal nerves, which run medially and superficially to the pedicle.
b. Recipient vessels in breast reconstruction
i. Can harvest internal mammary artery (IMA) and internal mammary vein (IMV) through the third interspace or by
partial resection of the third intercostal cartilage.
a) Start lateral to avoid coming down into the IMA.
b) Remove cartilage to the sternocostal articulation.
ii. Can use large perforators from IMA and IMV if available.
iii. Alternative recipient: Thoracodorsal vessels.
c. Other technical points
i. If possible, should orient flap such that the thicker central adipose tissue forms the medial and inferior portions of
the reconstructed breast.
ii. If preserved, can attach sensory nerves from the flap to an intercostal nerve.
iii. Flap is partially deepithelialized or deskinned depending on the amount of breast skin preserved.
iv. Zone IV is routinely discarded.
B. Anterolateral thigh flap (ALT or LCFAP-vl)
1. Indications: Often used in head and neck, upper and lower extremity reconstruction.
2. General features
a. Chimeric principle: Can raise multiple tissue components on different perforators from the lateral circumflex
femoral axis.
i. Vastus lateralis muscle
ii. Tensor fascia lata
iii. Rectus femoris (RF) muscle
iv. Iliac crest
b. Mosaic flap principle: Can harvest an adjacent flap and anastomose it to a branch of the LCFA (e.g., groin flap,
medial thigh flap).
c. Variations
i. Can raise flap with or without fascia.
ii. Can thin flap with one- or two-stage procedure to resurface shallow defects.
iii. Can use as a flow-through flap.
iv. Can use as an adipofascial flap.
v. Can be pedicled proximally for defects of perineum, lower abdominal wall, and greater trochanter.
vi. Can be pedicled distally for coverage around the knee.
d. Nerves: Can include anterior or lateral branch of lateral cutaneous nerve of the thigh to provide sensation.
e. Donor site
i. Can close primarily if flap width <8 cm.
ii. Alternatively, may repair with skin graft or V–Y local advancement flap.
3. Anatomy (Fig. 5-2)
a. Perforators originate from descending branch of LCFA.
b. LCFA lies in the intermuscular septum between RF and VL muscles.
c. Pedicle length typically 8 to 16 cm, diameter >2 mm.
d. Can often find 1 to 3 perforators approximately 5 cm apart and 1.5 cm lateral to a line drawn connecting ASIS to
superolateral patella. “Perforator B” is the perforator that is most consistently present, located around the midpoint.
4. Surgical technique
a. Can use Doppler to identify perforators preoperatively.
b. Design flap around perforator B with A and C perforators 5 cm proximal and distal to B perforator.
c. Make a longitudinal skin incision on medial side of flap, carrying on the dissection at the suprafascial level.
d. Enter the intermuscular septum distally between RF and VL to allow direct visualization of the descending branch
and location of perforators.
e. May leave a cuff of muscle to minimize damage and spasm of the vessel.
f. Take care to preserve the motor branch.
g. Can incorporate the lateral femoral cutaneous nerve if a sensate flap is desired.
C. Thoracodorsal artery perforator flap (TAP)
1. General
a. Can use as a perforator flap, muscle flap, chimeric flap pedicled on thoracodorsal vessels, flow-through flap, or
osteocutaneous flap with a segment of vascularized scapula.
b. Donor site can be closed for a flap width up to 10 cm.
c. If sensate flap is desired, can include lateral branch of intercostal nerve.

Figure 5-2. Vascular anatomy of the anterolateral thigh (ALT ) and anterior thigh musculature. T he descending branch of the lateral circumflex femoral artery (LCFA)
is the dominant vascular supply to the ALT flap in 57% to 100% of cases.

2. Anatomy: Descending branch of the thoracodorsal artery has the largest and most reliable perforating vessels.
a. Found along a line about 2 cm behind anterior border of latissimus dorsi muscle edge.
b. Perforators are located within 8 cm of neurovascular hilum and 4 cm inferior to tip of scapula.
3. Surgical technique: With patient in lateral decubitus position, make incision just anterior to the anterior border of
latissimus, which enables incorporation of a septocutaneous or musculocutaneous perforator.
D. SGAP flap
1. General
a. Advantages: Low donor site morbidity, longer vascular pedicle than the musculocutaneous flap, avoids need for vein
grafts, abundance of adipose tissue even in thin patients, hidden scar, and good projection of the reconstructed breast.
b. Donor site can be closed for flap widths up to 12 cm
c. Flap length usually 24 to 26 cm.
d. Potential for sensory reinnervation with nervi clunium superioris
2. Anatomy
a. Usually three perforators supply the SGA cutaneous territory
b. Pedicle length 3 to 8 cm.
c. SGA usually emerges from edge of sacrum approximately one-third of distance along a line drawn from the posterior
superior iliac spine (PSIS) to the greater trochanter.
3. Surgical technique
a. Identify perforators from SGA along a line drawn connecting PSIS and greater trochanter using Doppler.
b. Horizontal flaps produce a more favorable scar.
c. Flap is elevated from the muscle in the subfascial plane.
d. Perforators are approached from lateral to medial.
e. Usually a single large perforator is used.
f. When dissecting the pedicle, must eventually open the sacral fascia and ligate multiple communicating arterial and
venous branches.
E. Inferior gluteal artery perforator flap
1. Indications: Similar to SGAP flap
2. Anatomy
a. Usually has two to four perforators originating from inferior gluteal artery (IGA) supplying the cutaneous territory.
b. Pedicle 7 to 10 cm.
3. Surgical technique
a. Inferior limit of the flap is 1 cm inferior and parallel to the gluteal fold with the patient in standing position.
b. With the patient in lateral decubitus position, perforators are identified with Doppler.
c. Flap is elevated from muscle in subfascial plane.
d. Approach perforators from lateral to medial.
e. No need to expose sciatic nerve.
f. Should preserve the posterior femoral cutaneous nerve and the fat overlying the ischium medially.
g. When dissecting the pedicle, one must eventually open the sacral fascia and ligate multiple communicating arterial
and venous branches.

PEARLS
1. Perforator flaps are useful reconstructive tools as pedicled flaps, pedicled flaps in staged reconstruction, and as free tissue
transfer.
2. Donor site morbidity should be considered when planning reconstructive options, and closure may require local tissue
rearrangement or grafting.
3. A dogmatic, “cook-book” approach to perforator flaps should be avoided, and a detailed understanding of vascular anatomy
allows the surgeon to modify these flaps to fit a multitude of reconstructive needs.

QUESTIONS YOU WILL BE ASKED


1. What are the advantages of perforator flaps?
Reduced donor site morbidity, decreased postoperative pain, faster recovery, easier to tailor or thin for covering or filling defects,
and has longer pedicle than the parent musculocutaneous flap.
2. What is the difference between a direct and an indirect perforator?
Direct cutaneous perforators pierce the deep fascia to supply the skin without traversing any other structural tissues, whereas
indirect perforators traverse an intermediate structure (i.e. muscle) prior to piercing the deep fascia and supplying the skin.
3. What perforator flap options are available for breast reconstruction?
Options include the DIEP (deep inferior epigastric perforator), SIEA (superficial interior epigastric artery), TUG (transverse
upper gracilis), TAP/TDAP (thoracodorsal artery perforator), SGAP (superior gluteal artery perforator), IGAP (inferior gluteal
artery perforator), and LAP (lumbar artery perforator) flaps.

THINGS TO DRAW
1. Blood supply to the rectus abdominis muscle
2. Blood supply to SGAP flap

Recommended Readings
Saint-Cyr M, Schaverien MV, Rohrich RJ. Perforator flaps: history, controversies, physiology, anatomy, and use in reconstruction. Plast Reconstr Surg.
2009;123(4):132e–145e. PMID: 19337067.
Sinna R, Boloorchi A, Mahajan AL, Qassemyar Q, Robbe M. What should define a perforator flap? Plast Reconstr Surg. 2010;126(6):2258–2263. PMID: 21124168.
Wallace CG, Kao HK, Jeng SF, Wei FC. Free-style flaps: a further step forward for perforator flap surgery. Plast Reconstr Surg. 2009;124(6):e419–426. PMID:
19952709.
MICROSURGERY
I. DEFINITIONS
A. Microsurgery: Surgery with the aid of an operating microscope. Includes vascular, neural, lymphatic, otologic, and
ophthalmologic surgeries.
B. Microvascular surgery: Anastomosis of small vessels with illuminated magnification.
C. Reconstructive microsurgery: Free tissue transfer and replantation.

II. MICROSURGICAL EQUIPMENT


A. Microscope
1. Two heads for operator and assistant, independently adjustable.
2. Up to 40× magnification: Use moderate magnification (10× to 17×) for suturing.
3. Can also use 3.5× loupes alone without microscope for larger vessels (>1 mm).
B. Instruments
1. Fine jeweler forceps: For handling tissue; vessels should be handled by adventitia only. Available as straight, curved,
varied lengths/widths.
2. Curved scissors: For dissection and cutting adventitia
3. Straight scissors: For cutting suture
4. Needle holder: Curved tip, nonlocking easier to use, can also use angled forceps to hold needles.
5. Clamps (e.g., Acland microvascular approximator clamps).
a. Single
b. Double with adjustable bar for vessel approximation.
6. Vessel dilator: Thin, smooth tip to dilate intraluminally without damage.
7. Olive tip cannula: Blunt, rounded metal-tip cannula attached to syringe to flush intraluminally without damage.
8. Background: Colored plastic (yellow/blue/green) to contrast with vessel/suture, also available with built-in suction to keep
field dry.
9. Anastomotic coupler: Handheld device that anastomoses two vessel ends (usually vein) with interlocking stainless steel
pins mounted on a polyethylene ring.
a. Ring sizes vary from 1 to 4 mm allowing coupling of vessels from 0.8 to 4.3 mm.
b. Excellent patency rates, saves time versus hand-sewn anastomosis.
c. Helpful to use sizer prior to choosing coupler size.
10. Suture: Typically 7.0 to 12.0 nonabsorbable monofilament (nylon, prolene).
a. 8.0 for >1 mm (wrist vessels, internal mammary arteries, thoracodorsal, most head and neck vessels, larger nerves).
b. 9.0 to 10.0 for <1 mm (digital arteries/nerves).
c. 11.0 for <0.5 mm (distal digital vessels, pediatric).
C. Solutions
1. Heparin (10 to 100 U/mL in lactated Ringer’s solution (LR) or normal saline solution (NS)): Use to flush vessels, irrigate
field.
2. 2% lidocaine: Use to alleviate vasospasm.
3. Papaverine (30 mg/mL): Use for vasospasm, causes smooth muscle vasodilation (caution: precipitates with heparin).
4. If lidocaine and papaverine are used simultaneously, it can create precipitate.

______________
*De note s common in-se rvice e xamination topics
III. SETUP
A. Preoperative planning
1. Discuss with anesthesia provider the need for nerve monitoring, avoidance of pressors, blood pressure requirements, and
anticoagulation.
2. Check microscope/equipment.
B. Operator comfort
1. Can be seated or standing depending on location. Adjust microscope position for operator and assistant comfort. Adjust
sitting stool and table height as needed. Comfort is key.
2. Secure operative field to prevent motion (e.g., lead hand for replantation, suture-free flap to surrounding skin for
stabilization).
3. Stack towels to rest forearms/wrist to reduce tremor.
4. Place moist towels around operative field to wipe instruments as needed.
5. Adjust ocular distance and microscope focus in final position.
C. Use of microinstruments
1. Rest forearms/wrists in comfortable position.
2. Hold microinstruments lightly between thumb and forefinger like a pencil.
3. Microinstruments should be controlled primarily with fingers, minimal wrist/forearm motion.

IV. MICROVASCULAR ANASTOMOSIS


A. Vessel preparation
1. Exposure of vessels and early preparation can be done with loupes.
2. Once under scope, debride any traumatized areas with curved scissors.
3. Curved scissors to dissect vessel away from surrounding tissue to increase length, allowing for tension-free anastomosis.
4. Curved scissors to cut away periadventitia from vessel ends. Only cut away enough to allow suture placement.
Excessive stripping disrupts vaso vasorum and can damage vessel walls.
5. Release proximal clamp on artery to check for spurting flow.
6. Dilate vessel ends with smooth vessel dilator.
7. Flush lumen of debris/clot with heparinized LR/NS.
B. Goals for anastomosis
1. Evenly placed interrupted or continuous sutures circumferentially.
2. No “backwall” sutures—(accidentally grabbing the opposite wall through the lumen while suturing, thereby occluding the
lumen).
3. No tears in the vessel.
4. No leaks between sutures when clamps released.
C. Anastomotic techniques
1. End-to-end
a. Setup
i. Set vessel ends in double Acland clamps or single clamps in correct orientation for anastomosis, leaving enough
vessel exposed for suturing.
ii. Slide clamps together with hemostat to approximate vessel edges.
b. Halving technique: Place first two sutures 180 degrees apart at points furthest away from and then closest to you,
then place interrupted or running sutures along backwall, flip vessel over and complete front wall after checking
lumen for patency.
c. Triangulation: Place three sutures 120 degrees apart, leaving long tails. Use tails to retract while placing interrupted
sutures in between.
d. “Backwall-up”: Place first suture at deepest point on backwall, then suture up from each side toward the most
superficial point. Good for deep spaces.
2. End-to-side
a. Clamp donor vessel proximally and distally with single Acland clamps.
b. Slit donor vessel with no. 15 blade or scissors to create fishmouth incision.
c. Line up recipient vessel in orientation that avoids kinking/tension.
d. Suture toe and heel first with interrupted sutures.
e. Place running suture along backwall, then front wall.
Figure 6-1. Vessel suturing technique in microsurgery. A: T he “ back wall” has been sutured and the surgeon is now beginning to suture the “ front wall” of the
anastomosis. T he vessel dilator is placed into the lumen of the vessel, preventing the needle from inadvertently entering the back wall. B: T he surgeon passes the needle
through the other vessel wall at right angles. (© 2014 T he University of T exas MD Anderson Cancer Center, used with permission.)

D. Suture Technique (Fig. 6-1)


1. Enter vessel from outside at 90 degrees, push needle through vessel wall using curve of needle for guidance—do not
torque on needle or pull through, will tear delicate vessel wall. Can use vessel dilator inside lumen to provide counter
tension for suture placement. Be careful not to place any sharp instruments inside lumen.
2. Enter other vessel inside out directly across from last suture.
3. Pull suture through making sure not to pull up, leaving a short tail for tying.
4. Tie square knots with three throws just tight enough to approximate vessel edges.
5. Cut tails, but can leave some tails long to use as handles when placing other sutures.
6. Repeatedly check lumen to confirm that you are taking full-thickness bites and not backwalling. Use heparin flush to aid
in visualization and keep lumen clear.
E. Anastomotic coupler technique
1. Usually for veins, best for healthy vessels with approximately equal diameter and wall thickness.
2. Prepare vein ends same way as above, clamp donor vein with single Acland clamp.
3. Bring sizer under scope to determine size of coupler ring (1 to 4 mm). Sizer peg should be same as outer diameter of
vessel. Use largest size that will fit on smaller vessel.
4. “Ship to shore”: Pass recipient vein (“ship”) through coupler ring and anchor vessel walls onto steel pins. Confirm that
intima is completely everted and impaled onto each pin. Repeat with donor vein (“shore”).
5. Turn coupler knob clockwise until rings join each other and are ejected from device.
6. Squeeze rings together with hemostat to confirm secure placement.
F. Options if size discrepancy
1. Spatulation
2. Vein graft
3. Wedge excision out of larger vessel and subsequent anastomosis to small vessel.
G. Checking the anastomosis
1. Release distal clamp, check for backflow, repair any visible leaks.
2. Release proximal clamp by “flashing”—open for a moment to check for large leaks. Have suture ready to repair leaks.
a. If large, spurting leak, have assistant flush leak with saline continuously to identify exact location (most commonly
gap between sutures or tear in vessel wall), then repair. Continuous saline flush allows visualization of leak site during
repair.
b. If small leak or ooze from needle pokes, allow vessel to sit untouched for 5 minutes. Most small leaks will stop
without intervention.
3. Confirm patency of artery by direct visualization of flow in vessel proximal and distal to anastomosis.
a. Can Doppler vessel proximal and distal or feel for pulse.
b. Can also check distal tissue for bright-red bleeding from edges.
4. Confirm patency of vein by visualizing inflation of vein proximal and distal to anastomosis. Can also strip vein gently
with jeweler forceps and watch refill.

V. POSTOPERATIVE CARE
A. Flap monitoring
1. *Clinical evaluation (the gold standard)
a. Q1 hour checks × 24 to 48 hours by nurse, periodic checks by surgical team.
b. Arterial compromise: Pale, cool, slow, or no capillary refill
c. Venous congestion: Purple, tense, brisk capillary refill
2. Doppler
a. Handheld probe: Skin paddle Doppler site marked intraoperatively with prolene suture, ideally have audible arterial
and venous signal.
b. Implantable Doppler: Can be placed around artery or vein intraoperatively, connects to external flow monitor with
audible signal.
3. Commercial flap monitoring devices: Require expensive equipment, use is surgeon/facility dependent
a. Surface temperature monitoring.
b. Laser Doppler flowmetry.
c. Near-infrared spectroscopy.
d. Color duplex sonography.
e. Microdialysis.
B. Anticoagulation: Controversial, surgeon-dependent, no definitive data supporting use of any postoperative anticoagulants.
1. Heparin: Reduces platelet aggregation, activates antithrombin III, and lowers blood viscosity (Sample dose: 5,000 U IV
intra-op, 1,000 U/h postop × 5 days).
2. *Aspirin: Inhibits prostaglandin synthesis and platelet aggregation (Sample dose: 325 mg PO qday × 30 days,
first dose in PACU given PR).
3. Dextran: Volume expander, inhibits platelet aggregation, modifies fibrin (Sample dose: Dextran-40 at 25 mL/h × 5
days). Can cause flash pulmonary edema and acute renal failure.
C. Flap Salvage
1. Clinical examination by experienced observer is the gold standard for recognizing flap compromise.
2. If arterial or venous compromise suspected:
a. Remove dressings to release any constriction and inspect entire flap.
b. Release insetting sutures to alleviate pressure from tight closures, hematoma, swelling.
c. Return to OR expeditiously for exploration.
3. Intraoperative re-exploration
a. Release inset of a flap to inspect for hematoma, compression of vessels.
b. Inspect lie of vessels for kinks/twists/compression.
c. Check artery and vein for thrombosis, most commonly at anastomosis
i. Revise anastomosis as needed.
ii. Consider thrombolytics (streptokinase/urokinase).
iii. Consider postoperative anticoagulation.
4. If venous congestion continues with patent anastomosis, consider leeches (patient needs to be on antibiotics for
Aeromonas).

VI. MICRONEURAL SURGERY


A. Nerves are “coapted,” whereas vessels are “anastomosed.”
B. Nerve coaptation methods
1. General
a. Must be tension-free, otherwise a nerve graft is indicated.
b. In most cases of transection of small peripheral nerves, no difference is seen in outcomes following the various types
of repair.
2. Epineurial repair
a. Most common
b. Nerve edges are anatomically aligned and then sutures are placed at regular intervals. Surface vasculature and
fascicular patterns are used to guide alignment.
c. The needle should pass through the epineurium 2 to 3 needle breadths from the cut edge, avoiding deep penetration.
d. The first two sutures can be left long and used for manipulation.
3. Fascicular repair
a. Individual fascicles are coapted.
b. The theoretical advantage of greater anatomic alignment has not translated into superior outcomes.
4. Group fascicular repair
a. Indicated in the repair of larger nerves at levels that allow identification of specific branches.
b. Individual fascicular groups are coapted at the inner epineurial level.

VII. ENDOSCOPIC SURGERY


A. Overview
1. Allows the surgeon to operate through minimal incisions and less invasive techniques by augmenting visualization with an
endoscope.
2. Requires a cavity in order to introduce light which can then be reflected to the endoscope and allow for visualization
and may be maintained with the insufflation of gas (e.g., CO2 ) or fluid (e.g., saline).
a. Abdomen, thorax, joint.
b. Potential space is created subcutaneously.
3. Benefits
a. Less donor site morbidity and scar.
b. Shorter recovery (for selected procedures).
c. Allows improved visualization through small incision.
4. Disadvantages
a. Expense of additional equipment and longer operative duration.
b. Technically demanding with higher learning curve.
B. Instruments
1. Endoscope
a. Size: The diameter of the scope varies depending on the procedure performed (4 to 10 mm scopes). Larger scopes
have more fiber optic bundles and allow for greater visualization.
b. The lens may be straight (0 degree) or angled (e.g., 30 degrees or 45 degrees), depending on the visualization
required. Angled scopes may allow for enhanced viewing around obstructing structures.
2. Light source: Connected through fiber optic cables to the endoscope
3. Camera
a. Single-chip camera: Alternating pixels detect red, green, and blue.
b. Three-chip camera: Separate chips to detect red, green, and blue, providing a superior image.
C. Applications
1. Aesthetic surgery
a. Breast augmentation
i. Access through axilla, which may provide superior visualization of the subpectoral space.
ii. Either saline or silicone implants may be placed.
iii. Difficult to adjust the inframammary fold and may cause trauma to the implant.
b. Brow lift
i. Minimizes scarring, alopecia, paresthesias seen with coronal incision.
ii. Allows direct visualization of important structures.
c. Midface lift
d. Abdominoplasty
i. Ideal for patients with excellent skin quality, but require limited rectus plication.
2. Reconstructive surgery
a. Placement of tissue expanders (e.g., scalp)
b. Nerve harvest (e.g., sural nerve)
c. Skull reconstruction for cranial synostosis
d. Flap harvest (e.g., latissimus dorsi)
3. Hand surgery
a. Carpal tunnel release
b. Cubital tunnel release

VIII. ROBOTIC SURGERY


A. Initial concept developed by NASA for use on space missions, where devices can be manipulated remotely.
B. Should maintain at least equivalent precision and dexterity as a surgeon from afar, with some ability to supersede human
abilities.
C. Benefits
1. More rapid microsurgical manipulation.
2. Overcome physiologic tremor.
3. Bony fragments can be aligned to 0.1 mm.
4. Can compensate for moving targets (e.g., cardiac surgery).
5. Allows for greater dexterity in close spaces (e.g., pelvic surgery, pharyngeal procedures.
D. Current applications
1. Oropharyngeal reconstruction.
2. Urologic resection and reconstruction (e.g., prostatectomy).
3. Hepatobiliary procedures.
4. Cardiac surgery.

PEARLS
1. Check equipment function before the case begins (i.e., turn on the microscope).
2. Be comfortable: Take regular breaks, drink your usual amount of caffeine.
3. Set up the best position (scope, flap, chair height, etc.) before starting microsurgery.
4. Tight splints and dressings can kill flaps. Take the time to construct well-padded splints and dressings that do not put pressure on
pedicles and flaps.
5. Clinical examination is the gold standard for postoperative flap care. Have a low threshold for return to OR to evaluate potential
flap compromise. The window of opportunity to salvage compromised flaps is limited.

QUESTIONS YOU WILL BE ASKED


1. If arterial or venous compromise is suspected, what maneuvers should be undertaken?
a. Arterial: Use Doppler distal to check. Make sure vessel not in spasm, strip vessel. Ultimately usually need to take down
anastomosis (can open one side at a time if you think one backwall stitch or you just need to flush). Consider heparinizaiton
of large amount of clot in vessel.
b. Venous: Strip, redo. Often need additional venous anastomosis if the vein is draining but flap is still congested.
2. What are the options for postoperative flap monitoring? What is the gold standard?
a. Options: Physical examination, implantable Doppler, external Doppler, surface temperature monitoring, laser Doppler
flowmetry, near-infrared spectroscopy, color duplex sonography, and microdialysis
b. Gold standard: Physical examination
3. What is the mechanism of action of heparin, dextran, and aspirin?
a. Heparin: Binds antithrombin III inducing conformational change and inhibiting thrombin and factor Xa
b. Dextran: Exact mechanism unknown but thought to cause volume expansion, cause inactivation of von Willebrand’s factor,
impart negative charge on platelets, and cause fibrinolysis
c. Aspirin: Inhibits platelet aggregation though inhibition of cyclooxygenase. Low doses inhibit thromboxane without affecting
prostacyclin
4. What solutions should be available on the field during microvascular anastomoses?
a. 2% lidocaine
b. Heparin: (10 to 100 U/mL in LR or NS)
c. Papaverine: (30 mg/mL)

Recommended Readings
Grunwald T, Krummel T, Sherman R. Advanced technologies in plastic surgery: how new innovations can improve our training and practice. Plast Reconstr Surg.
2004;114(6):1556–1567. PMID: 15509950.
Pacella SJ, Codner MA. T he transaxillary approach to breast augmentation. Clin Plast Surg. 2009;36(1):49–61. PMID: 19055961.
Pratt GF, Rozen WM, Chubb D, et al. Modern adjuncts and technologies in microsurgery: an historical and evidence-based review. Microsurgery. 2010;30(8):657–666.
PMID: 20734321.
Rowe DJ, Guyuron B. Optimizing results in endoscopic forehead rejuvenation. Clin Plast Surg. 2008;35 (3):355–360. PMID: 18558228.
I. DEFINITION
A. Composite tissue consists of a “composite” of nonsolid organ tissues including skin, bone, muscle, nerve, and fat.
B. May also be referred to as a vascularized composite allograft (VCA). This is defined by the American Society of
Transplant Surgeons (ASTS) as nonautologous vascularized peripheral tissues including skin, muscle, nerve, tendon, blood
vessels, and/or bone as a functional unit.
C. Allotransplantation refers to the fact that these tissues are transplanted from one individual to another. This is in contrast
to autologous transplantation, where tissues of an individual are moved to another location on the same individual.

II. UPPER EXTREMITY/HAND TRANSPLANTATION


A. Background
1. First hand transplantation was performed in 1964 in Ecuador, which resulted in rejection requiring reamputation.
2. Subsequent hand transplantation was reported 35 years later in France. Graft was lost after 2.5 years in this instance.
3. Now over 60 upper extremity transplants and over 150 composite tissue allo-transplants have been performed including
cases of bilateral upper extremity transplantation.
B. Indications
1. Upper extremity transplantation remains experimental.
2. Patient compliance is extremely important. Patients must go through significant rehabilitation and must be adherent to
immunosuppression medications.
3. Patients should be otherwise generally healthy given the health risks associated with immunosuppression and the need
for intense postoperative rehabilitation
4. Patients must find use of prosthesis insufficient.
5. Body image is additionally cited as an indication for candidacy.
6. One report cites exclusion of patients with known psychiatric disorders, blindness, recent malignancy, hepatitis B/C
infection, or lack of economic support.
C. Surgical procedure
1. Surgical procedure consists of procurement from the donor and transplantation to the recipient. These require large
teams consisting of plastic and orthopedic surgeons, anesthesiologists, nurses, and solid organ transplant surgeons.
2. Donor procedure
a. Matching of gender and blood type is well documented, although further matching based on human leukocyte antigen
(HLA) is not well reported.
b. Upper extremity procurement from deceased donor requires amputation of the allograft proximal to the level of the
defect in the recipient. The integrity of the structures vital for survival and function of the graft must be ensured,
including bone, arteries/veins, nerves, and tendons.
c. A prosthesis is fitted to the deceased donor in order to avoid donor disfigurement after amputation of the allograft.
d. Must consider that deceased donor will also likely be donor for solid organs. Careful coordination with solid organ
transplant procurement team(s) is required.
e. The allograft is then perfused with cold solution to avoid warm ischemia.
f. Recent trials have demonstrated that bone marrow transplantation (BMT) from donor vertebral bodies combined with
immunosuppression prolongs allograft survival.
3. Recipient procedure
a. The recipient stump must be prepared for the allograft with opening of skin and preparation of the bony stumps.
b. Transplantation then proceeds in the general order of replantation, with bony fixation, extensor and flexor tendon
repair, nerve repair, vein repair, and finally arterial repair.
D. Immunosuppression and rejection
1. Immunosuppression medications are required to prevent rejection of the allograft. Rejection can occur either acutely
or chronically.
2. Induction immunosuppression consists of antithymocyte globulin and basil-iximab; these are anti-T cell antibodies.
Maintenance immunosuppression consists of tacrolimus, mycophenolate mofetil, and prednisone.
a. Tacrolimus is associated with elevated serum creatinine levels.
b. Prednisone is associated with hypertension, diabetes, dyslipidemia, and risk of malignancy.
3. Acute rejection appears to affect the skin first. It manifests as erythematous macules and diffuse redness.
Histologic analysis shows lymphocytic infiltrate consisting of T cells. It is graded according to the Banff score.
a. Grade 0 (no rejection): No or rare inflammatory infiltrates.
b. Grade 1 (mild rejection): Mild perivascular infiltration. No involvement of overlying epidermis.
c. Grade 2 (moderate rejection): Moderate-to-severe perivascular inflammation with or without mild epidermal and
adnexal involvement. No epidermal dyskeratosis or apoptosis.
d. Grade 3 (severe rejection): Dense dermal inflammation associated with epidermal involvement (keratinocyte
vacuolization, apoptosis, and necrosis).
e. Grade 4 (necrosis): Necrosis of epidermis or other skin structures.
4. Treatment of acute rejection consists of increased oral steroids or IV steroids, polyclonal or monoclonal antibodies,
and local immunosuppressants (topical).
5. The efficacy of generic versus brand immunosuppression medications has not been determined and is of question in the
solid organ literature.
6. Acute rejection can be monitored by visualization; biopsies of skin can be taken as needed.
7. Single-drug immunosuppression (tacrolimus) has been used in patients treated with donor bone marrow cells on
postoperative day 14.
8. Chronic rejection has not been defined in the literature. However, it would likely include intimal proliferation of
vessels, skin and muscular atrophy, and fibrosis of deep tissues.
E. Rehabilitation
1. Rehabilitation is similar to that after replantation. Passive mobilization is continued for 1 year. Patients may be started on
active motion within weeks after surgery.
2. Steroid use as part of immunosuppression impedes healing and may place tendon repair at risk if active motion is
performed too early postoperatively.
F. Outcomes
1. Immediate outcomes of interest include postoperative graft survival.
2. Immunologic outcomes of interest include acute or chronic rejection.
3. Long-term outcomes of interest include sensation, motor recovery (strength, function), and patient satisfaction.
4. Immunosuppression-related outcomes include development of any long-term sequelae (e.g., diabetes, hypertension,
malignancy, infection).

III. FACE TRANSPLANTATION


A. Background
1. Seventeen face transplantation procedures documented from 2005 to 2012.
2. First face transplant in November 2005 in France, has since been performed in France, the United States, Spain, and
China.
B. Indications
1. Significant facial deformity, although clear indications have not been delineated.
2. Facial deformity has been due to trauma (animal bites, weapons), congenital deformities, burns, and tumors.
C. Surgical procedure
1. Donor procedure
a. Surgical procedure is dependent on the structures required for transplantation.
i. May include bone, muscle, nerve, mucosa, skin.
ii. May include various aesthetic units, including nose, lips, cheeks.
b. Facial vessels or external carotid arteries reported as pedicles.
c. Facial nerve is transected and preserved distally to perform neurorrhaphy with the recipient facial nerve.
d. Consideration has been given to skin color and HLA matching.
2. Recipient procedure
a. Identify missing structures, as this guides donor operation.
b. Recipient vessels are identified.
c. Facial nerve trunks are identified.
d. Microvascular anastomosis performed between donor vessels and the recipient vessels.
e. Facial nerves are connected.
f. Sensory nerves (e.g., trigeminal branches) are connected if available.
D. Immunosuppression and rejection
1. HLA matching is reported in many of the facial transplant reports.
2. Induction regimen consisting of antilymphocyte serum (thymoglobulin) and methylprednisolone; thymoglobulin,
prednisone, tacromlimus, and mycophenolate mofetil.
E. Rehabilitation
1. Rehabilitation is similar to that after replantation. Passive mobilization is continued for 1 year. Patients may be started on
active motion within weeks after surgery.
2. Steroid use as part of immunosuppression impedes healing and may place tendon repair at risk if active motion is
performed too early postoperatively.
F. Outcomes
1. There are multiple outcome measures. While initially interest was focused on immediate postoperative graft survival and
immunologic outcomes, there has been an increasing interest in functional outcomes.
2. Two of the 17 patients have died due to lack of compliance with immunosuppression and posttransplant complications.
No graft loss or GvHD.

IV. ABDOMINAL WALL TRANSPLANTATION


A. Background
1. Involves transplantation of abdominal skin and/or muscle and/or fascia for abdominal wall support.
2. Described in both pediatric and adult patients in conjunction with solid organ transplants.
B. Indications
1. Described in pediatric multivisceral transplant recipients to provide abdominal wall support.
2. Described in adult patients with small bowel transplants.
3. May avoid donor site morbidity associated with autogenous free flaps, or risk of infection with open abdomen or
prosthetics.
C. Surgical procedure
1. May be taken with rectus muscle, fascia, subcutaneous tissue, and skin (vascularized myocutaneous abdominal wall
flap).
a. Bloody supply is from the deep inferior epigastric arteries.
b. Flap can be elevated on either the DIEA or more proximal femoral or iliac vessels.
c. These are then anastomosed to the recipient’s common iliac arteries.
d. Soft tissues are then closed with the flap in place.
2. May be taken only as posterior rectus sheath fascia
a. Perfused by the falciform ligament. May be taken en bloc with liver if liver transplantation is being performed.
b. Posterior rectus sheath fascia may be used to bridge the recipient’s fascia.
D. Immunosuppression
1. Induction therapy with alemtuzumab and maintenance with tacrolimus described for vascularized myocutaneous
abdominal wall.
2. Acute rejection treated with steroids.
3. Posterior rectus sheath fascia immunosuppression dictated by liver requirement and included methylprednisolone
induction followed by prednisone and tacrolimus maintenance.
E. Outcomes
1. Posterior rectus sheath fascia
a. Five (out of six) posterior rectus sheath fascia recipients have survived with complete allograft incorporation.
b. No documented rejection of the posterior rectus sheath fascia.
2. Vascularized myocutaneous abdominal wall flap
a. A total of 14 patients received 15 abdominal wall grafts.
b. Two grafts loss due to vascular thrombosis.
c. Five patients alive to date, one with failed abdominal wall graft; four with intact grafts. Deaths unrelated to abdominal
wall transplant.
d. Rejection treated in four patients.

V. BASIC SCIENCE RESEARCH


A. Immunology
1. Dendritic cells
a. Antigen-presenting cells (APCs) include Langerhans cells in the skin.
b. Acquire antigen in peripheral tissues.
c. Drain to lymph nodes via lymphatics.
d. Mature dendritic cells interact with T cells to induce an effector phenotype.
e. Immature dendritic cells interact with T cells and are believed to induce a tolerogenic phenotype.
2. T regulatory cells
a. CD4+CD25+FoxP3+ cell population.
b. May be induced or native (derived in thymus).
c. Inhibit effector function of T cells, mitigating rejection or graft versus host disease.
i. Express cytotoxic lymphocyte antigen 4 (CTLA4), which inhibits activity of APCs, preventing development of
effector T cells.
ii. CTLA4 can bind to co-stimulatory molecules (CD80 and CD86) to activate indoleamine 2,3-dioxygenase (IDO)
to deprive local environment of tryptophan and produce kynurenines, attenuating T cell proliferation.
iii. Produces IL-10 (immunosuppressive cytokine), which inhibits APC activity and promotes T cell conversion to T
regulatory cells.
d. Believed to exert their effects in the lymph node and allograft.
3. Mesenchymal stem cells (MSCs)
a. Found in bone marrow, adipose tissue, umbilical cord.
b. Multipotent, for example, may develop into multiple other tissue types.
c. May inhibit generation of T inhibitor 17 (TH17) cells from naïve CD4+ T cells.
d. Mediate effects via paracrine factors and cell contact.
4. Graft versus host disease
a. Complication associated with hematopoietic stem cell transplantation for malignancies.
b. Donor allogeneic T cells attack the host.
c. May be associated with vascularized BMT.
5. Chimerism
a. Full chimerism refers to the complete replacement of an organism’s hematopoietic cells (HSCs) with those of the
donor.
b. Mixed chimerism refers to the presence of both donor and recipient hematopoietic cells in the recipient.
c. Donor hematopoietic stem cells are isolated from the donor bone marrow. The recipient is conditioned using whole-
body irradiation, T cell depletion, co-stimulatory blockade, and immunosuppression followed by injection of the donor
HSCs.
d. Bone marrow cells have been injected into peripheral circulation in hand transplant patients with no evidence of
chimerism. Patients have been maintained on single-drug immunotherapy (tacrolimus).
6. Co-stimulatory blockade
a. T cell activation is dependent on antigen presentation by APC and interaction between B7-1/CD80 and B7-2/CD86
on APC with CD28 on T cells.
b. Results in IL-2 binding receptor and mTOR pathway activation T cell clonalization.
c. B7-1 and B7-2 have affinity for CTLA4 (see above) in addition to CD28.
d. CTLA4-Ig (belatacept) is a fusion protein between the extracellular domain of CTLA4 and IgG which may inhibit
co-stimulation by binding to B7-1 or B7-2.
e. CTLA4-Ig has shown efficacy in kidney transplantation clinical trials.
f. CD40/CD40L pathway involved in B cell activation. CD40 is on B cells while CD40L is on activated T cells.
g. Leukocyte function-associated antigen (LFA)-1 expressed on memory T cells interacts with intercellular adhesion
molecules (ICAMs) on APCs to stabilize interface between two cells.
B. Ischemia-reperfusion injury
1. Prolonged ischemia followed by reperfusion results in production reactive oxygen species.
2. This results in oxidization of proteins and upregulation of heat shock proteins (HSPs).
3. HSPs activate Toll-like receptors and may mediate innate immune response (e.g., neutrophils, macrophages, natural
killer cells).
4. Some experimental models have demonstrated more severe rejection following longer ischemia times.

VI. ECONOMIC CONSIDERATIONS


A. Cost of disability
1. This is an emerging area of research with respect to general reconstruction. Understanding the costs of specific
disabilities is complicated by various factors specific to the defect and the patient characteristics.
2. Hand/upper extremity
a. Does level of amputation associate with economic disability?
b. How does type of employment of recipient affect economic cost of transplantation (e.g., labor vs. desk job)?
3. Face
a. How is economic burden of facial disfigurement assessed? What is this economic burden?
b. What is the cost associated with multiple reconstructive procedures?
4. Abdominal wall: what is the economic burden of hernia in terms of lost productivity and reoperation?
B. Cost of immunosuppression
1. What is the cost of immunosuppression? What are the costs of generic versus brand immunosuppression medications?
2. What are the costs of managing complications associated with immunosuppression?
3. What are the costs of single-drug therapy (and associated complications) versus multidrug therapy (and associated
complications)?
C. Cost of surgery: these costs are related to time in the operating room and anesthesia. Cost comparisons looking at cost of
surgery must also look at the cost of multiple operations if traditional reconstructive methods are used.
D. Cost of rehabilitation: analyses of rehabilitation cost should again look at the cost of rehabilitation in the case of traditional
reconstructive methods as well.
E. Cost of complications: we need to first define complications, and what the rates of these complications are. This requires
further long-term investigations of the current experience with each particular type of composite tissue allotransplantation
(CTA) (e.g., hand vs. face). Following this, the cost of management strategies related to each of these complications must
be assessed.

VII. ETHICAL CONSIDERATIONS


A. Immunosuppression and rejection
1. Do the benefits of a non-life-saving transplant (e.g., hand/face) outweigh the risks associated with immunosuppression
(e.g., hypertension, diabetes, dyslipidemia, and malignancy)?
2. How do you define quality of life before and after transplantation?
3. What are the options if a patient has rejection which necessitates graft removal? Consider the implications of removing
the face.
B. Patient selection
1. How should patients be selected for transplantation? What are the screening mechanisms in place?
2. Who can we justify for exclusion from candidacy for this procedure? Should economically disadvantaged individuals be
excluded?
3. Should patients be screened based on employment? Are patients who perform labor-intensive jobs better candidates for
extremity transplantation?
4. How can we screen patients to avoid transplanting patients who are motivated by a desire for financial gain or publicity
from having this procedure?
C. Informed consent
1. As most surgeons are aware, it is difficult to inform patients about an operation with all of its potential complications.
How can we ensure that patients understand the full scope of this procedure?
2. Informed consent must include not only information regarding the procedure and its immediate postoperative
complications but also the need for intense physical rehabilitation (especially for upper extremity), and lifelong
immunosuppression. Patients must be aware of the potential complications from noncompliance and should understand
the challenges of compliance as well.
D. Procurement
1. How can we coordinate successfully with solid-organ transplant surgeons to ensure that procurement of composite
tissue allografts does not interfere with solid organ procurement?
2. Will procurement of composite tissue affect an individual’s likelihood of becoming a solid organ donor upon death?
3. How can we avoid disfigurement to the deceased donor?
4. How can we inform patients and deceased donor families about the benefit they will provide with donation of composite
tissue allografts?
E. Economics
1. Who should shoulder the costs associated with CTA? Should it depend on the type of allograft performed (e.g., hand vs.
face vs. abdomen)?
2. Should different economic costs of patient care be shouldered by separate institutions (e.g., surgery vs.
immunosuppression vs. complications vs. rehabilitation)?
3. Who are the potential payers for this procedure (e.g., patient, worker’s compensation/government/Medicare/Medicaid,
hospital, employer, private insurers, NIH, military)?

PEARLS
1. Treatment of acute rejection consists of increased oral steroids or IV steroids, polyclonal or monoclonal antibodies, and local
immunosuppressants (topical).
2. Prednisone is associated with hypertension, diabetes, dyslipidemia, and risk of malignancy
3. Induction immunosuppression consists of antithymocyte globulin and basiliximab; these are anti-T cell antibodies. Maintenance
immunosuppression consists of tacrolimus, mycophenolate mofetil, and prednisone.
4. Acute rejection appears to affect the skin first. It manifests as erythematous macules and diffuse redness. Histologic analysis
shows lymphocytic infiltrate consisting of T cells.

QUESTIONS YOU WILL BE ASKED


1. What is the most immunogenic tissue for transplantation?
Skin.
2. What is the difference between allotransplantation and autotransplantation?
Allotransplantation refers to the fact that these tissues are transplanted from one individual to another. This is in contrast to
autotransplantation, where tissues of an individual are moved to another location on the same individual.

Recommended Readings
Cavadas PC, Landin L, T hione A, et al. T he Spanish experience with hand, forearm, and arm transplantation. Hand Clin. 2011;27:443–453. PMID: 22051386.
Chung KC, Oda T, Saddawi-Konefka D, Shauver MJ. An economic analysis of hand transplantation in the United States. Plast Reconstr Surg. 2010;125:589–598.
PMID: 19910847.
Kaufman CL, Breidenbach W. World experience after more than a decade of clinical hand transplantation: update from the Louisville hand transplant program. Hand
Clin. 2011;27:417–421. PMID: 22051383.
Morelon E, Kanitakis J, Petruzzo P. Immunological issues in clinical composite tissue allotransplantation: where do we stand today? Transplantation. 2012;93:855–859.
PMID: 22538449.
Rohrich RJ, Longaker MT, Cunningham B. On the ethics of composite tissue allotransplantation (facial transplantation). Plast Reconstr Surg. 2006;117:2071–2073.
PMID: 16651986.
Schneeberger S, Landin L, Jableki J, et al. Achievements and challenges in composite tissue allotransplantation. Transpl Int. 2011;24:760–769. PMID: 21554424.
Siemionow M, Ozturk C. Face transplantation: outcomes, concerns, controversies, and future directions. J Craniofac Surg. 2012;23:254–259. PMID: 22337420.
Wood KJ, Bushell A, Hester J. Regulatory immune cells in transplantation. Nat Rev Immunol. 2012;12:417–430. PMID: 22627860.
I. INTRODUCTION
A. Definition
1. An artificial filling device is used to grow and expand local tissue to reconstruct an adjacent soft tissue defect when
primary closure is not possible.
2. A silicone elastomer reservoir is placed beneath the donor tissue and slowly filled over time with saline, causing the
overlying soft tissue envelope to stretch with a net increase in surface area per unit volume.
B. Advantages
1. Reconstruct “like with like” using donor and recipient tissues that share similarities in color, thickness, texture, and
hair-bearing patterns.
2. Larger soft tissue defects that would usually require a local flap for reconstruction can be closed primarily using
expanded local tissue, which simultaneously limits donor site morbidity.
3. A robust angiogenic response is achieved histologically within the expanded local tissue resembling an incisional
delay phenomenon.
4. Predictable amounts of donor tissue can be gained through the expansion process
5. As a reconstructive technique, it is versatile, reliable, and repeatable and can be applied to many regions of the body.
C. Disadvantages
1. Multiple operations (at least two for placement and removal of the expander) and outpatient visits are required.
2. Definitive reconstruction is delayed secondary to the expansion process.
3. Specific complications related to the presence of foreign material (e.g., infection, exposure, or extrusion).
4. Temporary contour deformity at the donor site that is often difficult to conceal (e.g., scalp and forehead
reconstruction).

II. HISTOLOGY
A. Soft tissue
1. Skin
a. *Epidermis
i. Increase in thickness through hyperkeratosis and acanthosis
ii. Increase in mitosis
iii. Narrowing of intracellular spaces
b. Dermis
i. *No change in thickness of papillary dermis, but there is a decrease in thickness of reticular dermis so
overall thinning
ii. Fibroblast and myofibroblast increase in number with thickened collagen bundles.
iii. Sweat glands and hair follicles spread out and demonstrate degenerative changes.
iv. Fragmentation and rupture of elastin producing striae
c. Clinically, expanded skin is often dry with pigmentary changes, and there is decreased appreciation of pain,
temperature, pressure, and light touch.
d. Changes in thickness of expanded skin are temporary, and return to baseline occurs approximately 2 years after the
expansion process.

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*De note s common in-se rvice e xamination topics

2. Muscle
a. *Decrease in mass
b. Decrease in thickness and mass.
c. Myofibril and myofilament disorganization.
d. No loss of function, but muscle injury has been reported during the expansion process (e.g., reduced brow elevation
due to frontalis damage).
3. Fat
a. *Decrease in thickness, especially subcutaneous fat.
b. Clinically, this manifests as reduced flap bulk.
c. Atrophic adipocytes are eventually replaced by fibrosis causing fat loss (30% to 50%) which is permanent.
B. Capsule
1. Formed by a foreign body reaction composed of parallel-oriented fibro-blasts intervening with a dense layer of
collagen bundles.
2. During removal of the expander, capsulotomy increases surface area and maximizes flap advancement.
3. Capsulectomy should be used judiciously to avoid interrupting the vascular supply to random-pattern flaps.
C. Vascularity
1. Expanded skin is hypervascular
2. Greatest density of blood vessels is found at the interface between the capsule and expanded local tissue.

III. BIOMECHANICS
A. Creep
1. Definition
a. The tendency of tissue to deform permanently under the influence of stress.
b. Can either be an acute (mechanical) or chronic (biological) response to sustained tissue stretch.
2. Mechanical
a. Acute tissue elongation due to reorientation of the collagen bundles in parallel with the applied force vector, and
recruitment of adjacent tissue from surrounding zones of skin laxity.
b. Mechanical creep is responsible for the initial gain in tissue length at the time of expander placement as a result of
the intraoperative fill volume.
c. Water is displaced out of ground substance and elastic fibers microfragment.
3. Biological
a. Chronic tissue elongation due to new tissue regeneration.
b. Both during and following completion of the expansion process, sustained tissue stretch leads to the addition of new
tissue within the expanded field by activating collagenogenesis, angiogenesis, and epidermal proliferation.
B. Stress relaxation
1. Stress is defined as the average force per unit surface area within the tissue.
2. Strain is defined as the amount of tissue deformation that occurs in response to stress.
3. Stress relaxation refers to the gradual decline in stress over time at constant strain in biological tissues. Clinically, this
is important because the acutely stretched tissue can relax before the next expansion, thereby preventing ischemia-
related complications of the overlying soft tissue envelope.

IV. PRINCIPLES OF TISSUE EXPANDER PLACEMENT


A. Fundamental design
1. Shape
a. Rectangular expanders are useful on the trunk and extremities, and result in the greatest amount of actual tissue
gain (approximately 40% of theoretical tissue gain).
b. Round expanders are most commonly used in breast reconstruction and result in the least amount of actual tissue
gain (approximately 25% of theoretical tissue gain).
c. Crescent expanders are useful in scalp reconstruction and gain more tissue centrally than peripherally.
d. Anatomic expanders differentially expand the overlying soft tissue envelope to more accurately recreate the body
part of interest (e.g., teardrop-shaped expanders used in breast reconstruction).
e. Custom expanders are designed for irregular defects, but may be more expensive.
2. Filling port
a. *Remote filling ports are connected to the tissue expander via silastic tubing and can either be placed
subcutaneously (most common) for percutaneous access or externalized for direct access. Crucial not to make tunnel
too wide or port will fall down back next to the expander making it difficult to fill.
b. Integrated filling ports are located within the expander, although this design may increase the risk of inadvertent
puncture of the outer shell.
c. Self-filling osmotic expanders do not have a filling port, but instead rely upon an osmotically active hypertonic
saline or hydrogel-based solution to gradually absorb fluid from the surrounding soft tissues over a 4- to 8-week time
period.
3. Permanence
a. Most tissue expanders are temporarily placed, and either later exchanged for a permanent saline or silicone
prosthesis, or removed completely to allow for rearrangement of the expanded local tissue.
b. A few permanent expanders are less commonly used in breast reconstruction, consisting of an empty inner core
designed to be remotely filled with saline, surrounded by an outer compartment filled with silicone gel.
B. Geometry of tissue expansion
1. Use the largest expander possible with a base diameter approximately two to three times that of the diameter of the
soft tissue defect to be reconstructed.
2. If the expander contains a base plate or rigid backing, this side should be placed along the floor of the pocket to
guide the direction of expansion outwards.
3. Multiple expanders are sometimes needed to reconstruct a single defect, depending on the availability of donor
tissue.
C. Donor site
1. The expander is usually placed adjacent and parallel to the long axis of the soft tissue defect; if placed in the extremities,
the expander should not cross any joints or impinge on joint motion.
2. Donor tissue must be well vascularized and free of unstable scar and must display no evidence of infection or
contamination.
3. Use cautiously in irradiated tissue or patients with poorly controlled diabetes mellitus, vascular disease, or connective
tissue disorders.
D. Expander pocket
1. The expander pocket can be developed in the subcutaneous, submuscular, or subgaleal planes depending on the location
of the soft tissue defect.
2. The size of the expander pocket should be individually tailored to allow the expander to lie completely flat with minimal
wrinkling.
3. Excessive dissection should be limited to prevent expander migration postoperatively, and meticulous hemostasis is
important to minimize hematoma formation.
E. Incision placement
1. *Incisions are placed radial to the expander pocket and perpendicular to the direction of expansion to
minimize tension on the incision during the expansion process; undue tension placed on the incision during expansion can
cause dehiscence and exposure of the expander.
2. Consider future reconstructive options when planning incision placement such that the incisions can easily be
incorporated into planned flaps or the tissue to be resected.
3. Endoscopic-assisted expander placement (refer to Chapter 6, “Endoscopic Plastic Surgery”) utilizes smaller incisions
and allows more direct visualization of the expander pocket, but at the expense of a steep learning curve and altered
depth perception.
F. Timing of expansion
1. Insert a 23G butterfly needle or Huber (noncutting) needle into the filling port perpendicularly; bigger needles should be
avoided because they can cause valve leak due to increased back pressure.
2. At the time of expander placement, an initial volume is infused intraoperatively to gently fill the expander pocket to
prevent seroma formation, and in the case of breast reconstruction patients, to maintain the shape of the overlying soft
tissue envelope.
3. The expansion process usually begins 2 to 3 weeks postoperatively and continues on a weekly basis thereafter.
4. Approximately 50 to 100 cc can be infused during each expansion, but regardless of the volume infused, the expander is
filled until the patient expresses discomfort or the overlying skin blanches.
5. The expansion process is complete based on surgeon preference when he/she deems there is enough donor tissue
available to reconstruct the soft tissue defect; however, this is often a difficult decision and additional “over” expansion is
often recommended to ensure adequate soft tissue coverage.

V. CLINICAL APPLICATIONS
A. Scalp and forehead reconstruction
1. Indications include traumatic, congenital, and oncologic soft tissue defects, as well as androgenic and burn alopecia;
*approximately 50% of the scalp can be reconstructed using tissue expansion without causing noticeable
thinning of the remaining hair.
2. The expander is usually placed in either the subcutaneous or subgaleal (more common) planes.
3. Incisions are camouflaged in either the frontotemporal hairline, brow line, vertical midline, or within relaxed skin tension
lines.
4. Following completion of the expansion process, the soft tissue defect is often reconstructed with a large rotation-
advancement flap; however, it is not uncommon for multiple rounds of tissue expansion to be required in a serially staged
process.
5. Caution should be observed when expanding near the temporal branch of the facial nerve to avoid stretching or
iatrogenic transection.
B. Facial defects
1. Indications are identical to scalp and forehead reconstruction.
2. The expander is placed in the subcutaneous plane centrally or over the parotidomasseteric fascia laterally.
3. Following completion of the expansion process, the soft tissue defect is often reconstructed with a local flap.
4. Caution should be observed when expanding near the zygomatic and buccal branches of the facial nerve and Stenson’s
duct.
C. Nasal reconstruction
1. Small soft tissue defects can be reconstructed using tissue expansion; most useful in the thin, mobile skin over the root or
dorsum of the nose.
2. When using a forehead flap, intraoperative tissue expansion of the forehead skin may allow for primary closure of the
donor site via mechanical creep.
D. Auricular defects
1. Indications include both congenital (e.g., microtia) and acquired causes (e.g., traumatic amputation, burns, or skin
malignancy).
2. The expander is placed in the subcutaneous plane.
3. The incision is placed along the postauricular hairline.
4. Following completion of the expansion process, thin, well-vascularized, non- hair-bearing skin can be easily draped over
the inserted neocartilaginous framework.
E. Neck reconstruction
1. The expander is usually placed above the platysma.
2. Caution should be observed when expanding near the marginal mandibular and cervical branches of the facial nerve.
F. Breast reconstruction (refer to Chapter 37, “Breast Reconstruction”)
1. Indications include both immediate and delayed reconstruction after acquired mastectomy defects.
2. Usually a two-stage procedure, in which the expander is later exchanged for a permanent saline or silicone prosthesis
once the expansion process is complete and tissue equilibration has been achieved, although a second procedure can
sometimes be avoided if the expander behaves as a permanent implant.
3. The expander is placed beneath the pectoralis major, and the inferolateral pole is covered by either serratus anterior
fascia or processed acellular dermal matrix scaffold.
4. Caution should be observed in irradiated tissue given increased postoperative expander-related complications including
infection, exposure, and extrusion.
G. Abdominal wall reconstruction
1. Similar to scalp reconstruction, approximately 50% of the abdominal wall can be reconstructed using a components
separation technique after the expansion process is complete.
2. The expander is placed either in the subcutaneous plane or between the external and internal obliques for myofascial
defects.
3. Due to the segmental innervation pattern of the abdominal wall, damage to any motor or sensory nerves is less likely to
have long-standing, debilitating consequences compared to the use of tissue expansion in the extremities.
H. Upper and lower extremity reconstruction
1. *Classically, the use of tissue expansion in the extremities is associated with higher complication rates,
especially in the lower limb.
2. The expander is placed above the deep investing fascia of the muscles.
3. Caution should be observed when expanding near named sensory nerves and superficial vessels due to the lack of a
segmental innervation pattern in the extremities.
4. There is an increased propensity to form keloids in the deltoid region.
5. The expander should not cross any joints or impinge on joint motion.
I. Flap pre-expansion
1. Pre-expansion of axial fasciocutaneous flaps facilitates coverage of larger soft tissue defects using expanded local tissue
and simultaneously limits donor site morbidity by allowing primary closure.
2. Pre-expansion of myocutaneous flaps improves safe flap transfer due to a robust angiogenic response within the
expanded local tissue resembling an incisional delay phenomenon.

VI. COMPLICATIONS AND TREATMENT


A. Major
1. Cellulitis and periprosthetic infection
a. Requires early and aggressive treatment with intravenous antibiotics.
b. If caught early, salvage of the expander may be possible with intravenous antibiotics alone; however, removal of the
expander is often needed due to decreased clearance of bacteria from around the expander.
c. If the infection becomes periprosthetic, removal of the expander is absolutely mandated.
d. Port site infections can sometimes be managed by externalizing the remote filling port.
2. Hematoma
a. Evacuation of the hematoma is necessary to prevent ischemia of the overlying skin flaps and bacterial superinfection.
b. Removal of the expander is often not necessary.
3. Expander exposure or extrusion
a. Requires removal of the expander if bacterial colonization is suspected.
b. Most commonly due to inadequate pocket creation.
c. Treat infection, if present.
4. Expander deflation
a. Usually presents clinically as a “flat tire,” and most often the result of iatrogenic puncture during insertion of the
filling needle.
b. Requires removal and replacement with a new expander.
5. Skin-flap ischemia
a. Avoid aggressive dissection during expander placement to prevent devascularization of the overlying skin flaps.
b. Avoid expanding too much during an individual session. If the overlying skin turns white, remove some fluid from the
expander.
c. Partial thickness necrosis can usually be managed with local wound care.
d. Full-thickness necrosis requires debridement of all devitalized tissue and reclosure to ensure adequate soft tissue
coverage of the expander.
e. Treat infection, if present.
B. Minor
1. Incorrect valve placement or valve turnover.
2. Inadequate expansion.
3. Pain during expansion.
4. Temporary contour deformity at the donor site.
5. Widening of surgical scars.
6. Transient neuropraxia of both motor and sensory nerves.

PEARLS
1. An exposed expander can sometimes be further expanded if not infected.
2. Methylene blue can be used to color the contents of the expander to help identify the valve correctly when filling and to detect
leakage more easily.
3. Expanded local tissue can be reexpanded 3 to 6 months later.
4. The epidermis is the only layer of skin that increases in thickness during tissue expansion.
5. The base diameter of the expander should be approximately two to three times that of the diameter of the soft tissue defect to
be reconstructed.
6. Approximately 50% of the scalp and abdominal wall can be reconstructed using tissue expansion.

QUESTIONS YOU WILL BE ASKED


1. Describe the phenomena of creep as it relates to tissue expansion.
Creep describes the biological response of cells which proliferate in response to continued mechanical stress.
2. Describe the histological changes seen with tissue expansion.
Gap junctions become disrupted, epidermis thickens, dermis becomes thinner.
3. Describe the contraindications to tissue expansion.
No absolute contraindications, but irradiated bed, infection, extremities in children are all relative contraindications.
4. What is the effect of tissue expander on overlying skin?
Blood flow increases, causing tissue expansion to mimic the delay phenomenon.

Recommended Readings
Austad ED, Pasyk KA, McClatchey KD, Cherry GW. Histomorphologic evaluation of guinea pig skin and soft tissue after controlled tissue expansion. Plast Reconstr
Surg. 1982;70(6):704–710. PMID: 7146153.
Cherry GW, Austad E, Pasyk K, McClatchey K, Rohrich RJ. Increased survival and vascularity of random-pattern skin flaps elevated in controlled, expanded skin. Plast
Reconstr Surg. 1983;72(5): 680–687. PMID: 6194539.
Huang X, Qu X, Li Q. Risk factors for complications of tissue expansion: a 20-year systematic review and meta-analysis. Plast Reconstr Surg. 2011;128(3):787–797.
PMID: 21572375.
Johnson T M, Lowe L, Brown MD, Sullivan MJ, Nelson BR. Histology and physiology of tissue expansion. J Dermatol Surg Oncol. 1993;19(12):1074–1078. PMID:
8282904.
Wilhelmi BJ, Blackwell SJ, Mancoll JS, Phillips LG. Creep vs. stretch: a review of the viscoelastic properties of skin. Ann Plast Surg. 1998;41(2):215–219. PMID:
9718160.
I. FAT GRAFTING
A. Background
1. Eugene Hollander documented the first known use of fat in surgical enhancement in 1912 when he used this technique in
patients presenting with lipoatrophy of the face.
2. Report of fat grafting that quoted poor outcomes in patients who had received autologous lipoaspirate transplants in the
1980s delayed acceptance of this technique.
3. Eventually, surgeons started using fat grafting to treat a variety of conditions, including radiation damage, vocal cord
impairment, breast capsular contracture, chronic ulceration, and, ultimately, burn injuries.
4. In general, “fat grafting” may be used to describe three alternatives.
a. Composite grafts of fat that have been minimally modified/processed.
b. Modified and processed portions of fat that can be injected after processing has been completed.
c. Highly sorted adipose-derived mesenchymal stem cells (MSCs) organized by fluorescence-activated cell sorting.
5. Adipose tissue composition
a. Macroscopically, at least five different types of adipose tissue exist: bone marrow, brown, mammary, mechanical,
and white. Each serves a distinct biological function.
b. Adipose tissue is composed mainly of fat cells organized into lobules
i. Mature adipocytes (90% volume)
ii. Stromal vascular fraction (SVF): preadipocytes, fibroblasts, vascular smooth muscle cells, endothelial cells,
resident monocytes/macrophages, lymphocytes, and adipose-derived stem/stromal cells (ASCs).
c. Adipocytes account for approximately 20% of all cells within the subcutaneous tissue.
d. Biochemistry
i. Adipocytes contain two receptors for catecholamines, which regulate fat storage.
ii. β-1 receptors—located in areas of metabolically active fat such as upper body, face, and breast—respond to
catecholamines by releasing lipase, splitting triglyercides into glycerol and fatty acids.
iii. α-2 receptors—located in diet-resistant areas such as the lateral thighs, buttocks, and abdomen—are antagonists
of β-1 receptors and block lipolysis.
B. Indications
1. Tissue augmentation in any subcutaneous location with tissue atrophy. Most commonly used in the face: nasolabial folds,
lips, malar region, and cheek.
2. Lipodystrophic syndromes and atrophic areas.
3. Breast reconstruction.
4. Breast augmentation.
5. Scar revision.
6. Hemifacial microsomia.

______________
*De note s common in-se rvice e xamination topics

C. Harvesting
1. Coleman technique
a. 3-mm incisions.
b. Blunt tip attached to 10-mL Luer-Lok syringe.
c. Cannula pushed through harvest site as surgeon uses manipulation to create gentle negative pressure by pulling back
on plunger.
d. Plunger removed and syringe placed in centrifuge.
2. Harvest can be done by liposuction.
3. Different providers have different preferences and beliefs about the effect of amount of suction during harvest, length of
canula, and size of collection tube but no studies have shown difference in adipocyte survival.
4. Donor site has not proven to affect outcome: Most commonly abdomen, buttocks, and thigh.
5. Superwet or tumescent techniques avoided to prevent trauma to graft during harvest. (Can use 1 mL of local
anesthetic per mL of fat harvest).
6. Can inject tumescent fluid after harvest for hemostasis and pain control.
D. Processing
1. Coleman technique: Lipoaspirate is loaded into 10-mL syringes.
2. Adipose tissue centrifuged at 3,000 rpm or 1300G for 3 minutes (though different providers use different settings).
3. Centrifugation: Separates aspirate based on density.
a. Less dense components: Adipocytes with part of stromal vascular fraction.
b. More dense blood, lymphocytes, as well as part of the stromal vascular fraction.
4. Blood and tumescent fraction drained from the bottom layer and the oil is decanted and wicked with a cotton pledget
for 3 minutes from the top layer.
E. Placement of fat graft
1. Smaller gauge used than harvesting.
2. Blunt tip allows less traumatic introduction (Coleman: 17G cannula with a 1-mL syringe, injecting tiny amounts with
each pass).
3. Fat should be placed with multiple passes laying down single layer of fat and avoiding clumping.
4. Each injection should be a new tunnel creating multiple levels in a three- dimensional manner.
5. If clump injected, flatten with digital manipulation.
6. Usually placed just under the dermis.
7. Augmentation over mandible and malar region just over periosteum.
8. Possible methods to improve survival
a. Greater exposure of each adipocyte to vasculature.
b. Diffuse infiltration with multiple passes.
c. Small amount of placement per pass.
d. Large surface area of contact between fat and surrounding tissue.
e. Pure fat.
f. Once you feel large open space with each pass, probably it is good to stop.
9. Three zones of healing among the adipocytes located in a newly fat-grafted bed
a. Necrotic zone.
b. Regenerating zone.
c. Surviving zone: Both adipocytes and ASCs survive.
F. Specific clinical uses
1. Facial volume correction
a. Injection of 16G needle stab incisions on each side of oral commissure and placement into upper lip, perinasal area.
b. Inject in vermilion of lip to roll out vermilion and give patient more red lip.
c. Submalar area with 18G blunt with 0.05 cc per pass.
d. Can use pickle fork to folds.
e. Periorbital rejuvenation: Inject along inferior orbital rim in plane close to the bone.
f. Temporal rejuvenation: Fat placed subcutaneously in plane above the temporalis fascia.
2. Breast augmentation
a. Three weeks of expansion via Brava System.
b. Injection using 14G Coleman side hole needle with multiple sites of injection along inframammary fold.
c. Fat injected subcutaneously and not directly into the breast tissue.
3. Breast reconstruction
a. Postmastectomy or postlumpectomy deformity can be used to improve contour irregularities in tissue expander and
autogenous breast reconstruction.
b. Tuberous breast deformity.
c. Poland’s syndrome.
a. Can harvest fat using in-line machine and liposuction.
b. Injection cannula 16G blunt.
c. Inject subdermal.
d. Often requires multiple stages for large deformities.
G. Graft survival and healing
1. Patients can have considerable postoperative edema due to multiple passes with injection.
2. In general, graft viability varies from as high as 70% to as low as 30%. Survival rate decreases with infection and
trauma.
3. Overcorrection needed to optimize results and account for graft loss. Overcorrection by 50% recommended (although
debated).
4. Final volume determined by
a. Interactions between multiple cell types, including ASCs, viable adipocytes, and necrotic adipocytes.
b. These cells stimulate maintenance of a set volume as determined by the original composite of tissue transferred into
the wound bed.
5. For most patients included in studies examining the effect of fat grafting after thermal or radiation injury, an average of
two treatments are needed.
6. Often the second fat transplantation occurs 3 months after the initial procedure.
H. Complications
1. *Glabellar injection can cause blindness.
2. Skin necrosis.
3. Fat resorption and necrosis.
4. Irregularities.
5. Unknown risk in breast cancer and head and neck patients.

II. ADIPOSE-DERIVED STEM CELLS


A. Can be isolated from adipose tissue harvested either by liposuction or by excision of tissue.
B. If harvested by liposuction, adipose tissue settles into two layers
1. Supernatant or processed lipoaspirate (PLA) layer: Consists of the suctioned adipocytes as well as their
surrounding endothelium and stroma.
2. The bottom layer or liposuction aspirate fluid: Consists of injected saline, erythrocytes, and denser pieces of the PLA
layer.
3. ASCs can be harvested from both layers; however, the yield of adherent ASCs is significantly higher in the
adipocyte layer than in the liposuction aspirate fluid cells.
a. Terms for adipose-derived “stem cells”: ASCs, adipose-derived adult stem cells (ADAS), adipose-derived adult
stromal cells, adipose-derived stromal cells (ADSCs), adipose stromal cells (ASCs), adipose MSCs (AdMSCs),
lipoblast, pericyte, preadipocyte, and PLA cells.
b. International Fat Applied Technology Society reached a consensus: ASCs to describe plastic-adherent,
multipotent cell population.
c. The exact location of ASCs is unknown: ASCs may exist within the perivascular tissue since they express similar
cell surface antigens to pericytes.
d. Culturing of these cells eventually results in the appearance of a relatively homogeneous population of
mesodermal or MSCs (usually after two to three passages) after nonadherent cells from SVF are washed away.
e. Beneficial impact of ASCs may be due to soluble factors produced by ASCs rather than their differentiation
capability toward different mature lineages.
f. ASCs secrete hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), transforming growth
factor-β (TGF-β), insulin-like growth factor (IGF)-1, basic fibroblast growth factor (bFGF), granulocyte–macrophage
colony-stimulating factor, tumor necrosis factor (TNF)-α, interleukin-6, interleukin-7, interleukin-8, interleukin-11,
adiponectin, angiotensin, and cathepsin D.
g. ASCs are mesodermal and can differentiate into adipogenic, osteogenic, chondrogenic, myogenic, cardiomyogenic,
angiogenic, tenogenic, and periodontogenic lineages.
h. ASC cell surface markers
i. Positive for CD44 (hyaluronate), CD90, integrin β1 (CD29), endoglin (CD105), and integrin α4 (CD49).
ii. Negative for the hematopoietic markers CD45, CD34, and cKit (CD117).
i. In vitro:
i. Isolated from floating portion of lipoaspirate or after finely mincing whole adipose tissue
a) Adipose tissue placed in 0.075% collagenase in Hank’s buffered solution in 37 degree shaking water bath for 1
hour venting every 15 minutes.
b) Collagenase neutralized with 10% fetal bovine serum (FBS) in PBS.
c) Tissue is then spun down in centrifuge.
d) Superior layer of adipocytes aspirated and cell pellet is resuspended in a medium and plated.
ii. ASCs display a cell doubling time of 2 to 4 days, and the medium should be changed every 2 to 3 days.
iii. Differentiation capacity and phenotype are similar to those MSCs isolated from bone marrow and umbilical cord
blood.
iv. On average, 45 mL of starting lipoaspirate can be plated onto 1 × 10 cm2 cell culture plates, which can be split to
three 10 cm plates 3 days later.
v. Osteogenic differentiation
a) Seed cells appropriately in plate size for desired experiment
1) 30,000 cells/well for a 12-well plate.
2) 100,000 cells/well for a 6-well plate.
3) 800,000 cells for a 10 cm plate.
b) After cells grow overnight in standard growth medium (SGM) (Dulbecco’s modified Eagle’s medium
(DMEM) + 10% FBS + 1% penicillin/streptomycin), change media to osteogenic differentiation medium
(ODM).
c) ODM: 10 mM glycerol β-phosphate, 0.25 mM ascorbic acid, 10% FBS, 1% penicillin and streptomycin, and
DMEM as given below.
d) DMEM: To make 100 × stock solutions (1 M G-2P and 25 mM AA2 )
1) 216 g G-2P in 1,000 mL medium or 43.2 g in 200 mL serum-free medium.
2) 4.4 g AA2 in 1,000 mL water or 0.88 g in 200 mL water.
3) Filtrate with 0.22-μm filtration device.
4) Aliquote 10 mL and transfer into 15 mL tube and store at –20°C for up to 3 months.
e) Length of differentiation
1) Human ASCs stain positive for alkaline phosphatase at 3 days and mouse ASCs around 7 days.
2) Bone mineralization by alizarin red can be seen by 7 days in human ASCs and 10 to 14 days for mouse
ASCs.
f) Bone morphogenetic proteins (BMPs)
1) Member of TGF-β.
2) Play a significant role in osteoblast differentiation and osteogenesis: BMP-2, BMP-4, and BMP-7.
3) Initiate their signaling cascade through bone morphogenic protein receptor types I and II.
4) These activated receptor kinases subsequently phosphorylate transcription factors Smad 1, Smad 5, and
Smad 8.

5) Activate Cbfa1 or Runt-related protein 2 (Runx-2) and OPN as well as stimulate osteogenic
differentiation.
6) Runx-2 and Osx are considered the master regulation genes for bone formation.
vi. Adipogenic differentiation
a) Inverse relationship between adipocytes and osteoblasts in bone marrow.
b) Peroxisome proliferators–activated receptor gamma (Pparγ) has been shown to play a key role in adipogenic
differentiation.
c) Data extremely variable for components and concentration of components. In general, includes DMEM+FBS,
insulin, and dexamethasone (Table 9.1). Some will also include indomethacin and IBMX, though more
common for bone marrow-derived MSC differentiation.
d) To assess adipogenic differentiation, use Oil Red O stain.
vii. Chondrogenic differentiation
a) Medium: High (4.5 g/L) glucose (DMEM-HG, Invitrogen) supplemented with 10% ITS + Premix Tissue
Culture Supplement (Becton Dickinson), 10−7 M dexamethasone (Sigma), 1 μM ascorbate-2-phosphate, 1%
sodium pyruvate, and 10 ng/mL TGF-β1.
b) Cells are grown as micromass with 1.25 × 106 cells/mL.
PEARLS
1. When harvesting fat for grafting, larger syringes or plunger-locking devices may create increased pressure that risks damage to
tissue.
2. Important to use many small passes for laying fat down to improve vascularity to fat grafts.
3. Once recipient site for fat grafting feels like a large open space, probably it is best to stop grafting.

QUESTIONS YOU WILL BE ASKED


1. What is the 6-month viability of fat grafting?
Around 50%
2. What is the most common complication after fat grafting?
Resorption
3. With fat grafting, why is it important for very small volumes to be injected with each pass?
To promote maximal contact between graft and surrounding bed

Recommended Readings
Coleman SR. Structural fat grafting: more than a permanent filler. Plast Reconstr Surg. 2006;118(3 Suppl):108S–120S. PMID: 16936550.
Gir P, Brown SA, Oni G, Kashefi N, Mojallal A, Rohrich RJ. Fat grafting: evidence-based review on autologous fat harvesting, processing, reinjection, and storage. Plast
Reconstr Surg. 2012;130(1):249–258. PMID: 22743888.
Locke MB, de Chalain T M. Current practice in autologous fat transplantation: suggested clinical guidelines based on a review of recent literature. Ann Plast Surg.
2008;60(1):98–102. PMID: 18281805.
PHARMACOLOGY OF LOCAL ANESTHETICS
I. CHEMISTRY
A. Local anesthetic (LA) molecules consist of three components, each of which contributes distinct properties to the
molecule:
1. Aromatic ring: Determines lipid solubility and hence potency.
2. Amine end: exists in either a tertiary form (lipid soluble) or a positively charged quaternary form (water-soluble)
depending on pH and determines the time of onset.
3. Intermediate ester/amide: determines pattern of biotransformation, allergic potential, and stability in solution.

II. MECHANISM OF ACTION


A. LAs reversibly block neural conduction in peripheral nerves by halting the propagation of action potentials.
1. *LAs prevent depolarization. Anesthetic molecules reversibly bind to Na + channels and inhibit Na+ influx,
thus preventing the depolarization threshold from being reached.
2. LAs have no effect on the resting or threshold potential, although the refractory period and repolarization may be
prolonged.
3. Sequence of anesthesia relates to nerve fiber biology (Tables 10-1 and 10-2):
a. Small diameter fibers more sensitive to LAs than larger diameter fibers. The distance of impulse propagation in small
fibers is shorter.
b. Myelinated fibers are more sensitive than unmyelinated fibers. Myelinated nerves need only to be block at several
nodes of Ranvier to inhibit impulse propagation, thus requiring smaller concentrations of anesthetic.
c. Nerves with higher firing frequency are more sensitive.
d. The affinity of LAs for Na+ channels depends on the state of the channel: Open state > inactivated state > resting
state.
e. Pain fibers have a higher firing rate and relatively longer action potential than motor fibers and are thus more
sensitive.

III. PHARMOKINETICS
A. Time of onset
1. The pKa of LAs determines the rate of onset
a. The pKa is the pH at which a solution of LA is in equilibrium, with half in the neutral base (salt) and half in the
ionized state (cation).
b. A decrease in pH shifts equilibrium toward the ionized form.
c. *The lower the pKa (closer to pH 7.4), the higher the concentration of nonionized LA at a given pH, and
therefore, the faster the onset.
d. Only the nonionized form crosses the plasma membrane.
e. After crossing the cell membrane, the LA is exposed to a more acidic intra-cellular environment and is converted to
its ionized state. The ionized molecule then binds to the sodium channel and blocks conduction.
f. *The addition of sodium bicarbonate will raise the pH of the solution and thus speed the onset of action.

______________
*De note s common in-se rvice e xamination topics
2. Infected and inflamed tissues have a low pH, which decreases the concentration of nonionized LA and reduces the
effect.
B. *Potency of an LA is determined by its lipid solubility
1. The aromatic ring determines the degree of lipid solubility.
2. As the lipid solubility increases, the ability of the LA to penetrate the plasma membrane increases.
C. Duration of action
1. LAs vary in their tendency to bind plasma proteins
a. When in circulation, LAs bind to α-1-acid glycoprotein.
b. LAs with higher affinity for protein binding remain bound to nerve membranes longer, increasing their duration of
action.
c. Binding to plasma proteins decreases the concentration of free drug in circulation, reducing the potential for toxicity.
d. As pH decreases, the affinity for plasma proteins is decreased. Thus, in conditions of acidosis or decreased serum
protein, there is a greater potential for toxicity.
2. Intrinsic vasodilatory effect reduces the duration of anesthesia
a. All LAs cause vasodilation, except cocaine, which causes vasoconstriction.
b. Vasodilation enhances removal of LA, thus shortening the duration.
c. *Epinephrine counters the vasodilatory effects of LAs and prolongs their duration of action

IV. CLASSES OF LOCAL ANESTHETICS (TABLES 10-3 AND 10-4)


A. Amino-esters
1. *Metabolized by circulating pseudocholinesterase, which causes shorter half-lives, except cocaine, which is
metabolized by the liver.
2. *Potential for allergic reaction. Breakdown product created by the action of serum pseudocholinesterases
on the amino ester includes para-aminobenzoic acid (PABA), which is very antigenic.
a. Majority of reactions are instead caused by anxiety, vasovagal responses, or accidental intravascular injection.
b. Less than 1% of reactions are true allergies.
3. Examples
a. *Cocaine: Vasoconstrictor; topical use only; useful intranasally for concurrent anesthesia and hemostasis.
b. Chloroprocaine: Rapidly metabolized; favored by obstetricians due to low fetal exposure.
c. Procaine (Novocaine): Rapid onset and short duration; not effective topically
d. Tetracaine (Pontocaine): Effective topically
B. Amino-amides
*Note: Amide LAs contain an “i” before the “-aine” in their names.
1. Metabolized in the liver. Half-lives are thus longer (2 to 3 hours).
2. True allergy is very rare.
a. Methylparaben is an antibacterial preservative sometimes used in LA cartridges that is metabolized to PABA.
b. There is no cross-reactivity between the amide and ester agents.
c. No longer contraindicated in patients with a family history of malignant hyperthermia.
3. Examples
a. Lidocaine (Xylocaine): Rapid onset; moderate duration; highly stable; non-irritating
b. Mepivacaine: Longer duration and more rapid onset than lidocaine.
c. Bupivacaine (Marcaine, Sensorcaine): Slow onset, long duration; high potency and toxicity; mixed with lidocaine for
rapid onset and long duration block. Preferentially blocks sensory versus motor fibers.
d. Ropivacaine (Naropin): Similar to bupivacaine, but less potent and less cardiotoxic.
e. Etidocaine (Duranest): Used for regional blocks; preference for motor over sensory fibers.
f. Prilocaine (Citanest): 40% less toxic acutely but its metabolite, o-toluidine, can cause methemoglobinemia

V. VASOCONSTRICTORS
A. Combined with LAs to provide local hemostasis and prolong anesthesia by delaying absorption. In doing so, they decrease
the potential for systemic toxicity and increase the safety margin.
B. Epinephrine is the most commonly used vasoconstrictor
C. Disadvantages with the use of epinephrine include the potential for tissue ischemia, tachycardia, hypertension, and
arrhythmias
D. Contraindications
1. Small volumes of LA with dilute epinephrine concentrations (≤1:200,000) may be safe for digital blocks. However, use is
contraindicated when digital perfusion is already compromised (e.g., diabetes, vascular disease, Raynaud’s disease,
trauma, infection).
2. Do not use on any skin flap with limited perfusion (e.g., delayed flaps).
3. Do not use in the penis.
4. Use caution when giving larger doses in patients with known cardiac disease, hypertension, diabetes, and thyrotoxicosis
and in patients taking β-blockers and/or monoamine oxidase inhibitor (MAO) inhibitors, as concomitant use has the
potential to cause a hypertensive crisis.

VI. DOSING AND CALCULATIONS (TABLE 10-4)


A. Epinephrine dosing
1. Expressed as a ratio of grams of solute in milliliters of solvent (e.g., a 1:100,000 concentration = 1 g epinephrine in
100,000 mL solution)
2. Typical epinephrine concentrations in anesthetic solutions = 1:400,000 (2.5 μg/mL), 1:200,000 (5 μg/mL), 1:100,000 (10
μg/mL), and 1:50,000 (20 μg/mL)
3. Plain epinephrine comes in either 1:1,000 (1 mg/mL) or 1:10,000 (0.1 mg/mL) concentration vials.
4. To prepare a 1:200,000 LA solution from plain epinephrine, 1:1,000 epinephrine must be diluted 200 times (a 1:10,000
solution must be diluted 20 times).
a. Example: Add 0.1 mL of 1:1,000 epinephrine to 20 mL of LA solution
b. Example: Add 2.5 mL of 1:10,000 epinephrine to 50 mL of LA solution
B. LA dosing
1. LAs come in various concentrations, for example:
a. Lidocaine: 1% (10 mg/mL), 2% (20 mg/mL), and 0.5% (5 mg/mL)
b. Bupivacaine: 0.5% (5 mg/mL) and 0.25% (2.5 mg/mL)
2. Maximum safety dose is increased by epinephrine.
3. Higher blood concentrations are associated with large volumes of dilute LA when compared to the same dose in a
smaller volume.
4. Mixing LAs
a. Mixtures of lidocaine and bupivacaine are commonly given to provide rapid, long-lasting effect.
b. The toxicity of a mixture of LAs does not exceed that of its individual components.
c. Allows smaller volumes of individual LAs to be used.
5. *Maximum volume allowed × patient weight (kg) × [LA]1 × maximum safety dose
a. Example: 2% lidocaine with epinephrine in a 80-kg man
i. 80 kg × 1 mL/20 mg × 7 mg/kg = 28 mL
b. Example: 0.5% bupivacaine with epinephrine in a 70-kg woman
i. 70 kg × 1 mL/5 mg × 3 mg/kg = 42 mL

VII. ADVERSE REACTIONS AND MANAGEMENT


A. Central nervous system (CNS) toxicity
1. Initial excitatory symptoms reflect escalating drug concentrations in CNS.
2. Increasing concentration begins to block inhibitory pathways in the amygdala, resulting in unopposed excitatory neuron
function. Symptoms: Muscular twitching, visual disturbance, tinnitus, light-headedness, tongue and lip numbness, anxiety,
feelings of impending doom, disorientation, shivering, and tremors
3. Increasing concentrations cause depression of medullary centers. Symptoms: Respiratory failure, hypotension,
bradycardia, arrhythmias, grand mal seizures, and coma.
B. Cardiovascular toxicity
1. The cardiovascular system is more resistant to the effects of LAs than the CNS.
2. LAs decrease myocardial excitation, the force of contraction, and the conduction rate.
3. Peripheral vasculature resistance is decreased secondary to arteriolar dilation.
4. Symptoms
a. Hypotension
b. Bradycardia
c. Arrhythmias
d. Ventricular fibrillation
e. Cardiovascular collapse
5. Cocaine differs from other LAs in that it blocks the reuptake of norepinephrine, resulting in vasoconstriction,
hypertension, and cardiac arrhythmias.
6. Bupivacaine and etidocaine have the greatest cardiac toxicity and can cause profound cardiovascular depression after
accidental intravascular injection.
a. Ropivacaine is similar to bupivacaine in onset and duration, but has a better safety profile in terms of cardiovascular
toxicity
C. Neuromuscular toxicity
1. LAs depress calcium activity, leading to decreased muscle excitability and contractility.
2. Reversible myotonic effects with direct injection into muscles.
D. Methemoglobinemia
1. Can be caused by prilocaine’s metabolite, o-toluidine
2. Manifests as shortness of breath, cyanosis, mental status changes, headache, fatigue, dizziness, and loss of
consciousness.
3. Arterial blood with elevated methemoglobin levels has a characteristic chocolate-brown color.
E. Allergic reaction
1. Most common adverse reaction
2. Often confused with patient anxiety, vasovagal responses, or accidental intravascular injection.
3. Signs and symptoms: Localized erythema, rash, pruritus, urticaria, edema, bronchospasm, and hypotension
F. Special considerations
1. Potential for toxicity is increased when amide anesthetics are used in patients with poor hepatic function or blood flow
(e.g., congestive heart failure, cirrhosis, hypothermia, general anesthetics, β-blockers).
2. Epinephrine can have deleterious effects in patients with cardiac disease, hypertension, and thyrotoxicosis and in patients
taking β-blockers and/or MAO inhibitors.
3. The toxicity of ester anesthetics is increased in patients with pseudocholinesterase deficiency.
G. Management
1. CNS toxicity
a. Stop injection
b. Ensure airway patency
c. Administer supplemental O2
d. Ensure adequate ventilation (hyperventilation may help by increasing the pH in the presence of metabolic acidosis
and hence decrease toxicity).
e. Confirm or establish IV access
f. Seizure control: Administer diazepam 0.1 mg/kg IV, thiopental 2 mg/kg IV, propofol 1 mg/kg IV, or succinylcholine
0.1 to 0.2 mg/kg IVP followed by intubation.
g. Assess cardiovascular status throughout.
2. Cardiovascular collapse
a. IV fluids for hypotension
b. Atropine for bradycardia
c. Manage arrhythmias according to ACLS protocols, except that additional lidocaine should not be administered.
d. Alert the nearest facility having cardiopulmonary bypass capabilities.
e. Consider treatment with lipid emulsion.
i. Bolus 1.5 mL/kg intravenously over 1 minute
ii. Continuous infusion 0.25 mL/kg/min
3. Methemoglobinemia
a. Administer 100% supplemental oxygen
b. Methylene blue 1% solution 1 to 2 mg/kg IV, administered slowly over 5 minutes.
4. Treat epinephrine-induced digital ischemia with phentolamine
5. Allergic reactions
a. Mild reactions
i. Treat with Benadryl 25 to 50 mg IV/PO in adults, 1 mg/kg IV/PO for pediatrics
b. Anaphylaxis
i. Airway management, IV fluids, supplemental oxygen
ii. Treat with 0.3 mL of epinephrine SC (1:1,000)
iii. Corticosteroids (125 mg methylprednisolone IVP or 60 mg prednisone PO)

NERVE BLOCKS
I. TEN WAYS TO DECREASE PAIN ASSOCIATED WITH INJECTION
A. Reassurance and distraction
1. Explanation, encouragement, and reassurance help decrease patient anxiety and thus pain perception.
2. Applying pressure or pinching skin near the site of injection stimulates local sensory A-fibers to inhibit stimuli from C-
fibers conveying pain to the spinal cord, partially blocking the transmission of pain associated with injection.
3. Talk about other things with the patient while preparing supplies.
4. Do not show the needle/syringe to the patient.
5. No surprises - tell the patient that you will let them when you are going to do the injection.
6. Don’t try to minimize the effect with words like “little pinch”.
7. Don’t tell the patient about an upcoming injection before leaving the room to go get supplies.
B. Prior application of topical anesthetic (e.g., eutectic mixture of local anesthetics [EMLA]) decreases pain associated
with injection.
C. Buffer solution with sodium bicarbonate (e.g., mix nine parts of LA with one part of sodium bicarbonate).
D. Warm the anesthetic solution to body temperature.
E. Use small gauge needle (25G or smaller).
F. Inject slowly and steadily.
G. Use the smallest volume of solution as possible.
H. Injecting into the subcutaneous tissue is less painful than infiltrating directly into the dermis.
I. Infiltrate through wound edges or introduce needle into previously anesthetized tissue (e.g., during field block).
J. Block nerves directly. A good knowledge of peripheral nerve anatomy helps avoid large volumes of LA.

II. UPPER EXTREMITY BLOCKS


A. Axillary block
1. Anesthetize the brachial plexus for procedures involving the elbow, forearm, and hand.
2. The axillary nerve and musculocutaneous nerve (which contains fibers of the lateral antebrachial cutaneous nerve)
emerge from the plexus above the puncture site and may be incompletely anesthetized.
3. With the patient lying supine, the arm is abducted 90 degrees and positioned on a cushioned surface in a relaxed manner.
4. The course of the axillary artery of the medial upper arm can be palpated dorsal from the medial bicipital groove.
5. Palpate the axillary arterial pulse and follow it proximally until it disappears under the pectoralis major.
6. The puncture site is located slightly above the axillary artery, at the highest point in axilla and slightly beneath the
pectoralis major muscle.
7. After disinfection and infiltrating the puncture site with LA, the needle is inserted parallel to the axillary artery at a 30-
degree angle to the skin.
8. The needle is advanced with index finger over the pulse until either.
a. A distinctive “click” is heard, consistent with penetration into the plexus sheath.
b. Paresthesia is elicited in the median, ulnar, or radial nerve distribution.
c. Arterial blood is aspirated; inject half of the LA behind the artery by advancing the needle and the other half in front
of the artery.
d. An attached nerve stimulator indicates needle tip placement within the sheath.
B. Bier block
1. Useful for procedures involving the forearm and hand
2. Technique
a. Place a double tourniquet on the upper arm and a peripheral IV distally.
b. Elevate the arm and exsanguinate with an ACE wrap all the way from the fingers to the tourniquet.
c. Inflate the proximal tourniquet and then remove the ACE bandage.
d. Slowly inject LA through the peripheral IV.
e. After 20 minutes (or sooner for patient discomfort), inflate the distal tourniquet and deflate the proximal one.
3. Anesthesia lasts as long as the tourniquet is inflated (maximum of 2 hours).
4. *Watch for signs of systemic toxicity caused by faulty tourniquet.
5. If a procedure lasts under 20 minutes, tourniquet deflation should be done in stages to avoid LA toxicity via IV bolus of
anesthetic.
C. Wrist block
1. Median nerve block
a. *The median nerve lies between the palmaris longus (PL) and flexor carpi radialis (FCR) (Fig. 10-1).
b. The PL is identified easily when the patient’s thumb is opposed to the little finger as the wrist is slightly flexed.
c. The injection is performed by introducing the needle between the PL and the FCR 2 to 3 cm proximal to the proximal
crease of the wrist.
d. Inject after feeling penetration through the flexor retinaculum.
e. If there is no PL (in 15% of hands), inject on the ulnar side of the FCR.
f. Avoid direct injection into the nerve by asking the patient to report any paresthesias.
2. Ulnar nerve block
a. The ulnar nerve is located just radial to the flexor carpi ulnaris (FCU) at the wrist crease (Fig. 10-2).

Figure 10-1. Median nerve block.


Figure 10-2. Ulnar nerve block.

b. The FCU can be palpated over the ulnar side of the wrist when the wrist is slightly flexed.
c. The ulnar artery is located just radial to the ulnar nerve. Given its close proximity to the nerve, one should always
aspirate prior to injection.
d. Injection is performed by introducing the needle ulnar and dorsal to the FCU.
e. The dorsal cutaneous nerve is blocked by subcutaneous infiltration extending from the injection site to the mid-
dorsum of the wrist.
3. The radial nerve (sensory branch) block
a. The superficial radial nerve is divided into several branches at the level of the radial styloid (Fig. 10-3).
b. Local anesthesia is injected subcutaneously from the first to the third extensor compartment at the level of the radial
styloid.
D. Digital block
1. Anatomy
a. The common digital nerves branch at the distal palmar crease and lie volar to the flexor tendons.
b. The digital arteries and nerves change orientation when entering the digits, with the nerve coming to lie volar to the
artery in the digits.
c. The radial digital nerve to the thumb crosses the A1 pulley.
2. Dorsal sensory branches should also be anesthetized
3. Dorsal approach (Fig. 10-4)
a. Subcutaneous wheal over the extensor tendon to block the dorsal nerves.
b. Two injections are made at the level of the distal palmar crease, one on either side of the digit—advance the needle
until the tip approaches the palmar skin surface and then withdraw while injecting slowly.
4. Volar approach (Fig. 10-5):
a. The needle is inserted vertically down to the flexor tendon. A subcutaneous wheal is placed directly over the flexor
tendon and then laterally near the digital neurovascular bundles.
Figure 10-3. Radial sensory nerve block.

Figure 10-4. Digital block—Dorsal approach.


Figure 10-5. Digital block—Volar approach.

Figure 10-6. Digital block—Sheath approach.


5. Sheath approach (Fig. 10-6)
a. At the level of the palmar digital crease, the flexor sheath is easily palpable.
i. Insert the needle vertically through the flexor tendon, down to the bone.
ii. With slight pressure on the syringe plunger, withdraw the needle slowly until there is a loss of resistance,
indicating injection into the potential space of the flexor sheath.
iii. Inject a few milliliters of LA.
iv. A fluid wave can be sometimes felt distally over the sheath.
b. This technique reliably results in digital anesthesia with one injection, but is not very effective in cases of sheath
violation, such as distal amputation.

III. FACIAL BLOCKS (FIG. 10-7)


A. Supraorbital nerve
1. The supraorbital nerve exits the supraorbital foramen at the superior orbital rim at the mid-pupillary line (approximately
2.5 cm from midline).
2. Palpate the supraorbital notch just under the mid-portion of the eyebrow and inject 2 to 3 mL; avoid injection into the
foramen.
B. Supratrochlear nerve
1. The supratrochlear nerve lies along the upper medial corner of the orbit approximately 1 cm lateral to midline and 1.5 cm
medial to supraorbital notch.
2. Inject just lateral to the root of the nose in the medial portion of the orbital rim.
3. Both the supraorbital and supratrochlear nerves can be blocked by horizontal infiltration 2 cm above the eyebrow.
C. Infraorbital nerve
1. The infraorbital nerve innervates the ipsilateral lower eyelid, nasal sidewall and ala, upper lip, and medial cheek.
2. An upper buccal sulcus or external approach may be used.
3. The infraorbital foramen is just medial to the mid-pupillary line approximately 0.7 to 1 cm below the infraorbital rim.

Figure 10-7. Supraorbital, infraorbital, and mental nerve block. (From Fischer JE, ed. Mastery of Surgery. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2012.)

4. For the intraoral approach, advanced the needle through the upper buccal sulcus in between the canine and first
premolar for about 1 cm, at which point 1 to 2 mL of anesthetic is injected just over periosteum.
D. Mental nerve
1. Innervates the lower lip and chin.
2. May be approached transorally or transcutaneously.
3. The mental foramen is located approximately 2.5 cm lateral to the midline just medial to the mid-pupillary line and
midway along the height of the mandible.
4. For the intraoral approach, advance the needle at the lower buccal sulcus between the first and second premolar, aiming
at the apex of the second premolar root.
E. Nasal anesthesia
1. External sensation is supplied by the infratrochlear (V1 ), external nasal (V1 ), and infraorbital (V2 ) nerves. Technique:
a. LA is injected along a line that starts from the nasolabial fold, continues lateral to the ala and along the base of nasal
sidewall, and ends at the radix.
b. Inject cranially and caudally for a regional block.
2. Internal sensation is supplied by the inferior posterior nasal nerve, superior posterior nasal nerves, nasopalatine nerve,
and branches of the ethmoidal nerves. Technique:
a. Either cotton pledgets dipped in 4% cocaine are placed directly on the nasal mucosa or LA is infiltrated directly
between the mucosa and perichondrium. Oxymetazoline nasal spray (Afrin) may also be used as a vasoconstrictor to
improve hemostasis during intranasal procedures.
F. External ear anesthesia
1. External ear is supplied by
a. Auricular branch of the vagus nerve (Arnold’s nerve)
b. Auriculotemporal nerve
c. Lesser occipital nerve
d. Great auricular nerve
2. Technique
a. Perform a field block via two injection sites cranially and caudally.
b. Inject anteriorly and posteriorly around the ear either in a ring-like fashion or in a diamond-shaped pattern.
c. May be difficult to obtain adequate anesthesia for the auditory canal and tympanic membrane.

IV. INTERCOSTAL BLOCK (FIG. 10-8)


A. Provides anesthesia for chest and upper abdominal procedures.
B. The second through seventh intercostal nerves are anesthetized.
C. Anatomy
1. The neurovascular bundle lies in the subcostal groove
2. At the mid-axillary line, the rib is relatively superficial and easy to palpate
3. *The intercostal vein is most superior (mnemonic: VAN = vein/artery/nerve)
D. The patient is placed supine with the arms abducted.
E. After negative aspiration of blood, injection of 3 to 5 mL of the LA is performed inferior to each rib in the mid-
axillary line.
Figure 10-8. Intercostal nerve block. T he star indicates site of injection. (From Mulholland MW, ed. Greenfield’s Surgery . 5th ed. Philadelphia, PA: Lippincott
Williams & Wilkins, 2011.)

F. Additional subcutaneous infiltration is occasionally necessary


1. Superomedially, for superficial cervical plexus.
2. Midline, due to crossing innervation of the intercostals.
G. Complications include intravascular injection and pneumothorax.

TOPICAL ANESTHESIA
I. COCAINE
A. Used for topical anesthesia and vasoconstriction for surgery of the nose, throat, and oral cavity.
B. Absorbed rapidly through mucous membranes.
C. Topical solution strengths include 4% and 10%.
D. Concentrations greater than 4% are generally not recommended due to difficulty in controlling dosage and increased risk
of toxicity.
E. The safe maximum dosage is reported to be 2 to 3 mg/kg.
1. Depends on the rate of absorption.
2. Spraying cocaine on surgical site leads to a more rapid absorption than application by pledgets.
3. Approximately one-third of the cocaine solution on pledgets is absorbed via the nasal mucosa.
F. Technique
1. Soak cotton pledgets in 4% cocaine solution. After being wrung out, use bayonet forceps to place pledgets in the nasal
cavity, flush with the mucosa.
2. Apply three pledgets per side.
3. Wait 10 to 15 minutes before removal.
II. EMLA (EUTECTIC MIXTURE OF LOCAL ANESTHETICS):
A. Indicated for use on normal intact skin or genital mucosa for superficial minor procedures.
B. Useful in children to minimize discomfort prior to injections or starting an IV
C. Consists of a eutectic mixture of 2.5% lidocaine and 2.5% prilocaine formulated as an oil-in-water emulsion.
D. Duration and depth of pain blockade are both a direct function of the application time.
1. Acceptable dermal analgesia is achieved 1 hour after application. Anesthesia reaches a maximum at 2 to 3 hours and
persists for 1 to 2 hours after removal.
2. Absorption is improved when applied under an occlusive dressing.
E. No local or systemic toxicity, but methemoglobinemia is a potentially life-threatening adverse effect in infants.

III. LMX4
A. Used to relieve pain caused by minor cuts, minor burns, sunburn, or insect bites, or prior to venipuncture.
B. Consists of 4% lidocaine delivered in liposomal vehicles, which enhances dermal penetration.
C. Similar to EMLA but faster onset and longer duration.

IV. VISCOUS LIDOCAINE


A. Used on mucosal surfaces to treat aphthous or radiation-induced ulcers or applied prior to performing an intraoral block.
B. Comes in 2 % solution. Used alone or in a compounded mixture as a mouthwash.
C. Anesthesia is achieved within 5 minutes. Duration of anesthesia is approximately 20 to 30 minutes.

V. LET
A. Useful for laceration repair; absorbs through the open surface of a wound.
B. Consists of Lidocaine 4%, 0.1% Epinephrine, and 0.5% Tetracaine in liquid solution.
C. Replaces tetracaine-adrenaline-cocaine (TAC).
D. Apply 1 to 3 mL to laceration with cotton swab. Apply remainder of dose to gauze and secure for 20 to 30 minutes.

VI. IONTOPHORESIS
A. Method of delivering a topical anesthetic using a low-voltage current to drive the transdermal delivery of lidocaine.
B. Lidocaine-soaked sponges are applied to intact skin, and electrodes are placed on top.
C. A low-voltage DC current is then applied to the skin.
D. Anesthetic effect occurs within 10 minutes and lasts approximately 15 minutes
E. The depth of anesthesia can reach up to 1 to 2 cm.
F. Disadvantages: Limited to small surface area, superficial burns are possible, and the equipment is comparatively complex.

PEARLS
1. Always verify anesthetic doses when solutions are prepared by others.
2. Wait 7 minutes after injection to allow epinephrine to take its hemostatic effect.
3. Perform injections with patients supine to avoid vasovagal response.
4. Premedicate children with ELA-Max or EMLA covered by occlusive dressing prior to injection or venipuncture.

QUESTIONS YOU WILL BE ASKED


1. How is epinephrine-induced digital ischemia treated?
Phentolamine
2. What are the key maneuvers that can be performed to minimize patient discomfort while administering LAs?
See Section I under nerve blocks. Maneuvers to minimize patient discomfort include reassurance and distraction, topical
anesthesia prior to injection, buffer solution, warm solution, small gauge needle, slow injection, small volume, inject into
subcutaneous tissues, inject in previous anesthetized tissues, and direct nerve blocks
3. What is the maximum dose of a mixture of 1% plain lidocaine and 0.5% bupivacaine that can be given to a 70-kg male? A 15-kg
child?
Maximum doses
a. 70-kg male: 35 mL of 1% lidocaine, 35 mL of 0.5% bupivacaine
b. 15-kg child: 7.5 mL of 1% lidocaine, 7.5 mL of 0.5% bupivacaine
4. Name examples of amino-ester and amino-amide LAs, and what is the most clinically relevant difference between the two
classes?
The major clinical difference between amino-amides and amino-esters is the potential for allergic reaction
a. Amino-amides examples: Lidocaine, mepicacaine, bupivacaine, ropivacaine, etido-caine, prilocaine
b. Amino-esters examples: Cocaine, chloroprocaine, procaine, tetracaine
5. What influences the duration of action of LAs? The potency? The time of onset?
The duration of action of an LA increases as its affinity for binding proteins increased. A higher pH increases binding protein
affinity and a lower pH decreases affinity. Potency of an LA increases with increased lipid solubility. The p Ka determines the
rate of onset. The lower the pKa, the higher the concentration of nonionized LA at a given pH, and therefore, the faster the
onset.

Recommended Readings
Chowdry S, Seidenstricker L, Cooney DS, Hazani R, Wilhelmi BJ. Plast Reconstr Surg. 2010; 126(6):2031–2034. PMID: 20697319.
Molony D. Adrenaline-induced digital ischaemia reversed with phentolamine. ANZ J Surg. 2006;76(12):1125–1126. PMID: 17199703.
Zide BM, Swift R. How to block and tackle the face. Plast Reconstr Surg. 1998;101(3):840–851. PMID: 9500408.
I. OVERVIEW
A. Laser is an acronym for light amplification by stimulated emission of
B. All lasers have four essential parts
1. A medium (gas, liquid, or solid) that can be excited by stimulated emission.
2. Power supply or a source of energy to excite the medium
3. Mirrors for amplification
4. Delivery system to deliver light to target
C. Laser light has three unique properties
1. Monochromaticity: Emission of single wavelength or narrow band of wavelengths
2. Coherence: Light waves are in phase temporally and spatially.
3. Collimation: Light waves travel in parallel without spreading even over long distances.
D. Lasers can be delivered in three modes
1. Continuous mode: A constant, uninterrupted beam. (Example: Argon lasers)
2. Pulsed mode: Single or train of pulses
3. Q-switched mode: Very short pulses at high peak power.
E. There are four outcomes when laser light hits the skin
1. Reflection: No biological effect
2. Scattering: Incoming beam is spread in all directions.
3. Transmission: Light passes through tissue unaltered.
4. Absorption: Light hits appropriate target (chromophore). Light is transformed into heat by interaction with tissue.
F. Theory of selective photothermolysis.
1. Energy of a specific wavelength is absorbed by a chromophore in tissue. Major chromophores in the skin are melanin,
hemoglobin, and water.
2. The time of laser exposure (pulse duration) is just shorter than the cooling time (thermal relaxation time) of the
chromophore.
a. Thermal relaxation time is the time required for the heated tissue to lose half of its heat.
b. If a pulse duration is longer than the thermal relaxation time, heat is not confined to target structure and can
damage the surrounding tissues.
G. Key parameters
1. Wavelength
a. Fixed and depends on the specific laser selected.
b. Lasers are selected based on the indication and target chromophore (e.g., pigment, water, melanin, hemoglobin).
i. Chromophores absorb the light, and heat is produced in order to create the clinical effect.
a) If no heat is produced, no clinical effect.
b) If excess heat is produced, scarring can result from thermal injury.
ii. Example: Darker skin has a greater amount of melanin and greater chromophore concentration. Therefore, it is
more likely to generate heat and thermal damage with laser therapy compared with lighter skin tones.

______________
*De note s common in-se rvice e xamination topics

2. Fluence
a. The amount of energy produced by the laser (J/cm2 ).
b. Selected by the practitioner
3. Pulse duration
a. How long the tissue is exposed to the laser.
b. Should be equal to or less than the thermal relaxation time.

II. LASER APPLICATIONS (TABLE 11-1)


A. The three main chromophores of the skin are water, hemoglobin, and melanin, and laser therapy is directed toward
these targets (Fig. 11-1).
B. Skin resurfacing
1. Can improve fine-to-medium wrinkles in patients with Fitzpatrick I or II skin (e.g., perioral rhytids) due to skin
contraction from collagen contraction and increased deposition and reorganization of collagen and elastin.
a. Results in thermal injury to the skin with wound healing.
b. Reepithelialization occurs through proliferation of progenitor cells within hair follicles and sweat glands.
c. Increased dermal collagen synthesis for 3 to 6 months.
d. Reorganization of elastic fibers into a parallel and tight configuration.
2. Contraindications
a. Relative: Smoking, previous resurfacing, diabetes, prior skin irradiation, active acne, hypertrophic scarring, skin
hypersensitivity, vitligo, and pigmentation disorders.
Figure 11-1. Wavelength depth of commonly used lasers. (Adapted from DiBernardo BE, Cacciarelli A. Cutaneous lasers. Clin Plast Surg. 2005;32:141–150.)

b. Absolute: Keloids, scleroderma, systemic lupus erythematosus, and isotretinoin use within the previous year.
3. Prophylaxis: *Valacyclovir or other similar antivirals for HSV prophylaxis for all patients.
4. CO2 laser: Ablative
a. Wavelength: 10,600 nm
b. Medium: Gas
c. Chromophore: Water
d. Pulsed or continuous wave modes
e. Water absorbs energy, converting light to heat which vaporizes or ablates tissue
f. Ablation threshold—the necessary amount of energy that achieves tissue vaporization. Ablation threshold for CO 2
laser is 5 J/cm2 .
g. Side effects
i. Long healing times
ii. Long period of erythema (weeks to months)
iii. Temporary hyperpigmentation
iv. Possible yeast, bacterial, viral infections
v. Contact dermatitis
vi. Risk of permanent hypopigmentation (infrequent)
vii. Risk of scarring (infrequent)
h. Indications: Photoaged skin, rhytids, acne scars, skin laxity, hypertrophic burn scars, some linear epidermal nevi,
sebaceous hyperplasia, and seborrheic keratoses.
i. Relative contraindications: Vitiligo, scleroderma, darker skin, unrealistic expectations.
j. Best candidate: Fitzpatrick type I or II skin.
k. Effects are similar to a controlled partial-thickness burn.
l. Fractional setting decreases amount of thermal injury but still stimulates tissue regeneration.
5. Erbium:yttrium–aluminum–garnet (Er:YAG)
a. Compared with the CO2 laser, more passes are required for the same depth of penetration, but with less thermal
damage.
b. *Wavelength: 2,940 nm
c. Medium: Solid
d. Chromophore: Water
e. Ablation threshold for Er:YAG laser is 1.6 J/cm2 .
f. Side effects
i. Long healing times
ii. Long period of erythema (weeks to months)
iii. Temporary hyperpigmentation
iv. Possible yeast, bacterial, viral infections
v. Contact dermatitis
vi. Risk of permanent hypopigmentation (infrequent)
vii. Risk of scarring (infrequent)
g. Indications: Rhytids, photodamage, acne scars, skin laxity
h. Best candidate: Fitzpatrick type I or II skin
C. Vascular lesions
1. Most commonly indicated for capillary malformations.
2. Selective photothermolysis targets hemoglobin and oxyhemoglobin molecules in order to shrink or eliminate blood
vessels.
3. Argon laser
a. Wavelength: 418 and 514 nm
b. Medium: Gas
c. Chromophores: Oxyhemoglobin and melanin
d. Painful for patient
e. Very popular choice in the 1980s for treatment of capillary malformations but now rarely used due to side effects
f. Side effects
i. Weeping, crusting, blistering after treatment
ii. Textural changes
iii. Hypertrophic scarring
iv. Pigmentary changes
4. KTP (potassium–titanyl–phosphate) laser
a. This laser is a long-pulsed, frequency-doubled Nd:YAG laser
b. Wavelength: 532 nm
c. Medium: Solid
d. Chromophore: Hemoglobin and melanin
e. For thicker pigmented lesions and vascular lesions. May have a role in resistant port-wine stains.
f. Similar response rates as pulsed dye laser (PDL) for some indications but main advantage over PDL is that purpura
rarely occurs—but scarring has been reported
g. Consider for resistant port-wine stain and large venous malformation
5. Flashlamp Pulsed Dye Laser
a. *Wavelength: 585 or 595 nm
b. Medium: Liquid (dye)
c. Chromophore: Oxyhemoglobin
d. Used to treat capillary vascular malformations, hemangiomas, telangiectases in rosacea, port-wine stains.
e. Side effects: Erythema/purpura for 7 to 14 days, hyperpigmentation, hypopigmentation.
f. Usually requires several treatments for lightening of vascular lesions.
g. Best results for port-wine stains depends on location and size.
i. Port-wine stains on the face and neck respond better than those on the leg and hand.
ii. On the face, port-wine stains on forehead and lateral face respond better than those on the middle of face.
iii. Chest, upper arm, and shoulder respond well
iv. Port-wine stain less than 20 cm2 at initial examination cleared more than those larger than 20 cm2 .
D. Pigmented skin lesions
1. Common pigmented skin lesions amenable to laser treatment: lentigines, ephelides, café au lait macules, thin seborrheic
keratoses, nevus of Ota, nevus of Ito, blue nevi.
2. May require multiple treatments, especially for lesions such as café au lait macules, nevus of Ota, nevus of Ito.
3. Treatment of melanocytic nevi is controversial and should be undertaken carefully because of concern for undiagnosed
dysplasia and melanoma being inadvertently treated and slowing diagnosis. As a result, diagnosis should be ascertained
prior to treatment.
4. Chromophore: Melanin
5. Although continuous wave lasers have been used in the past such as copper vapor or copper bromide, Q-switched lasers
are now the treatment of choice for pigmented lesions.
a. Q-switched ruby laser: 694 nm
b. Q-switched alexandrite: 755 nm
c. Q-switched Nd:YAG: 1,064 nm; use for patients with darker skin because of decreased risk of dyspigmentation
6. Complications: Pigmentary changes (hypopigmentation or hyperpigmentation), partial removal, infection, bleeding,
textural changes, scarring (< 5%)
E. Tattoo removal
1. Lasers in Q-switched mode are used for tattoo removal.
2. Chromophore: Tattoo pigment
3. Three types of lasers are currently used for tattoo removal.
a. Q-switched ruby: 694 nm
i. Useful for black, blue, and green pigments
ii. Can remove all colors except red and orange
b. Q-switched alexandrite: 755 nm
i. Useful for black, blue, and green pigment
ii. Can remove all colors except red and orange
c. *Q-switched Nd:YAG: 532 nm
i. Useful for red pigment
d. *Q-switched Nd:YAG: 1,064 nm
i. Useful for black and blue pigments
4. Absorption peak of pigment must match wavelength of laser, which heats the tattoo particles leading to fragmentation.
Phagocytes remove fragments.
5. Multiple treatments are necessary with treatments separated by 5 to 10 weeks. Complete clearance may not be
achieved.
6. Tattoos absorb in the following ranges
a. Red tattoos—505 to 560 nm
b. Green tattoos—630 to 730 nm
c. Blue green tattoos—400 to 450 nm and 505 to 560 nm
d. Yellow tattoos—410 to 510 nm
e. Purple tattoos—550 to 640 nm
f. Blue tattoos—620 to 730 nm
g. Orange tattoos—500 to 525 nm
h. Black and gray tattoos—600 to 800 nm
7. Practice care with cosmetic tattoos (e.g., tattooed lip liner) because oxidation of certain tattoo pigments (such as ferric
oxide and titanium oxide) with laser therapy may lead to darkening instead of lightening.
8. Complications: Pigmentary changes (hypopigmentation or hyperpigmentation), partial removal, infection, bleeding,
textural changes, tattoo ink darkening, scarring (< 5%)
F. Hair removal
1. Numerous lasers targeting unwanted hair include diode laser (800 to 810 nm), normal mode ruby (694 nm), alexandrite
(755 nm), and normal Nd:YAG (1,320 nm).
2. *Chromophore: Melanin
3. Using lasers with longer pulse duration achieves two goals.
a. Epidermal melanosomes are not affected.
b. The light-absorbing melanized bulb and shaft diffuses heat to surrounding follicle.
4. Lasers with higher fluences have better results for hair removal but higher fluences lead to higher discomfort and
complication risks.
5. Requires multiple treatments.
6. All lasers lead to hair reduction, not permanent hair removal.
7. Ideal patients have dark hair and fair skin. The treatment of light or white hairs remains a challenge.
G. Fractional photothermolysis
1. Only a portion of the epidermis and dermis is treated with columns of energy in order to create targeted areas of thermal
damage (microthermal treatment zones [MTZs]).
2. The untreated areas are a reservoir of collagen and promote tissue regrowth.
3. Allows for greater penetration with decreased risk of scarring.
4. Pattern density
a. Number of MTZs within the treatment area.
b. Greater number of MTZs yields a greater surface of the skin treated at each pass.
5. Energy
a. Depth of MTZ penetration into the dermis.
6. Nonablative fractional devices
a. Erbium-doped laser (1,550 nm)
b. Skin resurfacing, acne, striae, scarring, melisma, burn scars
c. Can be performed under topical anesthetic
d. Mild erythema and swelling for 2 days is most common. Can also result in facial edema, dry skin, flaking, superficial
scratches, pruritus, pigmentary changes, and an acneiform eruption.
e. Risk of herpes simplex virus and varicella zoster virus reactivation.
7. Ablative fractional devices
a. Ablative CO2 or erbium lasers
b. Fine rhytids, dyspigmentation, skin laxity
c. Can be performed under topical anesthetic with nerve block.
d. May result in prolonged erythema, hypopigmentation, and scarring, although the risks are less compared with fully
ablative therapy.

III. LASER SAFETY


A. Signs
1. Signs on room door should have information about laser, its wavelength, and energy.
2. A pair of appropriate eyewear placed on the door outside the room.
B. Eye protection
1. CO2 and Er:YAG lasers can injure cornea.
2. PDL and ruby lasers can injure retina.
3. Special glasses that match the emission spectrum of a laser must be worn by laser operator and other personnel in the
room.
4. Manufacturer of protective eyewear has the wavelengths of light for which protection is provided printed on goggles.
5. Patient can wear
a. Metal corneal eye shields if laser will be used around orbits.
b. Burnished stainless steel eye cups.
C. Fire risk
1. Prep solution should be nonflammable (avoid chlorhexidine or alcohol).
2. Surround the area to be treated with wet towels.
D. Laser plume
1. Ablative lasers create a plume.
2. Laser plume may contain bacteria and HPV.
3. Laser operator and personnel should wear surgical masks.
4. Use a smoke evacuator close to the site of procedure.

PEARLS
1. Vascular lesions are most effectively treated using PDLs (585 to 595 nm)
2. Tattoos can be effectively treated with Q-switched lasers, and the appropriate wavelength depends on the color and depth of the
pigment
3. Fractional technologies are increasingly popular for skin rejuvenation and resurfacing, and only treat a portion of the skin
surface. These techniques can potentially minimize patient side effects and complications.

QUESTIONS YOU WILL BE ASKED


1. What are the common complications of laser therapy?
Hypopigmentation, hyperpigmentation, HSV flare, and scarring.
2. What medication(s) should all patients undergoing cutaneous laser resurfacing receive as prophylaxis?
Valacyclovir
3. Which skin types are at greatest risk for side effects or complications following laser therapy?
Fitzpatrick IV and above

Recommended Readings
Alster T S, Lupton JR. Prevention and treatment of side effects and complications of cutaneous laser resurfacing. Plast Reconstr Surg. 2002;109(1):308–316. PMID:
11786830.
Chim H, Drolet B, Duffy K, Koshima I, Gosain AK. Vascular anomalies and lymphedema. Plast Reconstr Surg. 2010;126(2):55e–69e. PMID: 20679788.
DiBernardo BE, Cacciarelli A. Cutaneous lasers. Clin Plast Surg. 2005;32:141–150. PMID: 15814112.
Nelson AA, Lask GP. Principles and practice of cutaneous laser and light therapy. Clin Plast Surg. 2011;38:427–436. PMID: 21824540.
Wu EC, Wong BJ. Lasers and optical technologies in facial plastic surgery. Arch Facial Plast Surg. 2008;10(6):381–390. PMID: 19018058.
I. VARIABLES
A. Categorical variables (discrete variable)
1. Nominal variable: Variable with two or more categories but no intrinsic order. State of residence (Michigan, New
York, etc.) is a nominal variable with 50 categories.
2. Dichotomous variable: A nominal variable with only two categories. Presence of diabetes (yes/no) and male/female
are dichotomous variables.
3. Ordinal variable: Variables with two or more categories that can also be ordered or ranked. However, the orders or
rank are not continuous variables (see below). Results from a Likert scale can be considered an ordinal variable
(strongly agree/agree/neither agree or disagree/disagree/strongly disagree).
B. Continuous variables (quantitative variable)
1. Ratio variable: A variable that can be measured along a continuum and has a numerical value. A value of zero
indicates that there is none of that variable. Examples include distance in centimeters or height in inches.
2. Interval variable: A variable that can be measured along a continuum and has a numerical value. A value of zero does
not indicate absence of the variable. An example is temperature in degrees Fahrenheit, where a measurement of zero
degrees does not indicate the absence of temperature.
C. For purposes of a study, there are two broad classes of variables
1. Independent variable (experimental variable or predictor variable): A variable that is observed or is being manipulated
in an experiment or study
2. Dependent variable: The outcome of interest. A variable that is dependent or may be dependent on the independent
variable(s).

II. WORDS TO KNOW


A. p Value: The likelihood that the observed association occurred due to chance alone. p < 0.05 is commonly considered
“statistically significant.” When p = 0.05, what this is actually saying is that there is a 5% chance that the reported results
occurred due to chance (or, that there is a 95% chance that the results are real)
B. α: The likelihood of a type I error
C. β: The chance of a type II error
D. Power: A study’s ability to detect a difference if one is present. A study’s power is calculated as 1-β
E. Null hypothesis: The null hypothesis typically refers to the default position, for example, that there is no association
between two variables or that a treatment has no effect
1. The null hypothesis is often paired with an alternative hypothesis, which states that there is an association between two
variables or that a treatment does have an effect
2. The null hypothesis can never be proven. The data to be analyzed will either reject or fail to reject the null hypothesis.
F. Type I error: The null hypothesis is rejected but the null hypothesis is actually true. The likelihood of a type I error is equal
to your α value.
G. Type II error: Failure to reject the null hypothesis when the null hypothesis is false. The likelihood of a type II error is
equal to your β value.
H. Standard deviation (SD) is a measure of the dispersion of values in a dataset from the mean. A low SD implies that
values are clustered close to the mean. A high SD implies that values have wide dispersion around the mean.
1. Or, to put it another way, the SD reflects how close an individual observation will be to the sample mean
2. For a normal distribution, 68% of values lie within one SD and 95.5% within two SDs of the mean
I. Standard error of the mean (SEM) reflects how close the means of repeated samples will come to the true population
mean for a given sample size. SEM is calculated by dividing the SD by the square root of sample size
J. Confidence interval: A range into which you are sure your data fall
1. Typically reported as a 95% confidence interval, for example, that you are 95% sure that the true value lies between the
lower and upper borders of your interval
2. 95% confidence interval is calculated by taking the mean ± 1.96 × SEM

III. EVALUATING A DIAGNOSTIC TEST (Table 12-1)


A. Sensitivity measures a test’s ability to identify patients WITH disease
1. A test with high sensitivity is unlikely to give a false negative result
2. Sensitivity = A/(A + C)
B. Specificity measures a test’s ability to identify patients WITHOUT disease
1. A test with high specificity is unlikely to give a false positive result
2. Specificity = D/(B + D)
C. Positive predictive value (PPV) identifies the proportion of patients with a positive test result who actually HAVE the
disorder. PPV helps determine how confident you are that your patient has the disorder. PPV = A/(A + B)
D. Negative predictive value (NPV) identifies the proportion of patients with a negative test result who do NOT have the
disorder. NPV = D/(C + D)

IV. SAMPLE SIZE CALCULATION


A. This question is commonly asked: “How many patients do I need to determine if this intervention or treatment is
effective?”
B. Prior to initiating the study, define the intervention and outcome of interest. Additionally, define your tolerance for type I
and type II errors, typically 0.05 and 0.20, respectively.
1. For continuous outcome variables, you need an estimate of both mean and SD in the control and intervention groups
2. For dichotomous outcome variables, you need an estimate of event rate in the control and intervention groups
3. Pilot data (yours or someone else’s) are helpful to provide realistic estimates

C. Five values are required for sample size calculation for a dichotomous outcome. With these values, you (or your
statistician) can calculate the number of patients required in groups 1 and 2.
1. α
2. Power
3. Expected event rate in group 1
4. Expected event rate in group 2
5. Ratio of patients in group 1 versus group 2 (typically 1:1)
D. Five values are required for sample size calculation for a continuous outcome. With these values, you (or your
statistician) can calculate the number of patients required in groups 1 and 2.
1. α
2. Power
3. Expected mean and SD of outcome variable for group 1
4. Expected mean and SD of outcome variable for group 2
5. Ratio of patients in group 1 versus group 2 (typically 1:1)

V. STATISTICAL ANALYSIS
A. Univariate analysis looks for associations between two variables. Typically, one variable is a predictor variable and the
second is an outcome variable.
1. t-test compares a variable’s mean value between two groups. Example: Mean BMI was significantly higher in patients
who had a postoperative infection (30.9) when compared to patients who had no postoperative infection (24.8)
2. ANOVA can be used to compare a variable’s mean value between >2 groups. The Tukey t-test is used with an
ANOVA to identify means that are significantly different from one another
3. Chi-squared test compares differences in proportions or observed rates between two groups. Example: The observed
rate of DVT was significantly less in patients who received enoxaparin (4%) when compared to patients who did not
receive enoxaparin (8%)
4. Fisher’s exact test is a variant of the chi-squared test that can be used when the total number of outcome events is
low (<10)
B. Multivariable analysis examines the effect of an independent variable on an outcome of interest while controlling the
effect of other variables
1. Logistic regression is performed dichotomous (yes/no) outcome variables. Example: When controlling for the effects
of age, BMI, and smoking, presence of diabetes was an independent predictor of postoperative wound dehiscence
2. Linear regression is performed for continuous outcome variables (e.g., systolic blood pressure). Example: When
controlling for the effect of diabetes, smoking, and activity level, increased age was an independent predictor of
increased systolic blood pressure
C. Nonparametric statistics are required when the distribution of your outcome variable is not normal, or the variable itself is
nonlinear
1. Example: Nonparametrics are required to examine Likert scale values, an ordinal variable. Likert scales are often
arbitrarily assigned point values (e.g., strongly disagree (1), disagree (2), neither agree nor disagree (3), agree (4), and
strongly agree (5)). However, these point values are not actually a continuous variable because they do not have units.
Thus, you cannot use a t-test or linear regression techniques for analysis.
2. Examples of nonparametric statistics include the Wilcoxon rank–sum test, the Kruskal–Wallis one-way analysis of
variance, and the Mann–Whitney U test
D. Parametric versus nonparametric statistics
1. Parametric statistics assume that the underlying distribution of the variables is normal
2. Nonparametric statistics make no assumption about distribution of the variables

VI. DESCRIPTION OF RESULTS


A. Incidence: The rate of an event in a distinct time period. Example: 230,000 new cases of breast cancer will be diagnosed in
2012
B. Prevalence: The number or proportion of individuals in a population who have a disorder at any time point. Example: 20%
of individuals over the age of 65 have medication-controlled diabetes
C. Relative risk: The risk of an adverse event relevant to exposure. Calculated as (disease rate in exposed patients)/(disease
rate in nonexposed patients).
D. Odds ratio: A description of strength of association between two variables, typically a predictor and outcome variable
1. Odds ratio is a measure of effect size and is commonly reported in logistic regression analysis. If the 95% CI for an
odds ratio crosses 1, there is no significantly independent association.
2. Odds ratio is often confused with relative risk but the two are very different
E. Risk versus odds
1. For rare events (<10% incidence), risk and odds are essentially identical. For more common events, this is not true.
2. Example: Consider a deck of 52 playing cards. The risk of pulling an ace is 4/52. The odds of pulling an ace are 4/48.
For rare events, OR and RR are very close. However, the risk of pulling a black card is 26/52. The odds of pulling a
black card are 26/26. For common events, OR and RR are not similar.
F. Absolute risk reduction (ARR): (Event rate in control group) − (event rate in intervention group). This is the real
measure of effect size
G. Relative risk reduction: ARR/(event rate in control group). Relative risk reduction can be misleading. For example, a
drug that decreases an event rate from 0.1% to 0.075% has a 25% relative risk reduction but an absolute risk reduction of
only 0.025%.
H. Number needed to treat: The number of patients that must be treated to prevent one adverse outcome. Calculated as the
inverse of ARR. NNT = 1/ARR
I. Number needed to harm: The number of patients who need to receive a treatment to have one adverse event
1. Calculate the absolute adverse event rate: (adverse event rate in the intervention group) − (adverse event rate in the
control group)
2. NNH = 1/(absolute adverse event rate)

VII. STATISTICAL SIGNIFICANCE VERSUS CLINICAL IMPORTANCE


A. Do not always focus on statistical significance. Remember, by definition, the p-value indicates the likelihood that the
observed association was due to chance alone. The p-value says nothing about the importance or relevance of a
relationship.
B. Statistical significance is a measure of confidence. Effect size is a measure of importance
C. Statistically significant differences can be clinically meaningless. Large database studies often show significant
differences among clinically irrelevant results (like a BMI of 29.8 in the control group and BMI of 30.0 in the intervention
group).
D. Nonstatistically significant differences can still have a large effect size. When differences are large but the
differences were not significant, this represents an underpowered study (e.g., sample size was too small, also known as a
type II error). These studies can be used as excellent pilot data for your own, larger study

PEARLS
1. Investigators who do not have a formal background in statistics should collaborate with a statistician in all phases of a research
project
2. For dichotomous outcome variables, sample size calculation requires an estimate of the event rate in the control and treatment
groups
3. For continuous outcome variables, sample size calculation requires an estimate of the mean and standard deviation for the
outcome variables in the control and treatment groups
4. Pilot data are incredibly helpful in sample size calculation
5. Statistical significance is not the same as clinical relevance

QUESTIONS YOU WILL BE ASKED


1. Describe the difference between sensitivity and specificity.
Sensitivity examines a test’s ability to find patients WITH disease. Specificity examines a test’s ability to find patients
WITHOUT disease.
2. What is a type 1 error and a type 2 error?
A type I error rejects the null hypothesis when the null hypothesis is actually true.
A type II error fails to reject the null hypothesis when the null hypothesis is false.
3. What is the difference between incidence and prevalence?
Incidence refers to a disease rate within a certain time period (e.g., rate of post-operative MI at 30 days). Prevalence refers to
the proportion of the overall population who has disease at a certain time point. Incidence looks at NEW disease. Prevalence
looks at ALL disease.

Recommended Reading
Januszyk M, Gurtner GC. Statistics in medicine. Plast Reconstr Surg. 2011;127(1):437–444. PMID: 21200241.
I. SKIN EMBRYOLOGY
A. Epidermis: Ectoderm
B. Dermis: Mesoderm
C. Other cells
1. Melanocytes: Neural crest
2. Merkel cells: Neural cells
3. Langerhans cells: Mesenchymal

II. SKIN HISTOLOGY


A. Epidermis
1. Keratinocytes
a. Primary cell in epidermis
b. Start in basal layer (stratum germinativum or basale) and make their way to surface becoming a dead cornified layer
(stratum corneum).
2. Melanocytes
a. Found in basal layer
b. Protect against ultraviolet (UV) radiation
3. Merkel cells: Mechanoreceptors
4. Langerhans cells: Antigen-presenting cells in stratum spinosum
B. Dermis
1. Cell types: Fibroblast, macrophage, and mast cell
2. Papillary dermis
a. Similar thickness to epidermis
b. High content of type III collagen, less type I
c. Site of collagenase activity.
d. Intertwines with the rete ridges of the epidermis.
e. Contains terminal networks of Meissner corpuscles and capillaries.
3. Reticular dermis
a. Majority of the dermal layer
b. Mostly type I collagen bundles with elastic fibers between
c. Contains roots of the hair, sebaceous glands, sweat glands, receptors, nails, and blood vessels.
4. Tissue components
a. Collagen
i. Tensile strength
ii. Type I to type III—4:1 ratio in adult skin
iii. Immature scar type I to type III—2:1 ratio in adult skin.
b. Elastin
i. Interdigitates with collagen
ii. Important in skin recoil and decreases with aging
iii. Composed of the protein fibrillin
c. Ground substance
i. Noncellular component of extracellular matrix with fibers
ii. Composed of glycosaminoglycans (hyaluronic acid and proteoglycans)
______________
*De note s common in-se rvice e xamination topics

III. SKIN MALIGNANCIES


A. Generally grouped into three types (listed from most common to least)
B. Basal cell carcinoma (BCC)
C. Squamous cell carcinoma (SCC)
D. Melanoma
1. The ratio of BCC to SCC to melanoma is ≈40:10:1
2. Incidence of all three types is increasing; fortunately, the more common types (BCC and SCC) are far less aggressive
than melanoma
3. More than 20% of the US population develops a skin cancer during their lifetime
4. Each year in the United States, there are more new cases of skin cancer than combined new cases of breast, prostate,
lung, and colon cancers

BASAL CELL CARCINOMA (BCC)


I. EPIDEMIOLOGY
A. Incidence
1. BCC is the most common skin cancer, accounting for ≈80% of all skin cancers.
2. Roughly 2.8 million new cases per year in the United States.
B. Risk factors
1. Sun exposure (increased with lower latitudes, high altitude): 36% of BCCs originate from the area of previously
diagnosed actinic keratosis (AKs), but have distinct cells of origin.
2. Advancing age
3. Fair complexion
4. Long-term exposure to psoralens and UVA therapy (i.e., PUVA therapy for psoriasis)
5. Immunosuppression, most commonly seen in transplant patients
6. Nevus sebaceus of Jadassohn, a superficial skin lesion typically in the head and neck regions, presents as an irregular,
raised, yellow to pink, non–hair-bearing raised mass. They are usually present at birth or develop in early childhood, and
approximately 15% undergo malignant transformation to BCC.
7. Arsenic exposure
8. Syndromes associated with BCC
a. Basal cell nevus syndrome (Gorlin’s syndrome)
i. Autosomal dominant inheritance
ii. Multiple nevi/lesions often seen early in childhood with malignant degeneration more likely by the age of puberty.
iii. Skin pits on palms and soles, jaw cysts (odontogenic keratocysts), rib abnormalities, mental retardation
b. Xeroderma pigmentosum (XP): Patients have increased incidence of BCC, SCC, and malignant melanoma (see
above in melanoma section)
c. Albinism

II. BCC DISEASE BIOLOGY AND CHARACTERISTICS


A. Basal keratinocytes are the cell of origin, residing in the basal layer of the epidermis at the dermoepidermal junction.
B. No universal clinical precursor lesion
C. BCC is most common in areas with high concentrations of pilosebaceous follicles and thus >90% are found on the head
and neck.
D. Metastasis is rare—termed “barely a cancer” by some researchers
E. Morbidity is caused by invasion of the tumor into underlying structures, including the sinuses, orbit, and brain. Typically,
only a problem if neglected for many years.
F. Types of BCC
1. Nodular BCC
a. The most common type, usually presenting as a single lesion consisting of pearly papules with telangiectasias,
pruritus, and occasional bleeding.
b. Lesion breakdown over time leads to nodulo-ulcerative BCC (“Rodent ulcer”).
c. Histology demonstrates palisading nuclei.
2. Superficial spreading BCC
a. Slow-growing, erythematous, with minimal induration, and located primarily on the trunk.
b. It is easily confused with other scaly, eczematous dermatoses.
c. The lesions are shallow with a characteristic horizontal growth pattern and often present in multiples.
3. Morpheaform (sclerosing, fibrosing) BCC
a. Flat, often yellowish or hypopigmented, sometimes resembling scars or normal skin.
b. The true extent of the lesion is usually greater than the clinical appearance.
c. There is a high incidence of recurrence or incomplete excision due to “finger-like” extensions.
d. Margins of 1 cm or Mohs extirpation is warranted.
4. Pigmented BCC: Similar to nodular BCC; easily confused with melanoma due to its deep pigmentation and nodularity
5. Adnexal BCC
a. Uncommon and found in older individuals.
b. Tumors arise from sweat glands, and although they exhibit slow growth, they are locally invasive, with a high
incidence of local recurrence.

III. TREATMENT OF BCC


A. Standard surgical techniques: ≈95% cure rate
1. Wide local excision of BCC: 3- to 5-mm margins for nonaggressive types and 7-mm margins for morpheaform type.
a. Frozen sections may be used to confirm negative margins intraoperatively. False negatives are common. Surgeon
must have confidence in pathologist/ laboratory to use this modality.
2. Mohs surgery: Sequential horizontal excision with immediate frozen section testing by dedicated Mohs
dermatopathologist
a. *Indications include morpheaform BCC and/or lesions in aesthetically sensitive areas (nose, eyelid, lip,
etc.)
b. Advantages are tissue preservation and confirmation of complete excision.
B. Field therapies
1. Curettage and electrodessication can be used for BCC <1 cm that is NOT a recurrent disease or morpheaform type, but
leads to a widened scar.
2. Cryotherapy is effective for small BCC over bone or cartilage, tip of nose, or around the eye.
3. Radiation is effective but requires multiple visits. High cure rates (≈90%), but recurrence is relatively common many
years (10 to 15) later.
C. Topical Pharmaceuticals
1. Imiquimod: Immune stimulant. FDA-approved only for superficial BCCs, with cure rates between 80% and 90%. The
5% cream is applied 5 times per week for 6 weeks or longer.
2. 5-Fluorouracil (5-FU): Chemotherapy. FDA-approved for superficial BCCs, with similar cure rates to imiquimod. Five
percent liquid or ointment is rubbed onto the tumor 2 times per day for 3 to 6 weeks.
D. Adjuvant radiation therapy (after surgery): Useful for advanced, deeply invasive BCC

SQUAMOUS CELL CARCINOMA


I. EPIDEMIOLOGY
A. Incidence
1. Second most common skin cancer after BCC.
2. Roughly 700,000 new cases annually in the United States.
B. Risk factors
1. UV radiation: Sun exposure and tanning booth use; PUVA therapy for psoriasis
2. Chemical exposure, including some pesticides, organic hydrocarbons such as coal tar, fuel oil, paraffin oil, and arsenic
(in welding materials)
3. Viral infection: Some types of human papillomavirus (HPV); herpes simplex virus
4. Radiation: Long latency between exposure and disease.
5. Marjolin’s ulcer: SCC arising in a chronic wound (i.e., chronic burn scars and pressure sores) secondary to genetic
changes caused by chronic inflammation.
6. Impaired immunity: That is, immunosuppression for transplants and AIDS. Ratio of SCC to BCC in these patients is
2:1.
7. Fitzpatrick skin type

II. SCC DISEASE BIOLOGY AND CHARACTERISTICS


A. Precursor lesions
1. Actinic keratoses (AKs, or solar keratoses)
a. Erythematous macules and papules with coarse, adherent scale
b. Histologically resembles SCC in situ (pre-malignant)
c. AK is considered a precursor lesion; up to 5% progress to SCC; in turn, 65% of all SCC arise from sites of AKs
2. Bowen’s disease (SCC in situ)
a. Exhibits full-thickness cytologic atypia of the keratinocytes
b. Erythroplasia of Queyrat is SCC in situ of the glans penis.
3. Leukoplakia
a. Presents as a white patch on oral or other mucosa.
b. Malignant transformation occurs in 15%.
4. Keratoacanthoma
a. Benign skin tumor that is composed of squamous cells and keratin; may clinically resemble SCC.
b. Etiology is unknown but thought to originate from hair follicles.
c. Typically has a rapid 6-week growth phase followed by involution over the next 6 months. However, can progress to
SCC in 5% to 10% of cases.
d. Excision is the treatment of choice; may be difficult to differentiate from SCC histologically.
B. Types of SCC
1. Verrucous SCC: Slow-growing, exophytic, and less likely to metastasize.
2. Ulcerative SCC: Grows rapidly and is locally invasive.
a. Ulcerative SCC has very aggressive growth characteristics, raised borders, and central ulceration.
b. <50% 5-year survival if spread to lymph nodes in the head and neck.
3. Majorlin’s ulcer
a. Arise from chronic wounds (burn, pressure ulcer, fistula, osteomyelitis tracks)
b. Commonly metastasize to lymph nodes.

III. SCC TREATMENT OPTIONS


A. Standard surgical techniques: 90% to 95% cure rates; similar to BCC options
1. Wide local excision of SCC: 5- to 10-mm margins are usually sufficient. Frozen sections may be used to confirm
negative margins intraoperatively.
a. If <2 cm, low grade and extends to dermis, 4-mm margin
b. If >2 cm, grade 2 to 4, high risk or extension into fat, 6-mm margin
2. Mohs surgery: Sequential horizontal excision with frozen section testing. Highest cure rate for SCC: 94% to 99%.
a. Indications, include recurrent, high-risk SCC, and/or lesions in aesthetically sensitive areas (nose, eyelid, lip, etc.)
b. Advantages are tissue preservation and confirmation of complete excision.
B. Field therapies
1. Curettage, electrodessication, and cryotherapy are used much less in SCC treatment than in BCC treatment,
because of higher risk associated with missed deep tumor portions, and the risk of scarring obscuring SCC recurrences.
2. Radiation is reserved for unresectable lesions or for the very elderly. Cure rates vary widely. Cosmetic damage and
long-term risk of radiation must be considered.
3. Pharmaceuticals are being investigated for topical application, but not currently recommended for invasive SCC.
C. Regional lymphadenectomy
1. Indicated for clinically positive (palpable) nodes.
2. FNA: Confirm spread of SCC to palpable lymph node.
3. ELND: Indicated for a tumor extending down to parotid capsule or a large lesion contiguous with a draining nodal basin.
4. SLN biopsy: Considered for high-risk SCC without palpable nodes (controversial).
D. Adjuvant radiation therapy: Used postexcision for high-risk cutaneous SCC.

MELANOMA
I. EPIDEMIOLOGY
A. Incidence is increasing, faster than any other cancer in Western world
1. 2% to 3% increase in incidence per year in the United States as of 2009.
2. 75,000 new cases predicted to be diagnosed in the United States in 2012.
3. Lifetime risk in general population is 2% for children born today.
4. Less than 3% of all skin cancers, but cause of 75% of skin cancer-related deaths.
5. Prognosis of metastatic disease has changed little in past 40 years (unlike many other cancers).
B. Risk factors
1. Phenotypic include fair skin (Fitzpatrick I and II) (Table 13-1), freckling, light eye color, and light hair color (stronger
risk factor than eye color). Darker skin is protective against melanoma.
2. Geographic: High altitudes, lower latitudes have increased UV exposure, and therefore increased risk.
3. Gender: Females have lower risk and better prognosis; however, gender-based differences in risk are lessenings (Table
13-2). Lower extremity is the most common site in females; males more commonly have lesions on the head and trunk.

4. Race: Incidence is lower, but prognosis is worse for African-Americans, due to delayed diagnosis and/or worse disease
subtype.
5. Affluence: Unlike most cancer types, higher socioeconomic status correlates with higher risk.
6. History of UV radiation exposure (both UVA and UVB): Evidence for direct causality is less clear than for other
skin cancer types. A history of blistering sunburns, particularly in early life, correlates to increased risk of some
melanoma types.
7. Previous melanoma is a strong predictive factor and confers a 3% to 5% chance of developing a second melanoma.
8. Family history: Vast majority of melanomas are sporadic; however, some hereditary forms exist (see also Genetics
section below).
a. Familial melanoma (aka hereditary melanoma): Two or more cases of melanoma in first-degree relatives may
indicate familial melanoma, autosomal dominant transference with variable penetrance.
b. Dysplastic nevus syndrome (also known as familial atypical multiple mole and melanoma [FAMMM] syndrome):
Patients have a first- or second-degree relative with malignant melanoma and typically have at least 50 melanocytic
nevi. Mutations in CDKN2A typical. Patients need vigilant screening.
c. Xeroderma pigmentosum (XP)
i. Heterogeneous group of syndromes; due mutations in various DNA repair genes.
ii. DNA damage by UV leads to early death secondary to metastatic spread of skin tumors.
iii. Typically presents in childhood with multiple BCCs; SCCs and melanomas typically cause death.
iv. Restriction from sunlight exposure is mandatory, with aggressive surveillance/treatment of skin lesions.

II. MELANOMA DISEASE BIOLOGY AND CHARACTERISTICS


A. Precursor lesions
1. Melanoma is caused by multiple processes leading to malignant transformation of melanocytes.
2. Congenital nevi
a. Malignant potential is more dependent on histology than on size.
b. Giant hairy nevi: Confer a 5% to 20% lifetime risk of melanoma (difficult to predict risk accurately due to variability
in size/location); prophylactic excision (often serially) is recommended
3. Acquired melanocytic nevi
a. Typically appear at 6 to 12 months of age; usually <5 mm
b. Increase in number through the fourth decade then slowly regress.
c. The greater the number of nevi, the greater the chance of melanoma.
4. Dysplastic or atypical nevi
a. Often appear in puberty
b. Larger than common nevi (5 to 12 mm)
c. Commonly found in covered areas
d. May represent a precursor lesion and/or marker for increased risk for melanoma development.
5. Melanoma in situ / atypical junctional melanocytic hyperplasia (AJMH) Also termed “lentigo maligna”;
Hutchinson freckle
a. Melanoma precursor lesion; no penetration of atypical cells beyond epidermal junction.
b. May arise within dysplastic nevi
c. Needs to be fully excised; 5-mm margins are recommended, but re-excision is often needed.
6. Spitz nevus
a. Benign lesion most commonly found in children and young adults (formerly called juvenile melanoma). NOT a
melanoma precursor lesion.
b. Presents as a well-circumscribed, raised lesion with variable pigmentation.
c. Despite the lack of malignant potential, it is very difficult to distinguish histopathologically from melanoma.
d. Recent data indicate that Spitz nevi have mutations in the HRAS gene, distinct from the BRAF/NRAS mutations
seen in melanoma.
B. Genetic mechanisms
1. p16/CDKN2A gene: Tumor suppressor gene that is mutated or deleted in the majority of melanoma cell lines; mutations
found in some familial melanomas.
2. CDK4 gene: Cell cycle regulator-like CDKN2A; plays a role in melanoma progression in a small proportion of familial
and sporadic melanomas.
3. MC1R gene: Pigmentation gene; certain isoforms correlate with fair skin/poor tanning ability as well as increased risk of
melanoma.
C. Classification of melanoma types
1. Superficial spreading melanoma
a. Most common type, ≈70% cases
b. Intermediate in malignant potency
c. Most likely to arise from a preexisting nevus
d. Affects both genders equally
e. Median age at diagnosis is 50 years
f. Upper back in men and lower legs in women are most common sites
g. Irregular, asymmetric borders with color variegation
h. Radial growth phase early, vertical growth phase late
2. Nodular melanoma
a. Second most common: 15% to 30% cases
b. Most aggressive type
c. Typically do not arise from preexisting nevi
d. Men are affected twice as frequently as women
e. Median age at diagnosis is 50 years
f. No clear association with sunlight exposure
g. Typically bluish-black, with uniform, smooth borders
h. 5% are amelanotic—associated with a poorer prognosis because of delayed diagnosis
i. Vertical growth phase is a hallmark feature; no radial growth
3. Lentigo maligna melanoma (LMM)
a. 10% to 15% of cutaneous melanomas
b. Least aggressive type
c. Most clearly associated with sunlight/UV exposure
d. Head, neck, and arms of elderly (sun-exposed areas) typically affected
e. Women are affected more frequently than men
f. The median age at diagnosis is 70 years
g. Usually greater than 3 cm in diameter; irregular, asymmetric with color variegation, areas of regression may appear
hypopigmented.
h. Precursor lesion is lentigo maligna or Hutchinson freckle (histologically equivalent to melanoma in situ, or
AJMH): radial growth phase only. Transition to vertical growth phase marks development of LMM.
i. Malignant degeneration is characterized by nodular development.
4. Acral lentiginous melanoma
a. 2% to 8% of melanomas in Caucasians, 35% to 60% of melanomas in African-Americans, Hispanics, and
Asians
b. Presents in palms, soles, and beneath nail plate (subungual). Must be distinguished from melanonychia, a
benign, linear, pigmented streak in the nail, common in African and Asian populations. Due to the risk of melanoma,
biopsy of suspect lesions should be performed.
c. Median age at diagnosis is ≈60 years
d. Irregular pigmentation, large size (>3 cm) common
e. Most common site is great toe or thumb
f. Long radial growth phase, transition to vertical growth phase occurs with high risk of metastasis.
D. Noncutaneous melanoma
1. Mucosal melanoma
a. Mucosal melanomas represent <2% of melanomas, most commonly presenting within the genital tract, anorectal
region, and head and neck mucosal surfaces.
b. Difficult to detect; typically advanced at the time of diagnosis with poor prognosis.
c. Radical excision is of questionable benefit.
2. Ocular melanoma
a. Represent 2% to 5% of melanomas (most commonly noncutaneous melanoma)
b. Interference with vision leads to earlier diagnosis.
c. Melanomas of iris are similar to cutaneous melanomas in genetics/behavior; melanomas of the posterior uvea act
more like mucosal melanomas and have a worse prognosis.
d. The eye has no lymphatic drainage; therefore, no nodal metastasis is seen
e. The liver is the main site of metastatic disease
f. Treatment is by enucleation
E. Melanoma with an unknown primary
1. Represent 3% of melanomas
2. Diagnosis is by exclusion
3. Nodal metastases are the most common presentation
4. Prognosis is similar to metastatic melanomas with a known primary.

III. DIAGNOSIS AND STAGING OF MELANOMA


A. Physical examination is only 60% to 80% sensitive for diagnosing melanoma. Full-body photography to monitor atypical
nevi may increase sensitivity.
B. Common clinical features of melanoma lesions: (ABCDE)
1. Asymmetry
2. Border irregularity
3. Color variation
4. Diameter >6 mm
5. Enlarging/evolving lesion
C. Diagnosis of primary melanoma is made by histologic analysis of full-thickness biopsy specimens
1. Excisional biopsy is preferred for lesions <1.5 cm in diameter. If possible, excise lesion with 1- to 2-mm margins.
2. Incisional biopsy is appropriate when suspicion is low, the lesion is large (>1.5 cm) or is located in a potentially
disfiguring area (face, hands, and feet), or when it is impractical to perform complete excision. Incisional biopsy does not
increase risk of metastasis or affect patient survival.
3. Permanent sectioning is used to determine tumor thickness
4. Avoid shave biopsies, since they forfeit the ability to stage the lesion based on thickness.
5. Do not cauterize or freeze the specimen: Tissue destruction makes it impossible to evaluate thickness and margins.
6. Wide local excision for tissue diagnosis can decrease the efficacy of future lymphatic mapping because of disruption
of local lymphatics. Biopsy incisions should result in scars parallel to lymphatic drainage.
7. Orientation of biopsy incisions should also take definitive surgical therapy into consideration.
a. Extremity biopsies should use longitudinal incisions.
b. Transverse incisions are sometimes preferable for preventing contractures over joints.
c. Head and neck incisions should be placed within relaxed skin tension lines, keeping facial aesthetic units in mind.
D. Major prognostic factors: Tumor thickness, Nodal status, and Metastases—TNM (Table 13-3)
1. Breslow thickness is reported in millimeters; thus, it is more accurate and reproducible than Clark level and is a better
prognostic indicator.

2. Clark level is based on invasion through the histologic layers of the skin; more subjective.
E. Other significant prognostic factors
1. Anatomic location: Trunk lesions generally carry worse prognosis than those on the extremities.
2. Sex: For a given melanoma, women generally have a better prognosis; women are also more likely to have extremity
melanomas which carry a better prognosis.
3. Ulceration is a poor prognostic sign
4. Lymph node involvement or in-transit metastases are more significant than any other prognostic factors.
F. The American Joint Committee on Cancer has developed a staging system based on TNM classification (Table 13-4)

IV. MELANOMA TREATMENT


A. Definitive management of melanoma
1. Wide local excision is the treatment of choice.
2. Recommended surgical margins depend on tumor thickness (Table 13-5)
3. Subungual melanoma requires amputation proximal to the DIPJ for fingers and proximal to IP joint for the thumb.
B. Management of regional lymph nodes
1. Elective lymph node dissection (ELND) involves removal of clinically negative lymph nodes from the nodal basin.
No prospective survival benefit was seen except for a subgroup with 1- to 2-mm (intermediate thickness) melanomas.
2. Sentinel lymph node biopsy (SLNB)
a. In the sentinel node theory, a sentinel node will be the first lymph node seeded by tumor cells, and therefore, excision
of sentinel node(s) alone is adequate to determine nodal status. The morbidity of SLNB is considerably less than
ELND. Sentinel node(s) can be detected in >90% to 95% of patients. SLNB is now widely considered the standard
of care.
b. SLNB is performed in conjunction with wide local excision of the primary tumor. Lymphatic mapping is performed to
determine the first lymph node that drains the primary tumor site (sentinel node).
c. SLNB-positive patients undergo staged regional lymphadenectomy and may be candidates for adjuvant therapy.
d. Preoperative nuclear imaging is performed with radiolabeled colloid solution (technetium-99) injected intradermally at
the primary tumor. This can be done on the day of or day prior to surgery. Lymphoscintigraphic imaging localizes the
sentinel node basin(s) (some tumor sites can drain to multiple basins).
e. In the operating room, a lymphangiography dye (lymphazurin or methylene blue) can be injected intradermally at the
periphery of the primary tumor site prior to excision of the primary tumor.
i. Mark edges of the lesion before injection to avoid obscuring them with the dye and take care with the dye
because spills are difficult to manage.

ii. Potential sentinel nodes will appear blue when exploring the nodal basin, giving secondary confirmation to
localization with Geiger counter detection of Tc99 .
iii. Dye injection may briefly interfere with pulse-oximeter readings; alert anesthesiologist at the time of injection.
iv. Caution: Risk of allergy or anaphylaxis with dye injection
f. Following excision of the primary tumor, drapes, instruments, gowns, and gloves are changed and regional lymph node
basin(s) identified by lymphoscintigraphy are explored. All radioactive (“hot”) and/or blue nodes are excised.
g. Histologic analysis of sentinel node with immunohistochemical staining identifies micrometastases. Permanent
sections are required; frozen sections cannot reliably differentiate normal from neoplastic melanocytes.
C. Surveillance and treatment of melanoma recurrence
1. Asymptomatic patients should be seen every 3 to 4 months for 2 years, then every 6 months for 3 years, and then
annually. The most accurate way to detect metastatic disease is to take a thorough history.
2. Chest X-ray and liver function tests (LDH and alkaline phosphatase) are usually sufficient; more extensive work-ups
including CT scans have not altered outcomes.
3. Local recurrences typically occur within 5 cm of the original lesion, usually within 3 to 5 years after primary excision;
most often this represents incomplete excision of the primary tumor.
4. The most common sites of recurrence are the skin, subcutaneous tissues, distant lymph nodes, then other sites (lung,
liver, brain, bone, GI tract).
5. Re-excision is the primary treatment for local, small, isolated lesions
6. Surgery is effective for palliation in patients with isolated recurrences in skin, CNS, lung, or GI tract.
7. Chemotherapy: Complete remission is rare. Decarbazine (DTIC), carmustine, cisplatin, and tamoxifen in combination
are most frequently used. Isolated hyperthermic limb perfusion for extensive extremity cutaneous disease (melphalan
and tumor necrosis factor) is used at some centers.
8. Cytokine therapy has been demonstrated to produce relatively high levels of tumor response, albeit transient. FDA-
approved regimens include interferon-α (IFN-α) for stage III disease and interleukin-2 (IL-2) for stage IV disease;
however, these therapies demonstrate little or no improvement in overall survival.
9. Immunotherapies with monoclonal antibodies, tumor vaccines, and modified immune cells have been the
subject of active investigation for several decades. Despite a number of dramatic successes, these modalities have yet to
prove applicable.
10. Selective cell-signaling inhibitors (e.g., vemurafenib) have recently been developed and can produce dramatic tumor
responses in appropriately chosen patients. Increases in survival time, however, do not translate to improve overall
survival, as resistant melanomas return with added aggressiveness.
11. Mean survival with disseminated disease is 6 months. Respiratory failure and CNS complications are the most
common causes of death.

LESS COMMON SKIN CANCERS


A. Merkel cell carcinoma (MCC)
1. Rare, malignant neuroendocrine tumor arising within the dermis from cells of neural crest origin.
2. Incidence is increasing for unknown reasons; 1,500 cases per year in the United States.
3. Risk factors include age over 65; history of extensive sunlight exposure; fair skin; and immunosuppression (HIV; organ
transplants).
4. Recent research has implicated Merkel cell polyomavirus in 80% of MCC cases.
5. Presents as a purple to red papulonodule or indurated plaque; 50% involve the head and neck, 40% the extremities, and
10% the trunk.
6. MCC is aggressive, with radial spread, high local recurrence, and regional and systemic metastasis.
7. Treatment involves local excision with wide (up to 3 cm) margins; SLN biopsy, and postoperative radiation started
several weeks later.
8. Poor prognosis; 50% survival at five years.
B. Microcystic adnexal carcinoma
1. Pathophysiology is subject of debate, but many authors support dual follicular and eccrine differentiation.
2. Tumor is invasive and locally destructive.
3. Presents as a white to pink papule–plaque primarily on the head and neck.
C. Sebaceous gland carcinoma
1. Malignant tumor derived from adnexal epithelium of sebaceous glands.
2. Most are periocular; sebaceous gland carcinomas elsewhere are vanishingly rare.
3. Yellowish to pink, slowly growing papulonodule on eyelid (resembles chalazion).

SOFT TISSUE SARCOMAS


I. EPIDEMIOLOGY
A. 6,000 to 7,000 new cases are diagnosed annually in the United States
B. 1% of all malignancies in adults and 15% of those in children
C. 50% are located in the extremities
D. Risk factors
1. The majority of sarcomas have no identifiable predisposing genetic or environmental cause.
2. Radiation exposure
a. Associated with osteosarcomas and malignant fibrous histiocytomas.
b. Typically, there is a 10- to 20-year latency period after exposure.
c. Thorium dioxide (Thorotrast) is a contrast agent used in 1940 to 1950s for radiologic procedures; linked with a high
incidence of hepatic angiosarcoma.
3. Chemical exposure: Arsenic, vinyl chloride, and dioxin (contained in the Vietnam War era defoliant Agent Orange)
4. Genetic factors
a. Neurofibromatosis (von Recklinghausen syndrome): 5% lifetime risk of developing neurofibroma or
neurofibrosarcoma
b. Mutation in Rb1 tumor suppressor gene: Retinoblastoma (sarcoma of the eye)
c. Mutation in p53 tumor suppressor gene: Li–Fraumeni syndrome (variety of sarcomas)
5. Lymphedema
a. Following surgical procedures, radiation therapy, or parasitic infection; may also arise idiopathically.
b. 10- to 20-year latency for the development of lymphangiosarcoma.
6. Kaposi’s sarcoma: Strongly associated with HIV infection.

II. DIAGNOSIS
A. In contrast to ectoderm-derived carcinomas, sarcomas behave in a similar fashion regardless of the cell of origin.
B. Paucity of local symptoms often leads to advanced disease at diagnosis.
C. A pseudocapsule forms as the tumor expands and compresses adjacent tissue.
D. Major fascial planes typically act as barriers to local invasion.
E. Extremity sarcoma: Generally painless. Delay in diagnosis is common and patients are often erroneously treated for a
hematoma or “pulled muscle”
1. Suspicious findings include: Mass >5 cm, enlarging or symptomatic mass, mass present for >4 weeks.
2. MRI is the preferred imaging modality.
3. Pulmonary metastases are the most common location for metastatic disease.
4. Approximately 75% 5-year survival rate
F. Sarcoma of the abdomen or retroperitoneum
1. Can present with vague abdominal complaints: Fullness, early satiety, pain, weight loss, nausea, and vomiting
2. Metastatic disease: Most commonly to liver
3. Palpable mass in 80% of patients at the time of presentation
4. Median survival
a. Primary disease—72 months
b. Recurrent disease—28 months
c. Metastatic disease—10 months
5. Imaging
a. MRI with gadolinium contrast: Best technique for visualizing tumor and relationship to adjacent structures.
b. CT scan: Valuable for evaluating chest/abdomen/pelvis for metastatic disease and as a staging tool.
c. Angiography: For surgical planning
d. Chest X-ray: Evaluates for pulmonary metastasis
6. Biopsy of sarcomas: Performed for extremity lesions <5 cm

III. CLASSIFICATION AND STAGING


A. Subtypes are named for the cell of origin (Table 13-6). Fibrosarcoma is the most common sarcoma in adults and the second
most common in children.
B. Histologic type has little prognostic significance; histologic grade (including frequency of mitotic figures, cellular atypia, and
presence or absence of tumor necrosis) is the best for prognosis and therapy.
C. Staging criteria (Table 13-7)
1. Histologic grade is the most important prognostic indicator (see above). Low-grade tumors have less than a 15%
chance of metastasis; high-grade tumors metastasize in >50%
2. Tumors of larger size are more difficult to grade and have a greater chance of recurrence and dedifferentiation.
3. Nodal and distant metastases are associated with a similar prognosis and are classified as stage IV disease.
4. Five-year survival is on the order of 80% for stage I disease, 60% for stage II, 35% for stage III, and <10% for stage
IV

IV. SARCOMA MANAGEMENT


A. Extremities (especially the thighs) are the most common sites for sarcoma
1. Surgery
a. Complete resection with negative margins is the mainstay of treatment.
b. The pseudocapsule should not be entered.
c. Wide local excision (WLE) is the standard of care, with 3- to 5-cm margins of normal tissue proximally and distally.
En bloc resection of uninvolved fascial plane with tumor is performed for control of the other margins.
d. WLE is performed after excisional biopsy even if the margins are clear.
e. Major neurovascular structures are generally preserved for low-grade lesions, but are sacrificed and reconstructed
as needed for high-grade tumors.
f. There is no survival benefit of amputation compared to limb-sparing procedure.
2. Radiation therapy is not indicated for small (<5 cm) low-grade tumors due to excellent prognosis with WLE alone. It
can be used as primary therapy for patients who cannot tolerate or refuse surgery and is also useful as combination
therapy for sarcomas up to 10 cm.
3. Chemotherapy is of undetermined benefit in soft tissue sarcoma.
B. Retroperitoneal and intra-abdominal sarcomas have a uniformly poor prognosis. Excision with tumor-free margins is
curative, but difficult to achieve. Radiation is rarely used because surrounding organs cannot tolerate therapeutic doses.

PEARLS
1. SCC commonly affects the lower lip and upper eyelid; BCC characteristically affects the upper lip and lower eyelid.
2. Spitz nevus: Looks like melanoma (even under a microscope) but does not metastasize; if it spreads, then it is not a Spitz nevus
after all!
3. Perform full-thickness biopsies of pigmented lesions (i.e., punch or excisional) rather than shave biopsy or curettage so that the
depth of the lesion can be determined whether it is a melanoma.
4. Merkel cell carcinoma has increasing incidence and behaves much like an aggressive melanoma; unlike melanoma, Merkel cell
tumors respond to radiotherapy.
5. Fibrosarcoma is generally not sensitive to chemotherapy or radiation therapy.

QUESTIONS YOU WILL BE ASKED


1. Should you undermine the wound arising from excision of a suspected malignant skin lesion to facilitate wound closure?
No. It will permit spread of malignancy.
2. A 35-year-old breast augmentation patient also mentions a 5-mm, nonhealing wound on the face that has been present for two
months. What do you recommend?
Immediate biopsy.

Recommended Readings
Gulleth Y, Goldberg N, Silverman RP, et al. What is the best surgical margin for a basal cell carcinoma: a meta-analysis of the literature. Plast Reconstr Surg.
2010;126(4):1222–1231.
Netscher DT , Leong M, Orengo I, Yang D, Berg C, Krishnan B. Cutaneous malignancies: melanoma and nonmelanoma types. Plast Recon Surg. 2011;127:37E.
Stern RS. Prevalence of a history of skin cancer in 2007: results of an incidence-based model. Arch Dermatol. 2010;146(3):279–282.
I. EMBRYOLOGY
A. Ectoderm: Epidermis, pilosebaceous glands, apocrine glands, eccrine sweat glands, nails
B. Mesoderm: Langerhans cells, macrophages, mast cells, Merkel cells, fibroblasts, blood vessels, lymph vessels, fat cells
C. Neuro-ectoderm: *Melanocytes, nerves, specialized sensory receptors

II. ANATOMY
A. Epidermis—outer layer
1. Cell types: Keratinocytes, melanocytes, Langerhans cells, Merkel cells
2. Superficial to deep: Stratum corneum, lucidum, granulosum, spinosum, basale
B. Dermis
1. Cell types: Collagen, elastin, ground substance
2. Nerves, blood vessels, lymphatics, muscle fibers, pilosebaceous/apocrine/ eccrine glands
3. Two layers superficial to deep
a. Papillary—fibroblasts, mast cells, histiocytes, Langerhans cells, lymphocytes
b. Reticular—thicker than papillary dermis
i. Extends to underlying fat
ii. Contains elastin with interspersed large collagen fibers.

III. BENIGN LESIONS


A. Epidermal lesions
1. Epidermal nevus (linear nevus)
a. May be associated with developmental abnormalities. Ocular, central nervous, skeletal cardiovascular, urogenital
systems
b. Present at birth or early childhood.
c. Clinical presentation: Tan or brown warty papules
d. Anatomic location: Extremities
e. Treatment: Excision, laser therapy(CO2 ), dermabrasion, or cryotherapy
2. Inflammatory linear verrucous epidermal nevus
a. Present at birth or early childhood.
b. Clinical presentation: Erythematous, rough, scaly papules in linear array, extremely pruritic
c. Anatomic location: Extremities
d. Treatment: Excision or laser therapy (intense pulsed light)
3. Seborrheic keratosis
a. Derived from basal layer of epidermis. Cystic inclusions of keratinous material
b. Present in middle age around fifth decade.
c. Clinical presentation: Waxy, stuck-on appearance; warty papule or plaque May be yellow, light brown, dark brown,
or black in color
d. Anatomic location: Head, neck, and trunk
e. Treatment: Dermabrasion, cryotherapy, shaving, and excision

______________
*De note s common in-se rvice e xamination topics

4. Actinic keratosis
a. Occurs on sunlight-exposed skin
b. Most common pre-malignant skin lesion
i. *Approximately 5% to 20% will develop into squamous cell carcinoma
ii. May be present in transplant patients
iii. Require aggressive treatment due to high risk of malignant transformation.
c. Clinical presentation: Erythematous, rough, or scaly macules or papules
d. Anatomic location: Most commonly located on sunlight-exposed areas (scalp, ears, face, and hands)
i. Actinic chelitis (aggressive form involving lips)
ii. Histologically characterized by dyskeratosis, atypia in basal layer of epidermis
e. Treatment: Imiquimod 5% (Aldara) or 5-fluorouracil, cryotherapy, topical tretinoin
5. Verruca vulgaris
a. Common wart: Caused by human papillomavirus (HPV)
b. Clinical presentation: Scaly, rough appearance with a cap of friable keratotic material
c. Anatomic location: Variable. Lesions arise from stratum granulosum
d. Treatment: Cryotherapy, chemical ablation, or excision
6. Cutaneous horn
a. Clinical presentation: Well-circumscribed cone with hyperkeratotic features.
i. Resemble actinic keratoses
ii. Must be distinguished from squamous cell carcinoma
b. Anatomic location: Variable
c. Treatment: Excisional biopsy with careful evaluation of lesion base
7. Leukoplakia
a. Associated with chronic inflammation/irritation (Alcohol or tobacco)
b. *May degenerate into SCC
c. Clinical presentation: Mucosal lesion
i. White plaque exists on stratified squamous epithelium
ii. Cannot be wiped away
d. Anatomic location: Mucosal surface
e. Treatment: Removal of irritant, biopsy may be warranted
8. Keratoacanthoma
a. *Rapid growth phase followed by spontaneous regression
b. Clinical presentation: Firm, dome-shaped nodule
i. Prominent horn-filled central depression
ii. Keratin with thick epidermis
c. Difficult to distinguish from SCC
d. Treatment: Simple excision; may consider 5-fluorouracil for patients with multiple lesions.
B. Melanocytic lesions
1. Nevus of Ota
a. Found in patients with Asian ancestry
b. Appears at birth
c. Clinical presentation: Appears as large, blue-gray patch
d. Anatomic location: Areas innervated by first and second branches of trigeminal nerve
e. Treatment: Laser therapy (Q-switched Nd:YAG)
2. Nevus of Ito
a. Found in patients with Asian ancestry
b. Appears at birth
c. Clinical presentation: Appears as large, blue-gray patch
d. Anatomic location: Posterior shoulder and areas innervated by posterior supraclavicular and lateral cutaneous
brachial nerves
e. Treatment: Laser therapy (Q-switched Nd:YAG)
3. Nevus spilus
a. Appears at birth
b. Clinical presentation: Tan patch with speckled hyperpigmented macules and papules
c. Anatomic location: Commonly on trunk
d. Treatment: Observation, laser therapy (intense pulsed light), or simple excision
4. Spitz nevus (benign juvenile melanoma)
a. Appears in childhood or early adulthood
b. Clinical presentation: Pink or tan, dome-shaped, smooth plaque
c. Anatomic location: Commonly located on face
d. Treatment: Excision with margins to decrease recurrence risk (range from 1 to 2 mm to 1 to 2 cm depending on
concern for melanoma)
e. May be difficult to distinguish histologically from malignant melanoma
5. Junctional nevus
a. Nevus cells located at epidermal-dermal junction
b. Appears in childhood or early adulthood
c. Clinical presentation: Brown, evenly pigmented macule with well-defined borders
d. May be difficult to differentiate from melanoma
e. Anatomic location: Most commonly on trunk
f. Treatment: Simple excision
6. Compound nevus
a. Contains both junctional and intradermal components.
b. Appears in childhood or early adulthood.
c. Clinical presentation: Appears a dark-brown papule with regular borders
d. Anatomic location: Most commonly on trunk
e. Treatment: Simple excision
7. Intradermal nevus
a. Located entirely within the dermis.
b. Appears in the second or third decade of life
c. Clinical presentation: Appears as a flesh-colored or light tan papule
d. Anatomic location: Face or neck
e. Treatment: Simple excision
8. Common blue nevus
a. Appears during adolescence
b. Clinical presentation: Blue or blue-black papule
c. Anatomic location: Head, neck, and dorsum of hands/feet
d. Treatment: Simple excision
e. Cutaneous metastasis of malignant melanoma can resemble blue nevus
9. Cellular blue nevus
a. Appears after second decade of life
b. Clinical presentation: Blue-black papule
c. Anatomic location: Most commonly on buttocks
d. Treatment: Simple excision
10. Atypical (dysplastic) nevus
a. Patients with dysplastic nevi and a family history of melanoma in a first-degree relative are at a high risk of
melanoma.
b. Regular skin examination
c. Appear after puberty
d. Clinical presentation: Appears as a central brown macule with irregular pink rim.
e. More irregular pigmentation and borders compared with typical nevi.
f. Anatomic location: Trunk
g. Treatment: Excision with margins to prevent recurrence
i. Total body skin examination to rule out other lesions
ii. Sunscreen and avoidance of sunburning/tanning
C. Adnexal tumors
1. Background
a. Excised for aesthetic reasons
b. Normal relationship between epithelial and stromal components of skin altered
c. May be classified as nevus, adenoma, or epithelioma
d. May include sebaceous glands, hair follicles, apocrine, or eccrine sweat glands
2. Hair follicle tumors
a. Located in lower dermis and subcutaneous fat
b. Pilomatrixoma (calcifying epithelioma of Malherbe)
i. Typically seen in younger patients (<20 years old)
ii. Clinical presentation: Single, solid subdermal nodule
a) Positive tent sign—stretching of overlying skin yields multiple peaks
b) Difficult to distinguish from calcified masses or carcinoma.
c) On pathology shows epidermoid cells with basophilic and eosinophilic cells
iii. Anatomic location: Involves face and upper extremities
iv. Treatment: Excision (with up to 1 to 2 cm margins) with up to 10% recurrence rate
c. Trichofolliculoma (hair follicle nevus)
i. Clinical presentation: <1 cm and skin-colored
ii. Anatomic location: On face with thin pale hairs
iii. Treatment: Excisional biopsy for management
d. Trichoepithelioma
i. Involves patients after puberty
ii. Rasmussen syndrome is an autosomal dominant disorder that is a triad of multiple trichoepitheliomas, cylindromas,
and milia.
iii. Clinical presentation: Appears pink or flesh-colored
iv. May be difficult to distinguish clinically and histologically from basal cell carcinoma
v. Anatomic location: Multiple trichoepitheliomas may have symmetric distribution around face and eyes
vi. Treatment: Electrodesiccation
e. Trichilemmoma
i. Cowden disease (multiple hamartoma syndrome) should be suspected if patients have multiple such tumors
ii. Glycogen-rich epithelial cells surrounded by sheaths of cells resembling hair follicles on histology
iii. Clinical presentation: Smooth papule
iv. Anatomic location: Found on scalp or other hair-bearing regions. Association with nevus of Jadassohn if on scalp.
Warrants biopsy
v. Treatment: Laser therapy (CO 2 ), electrodessication with curettage, or simple excision due to similar appearance
with BCC and trichilemmal carcinoma
3. Eccrine tumors
a. Cylindroma (turban tumor or tomato tumor)
i. Appears in early adulthood
ii. Multiple cylindromas may indicate autosomal dominant cylindroma syndrome.
iii. Clinical presentation: Appears as firm, smooth pink nodules
iv. Anatomic location: Often located on scalp
v. Treatment: Laser therapy (CO2 ), electrodessication/curettage, cryotherapy, or simple excision
b. Eccrine poroma
i. Clinical presentation: Firm, papular or nodular lesions surrounded by rim of hyperkeratosis; may appear
pedunculated
ii. May resemble amelanotic melanoma and pyogenic granuloma
iii. Anatomic location: Found on palms and soles of feet
iv. Treatment: Simple excision
c. Syringoma
i. Appears in early adulthood
ii. May have increased incidence with Down’s syndrome
iii. Clinical presentation: Small papules ranging from yellow to pink in color. May be confused with xanthelasma or
trichoepithelioma
iv. Anatomic location: Most commonly appears in the periocular region (eyelids, upper cheek) but may involve trunk,
neck, or extremities
v. Treatment: Laser (CO2 ) or electrodesiccation
d. Eccrine spiradenoma
i. Appears in young adults
ii. Clinical presentation: Tenderness or pain with manipulation
iii. May be mistaken for glomus tumor
iv. Anatomic location: Appears as a single nodule on ventral upper half of body
v. Treatment: Simple excision if symptomatic
e. Eccrine hidrocystoma
i. Dilated and obstructed sweat ducts histologically
ii. Clinical presentation: Translucent vesicles
iii. Swell in heat/humidity; regress in cooler/dry climate
iv. Anatomic location: Appears on lower eyelids and upper cheeks
v. Treatment: Puncture to release pressure
4. Sebaceous tumors
a. Sebaceous nevus of Jadassohn
i. Appears at birth
ii. *After puberty, 10% to 15% degenerate into BCC. May also develop SCC or keratoacanthoma
iii. Clinical presentation: Appears as yellow/orange, waxy, smooth plaques prior to puberty
iv. Appear as rough, verrucous, orange plaques after puberty
v. Anatomic location: Most commonly found on scalp
vi. Treatment: Excision
b. Sebaceous hyperplasia
i. Appears in middle or late age
ii. Clinical presentation: Appears as shiny, small umbilicated, yellow-white papules
iii. May be covered with telengiectasia
iv. Anatomic location: Most common on face
v. Treatment: Cryotherapy, electrodesiccation, or laser (intense pulsed light or CO2 )
vi. May be excised due to similar appearance with BCC.
c. Sebaceous adenoma
i. Appears in middle age
ii. *May be associated with Muir-Torre syndrome—an autosomal dominant syndrome associated with
multiple keratoacanthomas, marked increase in visceral neoplasm
iii. Clinical presentation: Yellow nodules
iv. Anatomic location: Located primarily in head and neck
v. Treatment: Simple excision
5. Apocrine tumors
a. Apocrine cystadenoma
i. Contains brown or blue tinged fluid
ii. Clinical presentation: Appears as a single translucent nodule
iii. Anatomic location: Most common on face
b. Chondroid syringoma
i. Composed of sweat gland (epithelial) and cartilaginous elements (mesenchymal) on histology
ii. Treatment: Excisional biopsy
c. Syringocystadenoma papilliferum
i. Appears during childhood
ii. Clinical presentation: May be associated with nevus sebaceous
iii. Nearly 10% will harbor BCC
iv. Anatomic location: Most commonly found on scalp
v. Treatment: Excision
D. Smooth muscle tumor
1. Leiomyoma
a. Abnormal proliferation of smooth muscle
b. May become symptomatic with pain on exposure to cold/pressure
c. Clinical presentation: Appears as firm, pale intradermal nodules with brown hue
d. Treatment: Excisional biopsy
e. Local recurrence may occur
f. Malignant degeneration to leiomyosarcoma is rare
E. Cysts
1. Epidermal inclusion cyst (epidermoid cyst)
a. May be incorrectly called a sebaceous cyst; however, not sebaceous in origin
b. Appears in adulthood
c. Clinical presentation: Fluctuant, flesh-colored, well-circumscribed nodules
i. Punctum may be visible
ii. Contains foul-smelling keratinous debris
d. Anatomic location: Commonly found on face, neck, and trunk
e. Treatment: Simple excision if uninfected; if infected, perform incision and drainage with interval excision
2. Dermoid cyst
a. Appears at birth or early childhood
b. Clinical presentation: Similar to epidermal inclusion cysts. Lined with epidermal skin appendages
c. *Anatomic location: Most commonly found along supraorbital ridge, lateral brow, or nasal midline
d. Treatment: Excision
e. *Midline nasal mass differential diagnosis
i. Dermoid cyst, glioma, meningocele/encephalocele
ii. CT or MRI prior to excision to determine intracranial extension
3. Trichilemmal cyst
a. Pilar cyst
b. Appear in adulthood
c. Clinical presentation: Similar to an epidermal inclusion cyst
d. Anatomic location: Most commonly found on scalp
e. Treatment: Excision if uninfected; if infected, incision and drainage with interval excision
F. Fibrous Lesions
1. Dermatofibroma
a. Appears in adulthood
b. Clinical presentation: Brown-red indurated papule or nodule Positive dimple sign—when squeezed it sinks
c. Anatomic location: Most common lower extremities
d. Treatment: Simple excision
2. Angiofibroma
a. Clinical presentation: Pale, firm papule. May have telengiectasia or erythema
b. Anatomic location: Most commonly on lower third of face
c. Treatment: Simple excision for cosmesis
d. May be associated with tuberous sclerosis if multiple
3. Lipoma
a. May be present at any age
b. Clinical presentation: Painless, soft, flesh-colored nodule
c. Anatomic location: Commonly found in the trunk and extremities
d. Treatment: Simple excision
4. Dermatofibrosarcoma protuberans
a. Appears in middle age
b. Clinical presentation: As a reddish-brown, firm, nodular plaque
c. Anatomic location: More commonly found on trunk, extremities
d. *Treatment is radical excision due to locally aggressive behavior. Margins >3 cm if possible
e. Local recurrence is common; however, metastasis is rare.
5. Neurofibroma
a. Composed of Schwann cells and endoneurial fibroblasts.
b. May appear at any age
c. Clinical presentation: Soft, compressible, flesh-colored or pink nodules; button-hole sign (can be pushed deeper into
dermis)
d. Anatomic location: More common on the trunk and extremities
e. Treatment: Excision
f. Multiple neurofibromas may be associated with neurofibromatosis type I or II
i. *Type I—Cafe-au-lait spots, Lisch nodules (iris hamartomas), and optic nerve glioma
ii. Type II—bilateral acoustic neuroma

IV. OTHER DISORDERS


A. Calciphylaxis
1. Metastatic calcification resulting in calcification of blood vessels and necrosis of surrounding tissue.
2. Associated with renal failure
3. May appear at any age; more common in women
4. Clinical presentation: As necrotic ulcerations with red-blue mottling of skin (livedo reticularis)
5. Anatomic location: Common trunk and extremities
6. Treatment: Supportive care, phosphate-binding agents, parathyroidectomy, intravenous sodium thiosulfate, or excision
7. Excision often results in progressive calcification
B. Hidradenitis suppuritiva
1. Clinical presentation: Chronic inflammation and infection of the apocrine sweat glands. May result in chronic draining
sinus tracts and abscesses.
2. Anatomic location: Most commonly affects axillae, breasts, perineum, and buttocks.
3. Treatment: Topical clindamycin, oral or IV antibiotics, excision of involved tissue. Following excision, reconstruction can
occur via healing by secondary intention or by placement of a skin graft.
C. Xeroderma pigmentosum
1. Autosomal recessive disorder affecting DNA repair
2. High risk for SCC, BCC, and melanoma
3. Treatment: Avoidance of sunlight, isotretinoin, 5-fluorouracil, or excision of malignant lesions
D. Dystrophic epidermolysis bullosa
1. Hereditary disease with bulla formation of skin/mucosa following minor trauma
2. May result in encasement of digits with scar tissue
3. Treatment: Scar release/Z-plasty, topical steroids, avoidance of trauma
E. Cutis laxa
1. Defect in elastic fibers
2. Skin hangs loose from folds
3. Premature aging
4. Wound healing unaffected
5. Blepharoplasty and face lift can be beneficial
F. Pseudoxanthoma elasticum
1. Affects elastic fibers and collagen
2. Skin thickens and appears cobblestoned with mechanical stress
3. Wound healing is normal
G. Ehlers-Danlos syndrome (cutis hyperelastica)
1. Autosomal recessive or x-linked
2. Hyperextensible skin, severe joint laxity
3. Blood vessels are delicate
4. *Wound healing is abnormal: Approach surgery with caution
H. Acne vulgaris
1. Appears in younger patients
2. Clinical presentation: Comedones, inflammatory cysts, seborrheic plaques
3. Anatomic location: Face
4. Treatment: Topical retinoic acid, oral antibiotics, antibiotic pads, and oral isotretinoin (accutane). Isotretinoin—risk of
birth defects; patients must have two forms of contraception. Avoid if planning aesthetic facial rejuvenation with lasers
or peels.
I. Acne rosacea
1. Clinical presentation
a. Facial flushing (increased vascularity)
b. Thickened skin erythema, telangiectasia
c. Acne rosacea (papules and pustules)
d. Rhinophyma—nasal skin becomes erythematous with telangiectatic changes
2. Anatomic location: Affects forehead glabella, malar region, nose, chin
3. Treatment: Oral antibiotics, retinoic acid, dermabrasion, cryotherapy, laser (CO2 ), tangential excision (for Rhinophyma)
4. Reconstruct with secondary contraction versus skin graft
J. Pyoderma gangrenosum
1. Clinical presentation: Multiple superficial abscesses with significant ulceration and skin necrosis.
2. Should get a dermatology consult and biopsy to evaluate, though this is a diagnosis of exclusion.
3. Treatment: Broad spectrum antibiotics
4. Approach surgery with caution given chances that this could create a flare and spreading of the disease.
5. Harvesting STSG can also create a flare of the disease at the donor site.
6. Associated with ulcerative colitis

PEARLS
1. Keratoacanthomas are characterized by rapid growth and spontaneous regression; they are difficult to distinguish from
squamous cell carcinomas although they are not malignant.
2. Nevus sebaceous has a 10% to 15% risk of malignant degeneration into BCC. Excision is warranted.
3. Patients with cutis laxa do not have impaired wound healing and can be candidates for surgery, while those with cutis
hyperelastica have wound healing difficulties and may not tolerate surgery.
4. 5-Fluorouracil is a DNA synthesis inhibitor; imiquimod (Aldara) is an immunomodulator.
5. Excision is generally appropriate when definitive pathology and/or margins are required.
6. Keep in mind the amount of local anesthetic which can be used (e.g., 1% lidocaine vs. 1% lidocaine with epinephrine).
7. When drawing up lidocaine for excision, avoid displaying needle.
8. Identify lesion and its observable borders prior to injection with lidocaine to avoid obscuring the lesion boundaries.
9. Design excisions as ellipses with sharp corners to facilitate closure and avoid dog-earing.
10. Nylon stitches from the face should be removed in 5 days to avoid railroad tracks. Stitches on back should be left in for 2 weeks
to allow for more robust healing and to avoid splitting apart.

QUESTIONS YOU WILL BE ASKED


1. What is the recommended treatment of a nevus sebaceous?
Excision with clear margins.
2. What is the risk of malignant transformation of an actinic keratosis, and what type of skin cancer can it progress to?
Rates of AK progression to SCC were calculated at 0.6 percent at one year and 2.6 percent at four years. Of these SCCs, 75
percent were considered invasive and the remainder were in situ.
3. Patients with which of the following disorders should be approached with caution when considering surgical intervention: Cutis
laxa? Pseudoxanthoma elasticum? Ehlers-Danlos?
Patients with Ehlers-Danlos syndrome may suffer from excessive postoperative bleeding and poor wound healing and therefore
surgery is generally contraindicated.
4. What is the most common location of dermoid cysts?
Periocular region.
5. What malignancy can Spitz nevi appear histologically similar to?
Melanoma.

Recommended Readings
Lee EH, Nehal KS, Disa JJ. Benign and premalignant skin lesions. Plast Reconstr Surg. 2010;125:188e–198e. PMID: 20440130.
VASCULAR ANOMALIES
I. CLASSIFICATION: Classification of vascular anomalies was historically very confusing (i.e., “cavernous hemangioma”);
current nomenclature favors biology over tradition. Most vascular anomalies can be classified as one of the following:
A. Hemangioma
B. Vascular malformations
1. Arterial malformation
2. Venous malformation
3. Capillary malformation
4. Lymphatic malformation

II. HEMANGIOMA
A. Etiology: Benign proliferation of endothelial cells which is present after birth.
B. Most common tumor of infancy
1. Incidence: 1:10 infants
2. 10% of white infants
3. 2% of black infants
4. More common in females (3:1)
C. Most common location: Head/neck region
D. Stages of development—rapid postnatal growth, slow involution
1. Proliferating phase (0 to 12 months)
a. Endothelial cells and pericytes rapidly multiply (most significantly during 6 to 8 months of infancy)
b. VEGF and bVEGF are drivers of proliferation
2. Involuting phase (12 months to 10 years)
a. Progressive shrinking of lesion volume with deposition of fibrous tissue and degeneration of endothelial cells
(continues until 5 to 10 years of age)
b. Mast cells downregulate endothelial cell turnover
3. Involuted phase (>10 years): Loose fibrofatty tissue replaces previous parenchymal tissue
a. Approximately 50% of children experience complete involution by age 5.
b. Approximately 70% experience complete involution by age 7.
c. Minimal change expected after 12 years of age.
E. Diagnosis
1. Mainly based on history and physical examination findings: Lesion presents after birth and continues to enlarge in
infancy.
2. Ultrasound (US). Difficult to distinguish hemangioma from arteriovenous malformation (AVM) as both are high-flow
lesions. US shows shunting pattern of flow
3. MRI with contrast (gold standard test): Especially important if suspect visceral hemangiomas
F. Associated anomalies/syndromes and rare presentations
1. Spina bifida occulta: Associated with lumbar hemangioma
2. PHACES: Posterior fossa anomalies, Hemangiomas, Cardiac anomalies, Eye abnormalities, Sternal cleft

______________
*De note s common in-se rvice e xamination topics

3. Kasabach–Merritt syndrome: Hemangioma + thrombocytopenia


a. Platelet count <10,000, normal PT/PTT
b. Diagnosis can be confirmed with MRI
4. Maffucci’s syndrome: Enchondromatosis with multiple cutaneous hemangiomas
5. Von Hippel–Lindau disease: Retinal hemangiomas, hemangioblastomas of the cerebellum, visceral cysts, mental
retardation
6. Cutaneous visceral hemangiomas: Multiple hemangiomas (>5) should elicit concern for visceral hemangiomas
a. Congestive heart failure
b. Hepatomegaly (intrahepatic hemangiomas)
c. Anemia
7. Noninvoluting congenital hemangioma (“NICH”) grows in proportion to child, histologically similar to infantile
hemangioma (“regular hemangioma”, IH), except they do not express glucose transporter-1 protein (GLUT-1), whereas
IH do express GLUT-1.
8. Rapidly involuting congenital hemangioma (“RICH”). Involutes within 1 year of life, also histologically similar
appearance to IH and also GLUT-1 negative.
9. Kaposiform hemangioepithelioma (KHE): Causes platelet consumption, whereas NICH and RICH do not. KHEs
often have a lymphatic component and carry malignant potential.
G. Treatment
1. Observation—appropriate in most cases
a. Reassurance of parents and patients is critical
b. Take serial photographs to monitor progress
2. Indications for intervention
a. Bleeding/ulceration (5% cases). Most commonly occurs in lip or anogenital region
b. Major ulceration, destruction or distortion of surrounding structures, and/ or obstruction of vital structures (10%
cases). Most commonly occurs in eyelid, nose, lip, and ear.
i. Eye/eyelid: Obstruction can cause deprivation amblyopia in as little as 1 week; hemangiomas can directly distort
the cornea and damage vision.
ii. Airway: Subglottic hemangioma can cause stridor/obstruction of the airway.
3. Nonsurgical interventional treatment options
a. Laser therapy with pulsed dye laser (577 to 585 nm) which targets oxyhemoglobin
i. Goal is to lighten the hemangioma and involved skin.
ii. Does not reduce bulk or cause involution.
iii. Penetrates only 0.75 to 1.2 mm into the dermis.
b. Minor ulcerations/bleeding
i. Application of topical antibiotics and/or hydrocolloid dressing can speed healing.
ii. Pulsed dye laser can relieve pain and stimulate healing; if bleeding is noted after the procedure, parents should be
counseled to hold pressure to the area x10 min.
c. life-/limb-threatening lesions
i. Systemic corticosteroids
a) Historically has been considered first-line therapy for life-/limb-threatening hemangiomas.
b) 2 to 3 mg/kg/day given orally for 4 to 6 weeks
c) Initial response visible after 7 to 10 days
d) 85% of hemangiomas respond by regression or stabilization of growth after completion of corticosteroid
therapy.
e) Monitor for cushingoid facies, myopathy, cardiomyopathy, premature telarche, and hirsutism.
ii. Intralesional corticosteroid injection
a) 3 to 5 mg/kg of corticosteroid is injected into the lesion at low pressure.
b) Must be careful when injecting the eye to avoid occlusion of retinal artery.
iii. β-Blockers
a) Propranolol has recently been adopted by many centers and is highly effective at reducing tumor bulk during
the proliferative phase of the disease.
b) Its use appears to be well tolerated in infants and young children at a dose of 2 mg/kg/day, and use of
propranolol is becoming standard care in problematic lesions.
iv. Interferon α-2A
a) Second-line treatment
b) Effective in Kasabach–Merritt syndrome patients
c) Indications for use
1) Lack of response to corticosteroid therapy
2) Prolonged use of corticosteroid therapy
3) Complications due to corticosteroid therapy
d) 2 to 3 mU/m2 injected subcutaneously daily
e) Response seen over 6 to 10 months; 80% of patients demonstrate a response
f) Common side effects
1) Fever on initiation (pretreat with acetaminophen)
2) Transaminitis
3) Transient neutropenia
4) Anemia
5) Spastic diplegia—must stop interferon therapy immediately!
d. Vincristine (chemotherapy)
i. Second-line therapy (same indications as interferon)
ii. >80% response rate
iii. Administered through central line
iv. Side effects
a) Peripheral neuropathy
b) Complications due to central line placement
c) Sepsis
d) Line infections
e) Hair loss
4. Surgical treatment
a. Indications in infancy
i. Obstruction or deformation of critical/vital structures (e.g., eye, subglottic airway).
ii. Bleeding/ulceration unresponsive to pharmacologic treatments
iii. Easily excisable area with acceptable and predictable scar
b. Indications in childhood (as above, plus)
i. Excision necessary to address scarring caused by ulceration and fibro-fatty residual lesion.
ii. Staged excision and reconstruction for large lesions
c. Approach: Circular incision with purse-string closure versus lenticular incision.

III. VASCULAR MALFORMATIONS


A. Common features
1. Always present at birth (distinguishing factor from hemangiomas, which grow after birth and are not often seen at birth).
2. Vessels are inherently abnormal due to aberrant signal pathways that determine apoptosis and proliferation pathways.
3. 1:1 male:female ratio
4. Lesions grow proportionately to child and do not involute.
B. Diagnosis
1. Clinical history and physical examination
2. Imaging
a. US with Doppler
i. Differentiates slow-flow from fast-flow lesions
ii. Highly operator-dependent
b. MRI with contrast
i. Gold standard test
ii. Provides details on the anatomic distribution of the lesion along with unique sequences and signals used to
differentiate the types of vascular malformation
c. Arteriography
i. Invasive study
ii. Most often used in conjunction with planned embolization
C. Capillary malformations
1. Slow-flow lesion
2. Appearance: Regular, dilated, thin-walled capillaries localized to the papillary and superficial reticular dermis.
a. Must be differentiated from other common macular stains of the face (e.g., nevus flammeus).
b. The autonomic nervous system influences the development of this lesion, which is why it is often localized to distinct
nerve distributions (e.g., V1 nerve distribution with port-wine stains of the face).
3. Incidence: 0.3% of newborns. Most common location is on the face
4. 3:1 female:male ratio
5. Common associated syndromes
a. Sturge–Weber syndrome
i. Port-wine stain (capillary malformation) in V1/V2 distribution of the face
ii. Leptomeningeal malformations
a) Seizures
b) Contralateral hemiplegia
c) Warrants MRI of head
iii. Developmental delay
iv. Glaucoma and retinal detachment: Screen using biannual fundoscopic and tonometry examinations for 1 to 3
years, then yearly examinations
b. Klippel-Trenaunay syndrome
i. Capillary malformation and/or lymphatic-venous malformation (patchy port-wine stain on an extremity)
ii. Skeletal and soft tissue hypertrophy (axial/transverse) of an extremity
c. Parkes–Weber syndrome
i. Capillary malformation + AVM
ii. Soft tissue/skeletal hypertrophy
d. Cobb syndrome
i. Capillary malformation localized to the trunk
ii. Associated with spinal AVM
6. Treatment options
a. Observation
i. Lesions do not regress
ii. Can progress to “cobblestone” appearance
b. Pulsed dye laser
i. Typically requires multiple treatments
ii. 70% to 80% of patients respond with decrease in pigmentation of the lesion.
iii. More favorable results on the lateral face as compared to mid-face, trunk, and extremities.
c. Surgical excision. Must be used for management of soft-tissue/skeletal hypertrophy to address contour deformity.
D. Lymphatic malformations
1. Slow-flow lesion
2. Appearance
a. Anomalous lymphatic channels filled with lymphatic tissue which may be clustered into vesicles
b. Further classified as microcystic versus macrocystic
3. Most common cause of macroglossia, macrochelia in children. Can also cause facial asymmetry, distortion of
surrounding tissue, soft- tissue/skeletal hypertrophy.
4. Treatment options
a. Observation
i. Intralesional bleeding can be treated with NSAIDS for pain control and rest.
ii. Antibiotics indicated for cellulitis/other infections.
b. Sclerotherapy (mainstay treatment)
i. Lesion is instilled with ethanol, doxycycline, sodium tetradecyl sulfate
ii. Can be used effectively when macrocysts are present (large volumes of lymphatic fluid without small loculations
as seen on US or MRI). Microcystic disease, in which many small loculations are present, is not readily amenable
to sclerotherapy.
c. Surgical resection
i. Direct excision can be effective but carries a high likelihood of significant complications.
ii. Suction-assisted lipectomy has been used to debulk lesions.
iii. Complications often include
a) Cellulitis
b) Hematoma
c) Persistent drainage
d) Recurrence of vesicular lesions
e) Need for skin graft depending on extent of excision
E. Venous malformations
1. Slow-flow lesion
2. Appearance
a. Bluish, soft, compressible lesion which swells on dependent positioning; cluster of thin-walled veins with smooth
muscle surrounding, many veins lack valves.
b. Changes in hormone levels can cause enlargement
3. Must monitor for coagulopathy: Always perform coagulation profile studies as patients can develop DIC
4. Treatment
a. Observation
b. Compression therapy
i. Useful for pain and edema
ii. Minimizes phlebothrombosis
c. Sclerotherapy: Most effective if performed on small cutaneous lesions using ethanol.
i. Side effects: Blistering, full thickness necrosis, neural deficits
ii. Make sure no important neural structures are nearby if using ethanol sclerotherapy.
d. Surgical excision: Performed most commonly after sclerotherapy to improve cosmetic appearance or remove mass
tissue to optimize function.
F. Arteriovenous malformation
1. High-flow lesion
2. Appearance: Abnormal connections between arteries and veins
a. Arteries have thick, fibromuscular veins with prominent elastic lamina and stroma
b. Veins are “arterialized” and hyperplastic
3. Clinical features
a. Intracranial AVMs are more common than extracranial AVMs.
b. *Always present at birth, but NOT always apparent. Puberty and trauma can stimulate enlargement
c. Schobinger stages of development
i. Stage 1: Quiescence—bluish discoloration and warmth of skin with AV shunting noted on Doppler examinations.
ii. Stage 2: Expansion—AVM begins to enlarge and demonstrates bruit, thrill, and pulsations.
iii. Stage 3: Destruction—begins to bleed, cause pain, and destroy surrounding tissue.
iv. Stage 4: Decompensation—persistent destruction to surrounding tissue with cardiac failure.
4. Associated syndromes
a. Bannayan–Zonana syndrome: AVM + microcephaly + lipomas
b. Riley–Smith’s syndrome: AVM + microcephaly + pseudopapilledema
c. Osler–Weber–Rendu disease
i. Multiple cutaneous telangiectasias with visceral AVMs (most commonly in lungs, liver, brain)
ii. Often presents as frequent nosebleeds
5. Treatment
a. Observation: Used for small, clinically stable, asymptomatic lesions
b. Embolization with surgical excision
i. Used for Stage 3 to 4 lesions
ii. Ligation/embolization of proximal feeding vessels must never be performed. Can cause recruitment of nearby
vessels to exacerbate AVM.
iii. Wide local excision is necessary to minimize recurrence rates.
iv. Reconstruction with flaps is often necessary after excision.

LYMPHEDEMA
I. NORMAL LYMPHATIC SYSTEM
A. Structure
1. Superficial and deep lymphatic vessels
a. Superficial lymphatic system: Vessels have no valves and drain into the subdermal and subcutaneous lymphatic
systems.
b. Deep lymphatic system: Contain valves, located below the muscular fascia.
c. Superficial and deep systems are connected by lymph nodes.
d. Thoracic duct drains the lower extremities, left trunk, left upper extremity.
e. Right lymphatic duct drains the right head/neck region, right upper extremity, right thorax.
B. Function
1. Transport interstitial fluid into the vascular system.
2. Transport chylomicrons, triglycerides, and fat from the GI tract into the blood stream through the thoracic duct.
3. Clears foreign material and particles to present them to the immune system.

II. LYMPHEDEMA
A. Definition: Accumulation of protein-rich fluid within the interstitial space due to a decrease in at least 80% of lymphatic
function.
1. Postmastectomy Lymphedema:
a. Up to 10% women after breast cancer surgery have lymphedema.
b. More prevalent in cases involving XRT or radical mastectomies.
c. Thought to be less prevalent due to increased used of sentinal lymph node biopsy.
d. Presentation is a swollen, painful arm, which is at increased risk for infection.
2. Chronic lymphedema: Caused by persistent inflammation and fibrosis which then cause fatty and fibrous tissue
deposition.
3. Common locations
a. Lower extremities (90%)
b. Upper extremities (10%)
i. Occurs in at least 8% of women after mastectomy
ii. Occurs in at least 35% of women after axillary node dissection and radiation
c. Genitalia (<1%)
B. Differential diagnosis
1. Venous stasis
2. Conditions of fluid overload
a. Congestive heart failure
b. Renal disease
c. Liver disease
3. Diminished intravascular protein content
C. Diagnosis
1. History and physical examination
a. Recent surgery or trauma
b. Travel to a foreign country: Concern for Wuchereria bancrofti (filariasis)
c. Malnutrition
d. Examination
i. Nonpitting edema that usually affects hands/feet
ii. Usually not painful
iii. Minimal pigment change or ulceration
iv. Often unilateral (can measure limb circumference to document progression of disease)
v. Fluid protein content is 1 to 5 g/dL
vi. Positive stemmer sign: Inability to grasp the base of the second toe or finger due to thickening of the
subcutaneous tissues.
2. Diagnostic studies
a. Lymphoscintigraphy (Gold standard test): Sensitivity: 97%; specificity: 100%
b. Nuclear medicine study which maps the lymphatic system and can identify points of blockage
c. Lymphangiogram: Can cause worsening of disease due to injection of contrast.
d. CT scan: Can differentiate lymphedema from venous stasis based on thickness of skin/muscular compartment and
appearance of fluid.
e. Doppler/US: Use to rule out other causes of asymmetrical limbs (e.g., deep venous thrombosis, venous stasis).
3. Classification
a. Primary
i. Congenital (15%). Milroy’s disease: Congenital maldevelopment of lymphatic system causing lymphedema and
steatorrhea, defective cell-mediated immune system, familial disease.
ii. Lymphedema praecox (75%)
a) Onset at 1 to 35 years of age
b) Often occurs with puberty
c) Most often affects the lower extremity
iii. Lymphedema tarda (10%): Onset at greater than 35 years of age
b. Secondary. Caused by a mechanical obstruction/anatomic dysfunction of an otherwise normal lymphatic system
i) Infection: Wuchereria bancrofti
ii) Iatrogenic
a) Trauma to lymphatic channels
b) Excision of lymph nodes
c) Stenosis of channels due to radiation
iii) Trauma
iv) Other: Autoimmune diseases, malignancy (primary or metastasis to lymph nodes), benign growths
4. Complications
a. Cellulitis
i. Can progress aggressively to sepsis and death
ii. Initiate treatment immediately with oral antibiotics
iii. Have low threshold to start IV antibiotic treatment
iv. Consider prophylactic antibiotics in patients who have greater than three episodes of cellulitis per year
b. Ulceration (more common in venous stasis)
c. Thickening of skin/verrucous skin changes
d. Lymphangiosarcoma (<1% incidence): Must biopsy all concerning lesions
5. Treatment
a. Elevation with proper skin hygiene
i. Use low pH solutions and water-based products
ii. Useful for most patients
b. Compression
i. Bandages, stockings, massage, pneumatic compression devices
ii. Can reduce the volume of the extremity by 25% to 60% depending on the device used.
c. Surgical management
i. Indications
a) Significant loss of function
b) Frequent infections
c) Failure of conservative/medical management
d) Significant psychological morbidity
ii. Surgical options
a) To restore lymphatic flow
1) Lymphangioplasty
2) Flap transposition
3) Microsurgical anastomosis ± microlymphatic grafting
• Anastomosis of lymphatics to veins is most common technique; lymph node transfer is gaining in
popularity
• Traditionally considered not reliable; gaining renewed interest of late
b) To excise excess tissue
1) Charles operation: Excision of all tissue to the level of the muscle with skin grafting for coverage;
uncommonly performed today.
2) Staged subcutaneous excision: Skin flaps are maintained, only subcutaneous tissue is excised, most
commonly performed excisional technique.
3) Suction-assisted lipectomy: Liposuction techniques are used to remove subcutaneous tissues, commonly in
the upper extremity and in early disease stages.

TATTOOS
I. DEFINITION: Foreign material injected into the skin which penetrates the dermis and leads to a visible/permanent mark on the
skin

II. USE OF TATTOOS


A. Decorative tattoos
1. Professional—explosive growth in prevalence in the United States in last generation (one-third of all adults under age
30 have at least one); carbon base used for black dyes, variety of metals for other color pigments.
2. Amateur—variable depth; wider range of particle sizes, with larger particles refractory to laser
B. Cosmetic tattoos: Used to accentuate eyelids/eyebrows, mimic hair. Ferrous oxide is the pigment commonly used.
C. Reconstructive tattoos
1. Nipple-areolar complex reconstruction: Perform 2 to 3 months after implant-based reconstruction/flap reconstruction is
complete.
2. Vitiligo: Especially useful if large, focal areas are involved

III. METHODS OF TATTOO REMOVAL


A. Destruction of tattoo: Removal of epidermis and superficial dermis
1. Nd:YAG laser
2. Infrared coagulator
3. Chemical peels
4. Dermabrasion
5. Cryosurgery
6. Dermaplaning
B. Inflammatory removal: Induces removal or diffusion of pigment
1. Tannic acid
2. Oxalic acid
3. Urea
C. Surgical excision: Necessitates surgical scar in exchange for removal of the tattoo
1. Simple excision with primary closure for small tattoos
2. Excision with flap/graft coverage for larger ones
D. Laser removal of particular tattoo color pigments:
1. Red, orange, and yellow: Q-switched Nd:YAG (532-nm) or pulsed dye (510-nm) lasers
2. Black, blue, and green: Q-switched alexandrite (755-nm) and Q-switched ruby (694-nm) lasers.
3. Black: Q-switched Nd:YAG (1064-nm) is optimal for black pigment.

PEARLS
1. If the lymphedema progresses, application of intermittent pneumatic massage unless the extremity is infected, in which case
massage is deferred until the infection resolves. Manual lymph compression enhances drainage through unaffected lymphatics.
2. The lymphatic system is responsible for transporting protein and lipids from the inter-stitial space to the vascular system.
3. Q-switched Nd:YAG and Alexandrite lasers helpful for tatoo removal.
4. Pulsed dye laser (585 nm, 450 ms): treatment of choice for most vascular lesions.

QUESTIONS YOU WILL BE ASKED


1. What is the difference between timing of presentation of hemangiomas versus vascular malformations?
Vascular malformations are present at birth and continue to grow as the child ages. They do not involute. Infantile hemangiomas
present after birth and continue to grow until approximately one year of age after which time they often begin to involute. The
exception is congenital hemangiomas which are present at birth.
2. By what age do most hemangiomas involute?
Most hemangiomas involute by 5 to 7 years of age. Approximately 50% of lesions involute by age 5. Approximately 70% of
lesions involute by age 7.
3. What are the indications to perform operative intervention on a hemangioma?
1. Obstruction or deformation of critical structures such as the eye or airway.
2. Bleeding or ulceration that is unresponsive to pharmacologic management. 3. Easily excisable area with potential for an
acceptable scar.
4. What nerve distribution do port-wine stains usually affect?
V1 and V2 branches of cranial nerve V.
5. Name the different syndromes associated with hemangiomas and vascular malformations along with associated signs.
See Sections IIF, IIIC, and IIIF for details.

Recommended Readings
Chim H, Drolet B, Duffy K, Koshima I, Gosain AK. Vascular anomalies and lymphedema. Plast Reconstr Surg. 2010;126(2):55e-69e. PMID: 20679788
Pohl L, Kaiser K, Raulin C. Pitfalls and recommendations in cases of laser removal of decorative tattoos with pigmented lesions: case report and review of the literature.
JAMA Dermatol. 2013;149(9): 1087-1089. PMID: 23903803
INTRODUCTION
I. EPIDEMIOLOGY
A. Squamous cell carcinoma (SCC) is the most common cancer involving head and neck mucosal sites (accounts for 90% of
malignancies)
B. Most often occurs in the sixth and seventh decades of life
C. Incidence increases with age
D. Male to female ratio is approximately 2:1
E. Risk factors
1. Tobacco (including smokeless/chewing tobacco)
2. Alcohol: Synergizes with tobacco; increases risk by 10- to 15-fold
3. Human papilloma virus (HPV): Responsible for increasing incidence of oropharyngeal SCC
4. Epstein–Barr virus (EBV): Associated with nasopharyngeal SCC
5. Poor dental hygiene
6. Chronic irritation (i.e., ill-fitting dentures)
7. Plummer–Vinson syndrome (achlorhydria, iron deficiency anemia, dysphagia, mucosal atrophy)
8. Syphilis
9. Lichen planus
10. Chronic immunosuppression
11. Betel nuts: Common in Indian population

II. PATHOLOGY
A. Premalignant lesions
1. Require close follow-up; biopsy required to rule out invasive component
2. Leukoplakia
a. Clinical description of white patchy mucosa
b. Represents epithelial hyperplasia, usually secondary to trauma
c. May harbor dysplasia, carcinoma in situ, or invasive SCC
3. Erythroplakia: Clinical description of red “velvet-like” mucosal patches
a. Higher incidence of associated SCCA compared to leukoplakia
b. Biopsy required to rule out SCCA
4. Lichen planus
a. White, flat inflammatory papule involving oral mucosa
b. 5% undergoes malignant transformation
B. Gross variants of SCCA
1. Ulcerative type: Most common type of oral cavity SCCA
2. Infiltrative type
a. Often found in tongue SCCA
b. Diagnosis requires careful palpation
3. Exophytic type
a. Spreads superficially
b. Less aggressive/less likely to metastasize
C. SCCA histology
1. Three histologic variants (well, moderately, and poorly differentiated)
______________
*De note s common in-se rvice e xamination topics

2. Well-differentiated lesions have increased amounts of keratin and predict a better prognosis.
3. Nasopharyngeal carcinoma has a separate World Health Organization (WHO) classification.
a. WHO type I: SCCA; represents 25% of nasopharyngeal carcinoma
i. Not associated with EBV
ii. Worse prognosis
iii. Less sensitive to radiation
b. WHO type II: nonkeratinizing; 12% tumors
i. Associated with EBV
ii. Better prognosis
iii. Sensitive to radiation
c. WHO type III: Undifferentiated (includes lymphoepithelioma, anaplastic and clear cell variants); >60% tumors
i. Associated with EBV
ii. Better prognosis
iii. Sensitive to radiation
4. Verrucous carcinoma (Ackerman’s tumor)
a. Rare variant of SCCA
b. Most often involves buccal mucosa followed by gingival mucosa
c. Exophytic; papillary morphology
d. Deep infiltration and metastasis uncommon
e. Treatment
i. Surgical excision with only a few millimeters of margin
ii. Serial sectioning of pathology specimen necessary to rule out harboring invasive SCCA.
iii. Role of radiation controversial due to potential for transformation into an anaplastic/aggressive lesion.
D. Metastatic disease
1. Regional spread to cervical lymph nodes
a. Follows a predictable pattern depending on location of primary tumor.
b. Midline tumors can drain to bilateral nodal basins.
c. Poor prognostic factors include multiple lymph node involvement, presence of extracapsular spread (ECS), perineural
invasion, and matted nodes.
2. Distant metastasis is most often to lung, and sometimes to bone.

III. ANATOMY
A. Oral cavity
1. Extends from the skin-vermilion lip junction posteriorly to the junction of the hard and soft palate and circumvallate
papillae.
2. The oral cavity is divided into a number of subsites
a. Lips
b. Buccal mucosa
c. Upper and lower alveolar ridge
d. Retromolar trigone (RMT)
e. Floor of mouth (FOM)
f. Hard palate
g. Anterior two-third of tongue
B. The pharynx is divided into three subsites
1. Nasopharynx: Extends from the skull base superiorly to the soft and hard palate inferiorly; from the nasal
choanae/septum to the posterior pharyngeal wall. Subsites of the nasopharynx include:
a. Fossa of Rosenmuller
b. Torus and orifice of the Eustachian tube
c. Lateral and posterior walls
2. Oropharynx
a. Anterior border: Circumvallate papillae
b. Lateral borders: Tonsil, tonsillar fossa, and tonsillar pillars
c. Posterior border: Posterior pharyngeal wall
d. Inferior border: Floor of vallecula (space between base of tongue (BOT) and epiglottis)
e. Superior border: Soft palate
f. Weldeyer’s ring, within the oropharynx, includes lymphoid tissue of the palatine and lingual tonsils
3. Hypopharynx: Extends from floor of vallecula and aryepiglottic folds to inferior border of cricoid cartilage; contains
three subsites.
a. Pyriform sinuses
b. Posterior pharyngeal wall
c. Postcricoid region/pharyngoesophageal junction (least common)
C. Larynx: Three subsites
1. Supraglottis (30% of laryngeal SCCA)
a. Separated from glottis by horizontal plane through ventricle (space between true and false vocal cords).
b. Includes epiglottis, aryepiglottic folds, arytenoids, false vocal cords, and ventricles.
2. Glottis (50% to 70% of laryngeal SCCA)
a. Extends from ventricle to 1 cm below the free edge of the true vocal cord.
b. Includes true vocal cords, anterior, and posterior commissure.
c. “Transglottic” tumors cross glottis in continuity with another site
3. Subglottis: Extends from glottis to inferior border of cricoid ring.
D. Other spaces
1. Pre-epiglottic space
a. Bound superiorly by the hyoepiglottic ligament and vallecula, anteriorly by the thyrohyoid ligament, and posteriorly by
the epiglottis and thyroepiglottic ligament.
b. The infrahyoid epiglottis has numerous holes in the cartilage allowing cancer to easily spread from the larynx to this
space.
2. Paraglottic space
a. Potential space between the thyroid cartilage and medial mucosa wall of the pyriform sinus.
b. Continuous with pre-epiglottic space anteriorly and superiorly.
3. Reinke’s space: Between true vocal cord epithelium and thyroarytenoid muscle.
E. Lymphatic drainage levels of the neck (Fig. 16-1)
1. Level I (submental/submandibular triangle): Bound by anterior and posterior digastric muscles, inferior hyoid bone,
and body of the mandible.
2. Level II (upper jugular): Bound by skull base, inferior border of hyoid, stylohyoid muscle, and lateral border of
sternocleidomastoid muscle (SCM).

Figure 16-1. Lymphatic drainage levels of the neck. Level I, submental and submandibular lymph node groups; level II, upper jugular group; level III, middle jugular
groups; level IV, lower jugular group; level V, posterior triangle group; level VI, anterior compartment group. (From Fischer JF, ed. Mastery of Surgery. 6th ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2012.)

3. Level III (mid-jugular): Bound by inferior border of hyoid, inferior border of cricoid cartilage, lateral border of
sternohyoid, and lateral SCM.
4. Level IV (lower jugular): Bound by inferior boarder of cricoid cartilage, clavicle, lateral border of sternohyoid muscle,
and lateral border of SCM.
5. Level V (posterior triangle): Bound by apex of SCM and trapezius muscle, clavicle, posterior border of SCM, and
anterior border of trapezius muscle.
6. Level VI (upper mediastinum): Bound by the hyoid bone, suprasternal notch, and common carotid arteries.
IV. TUMOR, NODE, METASTASIS (TNM) STAGING SYSTEM
A. Clinical staging system
1. Stage denoted by Roman numeral (Table 16-1)
2. Takes into account T, N, and M levels to give a clinical stage
3. Treatment and prognosis are determined by stage
B. Primary tumor (T)
1. Oral cavity (OC)
a. TX: Cannot assess
b. T0: No evidence of tumor
c. Tis: Carcinoma in situ
d. T1: ≤2 cm
e. T2: >2 cm and ≤4 cm
f. T3: >4 cm
g. T4a: Invades adjacent structures (cortical bone, extrinsic tongue musculature, inferior alveolar nerve, floor of mouth,
maxillary sinus, facial skin).
h. T4b: Invades masticator space, pterygoid plates, skull base, or encases internal carotid artery.
2. Oropharynx (OP)
a. T1: ≤2 cm
b. T2: >2 cm and ≤4 cm
c. T3: >4 cm
d. T4a: Invades larynx, extrinsic tongue musculature, medial pterygoid muscle, hard plate, or mandible
e. T4b: Invades lateral pterygoid muscle, pterygoid plate, lateral nasopharynx, skull base, or encases carotid artery
3. Hypopharynx (HP)
a. T1: Tumor limited to 1 subsite or ≤2 cm
b. T2: Tumor involves more than 1 subsite or is >2 cm (and ≤4 cm) without vocal cord fixation
c. T3: >4 cm or vocal cord fixation or extension into esophagus
d. T4a: Invades thyroid/cricoid cartilage, hyoid bone, thyroid gland, esophagus, strap muscles/subcutaneous tissue
e. T4b: Invades prevertebral fascia, mediastinum, or encases carotid artery
4. Nasopharynx (NP)
a. T1: Confined to nasopharynx
b. T2a: Extends to soft tissues of OP/nasal cavity without parapharyngeal extension

c. T2b: Any tumor with parapharyngeal extension.


d. T3: Involves bony structures or paranasal sinuses.
e. T4: Intracranial extension, cranial nerve involvement, infratemporal fossa, hypopharynx, orbit, or masticator space.
5. Supraglottis
a. T1: Limited to one subsite with normal vocal cord movement.
b. T2: Invades mucosa of more than one adjacent supraglottic or glottic subsite or region outside supraglottis (BOT,
vallecula, medial wall of pyriform sinus) without vocal cord fixation.
c. T3: Tumor limited to larynx with vocal cord fixation or invasion of postcricoid area, pre-epiglottic space, paraglottic
space, or inner cortex thyroid cartilage.
d. T4a: Invasion through thyroid cartilage or invasion beyond larynx (i.e., trachea, deep extrinsic tongue musculature,
strap muscles, thyroid gland, or esophagus).
e. T4b: Invades prevertebral space, mediastinum, or encases carotid artery
6. Glottis
a. T1a: Limited to one vocal cord with normal mobility.
b.T1b: Involves both vocal cords with normal mobility.
c.T2: Extension to supraglottis or subglottis or impaired vocal cord mobility.
d.T3: Tumor limited to larynx with vocal cord fixation; invasion of paraglottic space or inner cortex thyroid cartilage.
e. T4a: Invasion through thyroid cartilage or invasion beyond larynx (i.e., trachea, deep extrinsic tongue musculature,
strap muscles, thyroid gland, or esophagus).
f. T4b: Invades prevertebral space, mediastinum, or encases carotid artery.
7. Subglottis
a. T1: Limited to subglottis
b. T2: Extends to vocal cord(s) with normal or impaired mobility
c. T3: Limited to larynx with vocal cord fixation
d. T4a: Invasion through thyroid cartilage or invasion beyond larynx (i.e., trachea, deep extrinsic tongue musculature,
strap muscles, thyroid gland, or esophagus)
e. T4b: Invades prevertebral space, mediastinum, or encases carotid artery
C. Regional lymph nodes (N)
1. Nx: Cannot assess
2. N0: No regional involvement
3. N1: Ipsilateral lymph node ≤3 cm
4. N2a: Single ipsilateral lymph node >3 cm but ≤6 cm
5. N2b: Multiple ipsilateral lymph nodes all ≤6 cm
6. N2c: Bilateral or contralateral lymph node ≤6 cm
7. N3: Lymph node >6 cm
D. Distant metastasis (M)
1. Mx: Cannot assess
2. M0: No distant metastasis
3. M1: Distant metastasis

EVALUATION
I. HISTORY
A. Duration of lesion or mass, and rapidity of enlargement, should be determined
B. Associated symptoms may include
1. Localized pain
2. Odynophagia (painful swallowing)
3. Otalgia (referred ear pain)
4. Hoarseness (indicating glottic involvement)
5. Dysphagia (difficulty swallowing)
6. Weight loss
7. Shortness of breath/stridor
8. Hemoptysis
C. Social history
1. Tobacco use (type; number of years)
2. Alcohol (type; daily amount consumed)—patient may require prophylaxis with benzodiazepines to prevent delirium
tremors (DTs) if hospitalization planned
D. Past medical history
1. Past history of head and neck SCCA
2. Previous exposure to radiation

II. PHYSICAL EXAM


A. Tympanic membranes: Middle ear effusion may indicate nasopharyngeal mass
B. Oral cavity
1. State of dentition is important for radiation and reconstructive considerations. Teeth may need to be extracted if they
have excessive caries prior to radiation therapy (post-XRT extraction can be inciting event in osteoradionecrosis).
2. Note size and location of suspicious lesions.
3. Comment on fixation of lesion to surrounding bone.
4. Describe extension of tumor by noting all structures involved
5. Deviation of tongue on protrusion indicates involvement of hypoglossal nerve (CN XII) ipsilateral to the deviation.
6. Trismus (inability to fully open mouth) indicates possible involvement of pterygoid muscle, masseter muscle, and/or
infratemporal fossa.
C. Oropharynx
1. Note size and location of suspicious lesions
2. Comment on fixation to surrounding bone
3. Describe extension of tumor
4. Palpate BOT and RMT because lesions can infiltrate and/or be difficult to visualize.
D. Larynx
1. Perform indirect examination with mirror visualization.
2. Direct visualization with flexible laryngoscopy should be performed.
3. Assess airway, nasal portion of the soft palate, vocal cord mobility, pyriform sinuses, epiglottis, and vallecula.
4. Anticipate potential need for surgical airway prior to treatment.
E. Neck
1. Careful palpation for cervical lymphadenopathy is performed.
a. Comment on node size, location, and fixation.
b. “Lymph nodes” greater than 3 cm are likely matted nodes.
2. A neck mass can also represent direct tumor extension.
3. Fixation of the larynx (loss of laryngeal crepitus and ability to move larynx side-to-side) is indicative of extralaryngeal
tumor extension.

III. LABORATORY STUDIES


A. CBC
B. Coagulation studies (PT, PTT)
C. Electrolyte panel
D. Liver enzymes, including alkaline phosphatase

IV. RADIOGRAPHIC STUDIES


A. CT scan of the neck with contrast (axial and coronal)
1. Evaluate tumor extension
2. Assess bony and cartilaginous invasion
3. Evaluate cervical lymph node involvement
4. Evaluate great vessel involvement/encasement
B. MRI is helpful in evaluating skull base involvement and neural invasion
C. Panorex is useful for evaluating mandibular bone involvement if the CT scan is equivocal
D. Chest X-ray is used to screen for pulmonary metastases
1. Any nodule requires further evaluation with chest CT.
2. Most surgeons advocate chest CT for any patient with recurrent SCCA or with advanced stage III/IV disease since it is
more sensitive than CXR.
E. Positron emission testing (PET)
1. Tissues with high metabolic rates (such as tumors) demonstrate increased uptake of radioactive 18-fluorodeoxyglucose
(FDG avidity).
2. May be helpful in differentiating post-radiation changes from tumor, and in working up occult nodal disease, pulmonary
metastasis, and secondary primaries.
3. Post-treatment response evaluation after chemoradiation (usually 12 weeks after completion).
F. Bone scan evaluates for metastatic lesions in patients with elevated alkaline phosphatase levels, recent fracture, or bone
pain.
G. Barium swallow is used to evaluate cervical esophageal involvement if rigid esophagoscopy cannot be performed.

V. HISTOLOGIC DIAGNOSIS
A. Biopsy of the primary tumor can be done in clinic setting with local anesthesia or in OR under general anesthesia depending
on anatomic location.
B. Fine-needle aspiration (FNA) of neck masses is used to assess cervical metastasis.

VI. DIRECT LARYNGOSCOPY (DL)


A. Formal evaluation of tumor extension under general anesthesia (“tumor mapping”).
B. Often provides better visualization compared to clinic exam because head and neck musculature is relaxed
C. Rigid esophagoscopy and rigid/flexible bronchoscopy can be performed at the same time to evaluate for synchronous
second primary lesions.
VII. ADDITIONAL CONSIDERATIONS
A. Cardiac clearance by cardiology team
B. Nutritional exam
1. Adequate nutrition is imperative for postoperative healing.
2. Patient may require supplemental nutrition.
3. If dysphagia/odynophagia will be problematic, consider nasogastric feeding tube placement.
4. If long-term nutrition will likely be a problem, consider PEG tube.
C. Dental exam: Patients undergoing radiation therapy will need poor dentition extracted prior to treatment in order to avoid
caries, abscess formation, and osteoradionecrosis.
D. Pulmonary function tests (PFTs) are required if a patient is being considered for laryngeal conservation surgery
(hemilaryngectomy, supracricoid, etc.).

TREATMENT
I. MULTIDISCIPLINARY TEAM MEMBERS
A. Surgical extirpative team
B. Surgical reconstructive team
C. Medical oncologist
D. Radiation oncologist
E. Radiologist
F. Speech therapist
G. Dentist/prosthodontist
H. Nutritionist
I. Physical therapist
J. Social worker

II. ORAL CAVITY AND PHARYNX (EXCLUDING NASOPHARYNX)


A. Single modality treatment (surgery or radiation therapy) for T1/T2 lesions
1. Surgery is favored for oral cavity tumors
a. Better locoregional control and overall survival versus radiation
b. Spares patient radiation side effects (see Complications section)
c. Reserves the use of radiation for recurrence
2. Surgery versus radiation for oropharynx lesions
a. Transoral laser and robotic surgery have evolved as additional options.
b. Chemoradiation of HPV+ advanced oropharynx SCC with excellent survival rates.
c. Patient compliance is imperative when selecting candidates.
d. Early lesions with a high rate of occult nodal metastasis (e.g., oropharynx) should include radiation to neck fields.
e. Disadvantages of XRT: The patient will miss ~2 months of work/activity and tumor recurrence may be difficult to
detect in the setting of postradiation changes.
B. Multimodality treatment for T3/T4 lesions
1. Surgery with radiation therapy (usually postoperative)
2. Organ preservation protocols involving chemotherapy (usually cisplatin and 5-FU) and radiation
3. Patients should be educated on available clinical trials

III. LARYNX
A. Glottic SCCA in situ
1. Initially can be treated with vocal cord stripping and close follow-up.
2. Recurrence requires repeat stripping, microlaryngeal excision, radiation, or partial laryngectomy depending on patient
history and tumor size.
B. Glottic T1/T2 SCCA
1. Primary radiation with 50 to 70 Gy over 5 to 8 weeks preserves voice quality compared to surgery.
2. Surgery with laser microexcision or partial laryngectomy has an overall cure rate of 80% to 85%.
3. Neck metastases are rare (8%) due to limited lymphatics in glottic region.
C. T3/T4 laryngeal tumors
1. Vertical partial laryngectomy versus total laryngectomy (depending on tumor location and pulmonary status) with
postoperative radiation.
2. Organ preservation protocols involving chemotherapy (usually cisplatin and 5-FU) and radiation have equal survival rates
versus primary surgery with postoperative radiation.
D. Subglottic SCCA
1. Nodal and cartilage involvement common because presentation is late (presentation often involves airway obstruction).
2. Total laryngectomy with bilateral neck dissections usually required.
3. Postoperative radiation often necessary given late presentation/advanced disease.
4. Stomal recurrence is common (paratracheal node dissection advocated to help prevent stomal recurrence).
E. Speech rehabilitation
1. Esophageal speech: Air released from esophagus vibrates against posterior pharyngeal wall to produce speech.
2. Tracheoesophageal puncture
a. A one-way valve is placed through posterior tracheal wall (~1 cm below stoma opening) into the esophagus.
b. Pulmonary air is diverted through the valve to vibrate against esophagealpharyngeal wall and produce speech.
c. Superior voice quality compared to esophageal speech.
d. Contraindication: Poor patient vision or dexterity; poor patient motivation.
e. Potential complications include leakage, granulation tissue formation, and Candida infections.
3. Artificial larynx (electrolarynx) electronically modulates and amplifies remaining vocal sounds to simulate speech.

IV. NASOPHARYNX
A. *Radiation to primary lesion and bilateral necks
B. Concomitant chemotherapy decreases the development of distant metastasis and improves both disease-free and overall
survival for advanced disease.
C. Salvage neck dissection required for persistent nodal disease following chemo-therapy and radiation.

V. MANAGEMENT OF THE NECK


A. Selective neck dissection
1. Neck dissection with preservation of one or more lymph node groups.
2. Indication: Used as a staging procedure in a patient without clinical evidence of nodal metastasis (N0 neck) in order to
determine the need for postoperative neck radiation.
B. Modified radical neck dissection
1. Removal of all ipsilateral cervical lymph node groups (levels I through V).
2. Preserves at least one of the following vital structures: The internal jugular vein, sternocleidomastoid muscle, or spinal
accessory nerve (CN XI).
3. Indication: Treatment of known cervical lymph node metastasis in which the internal jugular vein, SCM, and spinal
accessory nerve are not directly involved.
C. Radical neck dissection
1. Removal of all ipsilateral cervical lymph node groups (levels I through V).
2. Removal of all three vital structures: Internal jugular vein, sternocleidomastoid muscle, and spinal accessory nerve (CN
XI)
3. Indication: Treatment of advanced cervical disease including multiple, fixed lymph node metastases invading neck
structures.
D. Extended neck dissection: Involves additional lymph node groups beyond levels I–V or non-lymphatic structures such as
the hypoglossal nerve

VI. RECONSTRUCTION—SEE CHAPTER 16: “PRINCIPLES OF HEAD AND NECK RECONSTRUCTION”

VII. COMPLICATIONS
A. Surgical
1. Bleeding
2. Infection/wound breakdown/potential for carotid artery exposure
3. Scarring
4. Nerve paresis/paralysis (especially marginal mandibular branch of CN VII and spinal accessory nerve)
5. Fistula formation
6. Chronic aspiration
7. Trismus (limited mouth opening)
B. Radiation
1. Xerostomia (dry mouth secondary to salivary gland dysfunction; may be palliated with prosalivatory topical medications)
2. Mucositis: Patient may require PEG or Dobhoff tube for nutrition
3. Pharyngitis
4. Laryngeal and esophageal scarring/stenosis
5. Osteoradionecrosis: Treatment requires debridement, local wound care; ± antibiotics; may eventually require free tissue
transfer
6. Dental caries
7. Chronic aspiration

VIII. FOLLOW-UP
A. Routine appointments imperative because HNSCCA has a high rate of locoregional recurrence and of second primary
tumor development
1. First year: Every 1 to 2 months
2. Second year: Every 2 to 3 months

Figure 16-2. Subclavian and carotid arteries and their branches. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2010.)

3. Third year: Every 3 to 4 months


4. Fourth and fifth year: Every 4 to 6 months
5. Yearly thereafter
B. Yearly chest X-ray to evaluate pulmonary metastasis
C. Radiated patients require yearly TSH because of risk for hypothyroidism

QUESTIONS YOU WILL BE ASKED


1. What are branches of the external carotid artery?
Superior thyroid, ascending pharyngeal, lingual, occipital, facial, posterior auricular, maxillary, and superficial temporal
2. What is the relationship of CN XI to sternocleidomastoid?
The accessory nerve travels approximately 1 cm superior to Erb’s point
3. What is the difference between a modified and radical neck dissection?
Radical neck dissection sacrifices CN XI, IJ vein, and SCM. A modified radical neck dissection spares one or more of these
three structures
4. Draw branches of the external carotid artery (Fig. 16-2)
5. Draw the different levels of node dissection
Recommended Readings
Bernier J, Domenge C, Ozsahin M, et al. Postoperative radiation with or without concomitant chemo-therapy for locally advanced head and neck cancer. N Engl J Med.
2004;350:1945–1952.
Cooper JS, Pajak T F, Forastiere AA, et al. Postoperative concurrent radiotherapy and chemotherapy for high risk squamous cell carcinoma of the head and neck. N Engl
J Med. 2004;350:1937–1944.
Forastiere AA, Goepfert H, Maor M, et al. Concurrent chemotherapy and radiotherapy for organ preservation in advanced laryngeal cancer. N Engl J Med.
2003;349:2091–2098.
Funk GF, Karnell LH, Robinson RA. Presentation, treatment and outcome of oral cavity cancer: a National Cancer Data Base report. Head Neck. 2002;24:165–180.
Mork J, Lie AK, Glattre E, et al: Human papillomavirus infection as a risk factor for squamous-cell carcinoma of the head and neck. N Engl J Med. 2001;344(15):1125–
1131.
O’Malley Jr BW, Weinstein GS, Snyder W, et al. T ransoral robotic surgery (T ORS) for base of tongue neoplasms. Laryngoscope. 2006;116:1465–1472.
O’Sullivan B, Shah J. New T NM staging criteria for head and neck tumors. Semin Surg Oncol. 2003;21:30–42.
Pfister DG, Ang KK, Brizel DM, et al. National Comprehensive Cancer Network. Head and neck cancers. J Natl Compr Canc Netw. 2011;9(6):596–650. PMID:
21636536.
Robbins KT, Shaha AR, Medina JE, et al. Consensus statement on the classification and terminology of neck dissection. Arch Otolaryngol Head Neck Surg.
2008;134:536–538.
Shah JP. Patterns of cervical lymph node metastasis from squamous carcinomas of the upper aerodigestive tract. Am J Surg. 1990;160:405–409.
T he Department of Veterans Affairs Laryngeal Cancer Study Group. Induction chemotherapy plus radiation compared with surgery plus radiation in patients with
advanced laryngeal cancer. N Engl J Med. 1991;324:1685–1690.
EVALUATION OF A NECK MASS
I. HISTORY
A. Age of patient
1. Young patients are more frequently associated with congenital and infectious processes
2. Older patients more frequently have neoplastic and malignant processes
B. Duration and pattern
1. Date first noted
2. Growth pattern: Intermittent presence and fluctuations in size suggest a non-neoplastic process; slow growth followed by
rapid growth suggests a neoplastic process
C. Significant symptoms that may accompany a neck mass include
1. Otalgia, dysphonia, odynophagia, dysphagia, and generalized pain
2. Constitutional symptoms: Fever, chills, night sweats or weight loss
3. Hyper- or hypothyroid symptoms: Changes in energy level, mood, or temperature sensitivity.
D. Potential associations or causal agents
1. Exposure history: TB, animals (cats), radiation, or nickel
2. Recent infections: URI, sinusitis, dental problems, or recent dental procedures
E. Family history
1. Inherited syndromes
a. Multiple Endocrine Neoplasia type I *(MEN-I): Thyroid medullary carcinoma, parathyroid hyperplasia, and
pituitary tumors
b. Li–Fraumeni syndrome: Sarcoma and other malignancies
c. Basal cell nevus (Gorlin’s) syndrome: Multiple basal cell carcinomas and odontogenic keratocysts
d. Neurofibromatosis
2. Nonsyndromic family history of benign or malignant disease
F. Social history
1. Tobacco: Head and neck squamous cell carcinoma is six times more likely in smokers
2. EtOH: Potentiator especially in patients with a positive tobacco history

II. PHYSICAL EXAMINATION (requires a complete examination of head and neck; see also Chapter 14: “Squamous Cell
Carcinoma of the Head and Neck”)
A. Skin: Examine the scalp, ears, face, and neck for lesions or masses.
B. Eye: Proptosis, visual acuity disturbances, or extraocular movement changes may be a sign of an orbital mass.
C. Ear: Masses or effusions may indicate Eustachian tube obstruction
D. Nose: Inspect for nasal mucosa lesions and sinus discharge
E. Oral cavity/oropharynx
1. Inspect tonsillar pillars and posterior pharyngeal wall and perform mirror laryngoscopy or flexible laryngoscopy

______________
*De note s common in-se rvice e xamination topics

2. Palpate and inspect palate, tongue (dorsal, ventral, and base), floor of mouth, gingiva, buccal mucosa, and lips
3. Evaluate salivary flow (Stenson and Wharton ducts)
F. Neck
1. Inspection
a. Evaluation for symmetry and visible masses or lesions
b. Activation of musculature and symmetry on repose and while swallowing
c. Jugular venous distension may be seen with upper neck masses
2. Palpation
a. Anterior and posterior triangles (anterior and posterior to the sternocleidomastoid muscle), including lymph node
areas 1–5
b. All lymph node chains are examined for
i. Mobile versus fixed nodes
ii. Soft or doughy versus hard nodes
iii. Tenderness on palpation
3. Salivary gland palpation (see below)
4. Thyroid palpation
a. Performed from both anterior and posterior positioning
b. In repose and on swallowing
c. Evaluate size, symmetry, and consistency
G. Neurological evaluation of cranial nerve function
1. May assist in detection of an unknown primary
2. Nerve involvement may be an indicator of an aggressive neoplastic process

III. DIFFERENTIAL DIAGNOSIS OF NECK MASSES


A. *“80% Rule”
1. *80% of nonthyroid neck masses in adults are neoplastic, 80% of these are malignant, 80% of these are
metastases, and 80% of these are from primaries above the clavicles
2. *80% of neck masses in children are inflammatory or benign
B. *The type of neck mass is predicted by location
1. Midline: Teratoma, dermoid, or thyroglossal duct cyst
2. Anterior triangle: Branchial cleft anomaly or lymph node (site for nodal drainage of intra- and extraoral sites)
3. Posterior triangle: Lymph node (site for nodal drainage of intra- and extraoral sites)
4. Regional sites suggestive of local disease process
a. Thyroid
b. Salivary gland (parotid, submandibular, and sublingual)
C. Adenitis
1. Nodes greater than 1.5 cm in diameter are considered abnormal
2. Bacterial etiologies include Streptococcus, Staphylococcus, Mycobacterium, Catscratch fever (Bartonella),
Tularemia, and Actinomyces
3. Viral causes include Epstein–Barr virus (EBV), cytomegalovirus (CMV), herpes simplex virus (HSV), HIV, rhinovirus,
and adenovirus
4. Fungal infections are likely caused by Coccidiodomycosis
5. Toxoplasmosis can cause generalized or focal lymphadenitis.
6. Empiric therapy with antibiotics for 10 days to 2 weeks is indicated if the mass is inflammatory
a. Treat the most common causes in the differential diagnosis based on history, physical examination, and appropriate
diagnostic studies
b. Close follow-up of empiric treatment is required
c. Persistence of adenitis greater than 2 weeks requires additional work-up and treatment
D. Congenital neck masses
1. Branchial cleft anomalies
a. Arise from primitive branchial arches, clefts, and pouches
b. May include cysts, fistulas, or sinuses
c. *Cleft I: external auditory canal
d. Cleft II
i. Most common
ii. *Run under middle/lower sternoclydomastoid and over CN IX
iii. Runs under ECA and over internal carotid toward tonsillar fossa
iv. Third and fourth branchial cleft anomalies
e. Cleft III: Similar to cleft II but runs under ICA
f. Treated by excision of the cyst or sinus; may be complex in some cases of second branchial arch cysts, and may
course around the carotid artery
2. Thyroglossal duct cyst
a. Remnant of thyroglossal duct epithelium
b. *Occur anywhere from the foramen cecum of the tongue to the suprasternal notch
c. Often found in midline
d. Most commonly diagnosed in the first two decades of life
e. Treated by complete excision of the cyst tract, decreased recurrence rate if hyoid bone included in excision (Sistrunk
procedure)
3. Dermoid cyst
a. Teratoma-like cysts contain two rather than three (teratoma) germ layers
b. *Often presents as a midline doughy mass; most common in young adults
c. Usually amenable to local excision
d. Pre-op CT recommended to rule out
i. Extension of dermoid through posterior table which would require neurosurgical intervention
ii. *Glioma or encephalocele
E. Thyroid masses
1. Solitary nodule: Cyst, benign, or malignant neoplasm
2. Multinodular goiter: Toxic or non-toxic
3. Inflammatory/autoimmune: Reidel, Hashimoto, and De Quervain thyroiditis
4. Malignancy: Papillary carcinoma, follicular carcinoma, Hürthle cell tumors, medullary carcinoma, and anaplastic
carcinoma. The majority of thyroid cancers are low grade (papillary and follicular) and amenable to surgical excision.
Anaplastic tumors are associated with high mortality and are usually not treated surgically.
F. Neoplastic neck masses
1. Benign
a. Mesenchymal: Fibroma, lipoma, leiomyoma, rhabdomyoma, and neural tumors are usually amenable to resection
b. Salivary gland masses: See below
c. Vascular masses: Vascular malformation (not a neoplasm; actually a congenital anomaly), hemangioma,
lymphangioma (See Chapter 15: “Vascular Anomalies, Lymphedema, and Tattoos”)
2. Malignant
a. Sarcoma: Fibrosarcoma, liposarcoma, neurofibrosarcoma, and angiosarcoma. Usually amenable to surgical
management with or without radio-therapy (see Chapter 13: “Malignant Skin and Soft Tissue Lesions”)
b. Salivary tumors: See below
c. Lymphoma
3. Metastases
a. Primary regional site for head and neck malignancy spread is to cervical lymph nodes
b. Esophageal and lung tumors

IV. DIAGANOSTIC STUDIES


A. Ultrasound with Doppler: Useful for determination of cystic versus complex versus solid; shows association with
adjacent structures (thyroid, lymph nodes); and guidance for fine-needle aspiration (FNA). Ultrasound is excellent for
diagnostic imaging of thyroid disorders.
B. MRI: Best for the evaluation of primary lesions of palate, parotid, and retro- and parapharyngeal spaces
C. CT with contrast: Evaluation of nodes >1 to 1.5 cm, especially with necrotic center of greater than 3 mm; evaluation of
extracapsular extension of nodal disease
D. FNA is especially useful for thyroid masses and solid masses of the neck. Accuracy is highly dependent on operator and
cytopathologist experience.
E. Nuclear medicine studies: Thyroid uptake scans can be useful to determine whether a mass is actively sequestering
iodine (and therefore likely benign). Salivary gland scans (see below).
F. Indications for open biopsy of a neck mass
1. Persistent for greater than 3 weeks
2. Likely metastatic without evidence of primary tumor
3. Negative endoscopy with multiple random biopsies
4. Negative FNA
5. Probable lymphoma

SALIVARY GLAND NEOPLASMS


I. SALIVARY GLAND ANATOMY
A. Glands develop during the 6th to 8th week of gestation as oral ectoderm and nasopharyngeal endoderm
B. Parotid gland
1. *The parotid is located in the preauricular upper neck (tail) with deep and superficial lobes. The facial nerve
separates the lobes.
2. The surrounding fascia of the gland is an extension of the superficial layer of the deep cervical fascia
3. The gland consists predominantly of serous acini
4. *Stenson’s duct arises from the anterior border of the parotid and enters the oral cavity at the level of the
maxillary second molar
C. Submandibular (submaxillary) gland
1. Located in the submandibular triangle
2. Surrounded by the splitting of the superficial layer of deep cervical fascia
3. *Mucus and serous acini are, along with the parotid, responsible for the majority of saliva production.
4. Wharton duct arises from the medial gland and enters the oral cavity in the anterior floor of mouth
5. Closely associated with the lingual nerve which sends autonomic fibers to the gland
D. Sublingual gland
1. Located in anterior floor of mouth just below the mucosa
2. No fascial covering
3. Mucus acini
4. Drained by multiple ducts of Rivinus along its superior aspect entering the oral cavity. Occasionally, a coalescence of
these ducts form the Bartholin duct which empties into Wharton’s duct.
E. Minor salivary glands
1. 600 to 1,000 glands are located just below the submucosal layer of the oral cavity
2. No fascial covering
3. Mainly mucous-secreting glands
4. Simple ductal system which empties directly into the oral cavity

II. DIAGNOSIS OF SALIVARY GLAND PATHOLOGY


A. History
1. Findings favoring a diagnosis of neoplasm
a. Presence over an extended period of weeks to months
b. Pain is usually a sign of advanced disease
c. Slow but persistent growth or slow growth with sudden rapid phase indicates possible malignant transformation or
secondary infection with malignancy
2. Findings favoring an infectious processes. Rapid onset with signs of inflammation (warmth, erythema, and edema),
repeated episodes of inflammation, alcohol abuse, autoimmune diseases (i.e., Sjogren syndrome), HIV, xerostomia, and
dehydration
B. Physical examination findings
1. Findings favoring neoplasm
a. Discretely palpable firm mass especially when fixed to adjacent tissue
b. Facial nerve involvement/paralysis is a sign of malignancy
2. Findings favoring an infectious processes: Tenderness on palpation, evidence of duct obstruction, presence of a
stone, purulent discharge.

III. DIAGNOSTIC STUDIES


A. FNA
1. Accuracy is dependent on operator and cytopathologist experience
2. Accuracy in distinguishing benign versus malignant approaches 90% specificity
3. Indicated only if results may change decision to operate or extent of operation
B. MRI
1. Helpful for larger tumors (>3 cm) especially where there is a question of deep lobe parotid involvement
2. Visualizes delineation of poorly defined versus sharp margins (useful for distinguishing benign vs. malignant processes)
3. In general, benign lesions demonstrate low T1-weighted signal intensity but high T2 signal due to seromucinous content.
Malignant lesions show low T1 and T2 signal intensities.
4. Perineural invasion, nodal metastases, and dural involvement may be demonstrated
C. CT
1. CT for neoplastic salivary disease can be helpful in submandibular gland neoplasms; it may demonstrate bony invasion.
2. Helpful for stone identification in duct obstruction
D. Nuclear medicine studies
1. Of historical interest; of minimal use currently for salivary gland disease
2. Warthin’s tumor and oncocytoma usually have positive uptake of technetium-99

IV. *BENIGN SALIVARY NEOPLASMS


A. Pleomorphic adenoma (benign mixed tumor)
1. The most common salivary gland tumor (the most common malignantsalivary tumor is mucoepidermoid
carcinoma)
2. Represents 65% of parotid and submandibular and 40% of minor gland tumors. Usually occurs in patients with 30 to
50 years of age, presenting as a painless, slowly growing mass
3. *Treated with excision: Usually a superficial parotidectomy, submandibular gland removal, or local excision of minor
gland tumors. A cure rate of 95% can be expected when excised with clear surgical margins (enucleation of benign
mixed tumor results in recurrence).
B. Canalicular and basal cell adenoma (previously monomorphic adenoma)
1. Rule of 75%: Canalicular adenomas present in the upper lip in 75% of cases. Basal cell adenomas present in the
parotid gland in 75% of cases.
2. Female predilection 2:1
3. May resemble a mucocele, which is rare in the upper lip
4. Surgical excision is usually curative. Recurrence is rare and may actually represent multifocal disease.
C. Warthin’s tumor (papillary cystadenoma lymphomatosum)
1. *Most common site is the parotid gland
2. *Rule of 10’s (a gross simplification)
a. 10% of all parotid neoplasms are Warthin tumors
b. 10% are bilateral
c. 10 times risk in smokers
d. Male to female ratio is 10:1.
e. 10% are malignant
3. Usually Warthin’s tumors are treated with local excision with minimal margins, or with superficial parotidectomy
D. Oncocytoma
1. Rare neoplasm (less than 1% of all salivary tumors), predominantly found in older adults
2. Usually presents in the major salivary glands with 80% arising in the parotid
3. Surgical excision is usually curative, with minimal surrounding tissue taken to establish clear margins

V. MALIGNANT SALIVARY NEOPLASMS


A. Mucoepidermoid carcinoma
1. *Most common salivary malignancy (however, the most common salivary neoplasm is pleomorphic adenoma)
2. Mucoepidermoid tumors represent 10% of parotid and submandibular neoplasms and 20% of minor gland neoplasms
3. *Most (70%) are found in the parotid gland, but they may also arise in the submandibular and minor salivary glands
and intraosseous locations
4. Classified as low, intermediate, and high grade based on histopathology
5. Treatment is based on grade
a. Low: Surgical excision with negative margins; 90% cure rate
b. High: Treat like squamous cell carcinoma; 30% cure rate with neck dissection and postoperative radiation therapy
B. Adenoid cystic carcinoma
1. Represents approximately 10% of all salivary malignancies, and 40% of minor gland malignancy
2. Rare in the parotid; most common malignancy in the submandibular gland
3. Consists of cribriform, tubular, and solid histopathologic types
4. *Perineural spread is common which may include skip lesions (breaks in continuum) which are best seen
preoperatively with MRI
5. Treat with surgical excision and radiotherapy; 5-year survival is 70%, but 15-year survival is approximately 10%
C. Polymorphous low-grade adenocarcinoma
1. Almost exclusively found in minor salivary glands
2. Presents in hard/soft palate in 60% of patients; also presents commonly in upper lip and buccal mucosa
3. 70% female; commonly presents in 6th to 8th decade of life
4. Perineural invasion is common
5. Wide surgical excision is indicated, including bones when involved
D. Acinic cell carcinoma
1.Rare (1%), low-grade malignancy; metastasis is unlikely
2.95% arise within the parotid gland
3.Broad age range of presentation, from 3rd to 8th decade of life
4.Excision with superficial versus total parotidectomy, submandibular gland removal, or wide local excision of minor glands
is usually curative
5. Radiation therapy may increase local control
E. Malignant mixed tumors (carcinoma ex pleomorphic adenoma)
1. Results from malignant degeneration of pleomorphic adenoma (10% degenerate)
2. Often presents with rapid growth in previous slow-growing lesion
3. Pain and facial nerve involvement often present
4. Treated with excision, neck dissection, and radiation therapy. Five-year survival is 50%

VI. MALIGNANT NEOPLASM MANAGEMENT


A. Surgical treatment of local disease is usually accomplished with primary tumor control, that is
1. Total parotidectomy
2. Partial parotidectomy
3. Submandibular gland removal
4. Sublingual/minor gland removal
B. Indications for neck dissection
1. Dependent on low- versus high-grade primary tumor pathology
2. Dependent on clinical presentation
3. Primary lesion size >4 cm increases likelihood of nodal disease and need for neck dissection
C. Postoperative radiation therapy
1. Increases locoregional control in larger malignancies or close margins
2. 60 to 65 Gy usually administered postoperatively
3. Should be used in high-grade malignancies, resudual or recurrent disease, T3 or T4 parotid malignancies and invasion of
adjacent structures
D. Postoperative complications of salivary tumor excision
1. Sialocele
a. Presents as postoperative swelling with fluid collection
b. *Aspiration with placement of pressure dressing is usually successful for treatment
c. Botulinum toxin injection may be useful for resistant sialoceles
2. Facial nerve damage (see Chapter 24: “Facial Paralysis”)
a. *Damaged nerves should be immediately repaired if transection is noted intraoperatively, or grafted if a
branch is intentionally resected for malignant disease
b. *Loss of the marginal mandibular or temporal branches results in the most significant longstanding
deformity due to lack of arborization; the zygomatic and buccal branches have extensive arborization and the
distal branches will often recover function
c. The frontal/temporal branch is most important for eye closure and needs consideration for reconstruction if there is
evidence of inadequate arborization from the buccal/zygomatic branch
3. *Frey’s syndrome (auriculotemporal syndrome)
a. *Caused by reinnervation of sympathetic sudomotor (sweat) fibers by severed parasympathetic
(salivomotor) fibers normally directed to parotid gland
b. Results in preauricular gustatory sweating (sweating in response to salivary stimulation)
c. Demonstrated by Minor starch–iodine test (topical starch/iodine powder mixture turns blue with sweating)
d. Relatively common (up to 30%) in patients after parotidectomy when iodine tested but many fewer patients complain
of symptoms (<5%)
e. Initial treatment is topical antiperspirant prior to meals
f. Long-term treatment may require botulinum toxin (BoTox) injections for control
g. Thought to be caused by auriculotemporal nerve

PEARLS
1. 80% of nonthyroid neck masses in adults are neoplastic, and of those, 80% are malignant. However, 80% of neck masses in
children are benign.
2. Indications for open biopsy of a neck mass
a. Persistent for greater than 3 weeks
b. Likely metastatic without evidence of primary tumor
c. Negative endoscopy with multiple random biopsies
d. Negative FNA
e. Probable lymphoma
3. Slow-growing salivary gland lesions that suddenly begins rapid enlargement are often carcinoma
4. Mucoceles are common in the lower lip but rare in the upper lip.
5. Rule of 10’s for Warthin tumors
a. 10% of all parotid neoplasms are Warthin tumors
b. 10% are bilateral
c. 10 times risk in smokers
d. Male to female ratio is 10:1

QUESTIONS YOU WILL BE ASKED


1. What is the course of frontal branch of facial nerve?
The frontal branch can be roughly located along a line extending from the attachment of the lobule (approximately 5 mm below
the tragus), anterior and superior to a point 1.5 cm above the lateral aspect of the ipsilateral eyebrow. The frontal branch crosses
the zygoma approximately 1.5 cm anterior to the tragus. It runs superiorly to about 2 cm lateral to the lateral canthus. It runs
within the temporoparietal fascia (also known as the superficial temporal fascia).
2. What is the course of marginal mandibular nerve?
The marginal mandibular branch crosses the mandible within 1 cm of the facial notch.
3. What is the relation of marginal mandibular nerve to facial vessels?
The marginal mandibular nerve crosses superficial to the facial vein and artery.
4. Name five ways to find the main trunk of the facial nerve.
1) The tympanomastoid suture is the most reliable landmark (this is 6 to 8 mm lateral to the stylomastoid foramen).
2) It lies approximately 10 mm inferior and 10 mm deep to the tragal pointer.
3) Identify distal branches and follow proximally.
4) It lies approximately at the level of the digastric muscle (in the superficial to deep dimension).
5) Drill out the mastoid to identify the descending (intratemporal) segment.

Recommended Readings
Cooper DS, Doherty GM, Haugen BR, et al. Revised American T hyroid Association management guidelines for patients with thyroid nodules and differentiated thyroid
cancer. American T hyroid Association (ATA) Guidelines Taskforce on T hyroid Nodules and Differentiated T hyroid Cancer. Thyroid. 2009;19(11):1167–214.
PMID: 19860577.
Lima RA, T avares MR, Dias FL, et al. Clinical prognostic factors in malignant parotid gland tumors. Otolaryngol Head Neck Surg. 2005;133:702–708.
O’Brien CJ. Current management of benign parotid tumors—the role of limited superficial parotidectomy. Head Neck. 2003;25:946–952.
Scianna JM, Petruzzelli GJ. Contemoporary management of tumors of the salivary glands. Curr Opin Rep. 2007;9:134–138. PMID: 17288880.
Spiro RH. Salivary neoplasms: overview of a 35-year experience with 2,807 patients. Head Neck Surg. 1986;8:177–184.
T orsiglieri AJ Jr, T om LW, Ross AJ 3rd, et al. Pediatric neck masses: guidelines for evaluation. Int J Pediatr Otorhinolaryngol. 1988;16:199.
T racy T F Jr, Muratore CS. Management of common head and neck masses. Semin Pediatr Surg. 2007;16(1):3–13. PMID: 17210478.
Witt RL. Major salivary gland cancer. Surg Oncol Clin North Am. 2004;13:113–127.
RECONSTRUCTIVE GOALS
I. PATIENTS UNDERGOING HEAD AND NECK RECONSTRUCTIVE PROCEDURES ARE OFTEN
DEBILITATED, AND LONG-TERM SURVIVAL MAY BE POOR. Many cancer patients must also undergo
postoperative radiation or chemotherapy. Therefore, the goal is rapid reconstruction with optimization of function and low
morbidity, accomplished as a one-stage procedure whenever possible.

II. A MULTIDISCIPLINARY APPROACH IS NECESSARY IN PATIENTS WITH HEAD AND NECK CANCER.
The reconstructive surgeon is part of a team that includes medical, radiation, and surgical oncologists, pathologists,
nutritionists, and psychiatrists, and (if needed) speech therapists, dentists, and ophthalmologists.

III. IN ADDITION TO STANDARD RECONSTRUCTIVE CONCEPTS, SPECIFIC PRINCIPLES GUIDE HEAD


AND NECK RECONSTRUCTION PLANNING
A. Attempt to restore symmetry
B. Maintain structural integrity of the nose and ears, for both aesthetic and functional reasons (e.g., support for glasses,
nasal airflow).
C. Maintain competence of the oral and ocular openings, with particular attention paid to the risk of late scar
contractures.
D. Replace entire anatomic subunits when reconstructing larger defects for the best aesthetic outcome.
E. Maintain or restore independent speech, breathing, and swallowing functions whenever possible.

RECONSTRUCTION BY ANATOMIC REGION


I. CUTANEOUS DEFECTS OF THE HEAD AND NECK (See Section “Facial Reconstruction”)

II. THE MIDFACE


A. Goals
1. Restore the contour and projection of the region.
2. Recreation of the maxilla and the occlusive surfaces.
3. Separation of the oral and nasal cavities.
4. Provide support for the eye or a prosthetic replacement.
5. Maintain flow through the lacrimal system.
B. Prosthetics historically have been used extensively in the midface, either alone or in combination with tissue transfers.
Maxillectomy defects that do not involve the buttresses or the orbits can be managed effectively with a palatal obturator.
C. Regional flaps: The deltopectoral flap, the temporalis muscle flap, and the forehead flap can be used to address medium-
sized defects.
D. Non-vascularized bone grafts: Used to fill bony gaps. The graft must be covered with adequate well-vascularized tissue
and be rigidly fixed in position for success.

______________
*De note s common in-se rvice e xamination topics

E. Free tissue transfer


1. The radial forearm osteocutaneous flap: A vascularized piece of radius up to 10 cm in length can be harvested with the
flap and used for bony support.
2. Scapular osteocutaneous flaps, with or without a skin paddle, may include a portion of the latissimus muscle. They are
based either on the descending or on the transverse branches of the circumflex scapular artery and the angular branch
thereof.
3. Free fibula, rectus abdominis muscle, or omental flaps may also be useful in the midface.

III. THE MANDIBLE


A. Goals:
1. Restore facial contour
2. Maintain tongue mobility
3. Restore mastication and speech
B. Reconstruction of large defects can either be immediate or be delayed. Ideally, one would plan immediate reconstruction
under a single anesthetic. However, if there is a question as to surgical margin, or if the patient’s health demands it, a delay
before reconstruction may be advisable.
C. Choice of reconstructive technique depends on the defect size and location.
1. Small bone defects, especially lateral ones, may be addressed with either no repair or with autologous bone graft.
However, non-vascularized bone grafts tolerate radiation poorly.
2. Metallic implants (such as mandibular reconstruction bars) can serve as spacers to maintain position, but they often
ultimately fail or lead to complications, including exposure and infection.
D. Vascularized bone flap is the method of choice most bony defect reconstruction, particularly anterior ones. Such flaps
promote healing, resist resorption, and permit dental restoration with osseointegrated implants.
1. Free fibula flap (Fig. 18-1):
a. Segment of bone up to 40 cm long available, along with the overlying skin
b. Based on perforators from the peroneal artery (2 mm diameter, 6 to 10 mm length)
c. Causes minimal functional debility.
d. Leaves at least 6 to 10 cm of distal aspect of fibula to avoid destabilization of ankle.
e. Key landmarks: Head of fibula and lateral malleolus
f. Can leave small cuff of soleus and flexor hallicus longus muscles to avoid disruption of periosteum.
g. Important to identify and preserve common peroneal nerve at head of fibula and superficial peroneal between fibula
and extensor digitorum longus.
h. Can make osteotomies in fibula to allow for curve of flap.
i. Often secured in place with large mandibular plate and screws. These can be pre-fabricated pre-operatively based on
CT imaging. Screws should be unicoritcal and on opposite side of pedicle to avoid injury.
j. CT angiography or magnetic resonance angiogram (MRA) is used preoperatively to assess the arterial anatomy. The
leg opposite the defect is usually chosen to allow for optimal skin paddle and pedicle placement in the recipient neck.
h. Allows for osseo-integrated implants in the future.
2. Iliac crest bone flaps
a. Based on the deep circumflex iliac artery (1 to 3 mm diameter, 5 to 7 cm length), have a natural curve
resembling the mandible.
b. Both iliac crests can be used to perform a total mandibular reconstruction.
c. Can provide 16 cm length and for mandible should use 2 cm height.
d. Can use one or two cortices though inner cortex usually sufficient for mandible and allows for decreased donor site
morbidity.
e. Skin paddle marked over anterior iliac crease and can extend from ASIS to posterior axillary line.
Figure 18-1. Free fibula flap harvest, cross-sectional view. CT angiography or MRA is often used pre-operatively to assess the arterial anatomy. T he leg opposite the
defect is usually chosen to allow for optimal skin paddle and pedicle placement in the recipient neck.

3. Scapula
a. Pedicle: Subscapular artery (3 to 4 mm diameter, 4 to 6 cm length)
b. Bone size up to 15 cm
c. Very large skin pedicle and quality bone
d. Requires position changes to access
4. Radius, rib, and metatarsal are other donor options for vascularized bone transfers for the mandible

IV. THE NECK


A. Goals
1. Protect vital neck structures, that is, the great vessels of the neck and the trachea
2. Prevent regional complications, which include chylous fistula, oropharyngocutaneous fistula, carotid artery blowout, and
wound infection due to intraoral contamination
B. Pedicled pectoralis major flap: Useful for neck coverage
1. Origin: Medial clavicle, sternum, anterior ribs (second to sixth), external oblique, and rectus abdominis
2. Insertion: Upper humerus, 10 cm from humeral head on lateral side of intertubercular sulcus
3. Function: Adduction and medial rotation of arm
4. Maximal mobilization is achieved by dividing the insertion and clavicular attachments
5. Primary pedicle is the thoracoacromial artery off axillary artery
6. Secondary blood from internal mammary perforators, intercostal perforators, and lateral thoracic artery
7. Overlying skin may be transferred with the flap and should be positioned so minimal tension upon inset
8. Flap is dependable, but bulky
9. *Innervation: Medial and lateral pectoral nerves (named for origin in brachial plexus rather than region of
pectoralis muscle innervated).
C. Pedicled latissimus dorsi flap
1. Thinner flap than the pectoralis, and the skin paddle is more likely hairless
2. Donor defect is favorable, and a paddle up to 10 cm can be harvested with primary closure of the skin.
3. Disadvantage: Intra-op positioning change when used for anterior neck wounds
4. Origin: Broad aponeurosis from thoracolumbar fascia and spine of lower sixth thoracic vertebrae, sacral vertebrae,
supraspinal ligament, and posterior iliac crest.
5. Insertion: Intertubercular groove of humerus
6. Dominant pedicle: Thoracodorsal branch of the subscapular artery, the flap may be tunneled either below pectoralis
major or subcutaneously along the anterior chest.
7. Secondary pedicles: Posterior intercostal perforators, lumbar artery perforators
8. Innervation: Thoracodorsal nerve (C6 to C8)
9. Common complication: Seroma formation at the donor site; drains are mandatory; and fascial quilting and/or fibrin are
advocated by some to reduce seroma rate
D. Trapezius flap: Three different flaps can be raised:
1. *Superior trapezius flap: Based on the occipital artery and paravertebral perforators. It is the most reliable. Its skin
paddle extends laterally across the top of the scapula.
2. *Inferior trapezius flap: Relies on the descending branch of the transverse cervical artery (also called dorsal
scapular). It can be used either as a muscle or as a myocutaneous flap. Its point of rotation is posterior, at the base of
the neck.
3. Lateral trapezius flap: Based on the superficial transverse cervical artery over the acromion. It can be useful for small
lateral defects.
E. The deltopectoral flap
1. Supplied by first four perforators from the internal mammary artery.
2. A delay procedure will permit more lateral skin to be used safely.
3. Flap is thin and can reach the oral cavity.
4. Can raise up to a 10- × 20-cm fasciocutaneous flap.
5. Donor site often requires skin graft and less aesthetic closure.

V. THE ORAL CAVITY


A. Goals
1. Maintenance of oral competence.
2. Provision of support for the floor of the mouth.
3. Prevention of aspiration by maintaining or restoring sensation and mobility.
B. Tongue flaps: Can be used for closure of small intraoral defects, as long as care is taken not to tether the tongue.
C. Palatal or palatopharyngeal flaps: Can be used to fix small defects in the palate.
D. The free radial forearm flap
1. First choice for larger intraoral defects.
2. Based on the radial artery and venae comitantes and/or cephalic/basilic veins.
3. Ideal for intraoral lining due to flap thinness. It can be made sensate by attaching the lingual nerve to the lateral
antebrachial cutaneous nerve.
E. The pedicled latissimus dorsi flap: Can be used for extensive oral cavity defects
1. Advantage of large size, but the arc of rotation can limit its use in the oral cavity.
2. Alternatively, it can be used as a free flap.
3. *Based on thoracodorsal artery
F. The gastro-omental free flap: Provides a secreting mucosal surface useful in preventing post-radiation xerostomia.

VI. THE TONGUE


A. Goals: Maintenance/restoration of mobility, preserve speech, and swallowing function.
B. Reconstruction may not be necessary if the defect volume is low. The tongue heals exceptionally well; infection,
scarring, and tissue loss are rare.
C. Partial glossectomy
1. Can be repaired with “setback” procedures, using the lateral anterior tongue to provide bulk and support to the tongue
base.
2. Outcomes from these procedures can be excellent, provided that at least one hypoglossal nerve is maintained and oral
cavity obliteration can be achieved with the remaining volume.
D. Hemiglossectomy or anterior 2/3 glossectomy: Radial forearm free flap: Pliable tissue can be designed in a “rectangle
tongue template” to achieve oral cavity obliteration and premaxillary contact for oral intake.
E. Total glossectomy reconstruction requires larger volume. Primary goal to restore speech and swallowing function.
Adequate bulk in the oral cavity will help food propulsion and can seal against the palate. Choices for reconstruction are:
1. Rectus abdominis free flap: The large volume flap permits creation of two or three separate cutaneous islands for
complex reconstructions. A perforator-based rectus can help tailor the volume of free tissue transferred.
2. Latissmus dorsi: Can be used as either a free or a pedicled flap.

VII. THE HYPOPHARYNX


A. Hypopharyngeal and esophopharyngeal defects are either partial or circumferential (total).
B. For partial defects, options are
1. Primary closure
a. Care must be taken not to narrow the lumen excessively.
b. Width of mucosa must be at least 3 cm for primary closure (pharynx must permit passage of at least a 34 French
catheter for swallowing)
2. Skin or dermal grafts: May be used for partial defects of the lining of esophagus or pharynx. They are initially secured
with a stent to allow adherence and prevent stricture formation.
3. Pectoralis, latissimus, or trapezius muscles can be used to fill larger defects.
C. Circumferential reconstruction
1. Free jejunum: The historical flap of choice. A proximal segment is isolated on its mesentery and transferred to the
neck, where it is placed in an isoperistaltic orientation. Endoscopic jejunum harvest is possible. Complications include a
“wet” voice, halitosis, and dysphagia.
2. A tubed radial forearm flap: Particularly useful when jejunal harvest is not advisable. This reconstruction can be
associated with a high incidence of stricture formation if adequate dimensions are not harvested.
3. Gastric transposition or gastro-omental flaps: For patients with tumors with significant inferior extension. Outside
the scope of plastic surgery; typically performed by thoracic surgeons.

COMPLICATIONS
I. CHYLE LEAK
A. Dissection low in level iv places thoracic duct at risk
B. Presents with milky drain output when po intake starts
C. Usually noticeable within first 24-48 hours
D. *Treat with low/no fat diet or medium chain fatty acids and pressure dressing
E. If high output (>200 cc/8 hours)
1. Replace fluid loss and frequently check electrolytes.
2. Requires neck exploration to repair leak.
3. Octreotide can be used as adjunct in high output chyle leaks.
F. Fistula
1. Can occur at any site of repair or anastomosis involving oral cavity or pharynx.
2. Much higher incidence if previously radiated field.
3. Usually presents with doughy erythematous skin around pod 4 to 7 before frank salivary communication to skin.
4. Can be managed conservatively with continued npo, irrigations and local wound care; and if infected, culture-directed
antibiotics.
5. If great vessels at risk, salivary diversion (bypass tube) and/or tissue coverage required.
6. Requires assessment of thyroid function and nutritional status to optimize healing.
7. Delayed fistula (months/years postoperatively) must raise suspicion for recurrence.
8. Carotid blowout must be in the differential dx of bleeding in any head & neck patient, especially if history of radiation.
G. Classified as a spectrum
1. Exposed carotid with impending bleeding.
2. Sentinel bleed – smaller volumes may herald a large volume bleed.
3. Acute rupture – high morbidity and up to 50% mortality.
4. Requires large bore iv access, secure airway, blood products.
5. Interventional radiology important as diagnostic and therapeutic adjunct.
6. In exposed carotid or sentinel bleed, can assess stroke risk with balloon occlusion for possible elective embolization or
ligation.
7. Stents increasingly utilized but unknown duration of benefit.
8. Surgical ligation in cases of rupture but high risk of stroke.

PEARLS
1. Feeding via gastro-or jejunostomy tubes may be necessary for long-term management, particularly for patients who will require
radiation therapy.
2. Feeding tubes should be placed at the time of reconstruction.
3. A reliable speech therapist is invaluable for rehabilitation of head and neck reconstruction patients.

QUESTIONS YOU WILL BE ASKED


1. How do you diagnose and treat a chyle leak?
Send drain fluid for triglycerides. Treat by changing tube feeds or PO diet to nonfat or medium-chain triglycerides. Apply
pressure dressing to supraclavicular fossa. Octreotide may be used as an adjunct. If high output, you should consider fluid
replacement of losses. If >200 cc/shift then consider returning to OR to identify/ligate the leak.
2. How do you treat a fistula after a jejunal free flap?
There are varying approaches to treat a fistula. The patient should be made/kept NPO and given nutrition via tube feeds. The
wound should be kept clean, which can be done with irrigation. The patient’s thyroid function and nutrition should be optimized.
The saliva should be diverted medially to protect the great vessels (a salivary bypass tube is sometimes used).

THINGS TO DRAW
Draw fibula osteoseptocutaneous flap in cross section, noting the muscles, septae, and vascular pedicles (refer to Fig. 18-1)

Recommended Readings
Chepeha DB, Teknos T N, Shargorodsky J, et al. Rectangle tongue template for reconstruction of the hemiglossectomy defect. Arch Otolaryngol Head Neck Surg.
2008;134(9):993-998.
Cordeiro PG, Santamaria EA. Classification system and algorithm for reconstruction of maxillectomy and midfacial defects. Plast Reconstr Surg. 2000;105:2331-2346.
Disa JJ, Pusic AL, Hidalgo DA, et al. Microvascular reconstruction of the hypopharynx: defect classification, treatment algorithm, and functional outcome based on 165
consecutive cases. Plast Reconstr Surg. 2003;111:652-663.
Haughey BH. T ongue reconstruction: concepts and practice. Laryngoscope. 1993;103:1132-1141.
Haughey BH, Wilson E, Kluwe L, et al. Free flap reconstruction of the head and neck: analysis of 241 cases. Otolaryngol Head Neck Surg. 2001;125:10.
Hidalgo DA, Pusic AL. Free flap mandibular reconstruction: a 10-year follow up study. Plast Reconstr Surg. 2002;110:438-449.
Makitie AA, Beasley NJ, Neligan PC, et al. Head and neck reconstruction with anterolateral thigh flap. Otolaryngol Head Neck Surg. 2003;129:547-555.
T heile DR, Robinson DW, T heile DE, et al. Free jejunal interposition reconstruction after pharyngolaryngectomy: 201 consecutive cases. Head Neck. 1995;17:83.
Urken ML, Weinberg H, Vickery C, et al. T he neurofasciocutaneous radial forearm flap in head and neck reconstruction: a preliminary report. Laryngoscope.
1990;100:161-173.
Zbar RI, Funk GF, McCulloch T M, et al. Pectoralis major myofascial flap: a valuable tool in contemporary head and neck reconstruction. Head Neck. 1997;19:412.
I. EYELID ANATOMY AND PHYSIOLOGY (FIG. 19-1)
A. The primary function of the eyelids is protection of the globe.
B. The upper eyelid is dynamic, whereas the lower eyelid acts as a static sling.
C. Composed of three lamellae (Fig. 19-2): Well-vascularized external coverage (anterior), structural support (middle), and
mucosal lining (posterior).
1. Anterior lamella: Skin and orbicularis oculi muscle
a. Skin
i. Approximately 1-mm-thick—thinnest skin in the body
ii. Underlying subcutaneous tissue is exiguous and areolar
b. Orbicularis oculi muscle (Fig. 19-3)
i. Innervated by zygomatic branch (CN VII) on its undersurface
ii. Pretarsal portion: Assists with involuntary blink
iii. Preseptal portion: Assists with involuntary blink
iv. Orbital portion: Produces voluntary lid closure
2. Middle lamella: Preseptal fat, orbital septum, and orbital (postseptal) fat
a. Preseptal fat
i. Between the orbicularis oculi muscle and the orbital septum
ii. Upper eyelid: Retro-orbicularis oculi fat (ROOF)
iii. Lower eyelid: Suborbicularis oculi fat (SOOF)
iv. Increasingly ptotic with age causing fullness and hooding
b. Orbital septum: Anatomic boundary between eyelid and orbit
i. Multilayer fibrous membrane arising from the periosteal confluence of the superior and inferior orbital rims.
ii. Fuses with the levator aponeurosis in the upper eyelid and the capsulopalpebral fascia in the lower eyelid.
c. Orbital (postseptal) fat (Fig. 19-4)
i. Upper eyelid: Two compartments (nasal and central)—separated by the trochlea and superior oblique tendon.
ii. *Lower eyelid: Three compartments (medial, central, and lateral)—inferior oblique muscle separates
medial and central compartments.
iii. Medial compartment contains white fat with small lobules.
3. Posterior lamella (Fig. 19-5): Tarsal plate, retractor muscles, and conjunctiva
a. Tarsal plates
i. Composed of cartilaginous-like dense connective tissue
ii. Provides structural support and rigidity to the eyelids
iii. Superior tarsus: 1-mm-thick, 25 mm long, 10 mm tall
iv. Inferior tarsus: 1-mm-thick, 25 mm long, 4 mm tall
b. Upper lid retractors
i. *Levator palpebrae superioris:
a) Innervation: Superior division of CN III
b) Origin: Lesser wing of sphenoid, then broadens as aponeurosis at Whitnall’s ligament
c) Insertion: Superior tarsus and dermis forming supratarsal crease
d) Function: Acts as fulcrum providing 10 to 15 mm lid elevation

______________
*De note s common in-se rvice e xamination topics
Figure 19-1. Surface anatomy of the eye. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2010.)

ii. *Mueller’s muscle


a) Innervation: Sympathetic nervous system
b) Origin: Deep surface of levator aponeurosis
c) Insertion: Superior tarsal margin
d) Function: 1 to 2 mm lid elevation
c. Lower lid retractors
i. Capsulopalpebral fascia: Analogous to levator aponeurosis
a) Origin: Inferior rectus sheath, splits at inferior oblique muscle, then reunites as Lockwood suspensory ligament
(lower lid equivalent of Whitnall’s ligament)
b) Insertion: inferior tarsus
Figure 19-2. Cross section of the upper (A) and lower eyelids (B). (Redrawn from Tasman W, Jaeger EA, eds. Duane’s Opthamology on CD-ROM. 2006 ed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2006.)

Figure 19-3. Periorbital musculature.


Figure 19-4. Eyelid fat compartments and lacrimal gland.

Figure 19-5. Ligamentous and cartilage support structures of the eyelids.

ii. Inferior tarsal muscle: Analogous to Mueller’s muscle


a) Innervation: Sympathetic nervous system
b) Origin: Posterior capsulopalpebral fascia
c) Insertion: Inferior tarsal margin
d. Conjunctiva
i. Gliding surface of nonkeratinized squamous epithelium
ii. Palpebral conjunctiva: Posterior surface of the eyelid
iii. Bulbar conjunctiva: Anterior surface of the globe
iv. Superior and inferior fornices: Apices where the palpebral and bulbar conjunctiva meet
D. Lateral canthal tendon (LCT)
1. Originates at lateral margin of the superior and inferior tarsal plates
2. Crura fuse as a Y-shaped common tendon that inserts onto Whitnall’s tubercle, a bony prominence located 5 mm
within the lateral orbital rim
a. Eisler fat pad is anatomic landmark for Whitnall’s tubercle
b. Located in pocket between the orbital septum and LCT insertion
3. Other contributing structures: Pretarsal and preseptal portions of the orbicularis oculi muscle, lateral horn of the
levator aponeurosis, Lockwood suspensory ligament, and check ligament of the lateral rectus muscle
E. Medial canthal tendon (MCT)
1. Originates at medial margin of the superior and inferior tarsal plates.
2. Crura fuse as a tripartite common tendon prior to insertion.
a. Superficial Head: Anterior to lacrimal sac
i. Inserts onto frontal process of the maxilla
ii. Provides majority of support for the medial canthus
b. Deep Head: Posterior to the lacrimal sac
i. Inserts onto the posterior lacrimal crest
ii. Less developed compared to the superficial head
Figure 19-6. Arterial supply of the eyelids.

c. Vertical head: Forms roof of lacrimal sac


i. Inserts onto orbital process of the frontal bone
ii. Functions in the tear pump mechanism
F. Vascular system (Fig. 19-6)
1. Dual blood supply from both the external and internal carotid systems.
2. Marginal arcade is located 2 to 3 mm from the lid margin.
3. Peripheral arcade is located between the levator palpebrae superioris and Mueller’s muscle just above the superior
tarsal margin.
4. Upper lid: Primarily supplied by branches of ophthalmic artery (internal carotid).
5. Lower lid: Primarily supplied by branches of facial artery (external carotid).
G. *Sensory innervation (Fig. 19-7)
1. Upper eyelid: Ophthalmic division of CN V (V1)
2. Lower eyelid: Maxillary division of CN V (V2)

II. CLINICAL EYELID MEASUREMENTS


A. Palpebral fissure: Distance between upper and lower lid margins (10 mm vertically and 30 mm horizontally)
B. Marginal reflex distance (MRD): Corneal light reflex to lid margin
1. Upper eyelid rests slightly below the superior limbus (MRD1 = 4 mm)
2. Lower eyelid rests at the inferior limbus (MRD2 = 5 mm)
C. Lateral canthus sits 1 to 2 mm above the medial canthus
D. Distance between lash line and supratarsal crease is 8 to 12 mm (women > men).
E. Ideal amount of pretarsal show is 2 to 3 mm in primary gaze
F. Distance from upper lid margin to brow: 22 mm
F. Highest point of the upper lid margin is just nasal to the mid-pupillary line, while the lowest point of the lower lid margin
is just temporal to the mid-pupillary line.
G. *Asian upper eyelids are anatomically different than occidental upper eyelids.
1. *Absent supratarsal crease (lack of levator aponeurosis dermal insertion
2. *Decreased height of pretarsal segment (caudal fusion of orbital septum and levator aponeurosis)
3. *Increased fullness (increased amounts of ROOF and SOOF)
4. *Presence of epicanthal folds
Figure 19-7. Sensory innervation of the eyelids. (From Tasman W, Jaeger EA, eds. Duane’s Opthamology on CD-ROM. 2006 ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2006.)

III. PREOPERATIVE EVALUATION OF EYELID AND CANALICULAR FUNCTION


A. Visual acuity using a Snellen chart
B. Assessment of tear production and drainage
1. *Schirmer’s test
a. Place paper strip in inferior fornix for 5 minutes
b. Topical anesthetic can prevent reflexive tearing (false-positive)
c. More wetting on the paper strip means less eye dryness
i. Normal: Greater than 10 mm
ii. Abnormal: Less than 10 mm
2. Tear film break-up time
a. Add 2% fluorescein dye to the eye and observe junction of globe and lower lid margin for evaporation of tear film
using slit lamp
b. Longer time to evaporation means the tear film is more stable
i. Normal: Greater than 10 seconds
ii. Abnormal: Less than 10 seconds
3. *Jones dye test
a. Determines patent lacrimal system versus functional obstruction
b. Jones I
i. Place 2% fluorescein in the inferior fornix and a cotton-tip applicator in the inferior meatus of the nose for 5
minutes
ii. Presence of fluorescein (positive) indicates patency
iii. Absence of fluorescein (negative) indicates obstruction
c. Jones II
i. Gently irrigate the puncta with saline after a negative Jones I
ii. Presence of fluorescein (positive) indicates distal partial obstruction at the nasolacrimal duct
iii. Absence of fluorescein (negative) indicates proximal partial obstruction at the puncta or canaliculi
iv. Complete reflux indicates complete obstruction
C. *Snap-back test to assess for lower lid laxity
1. Pull the lower eyelid away from the globe. Upon release, it should immediately return to its normal position without
blinking.
2. If this takes longer than one second, then significant laxity is present.
D. *Hertel exophthalmometry evaluates the position of the anterior border of the globe in relation to the most
anterior point of the lateral orbit rim.
1. Enophthalmos: Less than 14 mm
2. Exophthalmos: Greater than 18 mm
3. Greater than 2 mm difference between eyes is clinically significant
E. *Vector refers to the position of the anterior border of the globe in relation to the most anterior point of the
inferior orbital rim on lateral view
1. Neutral vector: Vertical line (no inclination) from the cornea to the rim
2. Negative vector: Posteriorly inclined line from the cornea to the rim—increased risk of postoperative
ectropion.

IV. RECONSTRUCTION OF EYELID AND CANTHAL DEFECTS (FIG. 19-8)


A. Lid margin repair
1. Rule out globe (loss of turgor) and septal injury (presence of orbital fat)
2. Missing tissue is unusual—Gap is due to pull of orbicularis oculi muscle
3. Align lid margin using a vertical mattress suture (6-0 silk) at the gray line
a. Evert wound edges to prevent postoperative notching
b. Secure long suture ends under skin sutures away from the cornea
4. Strength layer—Repair the tarsus using 5-0 or 6-0 absorbable suture
a. Partial-thickness bites protect the cornea from suture irritation
b. Bury all suture knots closer to the skin than to the conjunctiva
5. Close skin using 6-0 nylon suture (no conjunctival sutures required)
6. Remove skin sutures in 5 days and lid margin sutures in 7 to 10 days
7. Complications: Notching (most common), trichiasis, and eyelash alopecia
B. Partial-thickness defects (Fig. 19-8)
1. Anterior lamellar defects
a. Less than 50%: Local tissue rearrangement
b. *Greater than 50%: Skin graft from contralateral lid (preferred)
c. Avoid vertical incisions to prevent postoperative lid retraction.
2. Posterior lamellar defects
a. Involves conjunctiva only: Primary repair for smaller defects and nasal/buccal mucosal or amniotic membrane grafts
for larger defects.
b. Involves tarsus and conjunctiva: Primary repair for smaller defects and nasal chondromucosal (septal cartilage), ear
cartilage, donor scleral, or hard palatal mucosal grafts for larger defects.
C. Full-thickness defects of the upper eyelid (Fig. 19-8)
1. Less than 25%
a. Primary closure with meticulous lid margin repair.
b. In elderly patients, pre-existing laxity may allow closure up to 40%.
2. Between 25% to 75%
a. Lateral canthotomy and cantholysis with primary closure.
b. Tenzel semicircular flap: Lateral canthotomy and cantholysis with advancement of lateral myocutaneous flap
c. Switch flap: Lid sharing between the ipsilateral lower eyelid and a central upper lid defect. Flap is divided and inset 3
weeks later.
3. Greater than 75%
a. *Cutler–Beard flap
i. First stage: Full-thickness flap is developed in the ispilateral lower eyelid below the inferior tarsus—flap width
equals the defect size—and passed beneath the lower lid margin into the upper lid defect (may include cartilage
for additional support).
ii. Second stage: Flap is divided and inset 3 weeks later.
Figure 19-8. Eyelid reconstruction. FT , full thickness; PT , partial thickness.

b. Paramedian or temporal forehead flaps are reserved for extensive upper lid defects when other local options are
not available.
c. Free tarsoconjunctival graft from contralateral lid
D. Full-thickness defects of the lower eyelid (Fig. 19-8)
1. Less than 25%: Refer to full-thickness defects of the upper eyelid
2. Between 25% to 75%
a. Lateral canthotomy and cantholysis with primary closure or Tenzel semi-circular flap.
b. Unipedicled myocutaneous Fricke transposition flap: Ipsilateral upper lid skin–muscle flap based on either a
medial or lateral pedicle is transposed into a lower lid defect.
c. Bipedicled myocutaneous Tripier flap: Similar to the Fricke flap, except based on both the medial and lateral
pedicles.
3. Greater than 75%
a. *Hughes tarsoconjunctival flap
i. First stage: Ipsilateral upper lid conjunctiva and a portion of the superior tarsus (must leave 4 mm for upper lid
support) are transferred into a lower lid defect and covered with a full-thickness skin graft. Mueller’s muscle is
included in smokers.
ii. Second stage: Flap is divided and inset 3 weeks later
b. Mustardé cheek rotation-advancement flap
i. Combine with mucosal graft for total lower lid defects.
ii. Anchor to the deep temporal fascia and the periosteum of the infraorbital rim to prevent postoperative ectropion.
iii. Subcutaneous plane: For a thinner flap
iv. Deep plane: Prevents distal flap necrosis in smokers
E. Lateral canthal defects (Fig. 19-8)
1. Produces a rounded lateral canthus and a shortened palpebral fissure.
2. Simple disruption: Primary repair if both ends of the LCT are present
3. Complex disruption: Canthoplasty if lateral end of the LCT is absent
a. Medial end present: Suture to periosteum of lateral orbital rim
b. Medial end absent: Use lateral tarsal strip or periosteal flap
4. Canthopexy for LCT laxity—slight overcorrection prevents recurrence.
5. A local flap, regional flap, or skin graft can be used for soft tissue coverage.
F. Medial canthal defects (Fig. 19-8)
1. Rule out injury to the canalicular system.
2. Simple disruption: Primary repair if both ends of the MCT are present
3. Complex disruption: Canthoplasty if medial end of the MCT is absent. *If avulsed, may require transnasal wiring
(posterosuperior to the posterior lacrimal crest) to prevent postoperative telecanthus.
4. Canthopexy for MCT laxity—slight overcorrection prevents recurrence.
5. A local flap, regional flap, or skin graft can be used for soft tissue coverage.

V. RECONSTRUCTION OF THE CANALICULAR SYSTEM


A. Lacrimal apparatus (Fig. 19-9)
1. Lacrimal gland
a. Located within the lacrimal fossa in the superolateral orbit.
b. Lateral horn of the levator aponeurosis separates the orbital and palpebral lobes with approximately 10 to 12 ducts
passing from the orbital lobe through the palpebral lobe into the superior fornix.
c. Supplied by the lacrimal artery, a branch of the ophthalmic artery.
d. The lacrimal vein empties into the superior ophthalmic vein.
e. Lacrimal nerve via ophthalmic division of CN V provides sensation.
f. Pterygopalatine ganglion provides parasympathetic innervation.
g. Superior cervical ganglion provides sympathetic innervation.
2. Tears
a. Tear film is composed of a trilaminar fluid layer
i. Outer lipid layer: Meibomian glands, accessory sebaceous glands of Zeis and Moll—prevents tear evaporation
ii. Middle aqueous layer: Lacrimal gland, accessory lacrimal glands of Krause and Wolfring—90% tear film
thickness
iii. Inner mucoprotein layer: Goblet cells—hydrophilic and facilitates tear film distribution across the globe
b. Functions of tear film
i. Provides lubrication to promote a smooth gliding surface
ii. Mechanically removes foreign bodies and other irritants
iii. Increases the refractive power of incoming light
iv. Provides 80% to 90% of the cornea’s oxygen requirement
v. Contains lysozyme that imparts antimicrobial properties
c. Tear pump mechanism
i. Lacrimal puncta open into the superior and inferior canaliculi at medial end of the upper and lower lids,
respectively
Figure 19-9. T he lacrimal system. (From Mills SE, ed. Histology For Pathologists. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.)

ii. Both canaliculi travel 2 mm vertically and then 6 to 8 mm horizontally before uniting to form the common
canaliculus
iii. The common canaliculus empties into the lacrimal sac through the valve of Rosenmüller
iv. The lacrimal sac empties into the nasolacrimal duct which travels 18 mm inferiorly before entering the inferior
meatus
v. Nasolacrimal duct opening is covered by a mucosal fold (valve of Hasner) to prevent reflux of air and nasal
contents
vi. *Eyelids open: Sac is empty, diaphragm is in resting position, canaliculi at normal length, and puncta
are open
vii. *Eyelids close: Diaphragm is pulled laterally creating negative pressure within the sac, the canaliculi
shorten, the puncta close, and the sac fills with tears
viii. *Eyelids reopen: Diaphragm returns to its resting position expelling tears into the nasolacrimal duct
B. Canalicular repair
1. Recommended to prevent postoperative epiphora
2. Identify both the proximal and distal ends of the lacerated canaliculus
a. Proximal end is more difficult to find, usually more posterior
b. Irrigation of the uninjured canaliculus aids in the identification of the proximal end by observing for the backflow of
saline
3. Use an indwelling silicone stent to bridge the laceration
4. Some authors recommend microsurgical anastomosis of the lacerated canaliculus over the stent, while others
recommend simple reapproximation of the orbicularis oculi muscle and repair of the MCT
5. The stent should be left in place for at least 12 weeks
C. Lacrimal bypass surgery for a blocked lacrimal drainage system
1. Silicone tube intubation: Obstructions at the lacrimal puncta
2. Conjunctivodacryocystostomy: Obstructions at the canalicular level
3. Conjunctivodacryocystorhinostomy: Also for obstructions at the canalicular level, or in patients with congenital absence
of the lacrimal sac—requires use of a permanent Pyrex glass tube (Jones tube)
4. *Dacryocystorhinostomy (DCR): Obstructions at the nasolacrimal duct
5. Canaliculodacryocystorhinostomy: Obstructions at the junction of the common canaliculus and lacrimal sac—
combination of DCR and microsurgical repair of the stenotic common canaliculus

VI. PTOSIS
A. Mechanics of eyelid function
1. Refer to Section “Eyelid Anatomy and Physiology”
2. True ptosis: Drooping of the lid margin below its normal anatomic position due to levator complex dysfunction.
3. Pseudoptosis: Lid margin appears low, but levator complex is normal
a. Brow ptosis
b. Enophthalmos (e.g., posttraumatic, iatrogenic)
c. Hypotropia (after an orbital floor fracture)
d. Blepharochalasis: Recurrent episodes of eyelid edema in young women which stretches the eyelid tissue over time
e. Contralateral exophthalmos with associated upper lid retraction (e.g., Graves’ ophthalmopathy)
f. Duane syndrome: Limited abduction of the affected eye due to absent CN VI and aberrant innervation of the lateral
rectus muscle by CN III, resulting in impaired movement followed by fibrosis of the extraocular musculature and
subsequent globe retraction
B. Preoperative evaluation of ptosis
1. Refer to Section “Preoperative Evaluation of Eyelid and Canalicular Function”
2. Degree of ptosis: Decrease in MRD1
a. Mild: 1 to 2 mm
b. Moderate: 3 mm
c. Severe: Greater than 4 mm
3. Levator function (excursion): Examiner uses nondominant hand to stabilize the patient’s brow and measures the
distance between the upper lid margin in maximal downgaze compared to maximal upgaze
a. Good: 10 to 15 mm
b. Fair: 6 to 9 mm
c. Poor: Less than 5 mm
4. *Elevated Supratarsal Crease: Levator dehiscence
5. CN III palsy or Horner’s syndrome (triad of miosis, anhidrosis, and partial ptosis)
6. Hering’s law of equal innervation
a. Severe ptosis may mask a contralateral mild ptosis because each levator complex receives the same amount of
neural input determined by the more ptotic eyelid.
b. If not recognized preoperatively, then it may become more prominent after corrective surgery because the amount of
neural input to both levator complexes will be diminished
c. Hering’s test: Examiner uses nondominant hand to stabilize the patient’s brow and elevates the ptotic eyelid with a
cotton-tip applicator while simultaneously observing for contralateral ptosis
C. Classification of ptosis
1. Involutional (senile)
a. Most common type of ptosis due to aging
b. *Levator aponeurosis stretches or dehisces from the tarsus, but dermal insertions are preserved causing the
supratarsal crease to rise
c. Levator function often remains good
2. Traumatic
a. Due to direct injury of the levator complex
b. Either the muscle itself or the nerve can be involved
3. Neurogenic (paralytic)
a. *Myasthenia gravis
i. Ptosis that worsens with activity and improves with rest.
ii. Diagnosed by the intravenous administration of edrophonium or neostigmine causing temporary relief of the ptosis.
b. CN III palsy or Horner’s syndrome can cause paralysis of the levator palpebrae superioris or Mueller’s muscle,
respectively.
4. Mechanical
a. Due to excess weight from tumor infiltration or dermatochalasis
b. Also caused by tissue edema in the early postoperative period
5. Congenital
a. Due to fibrofatty replacement of the levator complex.
b. The supratarsal crease may be absent.
c. Levator function often remains poor.
d. Classic finding on physical examination is lagophthalmos on downward gaze (i.e., the ptotic eyelid remains higher
than the contralateral side on downward gaze due to levator fibrosis).
e. Surgical correction is delayed until age 3 to 5 years unless corneal exposure risks ulceration or visual field obstruction
risks amblyopia.
f. *Associated with blepharophimosis syndrome, which consists of the triad of telecanthus, bilateral ptosis,
and epicanthus inversus.
g. Marcus Gunn jaw-winking phenomenon
i. Synkinetic movement of the upper eyelid and jaw due to aberrant crossover from the motor branch of the lateral
pterygoid muscle (mandibular division of CN V) to the superior division of CN III.
ii. At rest, the upper eyelid is ptotic, but with jaw opening it briefly elevates simulating a “wink”.
D. Nonsurgical Management of Ptosis
1. If myasthenia gravis is suspected, referral to a neurologist is warranted.
2. Alpha-adrenergic agonist drops if the cause is botulinum toxin injection or Horner’s syndrome (stimulates Mueller’s
muscle contraction).
3. If the patient wears eyeglasses, they can be modified with a projecting flange to support the drooping upper eyelid.
E. Surgical management of ptosis
1. Intravenous sedation is preferred to be able to wake the patient up during surgery and accurately assess the degree
of ptosis correction
2. Degree of ptosis and levator function determine the type of ptosis repair
a. Good levator function/mild ptosis
i. Levator plication: Levator aponeurosis is plicated—1:1 ratio of millimeter plication to ptosis correction suffices
for mild ptosis, but a 4:1 ratio is required for more severe ptosis.
ii. Levator advancement: Levator aponeurosis is released from its insertion on the tarsus and advanced—1:1 ratio
of millimeter advancement to ptosis correction suffices for mild ptosis, but a 4:1 ratio is required for more severe
ptosis.
iii. *Tarsoconjunctival mullerectomy (Fasanella-Servat procedure): Conjunctiva, tarsus, and Mueller’s muscle
are removed en bloc via a posterior approach—*4:1 ratio of millimeter resection to ptosis correction is
required. If the tarsus is spared, it is called the Putterman procedure.
b. Good levator function and moderate ptosis: Levator plication or advancement.
c. Good levator function and severe ptosis: Levator advancement only
d. Fair levator function and any ptosis: Levator advancement only
e. Poor levator function and any ptosis: *Frontalis sling or suspension
i. Most often used in cases of congenital ptosis
ii. Relies on movement of the frontalis muscle to provide lid excursion by slinging the upper eyelid to the brow
iii. Patients require nocturnal eye protection and lubrication due to lagophthalmos while sleeping.
iv. Our preference is to use autologous tissue (e.g., fascia lata, palmaris longus tendon), but alloplastic material can
also be used (e.g., silicone, Gore-Tex, Alloderm).
v. Modified Crawford technique
a) Four stab incisions are made just above the lash line and three just above the brow.
b) Two strips of fascia lata are tunneled beneath the orbicularis oculi muscle from the upper eyelid to the brow
forming two opposing triangles.
c) The degree of ptosis correction is tailored by tightening the knots to the desired tension.

VII. ECTROPION
A. Defined as eversion, or rolling outward of the lid margin.
B. Loss of normal lid-globe apposition leads to scleral show, keratinization of the exposed cornea and conjunctiva, and
ultimately loss of vision.
C. Nonsurgical management of ectropion
1. It is important to protect the cornea and prevent dryness with artificial tears, taping of the eyelid, and eye patches or
moisture shields.
2. If scarring is present, consider digital massage or steroid injections.
3. Punctal occlusion can help relieve dryness
4. Treat infection, if present
D. Classification and surgical management of ectropion
1. Involutional (senile)
a. Most common type of ectropion due to aging
b. *Hallmark feature is horizontal lid laxity
c. Surgical repair
i. Medial conjunctival spindle procedure: Medial conjunctiva and retractor muscles are horizontally excised.
ii. Kuhnt–Szymanowski procedure: Subciliary blepharoplasty combined with shield excision of redundant
orbicularis oculi muscle, middle lamella, and posterior lamella.
iii. *Lateral tarsal strip procedure (canthoplasty) (Fig. 19-10)
a) Lateral canthotomy followed by cantholysis of the inferior crus of the LCT.
b) A strip of lateral tarsus is then denuded and sutured to the periosteum of the lateral orbital rim with slight
overcorrection.
c) Excess skin and orbicularis oculi muscle is excised, and a commisuroplasty is performed.
iv. Standard canthopexy (Fig. 19-11 ): The lax LCT is retracted laterally and either plicated or sutured to the
periosteum of the lateral orbital rim. This technique differs from a canthoplasty in that no cantholysis is
performed.
2. Neurogenic (paralytic)
a. Due to a deficit in CN VII function
b. Neurotrophic keratitis associated with absent corneal sensation
c. Surgical repair
i. If poor Bell’s phenomenon, a tarsorrhaphy can be helpful
ii. Botulinum toxin injection of the levator palpebrae superioris or gold weight implantation may be a useful
adjunct in patients with lagophthalmos
iii. Mild cases: Lateral tarsal strip with or without midface lift
iv. Severe cases: A static sling is recommended
3. Cicatricial
a. Due to scarring in or around the anterior lamella
b. Surgical repair
i. If conservative measures fail (e.g., digital massage, steroid injections), then treatment involves surgical release of
the scar and lengthening of the anterior lamella once the scar is mature
ii. In some cases, tension can be reduced by local tissue rearrangement in the form of V-, Y-, or Z-plasties
iii. Additional tissue often needed in the form of local flap, regional flap, or skin graft (full-thickness preferred)
iv. Temporary traction suture taped to the forehead is used postoperatively to counteract downward pull of tissue
edema
Figure 19-10. T he lateral tarsal strip procedure.
Figure 19-11. Standard canthopexy.

4. Mechanical
a. Due to excess weight from tumor infiltration or dermatochalasis
b. Also caused by tissue edema in the early postoperative period
c. Surgical repair
i. Excision of the offending agent followed by eyelid reconstruction as outlined above depending on defect size
ii. If tissue edema is responsible, initial recommendations include head of bed elevation and expectant management.
Improves in 2 to 3 months when new lymphatic channels form.
5. Congenital
a. Least common type of ectropion due to vertical deficiency of the anterior lamella
b. Rarely an isolated finding—usually associated with blepharophimosis syndrome
c. May be complicated by a neurogenic (paralytic) component
d. Surgical repair
i. Manage initially with artificial tears and lubrication to see if it spontaneously resolves on its own
ii. May require a temporary tarsorrhaphy, but avoid prolonged use to prevent iatrogenic amblyopia
iii. Severe cases will require skin grafts or local flaps and are usually performed in conjunction with medial and
lateral canthoplasties and ptosis repair

VIII. ENTROPION
A. Defined as inversion, or rolling inward of the lid margin
B. Patients usually complain of epiphora, and corneal irritation occurs due to posteriorly directed eyelashes (trichiasis)
C. Nonsurgical management of entropion
1. Protection of the cornea is paramount with use of artificial tears, eye patches or moisture shields, and electrolysis or
argon laser to remove irritating eyelashes (or wear contact lens to deflect eyelashes)
2. Taping of the eyelid to the cheek may assist in everting the lid margin
3. Treat infection, if present
D. Classification and surgical management of entropion
1. Involutional (senile)
a. Most common type of entropion due to aging
b. *Hallmark features are horizontal lid laxity, disinsertion of the retractor muscles, and an overriding
preseptal segment.
c. Surgical repair
i. Quickert procedure: Multiple sutures are placed below and perpendicular to the lid margin to evert the eyelid.
Results are temporary and recurrence is expected.
ii. If horizontal lid laxity is the prominent finding, a lateral tarsal strip procedure is recommended.
iii. If vertical lid laxity is the prominent finding, reattachment of the capsulopalpebral fascia to the tarsus is required.
iv. Weis procedure: Full-thickness rotational procedure of the lid margin back to its normal position involving a
transverse blepharotomy and a lateral tarsal strip procedure.
2. Acute spastic
a. Due to ocular irritation or inflammation leading to sustained contraction or overactivity of the orbicularis oculi
muscle.
b. Surgical repair
i. Temporizing measures include taping of the eyelid, local anesthetic infiltration, or botulinum toxin injection into the
orbicularis oculi muscle, which can sometimes break the spasm and lead to resolution of the lid malposition
ii. If horizontal or vertical lid laxity also exist, then a lateral tarsal strip procedure or reattachment of the
capsulopalpebral fascia to the tarsus may be required, respectively
3. Cicatricial
a. Due to scarring in or around the posterior lamella.
b. More common in underdeveloped nations as a result of trachoma.
c. Surgical repair
i. Do not operate if the conjunctiva is actively inflamed.
ii. Treatment involves surgical release of the scar and marginal rotation. Conjunctiva is replaced with either nasal
mucosa, buccal mucosa, or amniotic membrane.
iii. If the tarsus is also missing or deformed, it can be fractured and repositioned, or replaced with an interpositional
graft
4. Congenital
a. Least common type of entropion due to vertical deficiency of the posterior lamella
b. Rarely an isolated finding caused by dysgenesis of the retractor muscles or structural abnormalities of the tarsus
c. *Commonly confused with epiblepharon in which a congenital horizontal redundant fold of skin is located
near the lid margin due to the abnormal insertion of the pretarsal orbicularis oculi muscle. No rotational lid margin
abnormality exists with epiblepharon and it may resolve spontaneously, which differs from congenital entropion.
d. Surgical repair
i. Congenital entropion: Transverse blepharotomy with marginal rotation is performed
ii. Epiblepharon: Elliptical excision of the redundant skin and muscle is performed

PEARLS
1. Asian upper eyelids have an absent supratarsal crease, more caudal fusion of the orbital septum with the levator aponeurosis,
increased amounts of ROOF and SOOF, and presence of epicanthal folds
2. Lateral canthotomy and cantholysis may facilitate primary closure of eyelid defects
3. In Graves’ ophthalmopathy, first perform orbital decompression, followed by strabismus surgery, and finally eyelid reconstruction
4. Take photographs both pre- and postoperatively for documentation
5. Avoid vertical scars on or near the eyelid to prevent postoperative ectropion
6. If levator function is good, the choice of ptosis repair is either levator plication or advancement
7. If levator function is poor, the choice of ptosis repair is frontalis sling or suspension
8. Aging is the most common cause of ptosis, ectropion, and entropion
9. The most important thing to remember about any eyelid procedure is to protect the cornea!

QUESTIONS YOU WILL BE ASKED


1. What is the most common complication following lower lid procedures?
Lower lid malposition
2. What structure attaches to the superior margin of the tarsus and is often visualized in cases of levator dehiscence?
Mueller’s muscle
3. Patients with a negative vector are at increased risk for what postoperatively?
Xerophthalmia
4. What ratio of levator plication/advancement is usually required for adequate ptosis correction?
4:1

THINGS TO DRAW
Draw the upper and lower eyelid in cross section.
Figure 19-2

Recommended Readings
Cherubini T D. Entropion and ectropion of the eyelids. Clin Plast Surg. 1978;5(4):583–591. PMID: 729343.
Codner MA, McCord CD, Mejia JD, Lalonde D. Upper and lower eyelid reconstruction. Plast Reconstr Surg. 2010;126(5):231e–245e. PMID: 21042070.
DiFrancesco LM, Codner MA, McCord CD. Upper eyelid reconstruction. Plast Reconstr Surg. 2004; 114(7):98e–107e. PMID: 15577335.
McCord CD Jr. T he evaluation and management of the patient with ptosis. Clin Plast Surg. 1988; 15(2):169–184. PMID: 3280214.
Spinelli HM, Jelks GW. Periocular reconstruction: a systematic approach. Plast Reconstr Surg. 1993; 91(6):1017–1024; discussion 1025–1026. PMID: 8479966.
I. HISTORICAL ORIGINS
A. References of total nasal reconstruction date as far back as 3000 BC India.
B. Local cheek flaps published in “Sushruta Samhita” by Sushruta (India, 700 BC).
C. Adjacent tissue rearrangements recorded by Celsus (Greece, ~40 AD) and Paulus Aegineta (Byzantine Greece, ~660 to
680 AD).
D. Italian method used the arm flap, originated by Branca in ~15th century Italy, published by Tagliacozzi in 1597.
E. Indian method using the forehead flap, originated in ~1440 in India and Nepal by Kanghiara or Mahrattas families, published
by “Madras Gazette” in 1700s Bombay, reproduced in English in “Gentleman’s Magazine” in 1794 England.

II. IMPORTANT FACTORS TO NOTE WHEN DEFINING THE DEFECT


A. Etiology of the defect
1. Skin cancer: Must have clear oncologic margins before reconstruction
a. Immediate reconstruction preferred after Mohs excision, and sometimes after frozen sections depending on tumor
type and aggressiveness, due to the possibility of false-negatives (know your pathologist and Mohs surgeon and the
reliability of their reports).
b. Delayed reconstruction (e.g., non-Mohs or melanoma resection)
2. Trauma, ischemic necrosis (e.g., secondary to rhinoplasty), and infection: Reconstruction proceeds when the
viability of the remaining tissue is certain

III. LOCATION OF THE DEFECT


A. Proximal, middle, or distal third of nose
B. Nasal subunits that are involved

IV. SIZE OF THE DEFECT


A. Less or greater than 1.5 to 2.0 cm (for choosing local flap vs. forehead flap).
B. *If more than 50% of a subunit is involved, then include the remainder of the subunit as part of the estimated
defect size (subunit principle).

V. TISSUE PLANES INVOLVED BY THE DEFECT


A. External nasal cover: Skin, subcutaneous fat, and submuscular aponeurotic system (SMAS)
B. Structural support: Perichondrium/cartilage and periosteum/bone
C. Internal nasal lining

ANATOMY
I. NASAL REGIONS (BY THIRDS)
A. Proximal third
1. Nasal bones and bony septum
2. Thin skin over the radix
3. Nasal bones thicker more proximally

______________
*De note s common in-se rvice e xamination topics
Figure 20-1. Nasal aesthetic subunits.

B. Middle third
1. Upper lateral cartilages and cartilaginous septum
2. Thin skin over the dorsum
C. Distal third
1. Lower lateral cartilages, nasal tip, alae, and caudal cartilaginous septum
2. Thick, less mobile, sebaceous skin over the nasal tip and alae

II. NASAL SUBUNITS (NINE TOTAL)


A. *Dorsum, two sidewalls, tip, two alae, columella, and two soft triangles (Fig. 20-1).

III. LAYERS (SUPERFICIAL TO DEEP)


A. Skin
B. Subcutaneous fat
C. SMAS (± musculature)
D. Deep fatty layer (very thin)
E. Perichondrium/periosteum
F. Cartilage/bone
G. Mucosa/mucoperichondrium

IV. RELEVANT VASCULAR SUPPLY —Major nerves and blood vessels of the external nasal covering run deep to the SMAS,
with a few exceptions (Fig. 20-2).
A. External carotid artery branches
1. Angular arteries
a. Branch of facial artery
b. Superficial to or within the SMAS
c. Supplies lateral surface of caudal nose
d. Gives off lateral nasal arteries
2. Superior labial arteries
a. Within the orbicularis oris muscle, or between the mucosa and muscle
b. Supplies nasal sill, septum, and base of columella
Figure 20-2. Arterial supply of external nasal cover.

3. Infraorbital arteries
a. Branch of internal maxillary artery
b. Supplies dorsum and lateral nasal side walls
B. Internal carotid artery branches
1. Dorsal nasal branch
a. Branch of ophthalmic artery
b. Supplies dorsum and lateral skin
2. External nasal branch
3. Supratrochlear arteries
a. Branch of ophthalmic artery
b. 1.7 to 2.2 cm from midline
c. Runs between corrugators and frontalis layers at orbital rim, becoming superficial to frontalis at mid-forehead level.
4. Supraorbital arteries
a. Branch of ophthalmic artery.
b. ~2.9 cm from midline
c. Runs through a notch or foramen with a superficial branch coursing superficial to SMAS and a deep branch coursing
deep to or within the SMAS.
C. Venous anatomy: Venous drainage parallels arterial supply. Note—The angular vein becomes the anterior facial vein and
communicates with the ophthalmic veins and cavernous sinus.
Figure 20-3. Innervation of nasal cavity. A: Sensory innervation of the lateral wall of the nasal cavity. B: Sensory innervation of the medial wall and the nasal
septum. (From Agur AMR, Dalley AF, eds. Grant’s Atlas of Anatomy. 11th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2004.)

D. Septal vasculature: Branches of the anterior ethmoidal artery, posterior ethmoidal artery, sphenopalatine artery, and
superior labial artery.
E. *Lateral nasal wall vasculature: Branches from anterior ethmoidal artery, posterior ethmoidal artery, and
sphenopalatine artery.

V. INNERVATION (FIG. 20-3)


A. Sensory
1. External cover: Branches from the ophthalmic (V1 ) and maxillary (V2 ) divisions of the trigeminal nerve
a. *Supratrochlear, infratrochlear, and external nasal branches of the anterior ethmoidal nerve (derive from
V1).
b. Infraorbital nerve (derives from V2 )
2. Septum: Branches of the anterior ethmoidal (V1 ) and nasopalatine nerves (V2 ).
3. Lateral nasal wall: Branches of the anterior ethmoidal (V1 ) and branches of the pterygopalatine nerve (V2 ).
B. Motor innervation to muscles of the SMAS layer is supplied by branches of the facial nerve (VII).

SURGERY
I. GENERAL OBJECTIVES (depending upon the defect, one or more of these objectives will need to be achieved)
A. Establish or repair bony/cartilaginous foundation
B. Restore internal nasal lining
C. Restore external cover
D. Maintain patent airway
E. Optimize aesthetic result

II. OPTIONS FOR BONE/CARTILAGE FOUNDATION


A. Midline (septal) foundation
1. L-shaped septal strut (fabricated from septal cartilage, bony septum, rib, outer table cranium, or iliac bone)
2. *Cantilevered graft (fabricated from septal cartilage, bony septum, rib, outer table cranium, or iliac bone) and secured
to the remaining nasal bones or frontal bone
3. *Septal pivot flap based superiorly per Millard or inferiorly per Burget and Menick.
4. Alloplastic materials such as vitallium, titanium, or porous polyethylene; we do not encourage the use of these due to
the high rate of exposure and infection.
B. Lateral structures (nasal bones, upper lateral cartilages, and lower lateral cartilages)
1. Use septal, conchal, or rib cartilage
2. Reconstruct native cartilage anatomy when possible
3. Bolster reconstructed areas that are prone to collapse (sidewalls, alae, and columella) with cartilage grafts
4. Maintain airway patency (spreader grafts)
5. Lateral crural strut graft
a. Measures 3 to 4 mm wide by 20 to 25 mm long
b. Lateral end spans from piriform rim to lateral crura
c. Positioned caudal to alar groove.
d. Useful for lateral crural malposition and alar retraction
C. Alar support
1. Alar batten graft
a. Used for alar collapse and external nasal valve obstruction.
b. Placed cephalad to alar rim.
2. Alar contour graft
a. Inserted through infracartilaginous incision into alar-vestibular pocket inferior to rim of crus.
b. Used to recreate external nasal valve.

III. OPTIONS FOR RESTORING NASAL LINING (For larger defects, one may combine multiple available options. Lining
must be restored because wound contraction caused by secondary healing always results in significant distortion of the nose
or synechiae.)
A. Residual nasal vestibular lining
1. Often more nasal lining is available than is apparent, especially with a contracted, secondarily healed defect involving the
alar rim.
2. Advancement of 2 to 3 mm of internal lining may be achieved; must use cartilage graft to provide rigid support to
prevent subsequent retraction.
3. Often carried out in a bipedicled fashion; donor site may need coverage with full-thickness skin graft.
B. Turnover flap
1. Most appropriate for situations when the external nasal cover is to be reconstructed with a forehead flap.
2. The external nasal cover is turned in (rather than discarded) to be used as lining.
3. The scarred nature of the external nasal cover in these situations make the “turnover flap” relatively avascular with
unreliable survivability.
4. Must be kept <1 cm in length.
C. Intranasal flaps for lining (generally contraindicated for smokers) (Fig. 20-4)
1. Ipsilateral septal composite flap
a. Based upon axial septal blood supply (septal branch off the superior labial artery) and includes septal
mucoperichondrium.
b. Appropriate for cases with unilateral defect involving the internal lining of the middle and upper vaults.
2. Contralateral septal composite flap (septal door flap) can also be used, where nasal septum and contralateral
mucoperichondrium is hinged on the dorsum and transferred into the defect such that the septal mucosa now lines the
airway. Based on anterior ethmoid artery.
D. Other flaps for lining
1. Inferior turbinate flap
a. May be used for small full-thickness alar defects.
b. Pedicle based upon the anterior attachment of the turbinate.
2. FAMM (facial artery musculo-mucosal) flap.
a. Good for lining the middle vault.
b. Consists of intraoral mucosa, submucosa, strip of buccinator muscle, deeper plane of orbicularis oris muscle, and
facial artery with its venae comitantes.
c. Based superiorly upon the alar base and centered over the facial artery.
d. 8 to 9 × 1.5 to 2 cm of tissue available; may be passed via a tunnel directly into the nose (without any external
scars).
Figure 20-4. Intranasal lining flaps. A: Bipedicle flap. B: Ipsilateral mucoperichondrial flap. C: Contralateral mucoperichondrial flap. D: Contralateral septal flap. E:
Composite flap.

3. Nasolabial flap
a. Rarely is used for nasal lining, usually in situations when all other options have been exhausted.
b. May perform delay to maximize chance of flap survival.
c. Disadvantages include thicker, stiffer tissue, and it cannot be thinned at initial transfer.
E. Forehead flap techniques for internal lining
1. Full-thickness skin graft
a. Used to line a full-thickness forehead flap (skin, subcutaneous fat, and frontalis muscle).
b. Cartilage grafts are NOT immediately placed under skin-grafted areas.
c. Reconstruction typically performed in three stages, and cartilage grafts are inserted under skin-grafted areas during
subsequent stages of reconstruction.
2. Folded forehead flap
a. For full-thickness unilateral and bilateral defects.
b. Can replace internal lining defects up to 3.5 cm.
c. Uses the most distal edge of the flap (often within the scalp) harvested superficial to frontalis muscle and folded over
on itself.
d. Best used in a three-stage reconstruction with cartilage grafts placed during the second stage.
3. Prelaminated forehead flap
a. Viable option for small- to medium-sized rim defect in elderly or debilitated patients for whom the priority is to
minimize the physiologic burden of each surgery (with less emphasis upon aesthetic outcome).
b. Each procedure may be done under light sedation or local anesthesia alone.
c. Preliminary operation involves application of a full-thickness skin graft to the distal deep surface of the flap under the
frontalis muscle along the proposed nostril margin of the planned forehead flap. Cartilage graft also placed between
the frontalis muscle and overlying external skin (providing rim support along nostril margin).
d. Usually requires at least three surgical stages.
4. Second forehead flap
a. May be used for large internal lining defects.
b. A second forehead flap may be used for lining of the forehead flap used for external cover.
c. Midline support may be established at initial surgery.
d. Lateral support (alar cartilage grafts) should be placed at subsequent thinning.
F. Free flap
1. Multiple available donor options
a. Radial forearm free flap
b. Temporoparietal fascia flap + skin graft
2. Usually needed with
a. Large and deep defects to central face (e.g., shotgun injury)
b. Major contamination, radiation injury, or immunosuppression
3. Requires a multiple staged reconstruction
a. Initial stages involve temporary external nasal cover (e.g., radial forearm free flap folded upon itself) and temporary
structural support (metal or cadaveric cartilage).
b. Final bony/cartilage support and external nasal cover (e.g., forehead flap) are placed at later stages.

IV. OPTIONS FOR RESTORING EXTERNAL NASAL COVER (MOST COMMON FOR SMALL DEFECTS)
A. Technical pearls
1. Convert circular defects into square defects with sharp corners (circular defects encounter concentric contraction when
healing).
2. Incisions should follow natural relaxed skin tension lines when possible; place upon junction of lateral nose and cheek
when possible; orient vertically or transversely upon glabella and nose.
3. No incisions on concavities
B. Smaller defects (less than 1.5 to 2 cm in greatest dimension)
1. Upper third/radix
a. Secondary healing
b. Primary closure (wounds smaller than 5 to 10 mm)
c. Integra ± full-thickness skin graft (preauricular or postauricular)
d. Local flaps
i. Single lobe transposition flaps (Banner, Romberg)
ii. Dorsal nasal flap and its variants (can actually reconstruct up to ∙2.5 cm defects)
a) Based laterally on angular arteries
b) Entire nasal dorsum rotated and advanced caudally
iii. Glabellar flap
2. Middle third/dorsum and sidewalls
a. Secondary healing
b. Primary closure (wounds smaller than 5 to 10 mm)
c. Integra dermal regeneration matrix ± full-thickness skin graft (preauricular or postauricular)
d. Consider cheek flap for recruitment of tissue onto sidewalls
e. Local flaps
i. Single lobe transposition flaps (Banner, Romberg)
ii. Dorsal nasal flap
iii. Nasolabial flap (Fig. 20-5): for sidewall/alar defects up to 2 cm
iv. V–Y advancement: Good for small defects along the alar groove
v. Rhombic flap
3. Nasal tip
a. Integra dermal regeneration matrix + secondary healing versus full-thickness skin graft from forehead.
b. Local flap—bilobed flap (Fig. 20-6)—does not reach the infratip lobule; should not be used to reconstruct defects
within 0.5 cm of nostril rim
i. For defects measuring 1.5 cm or less
ii. If the defect is within 1 cm of the nostril margin, some degree of rim distortion is expected.
iii. Maximum 50 degrees of rotation per lobe or 100 degrees total.
iv. Undermine widely above perichondrium/periosteum.
v. First lobe diameter should equal the defect diameter.
4. Alae
a. Local flap—nasolabial flap (Fig. 20-5)
i. For defects up to 2 cm
ii. Perform under general anesthesia (avoid distortion/blanching of local anesthetic)
iii. Immediate insertion of cartilage graft
iv. If entire alar subunit is to be reconstructed, it should be done in two stages.
b. Composite grafts (auricular donor site for chondrocutaneous tissue)
i. For full-thickness defects (external cover, fibrofatty tissue, and internal lining) involving the alar margin or soft
triangle.
ii. All portions of the placed graft must be within 1 cm from a wound edge (i.e., maximum theoretical limit of defect
is 2-cm diameter); ideal defect size is 1 cm or less. Donor graft is harvested slightly larger than defect to
accommodate expected contraction with healing.
iii. Reported survival rates ranging from 50% to 90%; ~30% failure or significant necrosis is to be expected.
iv. Helical crus for alar rim defect; other donor sites on the ear may be used.
Figure 20-5. T wo-stage nasolabial flap.

v. Improved graft take and aesthetic result when defect is allowed to heal secondarily and reconstructed in delayed
fashion.
vi *Graft is white initially; turns blue at 24 to 72 hours; then gradually becomes pink over subsequent
days.
C. Larger or adversely located defects (defects >1.5 to 2 cm or defects located upon the infratip lobule and within 0.5 cm
of nostril rim)
1. Forehead flap (Fig. 20-7)
a. Two-stage
i. Flap is partially thinned distally at the initial transfer (supratrochlear arteries become subcutaneous at level of mid-
forehead).
ii. Makes the flap more susceptible to necrosis.
b. Markings
i. Supratrochlear artery is found 1.7 to 2.2 cm lateral to midline and usually corresponds to vertical tangent of medial
border of eyebrow.
ii. Doppler out course in preoperative area.
iii. Create flap base about 1.5 cm (0.7 cm to each side of artery).
iv. Mark out rhytids so that they line up at the end of the case.
v. Curve the pedicle of the flap into non-hair-bearing areas.
vi. Template is created from the defect and placed at anterior hairline with flap centered over the supratrochlear
artery.
c. Surgery
i. Inject lidocaine with epinephrine into entire forehead and nose. Block nerve up into hairline where you are going
to take out standing cutaneous deformity (SCD).
ii. When injecting, do not infiltrate too much to avoid distortion.
iii. Place patient in 20 to 30 degrees of reverse Trendelenberg to decrease venous pooling.
iv. Prep the patient’s full face and scalp including the submental area.
v. Create template of the defect with Telfa or chromic paper.
Figure 20-6. Bilobed flap. Markings for blob flap (above). Undermining, elevation and trimming of flap during transposition (middle). Bilobe flap following inset
(below).
Figure 20-7. Forehead flap. A: Arteries (a.) of the forehead. T his richly anastomotic network provides the basis for the paramedian forehead flap (B).

vi. Place cut template from hairline upside down onto the nose so that it will rotate clockwise from right side or
rotate counterclockwise from left side.
vii. Use a suture to measure distal end of template to level of medial brow and then see if it reaches from medial
brow to distal recipient site.
viii. Pedicle is incised through skin, subcutaneous tissue, muscle, and f ascia, except not completely through the
galea at the distal part of the flap.
ix. Flap is elevated from superior to inferior.
x. Rapid dissection until reaching the corrugator at which point muscle is dissected away from underlying
periosteum bluntly (use spreading scissors).
xi. Once you are near the pedicle, enter the subfascial plane just superficial to periosteum of frontal bone.
xii. At the supraorbital ridge, score the periosteum and go under periosteum with periosteal elevator.
xiii. You may see the pedicle on deep surface of the frontalis muscle as it exits over or through the corrugator.
xiv. Undermine the entire forehead in both directions in subfascial plane.
xv. Make parallel vertical galeotomies 2 to 3 cm apart to help close the donor site, but avoid supraorbital nerve just
medial to temporal line.
xvi. If needed, use foley catheter balloon for intraoperative tissue expansion to facilitate closure of the donor site.
xvii. Use 2-0 Vicryl suture to reapproximate fascia moving from inferior to superior.
xviii. If cannot close the top, can leave open and place bacitracin.
xix. Cut out SCD from top of donor site into hair and use staple for the scalp.
xx. Tailor thickness of flap by thinning distal portion removing muscle and most of subcutaneous fat using a no. 15
blade.
xxi. Bevel out 45 degrees around the edges of the forehead flap.
xxii. The most distal aspect of flap should be skin only and progressively becomes thicker from most distal to most
proximal portions
xxiii. Inset flap with 4-0 monocryl in deep dermis followed by a running 6-0 nylon suture.
xxiv. Can wrap the raw part of flap with Integra
xxv. *Divide pedicle between 10 days and 3 weeks and inset flap.
xxvi. At second stage, can just thin distal flap and place back down or cut and inset pedicle and thin flap.
D. Columellar reconstruction—many options, none are ideal
1. Full-thickness skin graft from forehead (in situations without cartilaginous deficit)
2. Banked forked flaps and variants (soft tissue in the region of the columellar footplate/nasal floor/upper lip is rotated or
advanced onto the columella)
3. Nasolabial flaps
4. Tunneled labial mucosal flap
5. Composite chondrocutaneous grafts. Helical rim used for the columella
6. Forehead flap

V. COMPLICATIONS
A. Possible complications
1. Infection: Cellulitis ± purulent drainage; always consider the possibility of infection involving the underlying structural
grafts
a. Aggressive antibiotic treatment
b. Any abscess must be washed out
c. Persistent drainage suggests infection of structural grafts; investigate for internal lining defect
2. Necrosis of flap can be avoided by protecting the vascular supply to avoid ischemia.
a. Debride as needed
b. If flap cannot be salvaged with acceptable aesthetic result, plan on performing another flap.
B. Factors leading to complication
1. Inappropriate pedicle width (pedicle base should be 1.2 to 1.5 cm). Wider bases will encounter undue tension on rotation.
2. Flap design is too short or with pivot point too high (causing excess tension)
3. Excessive thinning at first stage leading to vascular compromise.
4. Excessive re-elevation of flap at stage II (do not elevate beyond 1 to 1.5 cm of the tip and nostril margin).
5. Smoking—three-stage approach is safer in smokers; avoid “intranasal flap” options for internal lining.
6. Radiation—can lead to severe atrophy, induration, or ulceration.
RHINOPHYMA
I. FEATURES AND ETIOLOGY
A. Most advanced stage of rosacea (1—frequent facial flushing; 2—thickened skin/telangiectasias/erythrosis; 3—acne
rosacea; 4-rhinophyma).
B. Predominantly male disease; prevalent among English/Irish ancestry, peak presentation at later than age 50, probably no
association with alcohol.
C. Disease begins with vascular instability of the skin; fluid is lost into interstitium; inflammation and fibrosis follows.
Dermal and sebaceous gland hypertrophy develop. Sebaceous ducts become plugged resulting in dilation and cyst
formation.
D. Therapies
1. Nonsurgical (will slow progression, but does not cure): both topical and oral antibiotics/retinoids
2. Surgical (goal is complete resolution, allow surgical site to heal secondarily)
a. Dermaplaning
b. Dermabrasion
c. Cryosurgery
d. CO2 and argon laser
E. Cutaneous malignancies (e.g., basal cell carcinoma, squamous cell carcinoma) can lie within the rhinophymatous tissue
F. *Oral retinoids (isotretinoin/Accutane) should be discontinued 1 year prior to surgery as they impair re-
epithelialization

PEARLS
1. If the blood supply to the columella is disrupted, the nasal tip relies on the lateral nasal arteries for blood supply
2. The forehead flap should become thicker when dissecting distal to proximal (subcutaneous to submuscular to subperiosteal)
3. The donor site of the forehead flap heals remarkably well by secondary intention.
4. The maximum rotation of a bilobed flap is 100 degrees
5. Defects of the nasal ala are best treated with a flap to prevent retraction and notching of the rim

QUESTIONS YOU WILL BE ASKED


1. What three things are required in all cases of nasal reconstruction?
Lining, support, and coverage.
2. What is the subunit principle of nasal reconstruction?
If 50% or more of a subunit is missing, then excise the remaining portion to achieve an optimal aesthetic outcome.
3. How far on either side of the midline is the supratrochlear artery located?
1.7 to 2.2 cm.
4. When should isotretinoin be discontinued in relation to nasal resurfacing procedures?
One year prior to surgery.

THINGS TO DRAW
Draw the nasal aesthetic subunits (Fig. 20.1).

Recommended Readings
Burget GC, Menick FJ. Nasal support and lining: the marriage of beauty and blood supply. Plast Reconstr Surg. 1989;84(2):189–202. PMID: 2748735.
Elliott RA Jr. Rotation flaps of the nose. Plast Reconstr Surg. 1969;44(2):147–149. PMID: 4895071.
Guo L, Pribaz JR, Pribaz JJ. Nasal reconstruction with local flaps: a simple algorithm for management of small defects. Plast Reconstr Surg. 2008;122(5):130e–139e.
PMID: 18971686.
Menick FJ. T he evolution of lining in nasal reconstruction. Clin Plast Surg. 2009;36(3):421–441. PMID 19505612
Millard DR Jr. Reconstructive rhinoplasty for the lower half of a nose. Plast Reconstr Surg. 1974;53(2):133–139. PMID: 4590746.
Rohrich RJ, Griffin JR, Adams WP Jr. Rhinophyma: review and update. Plast Reconstr Surg. 2002;110(3):860–869; quiz 870. PMID: 12172152.
Zitelli JA. T he bilobed flap for nasal reconstruction. Arch Dermatol. 1989;125(7):957–959. PMID: 2742390.
LIP RECONSTRUCTION
I. FUNCTIONAL AND AESTHETIC GOALS
A. Oral competence is the primary goal of lip reconstruction. Specifically, this includes maximizing oral aperture, mobility, and
sensation. Dribbling of saliva or food results from loss of lip function, sensation, or deficiency of the lower lip sulcus.
B. Restoration of static and dynamic symmetry. The lips are essential for facial expression and communication.

II. LIP ANATOMY


A. Layers: The lip consists of skin, a thin layer of subcutaneous tissue, orbicularis oris muscle, and mucosa
1. Vermillion
a. Unique tissue consisting of modified mucosa with relatively few underlying minor salivary glands
b. The “white roll” is the junction of the vermillion and the lip skin; *its continuity is critical during
reconstruction because even a 1 mm step off is noticeable at conversational distance
c. The posterior vermillion line (wet-dry border) is where the upper and lower lips meet when the mouth is closed. This
is the transition from oral mucosa to vermillion mucosa.
B. External anatomy (Fig. 21-1)
1. The lips are divided into four subunits
a. Philtrum: Between the philtral columns. The tubercle is the central portion of vermillion inferior to the philtrum.
b. Lateral wings: Between each philtral column and nasolabial fold
c. Lower lip: The entire lower lip is a single subunit
2. The labiomental fold separates the lower lip from the chin
3. The nasolabial folds confine the lateral extents of the upper lip
4. The normal intercommissural distance in an adult at rest is 5 to 6 cm. This width is approximately the distance between
the medial limbi of the corneas. Ideally, this width should also equal the distance from the stomion to the menton.
C. Muscular anatomy
1. Orbicularis oris muscles
a. The primary muscles for closure of the lips.
b. Function as a sphincter for the oral cavity and also act to evert the lips.
c. Originate from the modiolus and decussate at the midline in the lower lip; in the upper lip the muscles cross the
midline and insert into the opposite philtral column.
d. Innervation is by the buccal branches of the facial nerve.
2. The paired mentalis muscles
a. Principle elevators of the lower lip.
b. They arise from the lower border of the mandible and insert into the soft tissues of the chin below the level of the
labiomental crease.
c. Innervation is by the marginal mandibular branch of the facial nerve.

______________
*De note s common in-se rvice e xamination topics
Figure 21-1. External lip anatomy.

3. Lip elevators
a. Include the paired levator anguli oris, levator labii superioris, zygomaticus major, and zygomaticus minor muscles.
b. Innervation is by the zygomatic and buccal branches of the facial nerve.
4. Lip depressors
a. Include the paired depressor anguli oris and depressor labii inferioris muscles.
b. Innervation is by the marginal mandibular branch of the facial nerve.
c. *The paired platysma muscles also provide some lateral lower lip depression (e.g., during full denture
smile) and are innervated by the cervical branch of the facial nerve.
D. Sensation
1. Upper lip: The infraorbital nerve is the terminal branch of the maxillary division of the trigeminal nerve (V2 ) and exits
the maxilla at the infraorbital foramen in line with the pupil and 1 cm inferior to the infraorbital rim
2. Lower lip: The mental nerve is the terminal branch of the mandibular division of the trigeminal nerve (V3 ) and exits the
mandible at the mental foramen at the level of the second premolar.
E. Blood supply
1. Arterial
a. The superior and inferior labial arteries are branches of the facial artery. They form a rich vascular network that
spans circumorally and allows for the design of multiple flaps for lip reconstruction.
b. *The labial artery usually lies between the orbicularis oris muscle and mucosa within the vermillion
portion of the lip.
c. Superior labial artery is 10 mm from superior lip margin.
d. Inferior labial artery is 4-13 mm from lower lip margin.
2. Venous: Superior and inferior labial veins drain to the ipsilateral facial vein
F. Lymphatic drainage
1. *The upper lip and lower lateral lip segments drain into the submandibular nodes.
2. The central lower lip drains into the submental nodes.

III. APPROACH TO LIP DEFECTS


A. Etiology of lip defects: Cancer resection is the most common cause (>90%) and squamous cell carcinoma is the most
common neoplasm.
1. *Vermillion cancers (anterior to wet-dry line) behave like cutaneous tumors, but those posterior to this
landmark behave like intraoral tumors (higher risk of metastasis).
2. A surgical margin of 7 to 10 mm is recommended for squamous cell carcinoma. For basal cell carcinoma, a surgical
margin of 2 to 4 mm is recommended.
B. Reconstruction of lip defects requires consideration of
1. What tissue is missing: Vermillion, skin, orbicularis muscle, and mucosa
2. How much of the lip is missing: The proportion of total lip tissue missing is often described in thirds, superficial versus
full-thickness defect, involvement of commissure, and involvement of the philtrum.
3. Patient factors: Age of patient, tissue elasticity, lip redundancy, need for dentures, radiation, previous scars, tolerance
for complex reconstruction, and general health status
4. Lip defects that involve >30% of the lip may result in microstomia if closed primarily. Microstomia is a difficult
condition that impedes eating, use of dentures, and adequate oral hygiene.

IV. SUPERFICIAL LIP DEFECTS


A. Superficial defects of the skin: Usually do not cause functional deficits
1. Skin grafts can provide efficient coverage of superficial lip defects, but can result in inferior aesthetic results.
a. Split-thickness skin grafts contract more than full-thickness grafts.
b. Severe cases of retraction can lead to lip eversion and decreased oral competence.
2. Local tissue rearrangement techniques generally offer the best match in tissue thickness, color, and texture
a. Cheek advancement flaps combined with perialar excisions and lateral V–Y advancement flaps are commonly used
for upper lip skin defects.
b. Lower lip defects are often resurfaced with rotational flaps (e.g., bilobed) and transposition flaps (e.g., rhomboid).
c. If the defect is confined to the philtrum, consider healing by secondary intention or full-thickness skin grafting.
B. Vermilion defects
1. General principles
a. Before infiltrating local anesthetic, use a fine-tipped pen and mark the superior and inferior edges of the white roll.
b. Lesions of the vermillion are preferentially excised perpendicular to the white roll in order to facilitate alignment of
this landmark.
c. Local tissue rearrangements that involve skin only will require the use of one of the following techniques to repair the
vermillion.
2. Techniques for reconstruction
a. Small defects can be treated with musculomucosal V–Y advancement flaps (generally horizontally oriented).
b. Large defects (such as after vermillionectomy for precancerous lesions) involving the entire vermillion can be
resurfaced with a retrolabial mucosal advancement flap and dissected to the sulcus at a level between the orbicularis
oris muscle and the accessory salivary glands, which are included in the mucosal flap
c. Staged procedures that borrow mucosa from the upper lip (e.g., bipedicled mucosa flap, cross lip mucosa flap).
d. Staged tongue flap: Dorsal tongue for upper lip and volar tongue for lower lip.
e. For superficial vermillion defects <30% of the lip, the vermillion–skin border can be incised and the vermillion can be
directly advanced along the lip.
f. For more complex vermillion defects <30% of the lip, full-thickness excision can be performed.
Figure 21-2. Reconstructive algorithm for full-thickness lip defects.

V. TECHNIQUES FOR FULL-THICKNESS LIP RECONSTRUCTION (FIG. 21-2)


A. Full-thickness defects up to one-third of the lip: Primary closure is most appropriate
1. Shield or wedge excision: Preferred design around lip lesion for excision. Can be modified into a “W” on the lower lip
to limit the length of closure and prevent disruption of the labiomental or nasolabial creases.
2. Central upper lip defects involving the philtrum can be reconstructed with an Abbe flap to maintain aesthetic subunits.
3. Optimal repair and prevention of notching requires determined approximation of the orbicularis oris muscle, mucosa,
white roll, dermis, and epidermis.
B. Defects of one-third to two-third of the lip
1. Primary closure with skin excisions
a. For defects slightly larger than one-third of the lower lip, bilateral labiomental crease excisions (Schuchardt
procedure) can provide enough laxity for primary closure.
b. For the upper lip, bilateral perialar crescentic excisions with cheek advancement (Webster flaps) may allow for
primary closure.
2. Lip-sharing techniques
a. Abbe flap (Fig. 21-3): A two-staged lip-switch procedure where a full-thickness flap of up to one-third of the donor
lip can be used to reconstruct up to a two-third defect of the recipient lip. The flap is rotated 180° on its pedicle
(labial artery) and remains for about 3 weeks, when the pedicle is divided.
i. This technique can be utilized with upper and lower lip defects.
ii. Flaps are designed with their borders parallel to relaxed skin tension lines. The height of the flap should match that
of the defect. The width of the flap should be about half of the defect (to allow for proportional reduction of both
lips).
Figure 21-3. Abbe flap. A: An upper lip defect is being prepared. Complete excision of the lesion will produce a full thickness lip defect that can be reconstructed with
an Abbe flap. Markings are shown. B: T he Abbe flap has been rotated into the defect. T he flap is perfused by the labial vessels. C: After two or three weeks the flap is
divided and inset.

iii. Due to generous vascularity of the lip, the Abbe flap can be based on either a medial or lateral pedicle.
iv. Several millimeters of labial mucosa should be maintained around the pedicle to allow for venous drainage.
v. Despite denervation of the orbicularis oris muscle during harvest, motor and sensory function improves over the
first year.
vi. In the upper lip, an Abbe flap can be used for either philtral or lateral lip reconstruction.
vii. An Abbe flap can be performed in conjunction with labiomental crease incisions or perialar crescent excisions
for larger defects.
viii. In general, the artery is located at a level equivalent to the white roll on sagittal section.
b. Estlander flap (Fig. 21-4): A medially based lip-switch technique that is indicated in lip defects that demonstrate
commissure involvement
i. Principles of design similar to the Abbe flap. Again, the flap width should be about half the defect width for deficit
balance.
ii. Flaps are designed so that incisions lie within the nasolabial fold and are used with upper and lower lip defects.
iii. Despite being a one-stage reconstruction, there is often blunting of the reconstructed commissure and patients
often require commissuroplasty

Figure 21-4. A: Estlander flap. B: Reverse Estlander flap.


iv. Flap is not innervated and oral animation can be distorted.
v. Blood supply more tenouous than the Abbe flap because it comes from contralateral labial artery.
vi. Cuff of muscle should be maintained at rotation point to improve vascularity to flap.
3. Staircase technique: A one-stage operation most commonly used to reconstruct lower lip defects, but may also be
used for upper lip defects
a. A series of steps are designed originating diagonally from the defect along skin creases. Full-thickness rectangles or
squares of skin and subcutaneous tissue are excised under each step to allow for advancement of local tissue into the
defect.
b. The number and dimensions of the necessary steps are determined by the size of the defect and available laxity
c. This technique does not require violation of the orbicularis oris muscle or the opposite lip
4. Karapandzic flap (Fig. 21-5): A modification of the Gillies’ fan flap, *this one-stage technique preserves motor
and sensory function through meticulous dissection of the neurovascular pedicles and is ideal for large central
defects of up to 80% of the lower lip
a. For lower lip defects, circumoral incisions are made extending from the defect and curve up around the commissures
to include the nasolabial folds.
b. For upper lip defects, incisions are made along the nasolabial creases and extend down to the labiomental crease.
c. Bilateral opposing flaps are created and the incisions are limited to skin and subcutaneous tissue superficially and
separate incisions to release the mucosa.
d. The intervening neurovascular structures are bluntly dissected out with scissors and preserved as the soft tissues are
released to provide laxity to close the defect.
e. The Karapandzic flap may be used in cases with commissure involvement as the rotating donor lip tissue creates a
new commissure.
f. Because it is often used for large lip defects, the Karapandzic flap may lead to blunting of the commissures and
microstomia, which may require the use of lip-stretching appliances.

Figure 21-5. Karapandzic flap. T he flap elements are incised and elevated (left). Small Burow’s triangles may be excised to facilitate rotation. T he blood vessels and
facial nerve branches are preserved (inset). T he flaps are rotated into position and closed (right).

C. Subtotal and total lip defects


1. Combination of flaps
a. For the lower lip, two lateral Abbe flaps are used to reconstruct the lower lip while perialar crescent excisions with
cheek advancement are used to close the upper lip Abbe donor sites.
b. For the upper lip, an Abbe flap from the lower lip is used to reconstruct the philtrum in addition to bilateral perialar
crescent excisions with cheek advancement.
2. Karapandzic flap: Appropriate for very large defects if patients demonstrate sufficient tissue laxity.
3. Bilateral opposing cheek advancement: Many eponyms exist, but all are based on horizontal advancement of cheek
skin with removal of Bürow triangles. Excisions involve skin and subcutaneous excisions only to protect neurovascular
structures and preserve as much oral competence as possible. Buccal mucosa is used to reconstruct the vermillion.
a. Bernard–Burow for lower lip (Fig. 21-6): Two large Bürow triangles are excised lateral to the upper lip
b. Webster modification of Bernard–Burow for lower lip: Places triangular skin excisions adjacent and parallel to the
bilateral nasolabial folds, resulting in scars that are within natural skin creases and avoids violating the aesthetic
region of the chin
c. Bernard-Burow’s for upper lip: Four triangular skin excisions are needed, two perialar and two lateral to the
lower lip
4. Nasolabial flap: A long segment of skin and subcutaneous tissue is transposed to reconstruct full-thickness defects of
the upper or lower lip.
a. Requires a skin graft to line the inner surface at the first stage.
b. Flaps have a random blood supply and can be delayed if necessary.
c. Must account for significant contraction and therefore flaps should be made larger than the lip defect.
d. Reconstruction of the vermillion is necessary at a second stage.
e. Due to these limitations, this is not a preferred choice for subtotal or total lip reconstruction.
f. Blood supply thought to be from perforators off angular artery off of facial artery
5. Temporoparietal scalp flap
a. A regional option best suited for male patients providing full-thickness reconstruction.
b. Bilateral flaps based on the superficial temporal artery can be used for full lip reconstruction.
c. Like nasolabial flaps, a skin graft is needed to line the deep surface and the flaps can be delayed.
6. Free tissue transfer (e.g., radial forearm with palmaris longus tendon for static support for oral competence)

Figure 21-6. Bilateral modified Bernard–Burrow’s technique.

CHEEK RECONSTRUCTION
I. CHEEK ANATOMY
A. The cheek represents a relatively large area of the face delineated laterally by the preauricular skin, inferiorly by the
mandibular border, medially by the nasal sidewall and nasolabial fold, and superiorly by the lower eyelid and temple
B. Several descriptions of subunits exist, but the most straightforward one divides the cheek into three subunits:
1. Suborbital: Between the nasolabial fold and anterior sideburn, lower eyelid, and gingival sulcus.
2. Preauricular: Between ear and malar eminence, includes masseteric and parotid fascia.
3. Buccomandibular: Between the gingival sulcus and the border of the mandible, includes oral lining.
C. Muscle: The muscles of facial expression are connected by a contiguous fibrous sheet known as the superficial
musculoaponeurotic system (SMAS) which lies just deep to the subcutaneous layer. *Superiorly it is continuous with
the temporoparietal fascia (also known as superficial temporal fascia) and inferiorly it is continuous with the
platysma.
D. Innervation
1. Sensation to the cheek is mediated by branches of the maxillary (V2 ) and mandibular (V3 ) divisions of the trigeminal
nerve.
2. Motor function to the muscles of facial expression is imparted by the facial nerve (VII), which travels underneath the
superficial lobe of the parotid gland. More anteriorly, the distal branches are found just deep to the parotid masseteric
fascia.
E. Blood supply
1. The cheek is supplied predominantly by the facial artery, which gives off the angular artery.
2. The transverse facial artery branches from the superficial temporal artery and supplies the cheek superiorly.
3. Distally, these anastomose with the infraorbital artery and infratrochlear artery.
F. Retaining ligaments
1. There are two areas along the cheek where the skin and soft tissues are relatively fixed to the underlying bone.
2. The zygomatic ligament is found on the zygoma, just posterior and inferior to the malar eminence.
3. The mandibular ligament is found along the jaw line just posterior to the chin.
4. These ligaments resist advancement of cheek skin and may require release to allow for closure of cheek defects.

II. PREOPERATIVE CONSIDERATIONS


A. Patient factors such as smoking, diabetes mellitus, immunosuppression, history of radiation, and prior scars may compromise
wound healing or cause necrosis of local flap.
B. Defect size, complexity, surrounding skin quality, skin laxity, hair-bearing status, and orientation of relaxed skin tension lines
all affect the selection of the most appropriate reconstruction.
C. After excision of aggressive tumors (e.g., melanoma), a simpler reconstruction such as healing by secondary intention,
primary closure, or skin grafting may be preferred initially in order to allow for tumor surveillance.
D. Increased tension across the cheek will affect the appearance of neighboring facial units. For example, scar contractures of
the cheek commonly result in traction on the lower eyelid or upper lip, causing ectropion.

III. RECONSTRUCTIVE OPTIONS


A. Secondary healing
1. Reserved for selected cases where the defect is small and there is a reason to not perform primary closure.
2. Larger defects left to heal secondarily risk significant scar contraction that will lead to distortion and asymmetry.
3. Secondary healing leads to superior results in flat or concave areas (e.g., temple, preauricular) as opposed to convex
areas (e.g., malar eminence).
B. Primary closure: Small defects <1 cm in size can be reliably closed primarily, especially with skin undermining.
1. Elderly patients demonstrate increased skin laxity and therefore primary closure is often appropriate even for larger
cheek defects.
2. In general, undermining up to 4 cm beyond the defect borders increases recruitment of surrounding tissue; further
undermining does not contribute significantly to decreased wound closure tension.
3. Lesion excision and primary closure should be designed ideally along the relaxed skin tension lines.
4. Some lesions are positioned perpendicular to the relaxed skin tension lines: In these cases, it is better to accept an
unfavorably oriented scar than to create a much longer scar within the relaxed skin tension lines.
C. Skin grafts: Often the most efficient technique for covering larger cheek defects, skin grafts usually result in a poorer
cosmetic outcome compared to local flap reconstruction
1. Skin grafts are considered in unhealthy patients who cannot tolerate more complex reconstructive surgical options and
patients who require surveillance for recurrence of aggressive tumors
2. Healed skin grafts on the cheek will demonstrate a patch-like appearance, color mismatch, and contour deformity.
However, skin grafting is a preferred technique for temporal defects.
3. Full-thickness skin grafts will result in less secondary contraction and should be used whenever possible. When split-
thickness grafts must be used, a thick nonmeshed graft should be harvested to optimize cosmesis.
D. Local tissue rearrangement (see Chapter 4: “Flaps”): Local flaps are useful for moderate (2 to 3 cm) and large (>3 cm)
cheek defects. When designing a local flap, it is critical that the vector of maximum tension after closure of the donor site is
not in an unfavorable direction (e.g., pulling down the lower eyelid predisposing to ectropion). Often, many surgical options
will serve to close a cheek defect; the most appropriate reconstruction depends of the aforementioned preoperative
considerations.
1. Transposition flaps: These versatile reconstructions capitalize on the substantial mobility of the cheek skin. Skin and
subcutaneous tissue are borrowed from adjacent areas of relative laxity and the donor site is closed primarily. With
careful planning of incisions and donor site tension, drawbacks such as complex scarring, trapdoor deformity, and
irregularity in hair pattern can be minimized.
a. Banner flap
i. Simple transposition flap.
ii. Final scar is placed along the relaxed skin tension lines of the cheek and the apex of the banner is usually excised.
iii. Not the ideal choice because it typically results in a standing cutaneous deformity.
b. Rhomboid flap
i. Commonly used for coverage of defects on the lateral cheek and jawline.
ii. The classic rhomboid flap requires conversion of the defect to a rhombus with 60 and 120 degree angles.
iii. The donor flap is drawn from one of the 120 degree angles. The flap must be designed so that the vector of
maximum tension after donor site closure is placed favorably.
iv. Disadvantage: Multiple incisions create one or more scars that lie perpendicular to lines of relaxed skin tension.
c. Bilobed flap
i. Modification of the banner flap, the bilobed flap uses a second secondary flap to help close the donor site of the
primary flap.
ii. A pivotal arc of 90 to 110 degree is commonly used.
iii. These flaps may be used along the lateral and inferior cheek.
iv. Given the complex scarring, these flaps are generally not a first choice in cheek reconstruction.
2. Cheek advancement flap
a. Useful for preauricular defects, a flap of cheek tissue can be directly advanced into the defect with excision of
Bürow triangles at the base.
b. Variations of this advancement technique may be utilized depending on defect characteristics. One example is the O-
T flap, where a circular defect is converted into two opposing advancement flaps and the intervening standing
cutaneous deformity is excised.
3. V–Y advancement flap
a. Appropriate for defects of the medial cheek, alar base, and along the nasolabial fold, this flap survives on perforators
within the subcutaneous pedicle.
b. The flap may be designed with curved limbs that lie along the natural rhytids. With care, this flap is well-suited for
infraorbital defects, with low rates of ectropion and significant advantages over Mustardé-type flaps.
c. Sufficient subcutaneous dissection around the V–Y flap is required to achieve adequate mobilization for closure.
E. Regional flaps
1. Cervicofacial flap
a. Large (>4 cm) medial cheek defects that are inappropriate for other local tissue rearrangement options can be
repaired with a cervicofacial flap.
b. Various designs of cervicofacial flaps may be used depending on the size and location of the defect and flaps may be
based superiorly or inferiorly
c. Often a standing cutaneous deformity will need excision
d. Mustardé flap (Fig. 21-7)
i. For defects close to or including the lower eyelid, the incision may be carried into either the subciliary line or the
inferior orbital rim.
Figure 21-7. Mustardé cervicofacial flap.

ii. The incision is then taken beyond the lateral canthus and curves superiorly before extending inferiorly into the
preauricular crease.
iii. The flap should be anchored to the deep temporal fascia above the lateral canthus to reduce tension on the repair
and to prevent ectropion.
e. Cervicopectoral flap
i) Useful for very large cheek defects requiring significant advancement and rotation of donor tissue.
ii. Incisions are similar to a Mustardé flap but are extended onto the lower neck posteriorly and then over the
clavicle anteriorly.
iii. Anchoring sutures to inferior orbital rim periosteum and temporary Frost sutures can help prevent ectropion.
F. Tissue expansion
1. Provides skin that has good color and texture match and is well-vascularized and sensate to resurface large cheek
defects.
2. Tissue expansion in the head and neck region is associated with high complication rates.
3. Usually, lateral cheek and upper neck skin can be expanded to resurface defects resulting from excision of scars, large
benign lesions, or previous skin grafts.
G. Free flaps
1. Reserved for complex cheek defects involving multiple tissue layers or patients who are not suitable candidates for local
tissue rearrangements, such as patients with facial burns, patients who have had neck dissection, or patients
demonstrating significant radiation dermatitis.
2. A classic choice is the radial forearm free flap which is usually harvested with palmaris longus tendon for lip support.

PEARLS
1. When planning lip reconstruction, think about: What tissue is missing? How much of the lip is missing? What are the relevant
patient factors?
2. Before injection of local anesthetic into a lip or around a skin lesion, always think, “Do I need to first mark the vermillion border
or the edges of this lesion?”
3. When a cheek defect is close to the lower eyelid, always consider the vector of pull and the risk of ectropion
4. Be able to sketch various options for local flap designs (and their resultant scars) to reconstruct defects of the lip and cheek
5. For any given cheek defect, be able to list several possible reconstructive choices; know the pros and cons of each option

QUESTIONS YOU WILL BE ASKED


1. In the elderly, why is it important to consider oral stoma size when planning the reconstruction?
To ensure postoperative denture placement.
2. In order to reduce the risk of postoperative ectropion, what structure can the cervicofacial flap be anchored to?
Deep temporal fascia.
3. What is the most common complication of the Karapandzic flap?
Microstomia.
4. What secondary procedure do Estlander flaps sometimes require? Commissuroplasty to correct rounded commissure.

THINGS TO DRAW
Draw the surface anatomy of the lips.
See Figure 21-1.

Recommended Readings
Anvar BA, Evans BC, Evans GR. Lip reconstruction. Plast Reconstr Surg. 200715;120(4):57e–64e. PMID: 17805106.
Coppit GL, Lin DT , Burkey BB. Current concepts in lip reconstruction. Curr Opin Otolaryngol Head Neck Surg. 2004;12(4):281–287. PMID: 15252247.
Menick FJ. Reconstruction of the cheek. Plast Reconstr Surg. 2001;108(2):496–505. PMID: 11496195.
Schulte DL, Sherris DA, Kasperbauer JL. T he anatomical basis of the Abbé flap. Laryngoscope. 2001;111(3):382–386. PMID: 11224765.
I. EXTERNAL EAR ANATOMY AND DEVELOPMENT
A. Embryology of the External Ear
1. Auricle
a. Arises from six condensations of mesoderm known as the Hillocks of His during the sixth week of gestation
b. During the eighth week of gestation, the hillocks fuse, forming the rudimentary auricle
c. *Three anterior hillocks derive from the first branchial arch and give rise to the tragus, root of the helix,
and helix
d. *Three posterior hillocks derive from the second branchial arch and give rise to the antitragus, antihelix,
and lobule
e. The auricle forms in the lower neck and migrates cranially during mandibular development. Arrested growth results
in low-set ears.
2. External auditory canal
a. Ectodermal cells (first branchial cleft) initially coalesce forming a meatal plug and later degenerate before birth. If
degeneration does not occur, then congenital aural atresia or stenosis results
b. The outer one-third is fibrocartilaginous and the inner two-thirds are bony
c. In adults, it is sigmoid-shaped and approximately 25 mm in length and 10 mm in diameter
3. Tympanic membrane
a. Composed of the pars flaccida (small, triangular, flaccid) and pars tensa (large, oval-shaped, tense)
b. Contains an outer epithelial layer (ectoderm), middle fibrous layer (mesoderm), and inner mucosal layer (endoderm)
B. Surface topographic landmarks (Fig. 22-1)
C. Vestigial musculature
1. Intrinsic muscles include the helicis major and minor, tragicus, antitragicus, and the transverse and oblique auricular
muscles
2. Extrinsic muscles include the anterior, posterior, and superior auricular muscles
D. Vascular system (all branches of the external carotid artery)
1. Posterior auricular artery: *Dominant blood supply to both the anterior (through perforating branches) and
posterior surfaces of the ear
2. Superficial temporal artery: Supplies the anterior surface of the ear and forms numerous interconnections with the
posterior auricular artery, allowing ear replantation to base solely on either arterial network.
3. Occipital artery: Supplies the posterior surface of the ear (minor contributor) and the retroauricular skin
E. Venous and lymphatic system
1. Venous drainage follows the feeding arteries and empties into the retromandibular vein (external jugular system)
2. Sometimes the occipital vein drains into the internal jugular system
3. Lymphatic drainage parallels embryologic development
a. First branchial arch: Preauricular nodal basin
b. Second branchial arch: Retro- or infra-auricular nodal basins

______________
*De note s common in-se rvice e xamination topics
Figure 22-1. Surface anatomy of the ear. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2010.)

F. Sensory innervation
1. Great auricular nerve (C2, C3)
a. *Supplies the lower half of both the anterior and posterior surfaces of the ear
b. Arises at Erb’s point which is located 6.5 cm below the tragus along the posterior border of the sternocleidomastoid
muscle, and runs parallel to the external jugular vein
2. Auriculotemporal nerve (V3)
a. *Supplies the upper half of the anterior surface of the ear and the anterior aspect of the external auditory
canal
b. Ascends with the superficial temporal vessels
3. Lesser occipital nerve (C2)
a. *Supplies the upper half of the posterior surface of the ear
b. Arises above Erb’s point and ascends along the posterior border of the sternocleidomastoid muscle
4. Auricular branch of the vagus nerve (X, Arnold’s nerve)
a. *Supplies the concha and the posterior aspect of the external auditory canal
b. *A ring block will not provide adequate anesthesia to the concha; direct local infiltration is required
5. External auditory canal receives sensory innervation from cranial nerves V, VII, IX, and X
G. Clinical measurements of the ear
1. Approximately 85% of ear growth is achieved by the age of 3
a. Ear width reaches full size by the age of 10, while ear height continues to grow into adulthood
b. *In practical terms, near-adult size is routinely considered between the ages of 6 and 7
2. The ear is located roughly 6 cm, or a single ear-length, posterior to the lateral orbital rim
a. The superior aspect of the helix is at the level of the lateral brow
b. The inferior aspect of the lobule is at the level of the nasal ala
3. Average ear dimensions are 65 mm in height and 35 mm in width (ear width is approximately 50% to 60% of ear height)
4. Relative to the vertical, the long axis is inclined posteriorly 20 degrees
5. On frontal view, the helical rim is slightly lateral to the antihelical fold
6. Auriculocephalic angle: The angle formed between the midpoint of the lateral helix and the mastoid bone (normally
between 20 and 30 degrees)
7. Scaphoconchal angle: The angle formed between the scapha and the concha (normally less than 90 degrees)
8. Normal auricular projections include *10 to 12 mm at the upper third, *16 to 18 mm at the middle third, and
*20 to 22 mm at the lower third

II. RECONSTRUCTION OF CONGENITAL AURICULAR DEFORMITIES


A. Microtia
1. Epidemiology
a. Overall incidence is approximately 1 in 6,000 births
b. Male-to-female ratio is 2:1
c. *Right/left/bilateral ratio of 5:3:1
d. Most cases are isolated and sporadic; however, possible underlying causes include ischemia (e.g., acute vascular
obstruction), drugs (e.g., thalidomide, isotretinoin, retinoic acid), and infection (e.g., rubella)
e. *Syndromes commonly associated with microtia include hemifacial microsomia, Goldenhar syndrome, and
Treacher–Collins syndrome
f. Based on embryologic development, the inner ear is often spared, but defects of the external auditory canal and
middle ear are common
i. Hearing loss is predominantly due to atresia or stenosis of the external auditory canal, but can result from the
absence or structural abnormalities of the ossicular chain
ii. Accordingly, a conductive component (80%) is more prevalent than a sensorineural component (20%)
2. Classification
a. Many different classification systems have been proposed, but they are rarely clinically useful
b. Classification based on the severity of the deformity
i. Grade I: Small auricle with preserved surface topographic landmarks
ii. Grade II: Smaller auricle than grade I with malformed surface topo-graphic landmarks
iii. Grade III: Small sausage-shaped vertical remnant of skin containing a nubbin of hypoplastic cartilage superiorly
and a rudimentary lobule inferiorly
iv. Grade IV: Anotia, or total absence of the auricle
3. Timing of Repair
a. *Ear reconstruction is usually delayed until after the ear reaches near-adult size, so if no growth occurs in
the reconstructed ear postoperatively, it will still approximate the size of the contralateral normal ear when the patient
reaches adulthood
i. General rule of thumb is to wait until the patient requests surgery (i.e., not the parents) because then the patient is
aware of his or her deformity and is more likely to comply with the postoperative restrictions
ii. Brent technique: Performed at the age of 6
iii. Nagata technique: Performed at the age of 10. The patient’s chest circumference needs to measure at least 60
cm at the level of the xiphoid process.
b. In the presence of conductive hearing loss, coordination of operative care with an otolaryngologist is paramount
i. In cases of unilateral microtia with normal contralateral hearing, bone-anchored hearing aids (BAHAs) and
middle ear reconstruction are not routinely required
ii. *If unilateral conductive hearing loss is present, BAHA placement should be deferred until after ear
reconstruction to avoid compromising the vascularity of the skin envelope
4. Surgical management of microtia
a. Brent technique (four stages) (Fig. 22-2)
Figure 22-2. Brent technique for microtia reconstruction. Stage 1: A-D: T he base plate of the framework and the helix and the crura are carved from autologous costal
cartilage grafts. T he framework is implanted subcutaneously. Stage 2: A-B: T he lobule is created by transposing a flap from the microtia remnant or adjacent skin. Stage
3: A-C: T he ear is elevated and then a skin graft is placed on its posterior surface to increase lateral projection from the head. Stage 4: A-C: T he tragus is reconstructed
using a contralateral composite conchal cartilage graft, which is then secured to the previously placed framework.

i. Stage 1: A cartilaginous ear framework is carved from the synchondrosis of the contralateral sixth through eighth
ribs, which is then inserted into a subcutaneous pocket beneath the retroauricular skin
ii. Stage 2: Lobular transposition is performed
iii. Stage 3: Elevation of the ear framework, creation of the retroauricular sulcus, and coverage of the posterior
reconstructed ear with a full-thickness skin graft
iv. Stage 4: Conchal excavation and tragal reconstruction
b. Nagata technique (two stages)
i. Stage 1: A cartilaginous ear framework is carved from the synchondrosis of the ipsilateral sixth through ninth
ribs, which is then inserted into a subcutaneous pocket beneath the retroauricular skin. Lobular transposition and
tragal reconstruction are both performed during this initial stage
ii. Stage 2: Elevation of the ear framework, creation of the retroauricular sulcus, and coverage of the posterior
reconstructed ear with a tunneled temporoparietal fascial flap (TPFF) and split-thickness skin graft
c. Alloplastic ear framework
i. Options include silicone elastomer (Silastic, Cronin) or porous polyethylene (Medpor, Reinisch)
ii. Major advantage is no donor site morbidity, but higher rates of infection and extrusion
iii. Coverage with a TPFF decreases the complication rate
d. Ear prosthesis
i. Previously considered a poor option because adhesives are required for the prosthesis to “stick” to the patient’s
head
ii. With the advent of osseointegrated titanium implants, ear prostheses are now more practical and widely used
iii. *Indications include paucity of local tissue, radiation, burn, trauma, cancer, and in the elderly
iv. In the microtia patient, it is also indicated as a salvage attempt after failed autogenous reconstruction
v. Requires meticulous daily hygiene to prevent the skin-abutment interfaces from becoming inflamed/infected
5. Complications
a. Skin necrosis
i. Tips for minimizing risk include using a closed-suction drainage system, avoid pressure dressings, and do not raise
too thin of a flap when creating the subcutaneous pocket
ii. Small areas of partial-thickness necrosis can be managed conservatively with local wound care
iii. Larger areas of full-thickness necrosis require excisional debridement and coverage with a local flap
b. Infection
i. Early recognition and treatment are the mainstay of therapy
ii. *Superficial infections can sometimes be managed nonoperatively with antibiotics alone
iii. *Deep infections (i.e., gross purulence or suppurative chondritis) require irrigation of the
subcutaneous pocket, drain placement, and removal of the ear framework
c. Hematoma
i. *Classically presents as sudden onset unilateral ear pain
ii. Treatment is immediate clot evacuation
d. Hypertrophic scarring
i. Commonly occurs at the chest wall donor site
ii. It is important to design incisions that will not interfere with future breast growth and development in female
patients
e. Hair growth
i. Commonly occurs in patients with a low temporal hairline
ii. Our preferred treatment is preoperative laser hair ablation
f. Pneumothorax
i. If suspected intraoperatively, air within the pleural cavity can be evacuated using a red rubber Robinson catheter
ii. Rarely requires placement of a thoracostomy tube
iii. Chest plain film is obtained in recovery and on the first postoperative morning
g. Chest wall deformity
i. Usually more noticeable in thinner patients and when more donor rib cartilage is harvested
ii. Cartilage may regenerate if the perichondrium is left intact
h. Resorption of the cartilage graft
i. Usually due to infection or a tight, restrictive skin envelope
ii. If severe, may require regrafting
iii. Most cartilage grafts retain their size and shape, or grow slightly larger over time
B. Prominent ear (Fig. 22-3)
1. Underdeveloped antihelical fold
a. Most common cause of the prominent ear
b. Defined as a scaphoconchal angle more than 90 degrees
c. Typically results in prominence of the upper third of the ear
2. Conchal hypertrophy
a. Defined as excess conchal cartilage (more than 1.5 cm deep)
b. Typically results in prominence of the middle third of the ear
3. Protruding lobule
a. Least common cause of the prominent ear
b. Typically results in prominence of the lower third of the ear
4. Surgical management of the prominent ear
a. *In newborns less than 6 weeks of age, ear molding can be performed to help reshape the deformed ear
i. *Circulating maternal estrogens lend malleability to the ear cartilage, which persists longer in
breastfeeding mothers
ii. Soft putty is shaped into a custom mold that can be adjusted as the newborn grows (worn for several weeks to
months)
b. From our experience, the optimal timing for otoplasty is when the patient can actively participate in the decision for
surgery, which is usually around 6 to 7 years of age (similar to microtia patients)
c. The type of otoplasty performed will depend on the anatomic abnormality present, and often more than one technique
is required
d. Cartilage-scoring techniques
i. Based on Gibson and Davis’ Law, which states that cartilage bends away from the scored surface due to the
release of intrinsic stresses

Figure 22-3. Comparison of normal and prominent ear anatomy.

ii. Stenström: Anterior scoring via an anterior approach


iii. Chongchet: Anterior scoring via a posterior approach
e. Cartilage-suturing techniques
i. *Conchoscaphal (Mustardé) sutures: Recreate the antihelical fold using permanent mattress sutures,
thereby reducing upper-third prominence
ii. *Conchomastoid (Furnas) sutures: Reduce the auriculocephalic angle, and consequently middle-third
prominence, using permanent mattress sutures
f. Cartilage-incising or -excising techniques
i. A powerful tool in patients with stiffer ear cartilage or those with very severe deformities, but the major
drawbacks are palpable step-offs and an overly chiseled appearance
ii. Converse–Wood–Smith: Recreates the antihelical fold by first incising the cartilage and then placing permanent
mattress sutures
iii. Luckett: Similar to Converse–Wood–Smith, except that a crescent-shaped piece of skin and cartilage is excised
g. Lobule repositioning
i. Correction of upper- and middle-third prominences may reveal or accentuate prominence in the lower third of the
ear
ii. Webster: Repositions the helical tail next to the concha, but is often ineffective because the helical tail does not
extend into the lobule
iii. Other techniques involve either fusiform, wedge, or fishtail excisions on the posterior surface of the lobule, and
then suturing the fibrofatty tissue of the lobule to either the concha or mastoid periosteum
4. Complications
a. Recurrence
i. More common in patients with stiffer ear cartilage
ii. *Early recurrence is most likely due to suture pull-through or suture breakage
b. Asymmetry and contour irregularity
i. More common with cartilage-incising or -excising techniques
ii. Telephone deformity: Relative upper- and lower-third prominences of the ear caused by either overcorrection
of the middle third or undercorrection of the upper and lower thirds
iii. Hidden helix: The helix is unable to be seen on frontal view due to overcorrection of the upper and middle
thirds
c. Infection
i. Superficial infections can sometimes be managed nonoperatively with antibiotics alone
ii. If not recognized early, suppurative chondritis may develop leading to cartilage loss and residual deformity
iii. Spit sutures can be irritating and should be removed
d. Hematoma
i. *Classically presents as sudden onset unilateral ear pain
ii. Treatment is immediate clot evacuation
e. Keloids
i. More common in dark-skinned patients
ii. Treat initially with pressure earrings and steroid injections
iii. In severe cases, surgical excision and postoperative radiotherapy may be required
C. Cryptotia (Fig. 22-4A)
1. *Defined as adherence of the superior helix to the temporal skin with absence of the superior
auriculocephalic sulcus
2. Surgical correction involves release of the superior helix from the temporal skin and creation of a new superior
auriculocephalic sulcus using skin grafts or local flaps

Figure 22-4. Congenital ear deformities. A: Cryptotia. B: Stahl’s ear. C: Constricted ear.

D. Stahl’s ear (Fig. 22-4B)


1. *Defined as an abnormal third crus that arises from the antihelix and extends horizontally to the helical rim
2. The superior crus is often hypoplastic or absent
3. The scapha is malformed, while the concha is normal
4. Surgical correction involves wedge excision of the third crus with helical advancement
E. Constricted ear (Fig. 22-4C)
1. Also referred to as a cup ear or lop ear deformity
2. *Defined as an inadequate circumference of the helical rim causing the superior helix to fold over the scapha
3. Surgical correction involves detaching the superior helix from the scapha and reattaching it at the proper position and
angle
III. RECONSTRUCTION OF ACQUIRED AURICULAR DEFORMITIES
A. Epidemiology
1. Malignancy
a. The external ear is prone to sun exposure and development of cutaneous malignancies (10% of all head and neck
skin cancers)
b. Squamous cell carcinoma is the most common and has a higher rate of nodal metastasis compared to other head
and neck sites
c. *Chondrodermatitis nodularis chronica helicis
i. Common in elderly men related to trauma from sleeping
ii. Presents as a painful, inflammatory papule on the helix due to cartilage inflammation eroding through the overlying
skin
iii. Treatment is excisional biopsy, but the recurrence rate is high, so patients should avoid sleeping on the affected
ear
2. Trauma
a. Hematomas are caused by skin shearing from the cartilage
i. *Treatment involves immediate clot evacuation followed by a tie-over-bolster dressing to prevent
fluid reaccumulation between the perichondrium and cartilage
ii. If the clot is not evacuated, it will undergo fibrosis and calcification resulting in a cauliflower ear deformity
b. Simple lacerations should be minimally debrided to remove avascular tissue prior to wound closure
i. Small lacerations can be easily closed using a single-layer technique (i.e., skin-only closure)
ii. Large lacerations should be closed using a double-layer technique by first reapproximating the cartilage to reduce
tension on the wound edges
c. Avulsions and amputations can be considered for replantation depending on the quality of the avulsed/amputated
tissue, mechanism of injury, and the overall clinical status of the patient (i.e., a sharp laceration near the base of the
ear has the best chance of survival)
3. Burn and frostbite injuries
a. Burn
i. Initial management includes fluid resuscitation, local wound care, pressure relief, avoidance of pillow friction, and
topical application of *mafenide acetate due to its superior cartilage penetration (side effects include pain and
hyperchloremic metabolic acidosis due to carbonic anhydrase inhibition).
ii. Allow injured tissues to demarcate (may take days to weeks) prior to definitive reconstruction
iii. Small burns may heal secondarily with dressing changes
iv. Large burns with exposed cartilage require well-vascularized soft tissue coverage, and the choice of donor site
will depend on the zone of injury (e.g., if the temporoparietal fascia is injured, then it is not available for use)
v. *Complete auricular loss will require total ear reconstruction in a delayed fashion using either a
costal cartilage ear framework with a TPFF or pre-expanded local flap for coverage (if the local tissue
is not severely scarred), or an ear prosthesis with osseointegrated titanium implants
b. Frostbite
i. Initial management includes rapid rewarming, *use of nonsteroidal anti-inflammatory agents (reduces
thromboxane production), and topical application of mafenide acetate
ii. Allow injured tissues to demarcate (may take weeks to months) prior to definitive reconstruction
B. Partial-thickness defects
1. Presence of perichondrium
a. Small defects can heal secondarily with local wound care
b. Full-thickness skin grafts are recommended for larger defects
2. Absence of perichondrium
a. Most defects require coverage with a local flap
i. Helical rim: Same flaps used for full-thickness defects of the upper and middle thirds
ii. Conchal bowl: Trapdoor flap, postauricular island “revolving door” flap, and bipedicle advancement flap
b. Defects less than 1.5 cm near the helical rim can be converted to a full-thickness defect by wedge or shield excision
and closed primarily
3. Involvement of the external auditory canal
a. Stenosis is a common long-term complication
b. Treatment is application of a full-thickness skin graft over an acrylic mold used as a temporary stent
C. Full-thickness defects of the upper third
1. Primary closure
a. Commonly performed after wedge or shield excision of skin cancers involving the helical rim
b. To prevent buckling, a star-shaped resection pattern can be used
c. Limited to defects less than 1.5 cm to avoid a significant size discrepancy with the contralateral side
2. Contralateral chondrocutaneous graft
a. For defects up to 1.5 cm and is usually harvested from the contralateral helical rim or conchal bowl
b. The graft should be slightly larger than the defect to account for postoperative contraction
c. *Predictable pattern of color changes during graft take starting with white initially (ischemia), then blue
for 24 to 72 hours (venous congestion), and finally pink after 3 to 7 days (neovascularization)
3. Banner flap
a. A local transposition flap that can be based on either the pre- or postauricular skin
b. Performed with or without a cartilage graft; however, if the defect involves more than 25% of the helical rim, then
costal cartilage is required for support
4. Antia–Buch helical advancement (Fig. 22-5)
a. For defects up to 3 cm
b. A transcartilaginous incision is made in the helical sulcus along its entire length from the scapha to the lobule
preserving the integrity of the posterior skin
c. The posterior skin is then elevated off the remaining ear cartilage in a supraperichondrial plane until the entire helical
rim is mobilized as a chondrocutaneous composite flap (based on the posterior skin)
d. Additional length can be gained by performing a V–Y closure at the root of the helix
5. Chondrocutaneous composite flap
a. For defects involving the superior helical rim, especially when burn patients desire a stump to support their eyeglasses
and other local options are not available
b. Anterior skin and cartilage are rotated from the conchal bowl as a composite flap based on either the root of the
helix (Davis) or the lateral helical rim (Orticochea)
c. The donor site is skin grafted or left to heal by secondary intention
D. Full-thickness defects of the middle third
1. Similar to full-thickness defects involving the upper third of the ear, reconstructive options include primary
closure, contralateral chondrocutaneous graft, Banner flap, and Antia–Buch helical advancement

Figure 22-5. Antia–Buch helical advancement.

2. Tubed bipedicle flap


a. Based on the retroauricular skin and is performed with or without a cartilage graft in three stages
b. The flap is elevated and tubed with primary closure of the donor site. Three weeks later, one end of the tube is
divided and transferred into the defect. Finally, after an additional 3 weeks, the other end of the tube is divided and
transferred into the defect.
3. Dieffenbach flap
a. Similar to the tubed bipedicle flap, this flap is based on the retroauricular skin and is also performed in multiple stages
b. A cartilage graft is harvested and placed into the helical rim defect. The anterior surface of the graft is then covered
with a postauricular transposition flap. Three weeks later, the flap is divided at its base and inset using the additional
length of the flap to cover the posterior surface of the graft.
c. The donor site is skin grafted or closed by local tissue rearrangement
4. Converse “tunnel” technique
a. A prelaminated flap based on the retroauricular skin
b. A cartilage strut is tunneled beneath the retroauricular skin and secured to both ends of the helical rim defect. Three
weeks later, the cartilage strut is elevated along with the retroauricular skin still attached.
c. The donor site is skin grafted or closed by local tissue rearrangement
E. Full-thickness defects of the lower third
1. Many techniques have been described to reconstruct the lobule, but the basic premise involves the use of local flaps
folded over on themselves
2. The lobule normally does not contain any cartilage; however, contralateral auricular cartilage or nasal septal cartilage
can be placed subcutaneously as a graft to provide additional support and contour
3. If the lobule on the contralateral side is enlarged, sometimes it can be surgically reduced to match the reconstructed side
4. For cleft lobules, our preferred technique is wedge excision and primary closure with eversion of the wound edges to
prevent postoperative notching

IV. THE AMPUTATED EAR


A. Nonmicrosurgical options
1. Usually involves burying or banking cartilage in the temporal scalp, abdomen, or volar forearm for delayed reconstruction
2. Many techniques have been described, but often the results are inconsistent and the cartilage loses its definition over
time becoming flattened and warped
a. Baudet recommended removing only the posterior skin from the amputated segment and fenestrating the cartilage to
allow for greater imbibition and neovascularization. The cartilage was covered by a postauricular flap and later
divided at 3 months
b. Mladick recommended dermabrading the amputated segment, reattaching it, and then burying it beneath the
retroauricular skin. Three weeks later, the reconstructed ear was removed from its “pocket,” and the denuded areas
eventually re-epithelialized.
c. Destro and Speranzini recommended removing all the skin from the amputated segment except for the concha and
then made small round perforations in the cartilage. The cartilage was covered by a postauricular flap and later
divided at 3 months.
d. Park recommended removing all the skin from the amputated segment except for the helical rim. The cartilage was
then sandwiched between two flaps: a skin flap anteriorly and a fascial flap posteriorly, both based on the mastoid
region. The skin on the helical rim later necrosed, but was salvaged with additional operations.
B. Microvascular replantation
1. *Microvascular replantation provides a more natural-appearing reconstructed ear and is preferred to other
forms of delayed reconstruction
2. It is a technically demanding operation due to the small caliber of the vessels, and often venous outflow is a problem
3. Microvascular anastomosis is performed to either the posterior auricular artery or the superficial temporal artery. Both
can restore the blood supply to the entire amputated segment given the numerous interconnections that are present
between these two arterial networks.
4. If no vein can be found, or the veins are small, have a low threshold for starting leeches postoperatively

PEARLS
1. Patients with oropharyngeal cancer may complain of referred otalgia via Arnold nerve
2. A ring block will not provide adequate anesthesia to the concha; direct local infiltration is required
3. Children with microtia or prominent ears are usually operated on between the ages of 6 and 7 when ear growth is nearly
complete
4. For the burned ear, mafenide acetate is preferred due to its superior cartilage penetration, but its application can be painful and
beware of hyperchloremic metabolic acidosis from carbonic anhydrase inhibition
5. In newborns less than 6 weeks of age, ear molding can be performed to help reshape many deformed ears due to circulating
maternal estrogens lending malleability to the ear cartilage
6. Microvascular replantation may sacrifice the superficial temporal artery, which would impair the use of the temporoparietal
fascial flap in the future
7. Costal cartilage is often stiffer and more calcified in adults compared to children, thus the cartilaginous ear framework used for
total ear reconstruction in adults is usually carved en bloc.

QUESTIONS YOU WILL BE ASKED


1. What part of the ear is not anesthetized by ring block?
Conchal bowl due to CN X (it requires direct infiltration).
2. What is the most common reason ear replantations fail?
Poor venous outflow.
3. Why is it more difficult to use autogenous cartilage in the elderly for total ear reconstruction?
Calcification of the rib cartilage.
4. What is the most common complication of otoplasty?
Recurrence.

THINGS TO DRAW
Draw the surface anatomy of the ear.
Figure 22-1.

Recommended Readings
Antia NH, Buch VI. Chondrocutaneous advancement flap for the marginal defect of the ear. Plast Reconstr Surg. 1967;39(5):472–477. PMID: 5336914.
Brent B. Auricular repair with autogenous rib cartilage grafts: two decades of experience with 600 cases. Plast Reconstr Surg. 1992;90(3):355-374; discussion 375–376.
PMID: 1513882.
Brent B. T he acquired auricular deformity. A systematic approach to its analysis and reconstruction. Plast Reconstr Surg. 1977;59(4):475–485. PMID: 322165.
Janis JE, Rohrich RJ, Gutowski KA. Otoplasty. Plast Reconstr Surg. 2005;115(4):60e–72e. PMID: 15793433.
Pribaz JJ, Crespo LD, Orgill DP, Pousti T J, Bartlett RA. Ear replantation without microsurgery. Plast Reconstr Surg. 1997;99(7):1868–1872. PMID: 9180709.
SCALP RECONSTRUCTION
I. ANATOMIC LAYERS OF THE SCALP—ACRONYM SCALP (FIG. 23-1)
A. S: Skin
B. C: Connective tissue
1. Hair follicles, sweat glands, and fat cells
2. Connective tissue fibers between the galea and skin
C. A: Aponeurotic layer or galea aponeurotica: A fibrous tissue layer that is continuous with the frontalis and occipitalis and
temporoparietal (TP) fascia
D. L: *Loose areolar tissue: This layer allows the scalp to move on the cranium and is the most common plane of
scalp avulsion injuries
E. P: Pericranium/periosteum: A thick collagenous layer with firm attachments to the skull

II. SCALP VASCULAR SUPPLY (FIG. 23-2)


A. Internal carotid artery branches
1. Supraorbital artery
2. Supratrochlear artery
B. External carotid artery branches
1. Superficial temporal artery
2. Postauricular artery
3. Occipital artery
4. Extensive interconnections are present between branches and across the mid-line. These anastomoses allow potential
replantation of a scalp based on a single artery and vein.

III. SCALP INNERVATION (FIG. 23-3)


A. Motor
1. Frontalis: Frontal branch of CN VII
2. Occipitalis: Posterior auricular branch of CN VII
3. Temporalis: Deep temporal nerve of CN V
B. Sensation
1. Forehead and anterior scalp supplied by supratrochlear and supraorbital nerves (V1 )
2. Supraorbital nerve
a. Superficial division: Supplies skin of forehead and anterior hairline
b. Deep division: Innervates frontoparietal scalp
3. Temporal region supplied by zygomaticotemporal nerve (V2 ) and auriculotemporal nerve (V3 )
4. Posterior scalp supplied by greater and lesser occipital nerves (both are spinal nerves from C2 /C3 )
5. Ear and postauricular area supplied by great auricular nerve (cervical plexus from C2 /C3 )

IV. SCALP RECONSTRUCTIVE LADDER


A. Primary closure is an excellent option for defects less than 3 cm in diameter
1. Facilitated by wide undermining in the avascular subgaleal plane

______________
*De note s common in-se rvice e xamination topics
Figure 23-1. Anatomic layers of the forehead and scalp. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2010.)

Figure 23-2. Arterial supply to the scalp and face. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2010.)
Figure 23-3. Sensory innervation to the scalp and face. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2010.)

2. Scoring the galea allows additional advancement but may decrease the skin’s blood supply
B. Split-thickness skin grafting can provide coverage of a scalp defect but will not reconstruct hair-bearing skin.
1. Split-thickness skin grafting (STSG) can be placed directly on subcutaneous tissue, galea, or pericranium. If calvarial
bone is exposed, STSG is contraindicated.
2. If bare calvarium is present, the outer table can be burred and the STSG placed on the diploe.
3. Alternatively, Integra (a bilaminate bovine collagen construct) can be placed and a thin STSG placed at a second
operation in 2 to 3 weeks, once neovascularization of the construct has occurred.
4. STSG are technically easy and fast, making them a good option in systemically ill patients for whom cosmesis is of lower
importance.
C. Local flaps can provide coverage of defects between 3 cm and up to 30% defects of the scalp.
1. Many local flaps can be designed, including advancement flaps, rotation flaps, and bipedicled flaps.
2. Double-opposing rotation flaps (yin-yang) are also useful. Galeal scoring can increase flap length.
3. Orticochea’s three-flap and four-flap techniques are based on scalp axial blood supply and can cover up to 30% scalp
defects.
4. Local flaps provide superior cosmesis as hair-bearing skin is brought into the defect.
5. Flaps should be raised in the subgaleal plane, which keeps the pericranium as a “lifeboat” for STSG should the donor site
break down.
6. Similarly, STSG of the secondary defect may be necessary in order to cover the primary defect.
7. Local rotation and advancement flaps often create a dog-ear at the base. Do not excise the dog-ear as flap compromise
may result. The majority of these will flatten out over time.
D. Local axial flaps can be used for specific indications
1. Galeal flaps can be based on one or multiple axial vessels.
a. The flap is thin and pliable with minimal donor site morbidity.
b. They are particularly useful for three-dimensional (3D) intracranial defects.
2. TP fascia flaps are based on the superficial temporal vessels and can carry vascularized calvarium. Temporoparietal
(TP) fascial flaps are useful for 3D defects or, if bone is included, for periorbital or facial bony defects.
3. Temporalis muscle flaps are based on the deep temporal arteries. Temporalis flaps have limited use as rotation flaps for
anterior scalp and periorbital defects.
4. “Crane” flaps are interpolated flaps used to transfer soft tissue to the recipient site. Once vascularization occurs from
the recipient site, the flap is raised in a more superficial plane, leaving adequate soft tissue at the recipient site. The flap
is then replaced into the original donor site.
E. Tissue expansion is often used in secondary scalp reconstruction and can replace hair-bearing skin with hair-bearing skin.
1. Tissue expansion requires a staged approach with 2 to 3 months between operations.
2. Tissue expansion goal is to generate flaps that are 50% wider and longer than the defect.
3. Multiple rounds of tissue expansion may be required for large defects
4. *Up to 50% defects of the scalp can be reconstructed with tissue expansion before noticing alopecia
5. TEs are placed via incisions at the proposed flap margin, often at the junction of normal scalp and skin graft.
a. Dissection in the subgaleal plane should be just large enough to allow tissue expanders (TE) insertion.
b. Important not to have any sharp folds when placing TE.
c. A separate incision allows placement of a remote filling port over stable bone.
6. Hematoma, infection, and implant exposure are the most common complications of expansion. In children, pressure-
related deformation of the cranial vault may occur.
F. Regional muscle transfers are useful for defects in the mastoid, temporal and occipital regions but cannot reach the
frontal area or vertex
1. Pectoralis major muscle
2. Pedicled latissimus muscle can also be used for space-filling in orbital exenteration or other defects.
3. Trapezius muscle
G. Free tissue transfer is indicated for extensive wounds or wounds of the vertex and frontal region where regional muscle is
not available
1. Free latissimus is the workhorse for scalp coverage due to its broad, flat size, and long vascular pedicle that allows
anastomosis in the neck
2. Free omentum, rectus muscle, and parascapular flaps can also be used
3. Inclusion of a skin island may result in a bulky reconstruction. Both muscle and omentum can be skin-grafted.

V. SCALP TRAUMA
A. All wounds should be irrigated and debrided.
B. The scalp has excellent vascularity and may bleed extensively.
C. Closure of scalp wounds with full thickness sutures or staples will provide hemostasis.
D. Layered closure is usually unnecessary. For extensive wounds, closure of the galea may be necessary.
E. Healing by secondary intention is acceptable for small wounds.
F. *Scalp avulsion injuries most commonly occur in the loose areolar plane (e.g., between galea and periosteum).
Microvascular anastamosis is the standard of treatment for total and near-total scalp avulsions.
1. The scalp should be treated similarly to a replantable digit in the field: Wrap in moist gauze, place in a plastic bag, and
store on an ice slurry.
2. The entire scalp can often be replanted on one artery and vein. The superficial temporal system is preferred.
3. The ideal recipient vessels are contralateral to the zone of injury. Vein grafts are almost always necessary.
4. Contraindications to replantation include ischemia time >30 hours, failure to identify a suitable vascular pedicle, and
medical condition precluding prolonged operation and potential blood loss

CALVARIAL RECONSTRUCTION
I. ANATOMIC LAYERS OF THE CRANIUM
A. The cranium is composed of hard (cortical) external and internal tables that enclose the cancellous diploe layer.
B. Periosteum covers the superficial surface of the external table and the deep surface of the internal table.
C. Average bony vault thickness is 7 mm.
D. Temporal bone is thinnest. Occipital bone is thickest.

II. PRINCIPLES OF CALVARIAL RECONSTRUCTION


A. The goals are similar to all reconstructive efforts, namely, restoration of form and function. Specifically, this includes
restoration of aesthetic contour and protection of the brain.
B. The frontal region is most important aesthetically because it is not covered with hair-bearing skin. Additionally, frontal bone
contributes to the superior portion of the orbit.
C. Thick temporalis muscle can camouflage contour defects in the temporal region. Defects of up to 10 cm2 may not require
reconstruction.
D. The parietal and occipital regions require repair for protection of underlying structures; aesthetics in these areas are less of
an issue.

III. OPERATIVE PLANNING AND TIMING


A. Physical examination allows identification of aesthetic defects.
B. Preinjury photographs are helpful when available.
C. 3D CT allows visualization of all bony defects.
D. A patient’s 2D CT can be used to produce a lifesize anatomic model; the model assists in the planning process.
E. For defects that involve the frontal or ethmoid sinus, delay of reconstruction of 1 year is preferable to minimize infection
risk.
IV. ALLOPLASTIC CRANIOPLASTY MATERIALS
A. *Methyl methacrylate is formed by mixing a powdered polymer and liquid monomer. The substance hardens in an
exothermic reaction over 6 to 8 minutes and requires constant irrigation to avoid burning the dura.
1. Advantages: The technique is rapid and technically less demanding than bone cranioplasty. The substance’s contour is
stable and can be finely molded with a burr. Methyl methacrylate is radiolucent. No donor site. Relatively inexpensive.
2. Disadvantages: Methyl methacrylate is encapsulated, not incorporated, placing patients at a higher infection risk. The
exothermic reaction can burn the dura unless constantly irrigated.
B. Custom titanium or other alloplastic implants can be created by several companies based on a CT scan.
1. Advantages: Can be contoured to match patient’s individual features. Minimum surgical time as the implant is
prefabricated. No risk of dura burns. No donor site.
2. Disadvantages: Will not be incorporated and is prone to infection. Radiopaque and will cause scatter on imaging.
Expensive.
C. Porous polyethylene (MEDPOR) and hydroxyapatite are less commonly used to reconstruct calvarial defects. Porous
polyethylene is particularly useful for contour defects.

V. AUTOGENOUS CRANIOPLASTY MATERIALS


A. Bone is considered to be the ideal cranioplasty material by many surgeons.
1. Advantages include the potential for revascularization. Once revascularized, infection risk is minimal. No additional
expense.
2. Disadvantages include need for a second donor site, although the donor site is in the operative field if cranial bone
grafts are used. Graft harvest has a low but real risk of dural injury, CSF leak, and meningitis in experienced hands.
Bone graft may reabsorb and remodel over time.
B. Split rib grafts
1. Provide long, stable pieces of bone to bridge gaps.
2. Can be contoured with a Tessier bone bender to fit specific defects.
3. Donor site morbidity is minimal and some bones may regenerate if periosteum is left intact.
C. Calvarial bone graft
1. Best harvested from the thick parietal region.
2. The outer table can be separated from the inner table at the diploe layer using a side biting burr and osteotome.
3. Alternatively, a craniotomy can be performed and the bone flap split with a saw. Both flaps are then replaced.
4. The sagittal sinus runs in the midline. This site should be avoided for bone graft harvest.
5. Bone dust, obtained by diffuse burring of calvarium, can be applied directly to dura or used as a final onlay for
contouring.

VI. SOFT TISSUE IN CRANIOPLASTY


A. Some clinical circumstances require obliteration and infection control without cranial vault reconstruction.
B. Microvascular free tissue transfer may be required to provide soft-tissue bulk. This technique is useful when there is a
history of infection, extensive dead space, or communication between the intracranial cavity and sinuses. Options include
rectus muscle, latissimus muscle, or omentum.

PEARLS
1. The avascular loose areolar plane (subgaleal and supraperiosteal) is commonly dissected in scalp reconstruction. This plane is
also where scalp avulsion injuries occur.
2. In a noninfected and nonurgent setting, tissue expansion is the ultimate method to replace 50% of the scalp with hair-bearing
tissue.
3. Calvarial reconstruction requires careful preoperative planning, often with a 3D CT and medical modeling. Custom implant
creation requires several weeks of advance notice.
4. Bone grafts (split rib or calvarial) are the preferred method for calvarium reconstruction when clinically appropriate

QUESTIONS YOU WILL BE ASKED


1. How much of the scalp can be reconstructed with tissue expansion before noticing alopecia?
50%.
2. What are the advantages of using autogenous bone over alloplastic material for calvarial reconstruction?
Less infection and extrusion.
3. At what level is the scalp commonly avulsed?
Between the galea and periosteum.
4. What technique can be performed intraoperatively to improve rotation/advancement of scalp flaps?
Scoring of the galea.

THINGS TO DRAW
Name/draw the layers of the scalp.
Figure 23-1.

Recommended Readings
Chao AH, Yu P, Skoracki RJ, Demonte F, Hanasono MM. Microsurgical reconstruction of composite scalp and calvarial defects in patients with cancer: a 10-year
experience. Head Neck. 2012;34(12):1759–1764. PMID: 22331614.
Lin SJ, Hanasono MM, Skoracki RJ. Scalp and calvarial reconstruction. Semin Plast Surg. 2008;22(4):281–293. PMID: 20567704.
Mehrara BJ, Disa JJ, Pusic A. Scalp reconstruction. J Surg Oncol. 2006;94(6):504–508. PMID: 17061273.
I. FACIAL NERVE ANATOMY AND FUNCTION
A. The facial nerve, or cranial nerve VII, has separate motor and sensory divisions
1. Motor division
a. Originates from the facial motor nucleus within the pons
b. Dorsal neurons of the facial motor nucleus receive bilateral cortical input, while ventral neurons receive contralateral
cortical input only
i. An upper motor neuron lesion manifests as contralateral lower facial paralysis (i.e., the contralateral forehead
is spared due to its own ipsilateral cortical input)
ii. A lower motor neuron lesion manifests as ipsilateral total facial paralysis
2. Sensory division
a. Also referred to as the nervus intermedius
b. Originates from the geniculate ganglion at the junction of the labyrinthine and tympanic segments of the facial canal
c. Preganglionic parasympathetic secretomotor fibers originate from the superior salivatory nucleus within the pons
3. Intratemporal course
a. The motor and sensory divisions enter the facial canal at the internal acoustic meatus and join together as a common
trunk at the geniculate ganglion prior to exiting the stylomastoid foramen
b. Can be divided into three segments: labyrinthine (proximal), tympanic, and mastoid (distal)
4. Extratemporal course
a. From the stylomastoid foramen to the muscles of facial expression
b. *Three anatomic landmarks are commonly used to identify the main trunk of the facial nerve as it exits the
stylomastoid foramen
i. Tragal pointer: The nerve is located 1 cm inferior and 1 cm deep to the tragal cartilage
ii. Tympanomastoid suture: The nerve is located 6 to 8 mm medial to the end of the suture line
iii. Posterior belly of the digastric muscle: The nerve runs at the same depth as this muscle and is found
halfway between this muscle and the styloid process
iv. The styloid process itself is not a useful anatomic landmark because it is located deep to the nerve, resulting in a
higher incidence of nerve injury during its dissection
v. A small branch off the occipital artery is often encountered just lateral to the nerve; thus, brisk bleeding is usually
an indicator that the nerve is nearby
vi. Be careful in children—these anatomic landmarks can be distorted, and the nerve runs more superficial
c. The facial nerve gives off the posterior auricular nerve, stylohyoid branch, and digastric branch prior to entering the
parotid gland
d. Within the parotid gland, it lies between the superficial and deep lobes, and separates into the temporofacial
(upper) and cervicofacial (lower) divisions at the pes anserinus (Fig. 24-1)

______________
*De note s common in-se rvice e xamination topics
Figure 24-1. Facial nerve anatomy and facial musculature. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2010.)

i. Temporofacial (upper) division: Terminates as the temporal, zygomatic, and buccal branches
ii. Cervicofacial (lower) division: Terminates as the buccal, marginal mandibular, and cervical branches
e. Temporal branch
i. *Lies just superficial to the superficial layer of the deep temporal fascia (i.e., deep to superficial
temporal (tempo-parietal) fascia which is continuous with SMAS).
ii. *Follows the course of a line drawn from 0.5 cm below the tragus to 1.5 cm above the lateral brow
iii. Crosses the zygomatic arch over its middle third
iv. Especially prone to injury due to its location and lack of redundancy (i.e., it does not arborize)
f. Buccal branch
i. Lies deep to the SMAS where it arborizes and forms extensive interconnections
ii. *Most common facial nerve injury during rhytidectomy, but rarely symptomatic due to its redundancy
g. Marginal mandibular branch
i. Lies deep to the platysma muscle
ii. *Before crossing over the facial vessels, it runs along the inferior border of the mandible (80%) or 1
to 2 cm below it (20%)
iii. After crossing the facial vessels, it remains above the inferior border of the mandible
iv. Similar to the temporal branch, it is especially prone to injury due to its lack of redundancy
B. The facial nerve contains five types of nerve fibers
1. General visceral efferents (GVEs)
a. Provide preganglionic parasympathetic secretomotor function as part of the autonomic nervous system
b. Chorda tympani nerve: Sublingual and submandibular glands
c. Greater superficial petrosal nerve: Lacrimal, nasal, and palatine glands
2. Special visceral efferents (SVEs)
a. Voluntary motor control of muscles derived from the second branchial (hyoid) arch
b. Nerve to stapedius: Stapedius muscle
c. Posterior auricular nerve: Intrinsic ear muscles and the posterior auricular muscle (auricular branch), and the
occipitalis muscle (occipital branch)
d. Terminal branches: Stylohyoid muscle, posterior belly of the digastric muscle, and the muscles of facial expression
3. General somatic afferents (GSAs)
a. Transmit feelings of pain, light touch, and temperature
b. Posterior auricular nerve: External auditory canal
4. General visceral afferents (GVAs)
a. Transmit feelings of pain from the visceral structures as part of the autonomic nervous system
c. Greater superficial petrosal nerve: Soft palate
5. Special visceral afferents (SVAs)
a. Transmit the special sense of taste, or gustation
b. Chorda tympani nerve: Anterior two-thirds of the tongue
c. Greater superficial petrosal nerve: Soft palate
C. Muscles of facial expression (Fig. 24-1 and Table 24-1)
1. Four layers of facial musculature (from superficial to deep)
a. Depressor anguli oris, zygomaticus minor, orbicularis oculi
b. Depressor labii inferioris, risorius, platysma, zygomaticus major, levator labii superioris alaeque nasi

c. Orbicularis oris, levator labii superioris


d. Mentalis, levator anguli oris, buccinator
2. The muscles of facial expression can be viewed as a series of constrictors or expanders of the ocular, nasal, and oral
sphincters
3. *All muscles are innervated on their deep surface, except for the buccinator, levator anguli oris, and
mentalis (i.e., these muscles are inner-vated on their superficial surface)
4. Muscle movements on examination
a. Raises eyebrows: Frontalis
b. Closes eyelids: Orbicularis oculi
c. Smile: Zygomaticus major and minor
d. Purse lips: Orbicularis oris

II. ETIOLOGY OF FACIAL PARALYSIS


A. Facial paralysis can result from an anatomic lesion anywhere along the length of the facial nerve including proximal to,
within, or distal to the temporal bone
1. Proximal to the temporal bone (intracranial): Compressive masses tend to have an insidious onset, while acute
vascular obstruction accounts for most cases of sudden-onset facial paralysis
a. Neoplastic: Meningioma, cerebellopontine tumors, and bilateral acoustic neuromas in the setting of
neurofibromatosis type 2
b. Traumatic: Penetrating trauma and shear injury
c. Infectious: Encephalitis, meningitis, and intracerebral abscess
d. Vascular: Aneurysm, cerebrovascular accident, vasculitis, and intracerebral hemorrhage
e. Neurodegenerative: Amyotrophic lateral sclerosis and multiple sclerosis
f. Iatrogenic: Tumor extirpation
g. Congenital: Möbius syndrome and Goldenhar syndrome
i. *Bilateral underdevelopment of the facial and abducens nerves, usually accompanied by congenital
absence of the facial motor nucleus
ii. *Patients typically present with a motionless face and inability to abduct the eyes
iii. Other anomalies include club foot (most common) and features of Poland’s syndrome
2. Within the temporal bone (intratemporal)
a. Neoplastic: Cholesteatoma
b. Traumatic: Penetrating trauma and temporal bone fracture
i. Classified as either longitudinal (80%) or transverse (20%)
ii. Facial paralysis is more common with the transverse type
iii. Symptoms are usually due to swelling and compression of the nerve within the facial canal
c. Infectious: Acute otitis media/externa, mastoiditis, and Ramsay–Hunt syndrome—“herpes zoster oticus”
i. Characterized by unilateral facial paralysis, otalgia, and a painful vesicular rash in the external auditory canal
ii. Oral corticosteroids and antivirals for 10 days may be helpful, if started within 72 hours of symptom onset
d. Iatrogenic: Tumor extirpation
e. Systemic: Pregnancy, diabetes mellitus, neurosarcoidosis, hyperthyroidism, amyloidosis, and Melkersson–Rosenthal
syndrome—“cheilitis granulomatosa”
i. Characterized by recurrent granulomatous inflammation of the lips, facial paralysis, and plicated tongue
ii. Often associated with Crohn disease
f. Toxins: Lead poisoning and carbon monoxide
g. Idiopathic: Bell’s palsy
i. *Most common cause of unilateral facial paralysis in adults
ii. A diagnosis of exclusion thought to involve a viral-induced inflammatory process leading to edema and
compression of the nerve within the facial canal
iii. Higher incidence in pregnant and diabetic patients
iv. Rapid onset is characteristic, often described as appearing overnight
v. Most patients (85%) experience spontaneous recovery within 3 weeks, and the remainder of patients within 6
months
vi. *Observation is recommended for 3 weeks prior to performing any imaging or electrodiagnostic
studies
vii. Oral corticosteroids and antivirals are recommended within 72 hours of symptom onset
viii. Facial nerve decompression is controversial
3. Distal to the temporal bone (extratemporal)
a. Neoplastic: Parotid tumors
b. Traumatic: Penetrating trauma
i. *The general “rule of thumb” is that facial nerve exploration is not warranted for lacerations medial to
a vertical line dropped down from the lateral canthus
ii. *Exploration must be performed within 72 hours of injury (prior to neurotransmitter depletion) so that
the distal end can be identified by electrical stimulation
c. Infectious: Parotitis
d. Iatrogenic: Tumor extirpation
e. Obstetrical: Forceps delivery
i. May also be related to pressure from the maternal sacrum
ii. Produces a neuropraxia that is managed nonoperatively
f. Congenital: Congenital unilateral lower lip paralysis (CULLP)
i. Not considered a true congenital facial paralysis
ii. Caused by hypoplasia or absence of the lower lip depressors
iii. Typically presents with deviation of the lower lip toward the unaffected side with emotion (e.g., crying)
B. Bilateral facial paralysis is not as common as unilateral facial paralysis, but frequent causes include Lyme disease (most
common), Möbius syndrome, toxins, and any systemic condition including HIV infection.

III. DIAGNOSIS OF FACIAL PARALYSIS


A. Detailed history
1. Facial paralysis is a clinical diagnosis
a. Rate of disease progression: Gradual onset (e.g., neoplastic, neurodegenerative, systemic) versus rapid onset
(e.g., traumatic, vascular, infectious, iatrogenic, idiopathic)
b. Duration of symptoms: Health of the affected mimetic musculature as a result of prolonged denervation—key
factor in decision between a nerve operation or muscle operation.
c. The temporal relationship between symptom onset and the possible contributing factors (e.g., new medications,
exposure to toxins, history of recent surgery or trauma, chronic illnesses, infection) helps narrow down the
differential diagnosis list.
2. Use a “top-down” anatomic approach to document all of the patient’s complaints, so that each of them can be
individually addressed
a. Eye
i. Does the patient complain of eye discomfort, changes in vision, dryness, or excessive tearing?
ii. Can the patient close his or her eye on the affected side? (caused by paralysis of orbicularis oculi)
iii. Does the patient require the use of artificial tears?
b. Nose
i. Does the patient have any difficulty breathing out of his or her nose? (caused by paralysis of Levator labii
superioris aleque nasi and nasalis)
ii. Is it worse during inspiration or expiration?
c. Mouth
i. Does the patient complain of drooling?
ii. Does the patient have any difficulty speaking, especially when articulating bilabial plosives?
iii. Does the patient complain of a crooked smile?
B. Neuromuscular examination
1. Ask for a picture of the patient; routinely, subtle facial asymmetries exist prior to the diagnosis of facial paralysis
2. Classically, unilateral facial paralysis presents with symmetry at rest and asymmetry with spontaneous animation
a. Upper motor neuron lesion: Contralateral lower facial paralysis
b. Lower motor neuron lesion: Ipsilateral total facial paralysis
c. At rest
i. Smooth forehead with absence of wrinkles
ii. Brow ptosis with absence of true eyelid ptosis
iii. Paralytic ectropion with increased scleral show
iv. C-shaped nasal deformity with tip and phitral deviation toward the unaffected side.
v. Effacement and lack of definition of the nasolabial fold
vi. Drooping of the oral commissure
b. With spontaneous animation
i. Inability to elevate the brow (temporal branch)
ii. Lagophthalmos (zygomatic branch)
iii. Lack of nostril dilatation during inspiration (buccal branch)
iii. Inability to smile (zygomatic branch)
iv. Inability to whistle or puff out cheeks (buccal branch)
v. *Inability to expose lower dentition in a full-denture smile (either marginal mandibular or cervical branch
—asymmetry on pursing lips is also present in marginal mandibular palsy, but absent in cervical palsy);
additionally,the paralyzed side always corresponds to the lower lip that is more elevated (i.e., the lower
lip depressors are paralyzed).
c. Other associated physical findings may also be present
i. Xerophthalmia (greater superficial petrosal nerve)
ii. Hyperacusis (nerve to stapedius)
iii. Dysgeusia (chorda tympani nerve)
5. Preoperative evaluation of eyelid and canalicular function (refer to Chapter 17, “Eyelid Reconstruction”)
6. Synkinesis represents “miswiring” of regenerating SVE fibers to different mimetic muscles than which they were
intended
a. Produces synchronization of voluntary contraction between disparate muscle groups (e.g., eyelid closure with smile)
b. Crocodile tears refer to hyperlacrimation during chewing or salivation and are caused by “miswiring” of regenerating
GVE fibers to the lacrimal gland instead of the salivary glands.
7. The House–Brackmann facial nerve grading system is the most common classification scheme—I (normal) to VI
(complete facial paralysis)
a. Evaluates gross appearance and motion at the forehead, eye, and mouth
b. Limitations include its generalized assessment of facial nerve function, inability to detect small changes in facial
nerve recovery, and it does not address synkinesis.
C. Electrodiagnostic studies
1. Assist with prognostication and the decision between operative intervention versus continued observation
a. The normal side of the face is required for comparison and interpretation of results (i.e., less useful in bilateral cases)
b. Must allow at least 72 hours after symptom onset for Wallerian degeneration to occur in the distal segment
2. Nerve excitability test (NET)
a. Transcutaneous stimulation over the stylomastoid foramen until contraction of the paralyzed side is visualized at the
lowest current
b. Difference greater than 3.5 mA with the normal side is significant
c. Easy to perform, but highly subjective and examiner dependent
3. Maximal stimulation test (MST) is similar to the NET, except maximal current is used for comparison
4. Electroneurography (ENoG)
a. Compares amplitude of CMAPs between sides with greater than 90% axonal degeneration representing a poorer
prognosis
b. Most predictive test for facial nerve recovery
5. Electromyography (EMG)
a. Performed 2 to 3 weeks after symptom onset—at rest, with needle insertion, and with voluntary muscle contraction
b. Fibrillation potentials: Muscle denervation
c. Polyphasic potentials: Muscle reinnervation
D. Other imaging modalities
1. An audiogram should be obtained in all patients, and if abnormal, then the next step is magnetic resonance imaging and
referral to an otolaryngologist
2. In cases of trauma, computed tomography is helpful in ruling out temporal bone fractures

IV. NONSURGICAL MANAGEMENT OF THE PARALYZED FACE


A. Protection of the cornea
1. If dryness is not prevented, it can lead to ulceration and eventual blindness, especially if corneal sensation is impaired
a. Artificial tears can be helpful
b. Taping of the eyelid can provide some external support
c. Eye patches or moisture shields can reduce evaporative losses
d. Temporary tarsorrhaphy is required in refractory cases
2. Increased risk in patients with a poor Bell’s phenomenon
B. Botulinum toxin
1. Target-specific muscle groups on the normal side to achieve temporary facial balance while nerve regeneration occurs
2. Also used to treat synkinesis and blepharospasm
C. Oral corticosteroids and antivirals
1. Treats edema and compression of the nerve within the facial canal
2. Recommended within 72 hours of symptom onset
D. Physical therapy
1. Focuses on facial reeducation, especially if recovery is incomplete
2. Examples include EMG and mirror biofeedback
E. Although it does not treat the underlying cause, certain types of clothing and particular hairstyles can help mask or hide
facial asymmetries

V. SURGICAL MANAGEMENT OF THE PARALYZED FACE


A. Patients are divided into two treatment groups based on duration of symptoms—are the facial muscles still usable?
1. Less than 18 to 24 months: Nerve operations
2. Greater than 18 to 24 months: Muscle operations
B. Nerve operations
1. Ipsilateral facial nerve available
a. Primary nerve repair if no nerve gap is present
b. Nerve grafting if nerve gap is present
c. Incidence of synkinesis is increased with nerve grafting due to the presence of two coaptations instead of one
d. If a hostile wound environment exists or concomitant injuries are prohibitive to surgery, then the nerve ends should be
tagged for future exploration and repair.
2. Ipsilateral facial nerve not available
a. Cross-facial nerve grafting (CFNG)
i. A donor nerve graft (e.g., sural nerve) guides regenerating nerve fibers from a redundant facial nerve branch on
the normal side to a distal nerve stump on the paralyzed side
ii. Provides greatest potential for spontaneous animation
iii. Nerve growth is monitored by an advancing Tinel’s sign
iv. Indicated when proximal ipsilateral nerve stump is unavailable for grafting and distal stump is present and the
facial muscles are capable of function after reinnervation.
b. Nerve transfers
i. Powerful due to a greater number of nerve fibers being transferred compared to CFNG, but does not provide
spontaneous animation
ii. Donor nerves: XII, XI, masseteric branch of V, ipsilateral C7 root, and phrenic nerve
iii. Complications: Hemiglossal dysfunction (XII), shoulder droop (XI), and hemidiaphragm paralysis (phrenic nerve)
c. Babysitter procedure
i. If the ipsilateral facial nerve is not available and denervation time is between 6 and 18 months, a CFNG can be
combined with a minihypoglossal transfer
ii. XII “babysits” the facial muscles until the regenerating nerve fibers arrive from the CFNG
C. Muscle operations
1. Dynamic procedures restore facial movement
2. Static procedures achieve symmetry at rest
3. Upper face: Must address frontalis muscle
a. Supraciliary brow lift
i. Relieves brow ptosis by excising an ellipse of skin and frontalis muscle just above the eyebrow
ii. Alternatively, an endoscopic brow lift can be used
b. Botulinum toxin can temporarily reduce muscular tone in the contralateral normal forehead to match the paralyzed
side
4. Midface: Must address orbicularis oculi muscle and the nostril dilators
a. Upper eyelid
i. Gold weight implantation or palpebral springs achieve lid closure by gravity assistance. Weight is placed just
lateral of midline over the tarsus.
ii. In the supine position, the lids must be taped together
b. The lower eyelid is treated with lid-tightening procedures (refer to Chapter 19, “Eyelid Reconstruction”)
c. Nose
i. Nonanatomic alar contour grafts: Prevent external nasal valve collapse
ii. Spreader grafts: Prevent internal nasal valve collapse
d. Regional and free microneurovascular muscle transfers have been described to the midface, but the results are
less effective compared to smile restoration
5. Lower face: Must address zygomaticus major and lower lip depressors
a. Smile restoration is the primary goal of any operation performed on the lower face—based on patient’s age and
motivation level
b. Elderly
i. Static procedures are preferred
ii. Static slings establish oral symmetry in repose using grafts of temporalis fascia, fascia lata, palmaris/plantaris
tendon, or alloplastic materials
iii. Unilateral rhytidectomy for patients with lax skin
Figure 24-2. Examples of regional muscle transfer options for lower face reanimation in the adult. A: Masseter muscle transfer. B: Temporalis muscle transfer with
fascial extension (McLaughlin procedure). C: Temporalis muscle turndown with fascial strip (Rubin procedure). D: Sternocleidomastoid (SCM) muscle transfer. E:
Platysma muscle transfer.

c. Adults (Fig. 24-2)


i. Static slings or regional muscle transfers can be used
ii. Donor muscles: Masseter, sternocleidomastoid, and platysma muscles
iii. McLaughlin procedure: Transfer of the temporalis muscle insertion from the coronoid process with fascial
extension
iv. Rubin procedure: Temporalis muscle turndown with fascial extension
v. Although touted as dynamic procedures, excursion is not as dramatic as seen in free microneurovascular muscle
transfers
d. Young, highly motivated patients (Fig. 24-3)
i. *Best candidates for free microneurovascular muscle transfer
ii. Donor muscles: Gracilis (most common), latissimus dorsi, rectus abdominis, extensor digitorum brevis, serratus
anterior, and pectoralis minor
Figure 24-3. Free microneurovascular gracilis muscle transfer.

iii. Double-stage: CFNG is performed during the first stage and muscle is transferred 9 to 12 months later during the
second stage
iv. Single-stage: First stage is eliminated because the donor muscle has a long nerve for tunneling across the face or
is coaptated to the ipsilateral XII or masseteric branch of V.
e. Lower lip symmetry can be achieved with botulinum toxin injection (temporary) or surgical division (permanent) of
the contralateral lower lip depressors

PEARLS
1. Bell’s palsy is the most common cause of unilateral facial paralysis in adults (diagnosis of exclusion) and may be treated with
oral corticosteroids and antivirals if started within 72 hours of symptom onset.
2. Children are obligate diaphragmatic breathers, so avoid using the phrenic nerve during nerve transfers.
3. All mimetic muscles are innervated on their deep surface, except for the buccinator, levator anguli oris, and mentalis.
4. An upper motor neuron lesion manifests as contralateral lower facial paralysis, whereas a lower motor neuron lesion manifests
as ipsilateral total facial paralysis.
5. The paralyzed side of the face will display less fine wrinkling, but more tissue laxity (i.e., ptosis) compared to the contralateral
normal side.

QUESTIONS YOU WILL BE ASKED


1. What three anatomic landmarks help identify the facial nerve as it exits the stylomastoid foramen?
Tragal pointer, tympanomastoid suture, and posterior belly of the digastric muscle.
2. Describe how to find the temporal branch of the facial nerve.
Follows the course of a line drawn from 0.5 cm below the tragus to 1.5 cm above the lateral brow.
3. What structures are continuous with the SMAS?
Superficial temporal fascia (temporoparietal fascia) superiorly and platysma inferiorly.
4. What nerves are commonly used to reinnervate paralyzed facial muscles?
Contralateral VII, masseteric branch of V, and XII.

THINGS TO DRAW
Draw the course of the extratemporal facial nerve.
Figure 24-1.

Recommended Readings
Baker DC, Conley J. Regional muscle transposition for rehabilitation of the paralyzed face. Clin Plast Surg. 1979;6(3):317–331. PMID: 385211.
Harii K, Ohmori K, Torii S. Free gracilis muscle transplantation, with microneurovascular anastomoses for the treatment of facial paralysis. A preliminary report. Plast
Reconstr Surg. 1976;57(2):133–143. PMID: 1250883.
Rubin LR. T he anatomy of a smile: its importance in the treatment of facial paralysis. Plast Reconstr Surg. 1974;53(4):384–387. PMID: 4815693.
T erzis JK, Konofaos P. Nerve transfers in facial palsy. Facial Plast Surg. 2008;24(2):177-193. PMID: 18470829.
Wells MD, Manktelow RT . Surgical management of facial palsy. Clin Plast Surg. 1990;17(4):645–653. PMID: 2249385.
I. OVERVIEW
A. Cleft lip (CL) and cleft lip and palate (CLP) versus cleft palate (CP) only
1. CL and CLP are the same entity along a morphologic continuum (Fig. 25-1)
2. “CP only” is a distinct entity (see Chapter 26)
3. In addition, CLP has a separate pathophysiology from Tessier facial clefts (see Chapter 27)
B. Surgical treatment
1. Directed at restoring lip form and function, correcting nasal deformity
2. Goals
a. Lengthen medial lip element (in unilateral deformity)
b. Restore nasal width
c. Reconstitute orbicularis oris muscle
C. Cleft care requires a collaborative multidisciplinary team

II. EPIDEMIOLOGY
A. *Incidence of CL with or without CP
1. Caucasian ancestry: 1:1,000 live births
2. Asian ancestry: 1:500 live births
3. African ancestry: 1:2,000 live births
B. Demographics
1. Male:female = 2:1
2. Left:right:bilateral = 6:3:1
3. Risk factors
a. Fetal exposure to substances including phenytoin, EtOH, steroids, phenobarbital, diazepam, and isotretinoin
b. Maternal smoking
c. Parental age, especially advanced paternal age
d. Family history of clefting
C. *Genetics
1. Risk of clefting in subsequent children
a. If one child or one parent has CLP, there is a 4% chance of subsequent clefting in successive
pregnancies
b. If two children have CLP: 9%
c. If one child and one parent both have CLP: 17%
2. Most cases are sporadic, multifactorial, and no genetic cause is identified
3. CLP is syndromic in <15% of cases
a. Van der Woude’s syndrome
i. Is the most common syndrome associated with CL
ii. *Autosomal dominant, with variable penetrance
iii. *Associated with lip pits (accessory salivary glands)
iv. May also have absent second molar, syndactyly, abnormal genitalia, and popliteal pterygia

______________
*De note s common in-se rvice e xamination topics
Figure 25-1. T he spectrum of cleft lip—A: microform unilateral cleft lip; B: incomplete unilateral cleft lip; C: complete unilateral cleft lip; D: incomplete bilateral
cleft lip; and E: complete bilateral cleft lip with “ flyaway” premaxilla; F: right complete cleft and left incomplete cleft lip.

b. Waardenburg syndrome (sensorineural hearing loss, iris pigment abnormality, hair hypopigmentation, and lateral
displacement of medial canthi)
c. Trisomy 21 (Down syndrome)
d. Trisomy 13 (Patau syndrome)
e. Trisomy 18 (Edward syndrome)

III. EMBRYOLOGY
A. *Critical developmental period: 4 to 6 weeks
B. *CL is caused by failure of union between medial nasal process and maxillary prominence
C. Variable extent of clefting of the primary palate occurs (Fig. 25-1) in CL, including
1. Upper lip
2. Nasal floor (or nostril sill)
3. Alveolus
4. Hard palate (anterior to incisive foramen)
D. May involve the secondary palate (posterior to incisive foramen), and this combination is termed “cleft lip and palate”

IV. PATHOPHYSIOLOGY/EMBRYOLOGY
A. Interrupted mesenchymal migration and fusion of frontonasal, maxillary, and mandibular processes
B. Week 3
1. Genesis of branchial arches and growth of frontonasal prominence
2. Streaming of neural crest cells into mesoderm of early facial and frontonasal prominences and laterally in first and
second branchial arches
3. These neural crest cells are responsible for the fusion of facial prominences
C. Week 4 to 7
1. Medial nasal processes fuse with maxillary prominences to form philtrum and primary palate (failure causes CL)
2. Maxillary prominences become the lateral upper lip and maxilla and secondary palate
3. The two lateral palatine shelves that initially lie in a vertical plane adjacent to the tongue move into horizontal plane and
fuse at midline along with the primary palate (failure causes CP)
4. Nasal septum forms from fusion of medial nasal prominences and grow downward to join the fused palatal shelf

V. CLASSIFICATION OF CLEFT LIP


A. Severity/extent (Fig. 25-1)
1. Microform CL (“forme fruste” or “minor cleft lip”; Fig. 25-1A)
a. Vermilion notching, scar-like line or depression, lip shortening
b. ± Nasal deformity, usually mild
c. Surgery may or may not be indicated based on severity
2. Incomplete CL (Fig. 25-1B)
a. Intact nasal sill (termed “Simonart band”)
b. Intact alveolar ridge
3. Complete CL (Fig. 25-1C)
a. Clefting of the lip, nostril sill, and alveolus
b. Wider than incomplete clefts with greater cleft nasal deformity
4. Complete CLP
a. CL deformity is same as above
b. Includes CP (posterior to incisive foramen)
B. Unilateral versus bilateral
1. Unilateral CL
a. Greater segment
b. Lesser segment collapse, with medial and posterior displacement
2. Bilateral CL (Fig. 25-1D-F)
a. Central prolabium and premaxilla
b. May have “flyaway” premaxilla (Fig. 25-1E) and collapsed bilateral lesser segments
c. Variable severity per side (Fig. 25-1F)
d. More likely to be complete, wide clefts

VI. ANATOMY
A. Normal lip anatomy (see Chapter 21—Fig. 21.1)
1. Central philtrum demarcated laterally by philtral columns and inferiorly by Cupid’s bow and tubercle
2. Above the junction of vermilion–cutaneous border is mucocutaneous ridge (“white roll”)
3. Within red vermilion, noticeable junction demarcating dry and wet vermilion (“wet–dry border”)
4. Vertical height of upper lip = peak of Cupid’s bow to nasal sill
a. Newborn—10 mm
b. 3 months—13 mm
c. Adult—17 mm
5. Musculature
a. Orbicularis oris—primary muscle of lip, has two well-defined components (CN VII)
i. Deep (internal)
a) Fibers circumferentially from modiolus to modiolus
b) Functions as the primary sphincter for feeding
ii. Superficial (external)
a) Fibers run obliquely, interdigitating with the other muscles of facial expression to terminate in the dermis
b) Provide subtle shades of expression and precise movements of lip for speech
c) Fibers decussate in the midline and insert into the skin lateral to the opposite philtral groove forming the philtral
columns
d) Philtral dimple is depressed centrally because no muscle fibers directly insert into the dermis in the midline
e) Pars marginalis—portion of orbicularis along the vermilion forming the tubercle of the lip with eversion of the
muscle
b. Levator labii superioris
i. Fibers arise from medial aspect of infraorbital rim, insert near vermilion–cutaneous junction
ii. Medial-most fibers insert near the corner of the ipsilateral philtral column and vermilion–cutaneous junction
helping to define the lower philtral column and peak of Cupid’s bow
c. Nasal muscles
i. Levator labii superioris alaeque nasi arises along the frontal process of maxilla and inserts on the mucosal surface
of the lip and the ala
ii. Transverse nasalis arises along the nasal dorsum and sweeps around the ala to insert along the nasal sill from
lateral to medial and into the incisal crest and anterior nasal spine (ANS)
iii. These join with the oblique fibers of orbicularis and depressor septi
iv. Depressor septi arise from alveolus between the central and lateral incisors to insert into the skin of the columella
to the nasal tip and the footplates of the medial crura
6. Blood supply
a. Superior labial arteries, bilaterally; columellar branch centrally
b. Branch off from bilateral facial arteries
7. Sensory innervation: Upper lip, maxillary division of trigeminal nerve (CN V2 )
8. Motor innervation: Zygomatic and buccal branches of the facial nerve (CN VII)
B. Unilateral CL anatomy
1. Muscles
a. *Pathological insertion of orbicularis oris
i. Runs parallel along the edge of cleft and inserts on alar base (cleft side), base of columella (noncleft side)
ii. Responsible for nasal distortion and widening of cleft with smiling
b. Hypoplasia and disorientation of pars marginalis associated with disappearance of vermilion–cutaneous ridge (white
roll) at cleft margin
c. Deep fibers interrupted at the level of submucosa in both complete and incomplete clefts
d. Levator labii and nasalis muscles are similarly distorted
e. Incomplete cleft: If cleft is less than two-thirds of lip height, some superficial orbicularis fibers may traverse superior
lip across the cleft
f. Simonart’s band: Skin bridge (contains no muscle) in nasal sill across incomplete cleft
2. Vertical lip height is decreased on noncleft side
3. Disrupted Cupid’s bow
4. *Nasal abnormalities (Fig. 25-2)
a. Hypoplastic, flattened alar dome on the affected side
b. Lack of upper lateral cartilage overlap of lower lateral cartilage
c. Subluxed lower lateral cartilage with alar base displaced cephalad and posteriorly
d. Hypoplastic bony foundation (maxilla)
e. Caudal septum is pulled toward the noncleft side by aberrant insertion of orbicularis oris
f. Flattening of the nasal bones
g. Shortened columella, especially in bilateral cases
C. Bilateral CL anatomy
1. Two lateral components (lesser segments) of lip–alveolus–palate with an intervening prolabium and premaxilla that
varies in its degree of protrusion (mild vs. “flyaway”)
2. Widened alar bases, with laterally flared alar domes and malpositioned cartilages
3. Shortened columella (hallmark of cleft nasal deformity)
4. Obtuse nasolabial angle
5. Hypoplastic prolabium

Figure 25-2. The cle ft nasal de formity. T he lower lateral cartilage on the cleft side is abnormally shaped and improperly positioned. Numbers 1 and 7, hypoplastic,
flattened alar dome on the affected side; 2, lack of upper lateral cartilage overlap of lower lateral cartilage; 3, subluxed lower lateral cartilage with alar base displaced
cephalad and posteriorly; 4, hypoplastic bony foundation (maxilla); 5, the caudal septum is pulled toward the non-cleft side; and 6, flattening of the nasal bones.
6. Absence of normal labial–gingival sulcus in premaxillary segment
7. Total absence of orbicularis muscle in prolabial segment results in the absence of philtral dimple/columns/white ridge and
median tubercle
8. Absence of Cupid’s bow
9. Aberrant insertion of lateral lip orbicularis oris muscle into alar bases
10. Aberrant dry and wet vermilion on prolabial segment

VII. INTERVENTION
A. Initial evaluation
1. Reassure parents and family
2. Explain surgical goals and timing of interventions
3. Evaluate for associated anomalies (especially with isolated CP)
4. Consultations
a. Genetics
b. Social work
c. Feeding/nutrition
i. Monitor for appropriate weight gain
ii. May require Haberman bottle or cross-cut nipple to reduce the work of feeding, especially with CP
d. Otolaryngology
i. Eustachian tube dysfunction (see Chapter 26) often requires myringotomy tubes
ii. Repeat otitis media affects hearing and speech development
B. Preoperative molding may be used to bring cleft segments together to minimize tension during repair
1. Taping
a. Applied across both segments of the lip
b. Requires compliant and reliable parents
2. Lip adhesion: Suturing cleft margins together
a. Incisions should be made in region that will be discarded at subsequent operation (mark key landmarks)
b. Goal: Turn a complete CL into an incomplete CL
c. Definitive lip repair performed several weeks to months later
3. Nasoalveolar molding (NAM)
a. Custom fabricated oral appliance with nasal stents adjusted weekly
b. Goals of NAM are similar to the above methods; NAM positions nasal cartilages and alveolar processes to facilitate
closure
c. *NAM can lengthen deficient columella
d. Takes advantage of increased plasticity of neonatal cartilage
i. First 2 to 3 months of life
ii. High circulating maternal estrogen
4. Active presurgical infant orthopedics
a. Orthodontic appliance (Latham device) rigidly fixed to palatal segments
b. Parents adjust daily to bring alveolar segments into alignment
c. Removed at the time of definitive lip repair
C. Timing of CL repair
1. 3 months of age, generally accepted
2. “Rule of Tens” (historical criteria) for suitability for surgery
a. 10 weeks old
b. 10 pounds
c. Hemoglobin10 mg/dL
3. May delay in syndromic patients with systemic concerns
4. CP repair and secondary alveolar grafting (see Chapter 26)

VIII. OPERATIVE TREATMENT


A. Goals of unilateral repair
1. Lengthen medial lip element
2. Reconstitute orbicularis oris
3. Restore Cupid’s bow, aligning white roll and wet–dry vermilion
4. Correct nasal deformity (primary rhinoplasty)
a. Upright caudal septum
b. Narrow alar base on the cleft side
c. Establish convexity of lower lateral cartilage on the cleft side
d. May use nasal conformers to maintain shape
B. Goals for bilateral repair
1. Symmetry
2. Reconstitute orbicularis oris across premaxilla
3. Achieve proper prolabial size and shape
a. ~10 mm height
b. ~3 mm from midline to each Cupid’s bow peak
4. Formation of median tubercle from lateral lip vermillion–mucosa (see “Techniques” later)
5. Correct nasal deformity (primary rhinoplasty)
a. Narrowing alar base is key difference in emphasis from unilateral technique
b. Nasal conformers also used
C. Key landmarks: Intraoperative tattooing (e.g., with methylene blue and quill pen)
1. Alar bases (i.e., subalare: Alar insertion point onto upper lip)
2. Columellar–labial junction
3. White roll
a. At the peak of Cupid’s bow on non-CL
b. At the trough of Cupid’s bow (tubercle) on non-CL
c. Additional mark equidistant from the trough to the peak on medial cleft element
i. Define peak of Cupid’s bow for CL segment
ii. Peaks are approximately 3 mm from the trough on each side
d. Noordhoff’s point: Vanishing point of white roll on CL segment
i. Most critical and difficult point to identify
ii. Should correspond to region of thickest vermillion and robust white roll
iii. In bilateral cases, this is marked on each cleft segment
D. Mark lines for preferred repair type
E. Infiltrate tissue with local anesthetic + epinephrine
F. Cut on the inside of your marks so they remain visible
Figure 25-3. Example of surgical repairs of the unilateral and bilateral cleft lip deformities. A: Preoperative markings for the unilateral lip repair. B: Postoperative
result for unilateral lip repair. C: Preoperative markings for the bilateral lip repair. D: Postoperative result for bilateral lip repair.

IX. CHEILOPLASTY TECHNIQUES (FIG. 25-3)


A. Unilateral CL repair variations. Note most are Z-plasty-based reconstructions
1. Straight-line repair (Rose–Thompson): Excision of cleft margin and primary straight-line closure; Rose–Thompson
repair incorporates Z-plasty to establish normal vertical height of the lip
2. Quadrangular flap (Le Mesurier): Uses a back-cut above Cupid’s bow and a laterally based inferior rectangular flap
to fill in the rotational defect of the medial lip element
3. Triangular flap (Randall-Tennison, Trauner, and Skoog): Incorporates Z-plasty to restore vertical height
a. May result in excess vertical length
b. Places scar in the center of lip with oblique portion crossing philtrum
4. Rotation advancement
a. Poole
i. Similar to Millard which moves cleft advancement flap back-cut inferi-orly ~3.5 mm
ii. May place scar in undesirable area in center of upper lip
b. *Millard (Fig. 25-4)
i. Most commonly used repair currently in the United States
ii. Incorporates the Z-plasty superiorly
iii. “Cut-as-you-go” technique
a) C-flap back-cut is variable
b) Determined intraoperatively
iv. Medial lip rotated downward
v. C-flap (“c” is for columella)
a) Rotated to create the nasal sill, or
b) Used to lengthen the columella (more common)

Figure 25-4. Unilateral cleft lip deformity, with preoperative markings for (Millard) repair. For clarity, descriptive anatomy is used in place of numbers. First, mark the
peak of the Cupid’s bow on the noncleft side. T hen mark the nadir of the Cupid’s bow. Extrapolate the proposed peak of the Cupid’s bow in the cleft equidistant from
the nadir of the Cupid’s bow. Next, mark the superior point of the philtral column on the noncleft side: T his is the height of the normal philtral column that you must
achieve with the cleft side! You also need to establish the normal width of the nostril floor. To do this, mark the midpoint at the columellar–labial junction and then
mark subalare: the alar insertion point on the normal side. T his distance must equal the distance between subalare on the cleft side (please go ahead and mark this now)
and your midline columellar–labial mark. T he defect in the nasal floor will need to be closed to close this distance. At the junction of the nasal floor and the lip skin,
mark off a proposed “ wedge excision” (two marks here) that will achieve this. … Noordhoff ’s point: the point at which the white roll begins to fade and where the
vermillion begins to thin toward the cleft must now be marked. T his last point is the point that only your attending can correctly mark preoperatively. In the Millard
repair, the incision is made through the vermillion to the new Cupid’s bow peak and then up toward the columellar midpoint. A back-cut via “ cut-as-you-go” is then
made toward the open circle. Again, only your attending knows how far to make this back-cut. T his releases the lip, thereby lengthening the non-cleft side. Care must be
taken to avoid crossing the noncleft philtral column. On the cleft side, the incision is carried through the vermillion and Nordhoff point, to the superior-medial most
point on the cleft lip, then back laterally toward subalare along the skin/nostril sill junction. Nasal dissection for primary rhinoplasty is then performed through these
incisions. Once the muscle is dissected free of the skin and mucosa, and disinserted from its abnormal attachments, it can be reapproximated transversely in the midline.
T he mucosa is also closed in a separate layer, using the M-flap, and then the L-flap is used for nasal lining. T he C-flap rotates toward the columella for inset, and closure
of the lip commences with the white roll. (A, Advancement flap; R, Rotationflap)

vi. *Nasal lining is repaired with L-flap from mucosal portion of lateral segment (“l” is for lining)
a) This is required because the cleft ala is posteriorly displaced (Fig. 25-2)
b) When ala advanced forward to desired position, mucosal defect must be filled to prevent contraction
c) May also be filled with turbinate flap
vii. Gingivolabial sulcus is augmented with M-flap from mucosal portion of medial segment (“m” is for mucosa)
viii. Scar follows the line of philtral column and preserves Cupid’s bow
ix. Orbicularis oris muscle repair is important to restore dynamic lip function
a) Muscle fibers are inappropriately inserted into the alar base and columella
b) Must be completely disinserted and repaired in a transverse position
x. Primary rhinoplasty
a) Diffuse undermining of alar cartilage
b) Transnasal suture techniques to secure desired position
c) May use nasal conformers to maintain shape
xi. Common pitfall: Inadequate rotation and inadequately corrected vertical lip height on non-cleft side; “whistle
deformity”
c. Fisher repair (anatomic subunit, Fisher DM; Plast Reconstr Surg. 2005) is editor’s preferred technique (Fig. 25-5)
i. Markings are similar to Millard but closure lines are placed along anatomic subunits
ii. Stresses the importance of complete leveling of the Cupid’s bow
a) a = greater lip height
b) b = lesser lip height
c) c = difference between “a” and “b”

Figure 25-5. Unilateral cleft lip Fisher repair. T he height of the greater lip segment is measured from white roll to the apex of philtral column “ a.” T he height of the
lesser lip segment is similarly measured “ b.” T he difference between “ a” and “ b” is made up with a triangle from the cleft lip element “ c.” Because of the Rose–T homson
effect, 1 mm is subtracted from triangle “ c.” Noordhoff point is marked on the cleft side. From the proposed location of the philtral column apex on the cleft side, the
length “ b” is marked with a compass so that it coincides with Nordhoff point and the triangle “ c.” A back-cut is made beneath “ a” to admit the triangle “ c.” A similar
triangle may be required in the vermillion to augment the thickness of the vermillion on the medial aspect of the cleft.

iii. A white roll triangular flap (a “Nordhoff triangle” or “c”) is used to achieve Cupid’s bow symmetry
iv. The equation: a − b − 1 mm = c
a) Accounts for 1 mm lengthening effect
b) “Rose–Thompson” effect: Lip repair via closure as an ellipse will “automatically” lengthen the incision
v. Vermilion height is equalized by using a similar triangle as a vermilion flap
B. Bilateral CL repair (Fig. 25-6)
1. Measurements and maneuvers (Millard repair)
a. Prolabium is used to create the philtrum only
b. Prolabial white roll and vermillion are discarded; the remaining prolabial mucosa is rolled inward to reconstruct the
central gingivolabial sulcus
i. Prolabial vermillion lacks minor salivary glands
ii. Using this tissue results in dry, chapped, keratotic “patch”
iii. Prolabial vermillion previously used in Manchester repair (of historical interest)
c. Tip: Make width of philtral flap near columella 1 to 2 mm narrower than inferior portion near white roll to allow for
subsequent widening
Figure 25-6. Bilateral cleft lip deformity, with preoperative markings. T he most inferior point on the prolabium is marked; this will become the trough of the Cupid’s
bow. T he proposed peaks of the Cupid’s bow are marked approximately 3 mm lateral, on each side, to this point. T he center of the columellar–labial junction is also
marked, and 2 mm lateral to this, on each side, a mark is also made. Draw a neck-tie that connects these dots. On the lateral lip elements, Nordhoff points are defined
and marked above the white roll. About 3 mm lateral to these points, a mark is made that will allow (a) and (a’) to coincide upon closure. Mark subalare bilaterally. T he
height of the philtrum (b) is transferred to each lateral lip element (b’). Line (c) is marked extending into the nasal floor and (c’) is made to equal length. A similar
concept to the unilateral repair is applied to the nasal floor in the bilateral repair, in that a wedge must be taken from the floor to narrow it. T his corresponds to (f) and
(f ’). T he prolabial skin inside of the original markings is discarded and the mucosa is used for lining. Lines (e) and (e’) are made to close the distance in vertical lip height
to subalare. T he lateral lip elements rotate downward, forming the tubercle in the midline.

d. Cupid’s bow and tubercle reconstructed from lateral lip segments, which are advanced medially beneath the elevated
philtral flap
e. Alar cinch suture to reposition alar bases
f. Common pitfall(s)
i. Inadequate columellar length
ii. Poor projection of tubercle
iii. May have significant widening of the prolabium

X. SECONDARY PROCEDURES
A. Secondary cheiloplasty
1. Hypertrophic scars
a. Consider massage
b. Silicone sheeting
c. Steroid injections, prior to operative intervention
2. Short scar/lip
a. May be amenable to the addition of Z-plasty
b. Likely requires complete revision
3. Deficient tubercle
a. Most common encountered following bilateral repair
b. Likely requires Abbe flap
i. Lip sharing procedure from the lower lip
ii. Usually performed after maxillary growth or Le Fort I advancement
B. Secondary rhinoplasty
1. May be performed at any age, but commonly at skeletal maturity
2. Open approach requires creative use of preexisting incision or judicious planning of transcolumellar incisions
3. Requires stable bony foundation for the base of nasal pyramid (i.e., previously suitable alveolar bone grafting to address
maxillary deficiency)
4. Must address poor tip projection and abnormal alar position
5. Columella and caudal septum may require repositioning to the cleft side and suturing to the ANS
6. Requires addition of anatomic and nonanatomic cartilage grafts
a. Alar contour grafts
b. Onlay tip grafts
c. L-strut grafts
7. Severe septal deviation may require aggressive submucous resection of ethmoid in addition to septal cartilage (used for
grafts)
8. Spreader grafts often needed for airway patency at internal nasal valve (see Chapter 30)

QUESTIONS YOU WILL BE ASKED


1. Describe basic CLP epidemiology
a. Asians>Whites>Blacks
b. Left:right:bilateral; 6:3:1
2. What are key timepoints and events in CLP embryology?
a. 4 to 7 weeks, critical period
b. Cleft lip: Failure of fusion medial nasal process and maxillary prominence
c. Cleft palate: Failure of fusion palatal shelves
3. What is most common CLP syndrome and what are the findings?
a. Van der Woude
b. Autosomal dominant with lip pits and CLP
4. What is pathologic anatomy of cleft nasal ala?
a. Posterior and superior displacement
b. Loss of convexity of lower lateral cartilage
5. What is primary goal of unilateral cleft lip repair?
a. Increase the height of medial cleft lip segment
b. Restore continuity of orbicularis
c. Reposition alar base(s)
6. Draw Unilateral and Bilateral CL markings.
See Fig.24-4, 24-5

THINGS TO DRAW
1. Key anatomical landmarks in CLP
2. Unilateral and bilateral Millard repair techniques

Recommended Readings
Fisher DM. Unilateral cleft lip repair: an anatomical subunit approximation technique. Plast Reconstr Surg. 2005;116(1):61-71. PMID: 15988248.
Millard DR Jr. Complete unilateral clefts of the lip. Plast Reconstr Surg Transplant Bull. 1960;25: 595-605. PMID: 14422441.
Millard DR Jr. Refinements in rotation-advancement cleft lip technique. Plast Reconstr Surg. 1964;33:26-38. PMID: 14104544.
Mulliken JB. Primary repair of bilateral cleft lip and nasal deformity. Plast Reconstr Surg. 2001;108(1):181-194; examination 195-196. PMID: 11420522.
I. OVERVIEW AND EPIDEMIOLOGY
A. Isolated cleft palate (CP) must be differentiated from cleft lip and palate (CLP)
B. CP
1. 0.5 in 1,000
2. Involves the secondary palate only (posterior to incisive foramen)
3. No ethnic variation in incidence
4. *Often syndromic
a. DiGeorge syndrome (Shprintzen)
i. Most common
ii. Cardiac defects
iii. Chromosome 22q deletion
b. Stickler syndrome
i. Autosomal dominant
ii. Mutation in type 2 collagen
C. CLP (see Cleft Lip (chapter 25) for further information)
1. The vast majority of cleft lips arise spontaneously and are not inherited.
2. Ethnic variation in incidence (Asians > Whites > Blacks)
3. Syndromic conditions are rare (e.g., Van der Woude’s syndrome)
4. Predominantly sporadic
5. Always involves the primary palate, with variable involvement of the secondary palate
a. Forme fruste
b. Cleft lip and alveolus
c. Complete CLP

II. NORMAL PALATE ANATOMY


A. Hard palate (bony palate; Fig. 26-1)
1. Incisive foramen, through which passes
a. Nasopalatine nerve
b. Sphenopalatine artery
2. Primary palate
a. Anterior to incisive foramen
b. Forms with fusion of bilateral palatine process of maxilla
3. Secondary palate
a. Posterior to incisive foramen
b. Fusion of bilateral horizontal plates of palatine bone
c. Greater palatine foramen, through which passes greater palatine nerve and artery (blood supply to anterior
palatoplasty flaps)
c. Isolated CP involves this region and the soft palate
B. *Soft palate (velum; Fig. 26-2): Mucosa and muscles involved in velopharyngeal (VP) closure (with corresponding
innervation)
1. Levator veli palatini (LVP, CN X)
a. Lifts velum against posterior pharynx (“genu” action)
b. Key muscle involved in VP closure
______________
*De note s common in-se rvice e xamination topics
Figure 26-1. Anatomy of the hard palate. A: Normal palatal anatomy with all soft tissue removed. B: Palatal anatomy with anterior (hard) palate soft tissue removed.
C: Palatal anatomy with soft tissue intact, depicting neurovascular supply to palatal muscles and to mucosa. (From Moore KL, Dalley AF, Agur AM, eds. Clinically
Oriented Anatomy. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.)

Figure 26-2. Normal palate muscle anatomy. Views of the palatal muscles and their interaction with the pharyngeal constrictors as shown from (A) inferior and (B)
posterior views. (From Moore KL, Dalley AF, Agur AM, eds. Clinically Oriented Anatomy. 6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010.)

c. Normally oriented transversely across velum to decussate with contralateral muscle in midline, but in CP it is oriented
longitudinally; aberrant/anomalous insertion
2. Tensor veli palatini (CN V)
a. Travels around hook or hamulus (sphenoid bone)
b. Tendon often divided in repair to reduce muscle closure (intravelar veloplasty [IVV]) tension
c. Function: Open eustachian tube
3. Palatoglossus (CN X)
a. Originates from the tongue, passes through anterior tonsillar pillar, and inserts on anterior velum
b. Function: Palate depression
c. Used in dynamic sphincter pharyngoplasty (DSP)
4. Palatopharyngeus (CN X)
a. Originates from posterior pharynx, passes through posterior tonsillar pillar, and inserts on velum
b. Function: Palate depression
c. Used for dynamic sphincter pharyngoplasty
5. Musculus uvulae (CN X)
a. Originates from behind the levator to the tip of uvula
b. Function: Uvula shortening and elevation
6. Superior pharyngeal constrictor (CN X)
a. Broad muscle coarses anteriorly within the pharyngeal wall
b. Insertion: Velum
c. Function: Medial movement of lateral pharyngeal wall
C. Vascular supply
1. *Greater palatine arteries are primary blood supply for palatal mucosa
a. Pedicle for most palatoplasty flaps
b. Located medial to maxillary tuberosity in hard palate
2. Lesser palatine arteries: Supplies soft palate
3. Sphenopalatine artery
4. Ascending pharyngeal artery off of external carotid and ascending palatine branch of facial artery
D. Innervation
1. Hard palate: Greater palatine (CN V) and nasopalatine nerves (CN V)
2. Soft palate: Lesser palatine nerve (CN V)

III. CP ANATOMY AND CLASSIFICATION


A. Variable severity
1. Bifid uvula only
2. *Submucous cleft triad: Intact mucosa with aberrant musculature
a. Bifid uvula
b. Hard palate notch (palpable on exam)
c. Zona pellucida: Pale midline mucosa
3. Cleft velum only (soft palate, Veau type I)
4. Cleft of velum and bony palate (soft and hard palate, Veau type II)
5. Primary palate clefts (a component of cleft lip and cleft palate)
a. Lip, nostril sill, alveolus, and primary palate
b. May progress to secondary palate posteriorly
i. If unilateral complete, Veau III
ii. If bilateral complete, Veau IV
6. Secondary palatal cleft
B. Anomalous insertion of tensor and LVP
1. Eustachian tube dysfunction and decreased middle ear drainage
a. Recurrent otitis media leading to hearing loss
b. Myringotomy tubes
i. Placed in 95% of CP patients
ii. Often at time of CP repair
2. Instead of decussating in midline, LVP muscles oriented anteroposteriorly , inserting onto posterior margin of
hard palate

IV. PALATAL EMBRYOLOGY


A. Primary palate (fifth week)
1. Lip, alveolus, nostril sill, and hard palate anterior to incisive foramen
2. Medial and lateral nasal prominences of frontonasal process migrate and fuse to form median palatine process
3. Median palatine process forms from fusion of bilateral median nasal prominences and becomes premaxilla
B. Secondary palate (5th through 12th weeks)
1. Posterior to incisive foramen and soft palate
2. Bilateral palatine processes develop from medial maxillary process
3. Lateral palatine processes hang vertically then lift horizontally
a. Right lateral palatal process becomes horizontal before left, which may explain higher incidence of left-sided clefts
b. Fusion takes 1 week longer in females, which may explain increased incidence in females
4. Fusion starts at incisive foramen and moves posteriorly. When interrupted, CP results.

V. ETIOLOGY
A. Genetics
1. CP: Autosomal recessive with contributing genes
2. CLP: Polygenic, usually sporadic
B. Environment
1. Smoking: Inconclusive but many studies have implicated its role
2. Teratogens: Alcohol, isotretinoin increases the risk
3. Folate and B6 may be protective
C. Primary retrognathia. Pierre Robin sequence
1. Wide, U-shaped clefts
2. Difficulty maintaining airway
3. Lateral palatine processes unable to fuse due to glossoptosis (posterior displacement of tongue) causing CP

VI. INITIAL EVALUATION


A. Feeding and weight gain
1. Haberman or cross-cut nipple required due to poor oral suction
2. Palate repair is often performed at age 1 year, but may be carried out later if the patient is a poor operative candidate
B. Mandibular anatomy
1. Often normal
2. *Primary retrognathia (Pierre Robin sequence)
a. Prone positioning to relieve glossoptosis and airway obstruction
b. Continuous pulse oximetry and polysomnography to evaluate obstructive sleep apnea (OSA)
c. pH probe to evaluate gastroesophageal reflux
d. Nutrition consultation for failure to thrive, possible feeding tube
e. Direct laryngoscopy to determine additional airway pathology (e.g., subglottic stenosis)
f. Consider early mandibular distraction
i. May perform while intubated, if airway unstable
ii. Distraction until air leak, then subsequent extubation
g. Often delay CP repair for airway concerns until further mandibular growth
h. May require early tracheostomy (secondary strategy), after which CP repair may proceed at standard age
C. Patient examination
1. Use penlight and tongue depressor
a. Crying infant is easier to examine
b. Place child supine and upside-down on parent’s lap
2. Look for bifid uvula and palpate cleft to determine bony involvement
3. Vomer may be visible in nasopharynx in cases of bilateral CLP (Fig. 26-3A)

VII. GOALS
A. Closure of cleft
1. Separate oral and nasal cavities
2. Prevent aerophagia and reflux of oral contents into nasopharynx
B. Speech/VP competence
1. Requires competent VP mechanism
a. Contact of velum against posterior pharynx
b. “Genu” action describes physiologic motion of palate
2. Operative goals: Increased palatal length and muscle repositioning
3. Prevent maladaptive compensatory misarticulations
a. Perform repair at 1 year of age
b. Timing of speech milestone (first words)
4. May lead to OSA in some patients
C. Hearing
1. Otitis media
a. Eustachian tube dysfunction: Abnormal LVP origin impairs “milking” action, which leads to poor venting of middle
ear
b. Permanent impairments result with recurrent infection
2. Myringotomy performed at time of CP repair
D. Facial growth
1. *Palate repair in early childhood may adversely affect maxillary growth, but this drawback is outweighed by
the improvements in speech achieved by early correction
2. Early secondary palate and delayed primary palate repair has been advocated (controversial two-stage approach)
3. *Patients may require orthognathic surgery in adolescence (Le Fort I advancement; see Chapter 29) for midface
hypoplasia and class III malocclusion
Figure 26-3. Von Langenbeck palatoplasty. A: Preoperative appearance of bilateral cleft palate, surgeons view. Incisions are planned along the cleft margins and in the
vomerine mucosa (midline). Lateral relaxing incisions are also shown. T he dotted lines anteriorly would be incised to convert this bipedicled technique to a unipedicled
island flap (Bardach) repair. In the soft palate, a straight-line repair (IVV) is planned. B: Appearance of palate after closure of oral mucosa, muscle, and nasal mucosa.
Cellulose material has been placed into the lateral defects for hemostasis. (Photos courtesy of Dr. Craig Birgfeld.)

VIII. REPAIR TECHNIQUES


A. In CLP, both the primary and secondary palates require repair
1. The entire palate must be elevated for cleft closure
2. Nasal and oral mucosa are repaired in layers over primary palate
B. In isolated CP, only the secondary palate requires repair
1. Often involves dissection in the velum only
2. In wide clefts, total palatal elevation may be required for tension-free closure
3. Nasal mucosa, muscle, and oral mucosa repaired in layers over secondary palate
C. The repair technique used in the primary palate may be chosen independently from the repair technique used in the
secondary palate
D. Dingman mouth gag, neck extension with shoulder roll, Trendelenburg positioning all used to maximize exposure
E. Secondary palate repair techniques
1. Straight-line repair or intravelar veloplasty (IVV) (Fig. 26-3)
a. Useful in wide clefts
b. Three-layered closure
c. Relieve aberrant insertion of LVP from hard palate and rotate posteriorly
d. IVV: LVP dissection, disinsertion from hard palate, and muscle repair in soft palate midline
e. Adverse sequelae: Potential for short palate and subsequent VP insufficiency (VPI)
2. Furlow palatoplasty or *double-opposing Z-plasty (Fig. 26-4)
a. Opposing myomucosal Z-plasty flaps for both oral and nasal closure
i. Oral myomucosal flap is on the patient’s left
a) Conventional technique
b) Remember: Easier for right-handed surgeon to elevate the left-sided myomucosal triangle first
ii. Nasal myomucosal flap is on the patient’s right
b. Rotation of triangles will “automatically” bring LVP muscles into anatomic alignment (recall: anomalous LVP
insertion)
c. Lengthens soft palate
d. Adverse sequelae: Sacrifice of width in order to gain length; may not be possible in wide clefts (consider IVV)
e. May cause sleep apnea.
F. Primary palate repair techniques
1. Von Langenbeck repair (Fig. 26-3)
a. Bipedicle mucoperiosteal flaps
i. Anterior pedicle: Blood supply via sphenopalatine a.
ii. Posterior pedicle: Blood supply via greater palatine a.
b. Parallel incisions are made along cleft margin lingual to alveolus
c. Lateral relaxing incisions left open to heal secondarily
d. Nasal and oral mucosal flaps are mobilized to midline and sutured in separate layers
e. Adverse sequelae: Potential for maxillary growth restriction, high tension repair, which may lead to dehiscence
2. V-Y pushback (Veau–Wardill–Kilner)
a. Bilateral pedicled posteriorly
b. V-Y advancement posteriorly
c. Lengthens palate for speech
d. Adverse sequelae: Potential for maxillary growth restriction
3. Two-flap palatoplasty (Bardach repair, Fig. 26-4)
a. Requires elevation of entire palatal mucosa: Island flap based on greater palatine a.
b. May be used in wide cases of isolated CP to gain extra mucosa for closure
c. Most common repair in CLP
d. Adverse sequelae: Anterior areas heal secondarily causing maxillary growth restriction
G. Additional maneuvers for wide clefts
1. Infracture of the hamulus can bring lateral elements toward midline
2. Osteotomize medial to greater palatine foramen for increased pedicle length
3. The periosteal sheath around pedicle can be released with meticulous dissection to gain additional pedicle length

IX. ADJUNCTIVE TECHNIQUES


A. Buccal fat pad flaps
1. Small incision made posterior to maxillary tuberosity
2. Fat “teased” from buccal space with gentle spreading motion
3. Can be spread to cover surprisingly large surface area
4. Mucosalize secondarily
Figure 26-4. Furlow double-opposing Z-plasty. A: Preoperative appearance of unilateral cleft palate, surgeons view. Incisions are planned along the cleft margins, with
lateral relaxing incisions shown. T he hamulus (white circle) has been marked bilaterally so as to design the Z-plasty incisions. T he base of the right uvula is the other
landmark. Recall that the left Z-plasty flap is the oral myomucosal flap. T his will be easiest to elevate for the right-handed surgeon. Inset: diagrammatic representation
of incisions and abnormal LVP musculature in a case with isolated CP. B: Appearance of palate after closure of the nasal layer including the right-sided myomucosal flap.
T he oral layer and left-sided myomucosal flap is retracted. Inset: diagrammatic representation of first Z-plasty closure. C: Final appearance of Furlow palatoplasty after
closure of the second Z-plasty. Inset: Normal anatomic relationship of the LVP has been restored. (Photos courtesy of Dr. Craig Birgfeld.)
B. Vomer flaps
1. Based superiorly
2. Used for nasal mucosal closure anteriorly in all CLP repairs
C. Turbinate flaps
1. Can be based superiorly or inferiorly
2. Used for nasal mucosal closure of primary palate in CLP repair
D. Facial artery myomucosal flap
1. Intraoral mucosal flap based on facial a.
2. Often used to repair palatal fistulae secondarily
E. Gingivoperiosteoplasty
1. Rarely used
2. May be indicated at time of lip repair to close alveolar segments
3. Only feasible if greater and lesser segments are within ~1 mm of each other
F. Other techniques
1. Two different techniques may be used simultaneously for repair of the primary palate, one on each side
2. For example, a bipedicled Von Langenbeck (bipedicle flap) repair may be used on the lesser segment of the cleft, while
a one-flap Bardach (unipedicle island flap) repair is used on the greater segment

X. ALVEOLAR CLEFT BONE GRAFTING


A. *Performed prior to eruption of permanent dentition (~7 years of age)
B. Goals
1. Enables stable support of incoming permanent dentition
2. Provides bony support to deficient cleft nasal alar base
3. Allows for closure of nasoalveolar fistula
a. Often unable to be repaired during cleft lip or cleft palate
b. Prevents nasal regurgitation
C. Requires cancellous bone graft from iliac crest
1. Incision is made parallel and below iliac crest
2. Cartilage cap over ilium is split
3. Curettes used to “scoop out” cancellous bone
D. Intraoral flap dissection
1. Incision made just above attached gingiva/papillae, up into cleft on each side
2. Nasal floor and palatal mucosal closure performed
3. A back-cut is made into unattached gingiva near last molar
4. Subperiosteal dissection along maxilla
5. Cancellous bone is packed into cleft defect
6. Periosteal cuff is then released from the underside of the flap to relieve tension as it is rotated into the cleft defect for
anterior labial mucosal closure

XI. POTENTIAL COMPLICATIONS OF CP REPAIR


A. Acute airway obstruction
1. Bleeding/aspiration/laryngospasm
2. Tongue swelling; reperfusion injury from Dingman mouth gag
3. Reintubation in immediate perioperative period is ~1%
4. Place tongue stitch and possibly nasopharyngeal airway postoperatively
5. Pulse oximetry overnight
B. Dehiscence of palatal flaps, may be due to
1. Undue tension
2. Poor flap vascularity
3. Inadequate or overzealous suturing
C. Palatal fistula
1. Reported from 5% to 50%
2. Most common in cases of wide bilateral CLP
3. *Hard/soft palate junction is the most common location
4. Single-layer closure may be risk factor
D. Midfacial growth restriction
1. Intrinsic midface growth problems are present in children with CP or CLP
2. Scarring/secondary healing from palate repair exacerbates maxillary growth restriction
3. May be reduced by avoiding secondary intention healing
a. Limit undermining when possible
b. Use buccal fat pad flaps to close lateral open areas
4. Timing of palate repair: As late as possible to allow maximal growth, but before the emergence of speech
F. Hyponasality: Less common than VPI; related to overaggressive closure of velopharynx
G. VPI
1. Incomplete closure of velum
a. Air escape through nasopharynx
b. Hypernasal speech
2. 20% incidence following palatoplasty
3. Due to inadequate palatal length and/or poor muscle function
4. Patient develops maladaptive compensatory substitutions of abnormal for normal sounds in order to be
understood, especially
a. Pharyngeal fricatives
b. Glottal stops
5. Treatment
a. Obturator (prosthesis) to fill areas of tissue deficit
b. Posterior pharyngeal flap (PPF)
i. Static, nonphysiologic technique
ii. Myomucosal flap from posterior pharynx
a) Mucosa and superior pharyngeal constrictor m.
b) Superiorly based and sutured to soft palate
iii. Appears as a tissue “bridge” with two lateral ports
iv. Requires the patient to have movement of lateral walls
c. DSP
i. Dynamic technique
ii. *Superiorly based myomucosal flaps from posterior tonsillar pillar flaps (palatopharyngeus m.)
iii. Crossed and overlapped (to variable degrees) in midline
iv. Indicated with absent or minimal medial excursion of lateral walls
v. Appears as a single port
d. Posterior pharyngeal fat grafting (PPFG)
i. Hand-assisted liposuction
ii. Injection into submucosa of postpharyngeal wall to narrow distance to velum
H. OSA
1. Increasingly diagnosed in CP population
2. More likely following secondary speech operations: PPF, DSP, and PPFG

QUESTIONS YOU WILL BE ASKED


1. What is the effect of palatoplasty on maxillary growth?
Causes maxillary growth restriction
2. What is the most common location for a palatal fistula?
At the junction of hard and soft palate
3. What is the blood supply to the hard and soft palate?
Hard palate: Greater palatine artery. Soft palate: Lesser palatine artery, ascending pharyngeal artery, and ascending palatine
branch of facial artery

THINGS TO DRAW
Draw out a furlow palatoplasty.
See Fig. 26-4

Recommended Readings
Fisher DM, Sommerlad BC. Cleft lip, cleft palate, and velopharyngeal insufficiency. Plast Reconstr Surg. 2011;128(4):342e-360e. PMID: 21921748.
Furlow LT Jr. Cleft palate repair by double opposing Z-plasty. Plast Reconstr Surg. 1986;78(6):724-738. PMID: 3786527.
Liau JY, Sadove AM, van Aalst JA. An evidence-based approach to cleft palate repair. Plast Reconstr Surg. 2010;126(6):2216-2221. PMID: 21124164.
I. CRANIOFACIAL EMBRYOLOGY AND DEVELOPMENT
A. Skeletal tissues of head and face derive from mesenchyme and cranial neural crest cells
B. Bone formed through both endochondral and intramembranous ossification (Fig. 27-1)
1. Skull development starts at 23 to 26 days of gestation
2. Neurocranium: Develops into calvarium and provides bony encasement around the brain
a. Membranous neocranium: Precursor to cranial vault
i. Paired frontal, parietal, squamosal temporal, and superior occipital bone
ii. *Bone formation through intramembranous ossification (direct ossification of mesenchyme)
b. Cartilaginous neocranium: Precursor to skull base
i. Includes sphenoid, ethmoid, mastoid, petrous portion of temporal bone, and inferior occipital bone
ii. *Bones develop through endochondral ossification (ossification of cartilaginous precursor)
3. Viscerocranium: Precursor to the bones of the facial skeleton
a. *Derived from neural crest cells of the first pharyngeal arch (Meckel cartilage)
i. Maxillary process (dorsal portion of first pharyngeal arch) forms premaxilla, maxilla, zygoma, and squamous
temporal bone
ii. Mandibular process (ventral portion of first pharyngeal arch) forms the mandible, malleus, and incus
b. *Second pharyngeal arch (Reichert cartilage) gives rise to stapes, styloid process of the temporal bone and
lesser horn and superior body of the hyoid bone
c. Bone formation through intramembranous ossification
C. Cranial sutures
1. Fibrous joints between calvarial bones
2. Metopic, sagittal, coronal, lambdoid, and squamosal (Fig. 27-1)
a. Permit deformational changes (i.e., passage through birth canal)
b. Consist of adjacent osteogenic fronts, interposed mesenchymal tissue, and underlying dura mater
c. Allow for head expansion during development
i. *Primary stimulus for skull growth is brain growth
ii. Brain is 25% of adult size at birth, 50% at 6 months, and 75% at 1 year
iii. Full adult volume by ~2.5 years
3. Fontanelles (infantile “soft spots”) are the confluence of two or more cranial sutures
a. Anterior fontanelle (bregma): Closes around 2 years of age
b. Posterior fontanelle (lambda): Closes around 2 months of age

______________
*De note s common in-se rvice e xamination topics
Figure 27-1. Major bones, fontanelles, and cranial sutures of the newborn skull as seen from (A) superior and (B) lateral views. (Modified from Sadler T. Langman’s
Medical Embryology. 9th ed. Image Bank. Baltimore, MD: Lippincott Williams & Wilkins; 2003.)

4. Suture fusion sequence


a. Metopic: 3 to 9 months (only suture to obliterate during childhood)
b. Sagittal: 20 to 22 years
c. Coronal: 23 to 24 years
d. Lambdoid: 26 years
D. Sinus development (Table 27-1)

II. CRANIOSYNOSTOSIS
A. Premature fusion of the cranial sutures
B. *Virchow’s law
1. Growth restriction occurs perpendicular to the affected suture
2. Compensatory skull growth occurs parallel to the affected suture
C. Nonsyndromic (primary) craniosynostosis
1. Isolated suture fusion without associated abnormalities
2. Largely sporadic pattern of occurrence (incidence 0.6 in 1,000 live births)
D. Syndromic craniosynostosis
1. Heterogeneous group of disorders marked by premature suture fusion
2. Associated dysmorphic features and congenital abnormalities
3. Genetic heritability patterns (e.g., autosomal dominance, autosomal recessive, and X-linked)
4. Linked to specific gene mutations in some cases (see below)
E. Secondary craniosynostosis: Premature suture fusion due to other disease processes
1. Hyperthyroidism
2. Idiopathic hypercalcemia
3. Rickets
4. Microcephaly
5. Mucopolysaccharidoses
6. Hematologic disorders (thalassemia, polycythemia vera, and sickle cell)
7. Iatrogenic (e.g., after shunt placement for hydrocephalus)
F. Diagnosis, workup, and consultations
1. History
a. Abnormal head contour
b. Sleep disturbances
c. Regression or failure to meet developmental milestones
2. Physical exam
a. Palpable ridge along synostotic sutures
b. Lack of movement along sutures with palpation
c. Dysmorphic facial features or facial asymmetry
d. Abnormal head circumference when compared with age-predicted norms
e. Poorly defined, absent or bulging fontanelles
f. Fundoscopic examination for papilledema
3. Evaluate for elevated intracranial pressure (ICP)
a. Approximately 10% of single suture synostosis and 40% of patients with multisuture synostosis have elevated ICP
b. Irritability, growth impairment, inconsolability, vomiting, bulging fontanelles, and papilledema
c. Requisite neurosurgical consultation in all confirmed patients
4. Imaging: CT scan
a. Routinely used in diagnosis
b. Three-dimensional reformatting for preoperative planning
c. Evidence of elevated ICP may be manifested as hydrocephalus or luckenschadel (“copper beaten”) skull
5. Genetics evaluation
6. Neuropsychological evaluation to determine baseline cognitive functioning
7. Speech and audiology assessment should be performed to ensure ongoing language acquisition during development

III. NONSYNDROMIC CRANIOSYNOSTOSIS


A. Metopic synostosis
1. Relatively uncommon: <10% of craniosynostosis
2. Deformity: Trigonocephaly
3. Associated findings: Keel-shaped skull with pointed forehead, frontal bossing, bitemporal narrowing, hypotelorism, and
recessed superior orbital rims
B. Sagittal synostosis
1. *Most common: >50% of craniosynostoses
2. Male predominance: 4:1 male/female ratio
3. Sporadic with 2% genetic predisposition
4. Deformity: Scaphocephaly (dolichocephaly)
5. Associated findings: Increased AP length of skull, “boat-like” appearance, decreased biparietal width, and frontal and
occipital bossing
C. Unilateral coronal (unicoronal) synostosis
1. Second most common: 20% of craniosynostosis
2. Deformity: Anterior plagiocephaly
3. Associated findings: Ipsilateral frontal bone flattening, contralateral compensatory frontal bossing, shortened AP
dimension on affected side, anterior displacement of ipsilateral ear, and deviation of nasal tip to contralateral side
4. *Harlequin eye deformity
a. Lack of ipsilateral descent of greater wing of sphenoid during development
b. Pathognomonic for unicoronal synostosis
D. Bilateral coronal (bicoronal) synostosis
1. *Most commonly associated with syndromic craniosynostosis (such as Crouzon’s and Apert syndromes)
2. Deformity: Brachycephaly
3. Associated findings: Frontal bossing with vertical elongation of frontal bones, widening of anterior cranial base, shortened
AP skull dimension, occipital flattening, shallow orbits, and hypertelorism
E. Lambdoid synostosis
1. Least common: <3% of craniosynostosis
2. May be unilateral or bilateral
3. Deformity: Posterior plagiocephaly
4. Associated findings: Flattening of ipsilateral occiput, posterior and inferior displacement of ipsilateral ear, and
contralateral occipitoparietal bossing
F. Multiple suture synostosis
1. Usually occurs as a feature of syndromic craniosynostosis
2. Dysmorphic features depend on the pattern of involved sutures
3. Pansynostosis: Fusion of all cranial sutures
a. Nonsyndromic pansynostosis
i. Inadequate volume expansion secondary to impaired brain growth
ii. Skull is normocephalic in contour but microcephalic in volume
b. Syndromic pansynostosis
i. Normal brain growth which is constrained by the fusion of all sutures
ii. Kleeblattschädel deformity: Clover leaf skull
a) Ballooning of cranial vertex and squamosal sutures
b) Often requires immediate surgical decompression following birth to avert neurologic compromise
c) May require cerebrospinal fluid (CSF) shunt
d) C-spine must be evaluated for additional abnormalities

IV. DEFORMATIONAL PLAGIOCEPHALY (POSITIONAL HEAD DEFORMITY, OR POSITIONAL


PLAGIOCEPHALY)
A. Results from external pressure applied to the pliable fetal or infant skull
B. *Must be differentiated from lambdoid or coronal synostosis (Fig. 27-2)
C. Causes
1. Supine sleeping position: Recommended to decrease the risk of sudden infant death syndrome. This is the most common
cause of positional plagiocephaly.
2. In utero compression
3. Vertebral abnormalities
4. Congenital muscular torticollis (often occurs with deformational plagiocephaly)
5. Ocular torticollis: Visual field deficits causing preferential head positioning
D. Treatment specific to the underlying cause
1. Supervised prone positioning (“tummy time”), physical therapy, stretching and possible muscle release for torticollis,
head and neck rotation while feeding, encouraging looking to affected side by positioning infant
2. Shaping helmets
a. Fitted to widest skull dimension
b. Compensatory growth occurs due to external forces applied by helmet
c. Must be worn for >23 hours per day
d. Effective if worn for 2 to 3 months or longer
e. Less effective after 18 months of age; early helmeting is much more effective
f. Multiple helmet fittings required as cranial contour improves

V. SYNDROMIC CRANIOSYNOSTOSIS
A. Apert syndrome (Fig. 27-3A)
1. Genetics
a. Autosomal-dominant inheritance but vast majority of cases represent sporadic mutations
b. *FGFR2 mutation (chromosome 10)
Figure 27-2. Distinguishing features of deformational and synostotic plagiocephaly.

2. Craniofacial features
a. Bicoronal craniosynostosis, turribrachycephaly (short AP skull dimension, wide transverse dimension, and increased
vertical excess of skull), orbital hypertelorism, proptosis, midface hypoplasia with class III malocclusion, “parrot
beak” nose, high arched palate, occasional cleft palate, and acne
b. Elevated ICP common
3. *Extremities: Severe complex syndactyly of hands and feet in which most or all digits are fused, including
phalanges; all interphalangeal joints of fingers are stiff; lack PIP joints; also often have stiffness affecting elbow and
shoulder joints; 4 to 5 metacarpal synostosis; and radial clinodactyly of the thumb
4. Mental status: variable
B. Crouzon’s syndrome (Fig. 27-3B)
1. Genetics
a. Autosomal dominant
b. FGFR2 mutation
2. Craniofacial features
a. Coronal and lambdoidal synostosis, turribrachycephaly, exorbitism/proptosis leading to exposure keratitis, midface
hypoplasia, class III malocclusion
b. Features less severe than Apert
3. Conductive hearing loss due to cranial base abnormalities
4. *Extremities: normal
5. Mental status: variable
C. Saethre–Chotzen syndrome
1. Genetics
a. Autosomal dominant
b. TWIST-1 mutation
2. Craniofacial features: Asymmetric coronal synostosis, shallow orbits, telecanthus, ptosis of eyelids, midface
hypoplasia, deviated nasal septum, low hairline
3. Extremities: Partial syndactyly
4. Mental status: Usually normal
Figure 27-3. A: Apert syndrome. B: Crouzon’s syndrome. C: T reacher–Collins syndrome. D: Goldenhar–Gorlin’s syndrome (From Gold DH, Weingeist TA. Color
Atlas of the Eye in Systemic Disease. Baltimore, MD: Lippincott Williams & Wilkins; 2001.)

D. Pfeiffer’s syndrome
1. Genetics
a. Autosomal dominant
b. FGFR1, FGFR2, FGFR3 mutations
2. Craniofacial features: Turribrachycephaly, coronal and/or sagittal synostosis, shallow orbits, hypertelorism,
downslanting palpebral fissures, and midface hypoplasia
3. *Extremities: Broad thumbs and great toes, partial syndactyly of digits 2 and 3
4. Mental status: Variable
E. Jackson-Weiss syndrome
1. Genetics
a) Autosomal dominant
b) FGFR2 mutation
2. Craniofacial features: Highly variable, may appear similar to other syndromes
3. Extremities: Broad great toes or syndactyly of toes
F. Carpenter syndrome
1. Genetics: Autosomal recessive (most syndromic craniosynostosis are AD)
2. Craniofacial features: Variable suture synostosis, flat nasal bridge, low set ears, abnormal globe, and canthi
3. Extremities: Brachydactyly, syndactyly of hands and feet, and short stature
4. Mental status: Impaired
G. Boston-type craniosynostosis
1. Genetics
a. Autosomal dominant
b. MSX2 mutation
2. Craniofacial features: Craniosynostosis, soft palate cleft
3. Extremities: Short first metatarsal head, triphalangeal thumb

VI. FUNCTIONAL SEQUELAE OF CRANIOSYNOSTOSIS


A. Central nervous system
1. Varying degrees of cognitive impairment
2. Possible elevations in ICP (neurosurgical consultation is requisite in all patients)
B. Ocular
1. Exorbitism may lead to exposure keratitis and visual compromise
2. Strabismus
3. Bony orbit and ocular abnormalities may lead to deprivation amblyopia
C. Airway
1. Midface hypoplasia may result in varying degrees of airway compromise: From obstructive sleep apnea to critical airway
stenosis
2. Tracheostomy may be required
3. Monobloc or Le Fort III advancement may also be required
D. Abnormal speech and hearing

VII. TREATMENT
A. Multidisciplinary team includes plastic surgeon, neurosurgeon, otolaryngologist, pediatrician, oral surgeon, orthodontist,
pediatric dentist, ophthalmologist, geneticist, child neuropsychologist, speech therapist, social worker, dietician, and nurses
B. Preoperative considerations
1. Parents should be engaged in operative plan of care
2. Preoperative hematocrit with type and cross (~80% perioperative transfusion requirement)
3. Two large-bore peripheral intravenous lines, urinary catheter, and arterial line
4. ICU bed for 24 to 48 hours postoperatively
5. Perioperative antibiotics
6. Perioperative steroids may be used to decrease swelling
7. Prone versus supine positioning depending on involved suture(s) and surgeon preference
a. Special head rest may be necessary
b. Modified prone positioning
i. Greater exposure
ii. Preoperative cervical spine films required to rule out craniovertebral abnormalities
8. Ophthalmic ointment and corneal shields
9. Anesthetic considerations
a. Warming device to maintain normothermia
b. Hypotensive anesthesia
c. Cell saver devices for directed autotransfusion
d. Anti-fibrinolytics (Amicar) and erythropoietin have been used to mitigate bleeding risk
C. Operative interventions
1. Timing: 3 months to 1 year of age (earlier if evidence of elevated ICP)
2. Earlier operation: Patient maintains capacity for dural-induced ossification of small cranial defects
D. Postoperative care
1. ICU monitoring for 24 to 48 hours
2. Regular neurologic checks every 1 to 2 hours
3. Serial hematocrits to evaluate ongoing bleeding
4. Electrolyte abnormalities (especially sodium) due to disruption of hypothalamic-pituitary axis
a. SIADH (syndrome of inappropriate antidiuretic hormone): Low serum sodium, treat with fluid restriction, salt tabs, or
increased sodium in IV fluids
b. Diabetes insipidus: High serum sodium and increased urine output. Treat with fluid resuscitation due to the risk of
dehydration.
5. ICP monitoring (only in select cases)
6. Postoperative fever is very common; postoperative infection is rare
7. Other complications: Venous air embolism, dural lacerations, CSF leak, visual changes, seizures, meningitis, and death

VIII. CRANIOFACIAL (TESSIER) CLEFTS


A. Etiology
1. Lack of fusion of facial processes
2. Lack of migration of mesoderm
3. Possible amniotic banding
B. Extremely rare
1. Incidence: 1:100,000 births
2. *Tessier classification (Fig. 27-4)
3. “Oculocentric”
a. Cranial clefts extend superiorly from the lid margin
b. Facial clefts extend inferiorly from the lid margin
c. Corresponding cranial and facial clefts sum to 14 (e.g., 0 and 14, 1 and 13, and 6 and 8)
d. Tessier 7 cleft
i. Most common of all craniofacial clefts
ii. *Findings: ipsilateral microtia and macrostomia
e. Clefts 0-3: Oral-nasal, Clefts 4-6: Oral-Ocular, Clefts 7-9 Lateral facial
C. Soft-tissue abnormalities predict the underlying bony clefts (e.g., irregular hairline and lid margins)
D. Clefts may involve globe (coloboma) and extraocular muscles

IX. BRANCHIAL ARCH SYNDROMES AND HEMIFACIAL MICROSOMIA


A. Heterogeneous group of syndromes involving Tessier clefts 6, 7, and 8
B. Includes Treacher–Collins–Franceschetti complex, Goldenhar syndrome, and hemifacial (craniofacial) microsomia
Figure 27-4. T essier classification of craniofacial clefts.

C. Etiology
1. Vascular insults during embryogenesis (i.e., stapedial artery thrombosis)
2. Teratogens: Thalidomide and retinoic acid
3. Maternal diabetes
D. Treacher–Collins–Franceschetti complex (mandibulofacial dysostosis, Fig. 27-3C)
1. Genetics
a. Autosomal dominant
b. TCOF1 mutation (chromosome 5)
c. *Craniofacial features: Features are bilateral and symmetrical, Tessier clefts 6 to 8, with hypoplasia of body and
arch of zygoma, mandibular hypoplasia, retrusion of chin, prominent facial convexity, hypoplastic lower eyelids with
coloboma (congenital cleft of eyelid), absence of medial lower eyelashes, and downslanting palpebral fissures, and
upper eyelids show tissue redundancy and pseudoptosis
2. Associated abnormalities
a. Microtia and middle ear anomalies result in conductive hearing loss
b. Cleft palate
c. Abnormalities of hairline
d. Airway compromise
i. Decreased pharyngeal diameter secondary to mandibular hypoplasia
ii. May necessitate early airway intervention
3. Mental status: Normal intelligence
E. Hemifacial (craniofacial) microsomia and branchial arch syndrome
1. Genetics
a. Largely sporadic, occasional familial clustering
b. Incidence: 1 in 4,000 to 5,000 live births
c. Male predominance
d. Bilateral involvement in 10% to 15% of cases
2. Craniofacial features
a. Variable hypoplasia of the skeleton and overlying soft tissues
b. Characteristic mandibular deformity ranging from mild hypoplasia to complete absence of the ramus, condyle, or
temporal mandibular joint
c. Maxillary hypoplasia, upward occlusal cant on affected side, cross bite, open bite, and macrostomia
d. “C” deformity on frontal facial view
e. Orbital dystopia and upper lid colobomas
f. Facial muscle atrophy and weakness
g. External ear abnormalities with variable middle and inner ear anomalies
3. Mental status: Mental deficiency in 10% of cases
4. Treatment
a. Mild cases may not require treatment
b. Mandibular distraction osteogenesis during early adolescence
c. Le Fort osteotomy, bilateral split osteotomy of mandible, and genioplasty may be required in skeletally mature patients
d. External ear reconstruction
e. Audiologic evaluation and treatment for hearing loss
F. Goldenhar-Gorlin’s syndrome (oculoauriculovertebral dysplasia; Fig. 27-3D)
1. Genetics: Majority of cases are sporadic
2. Craniofacial features
a. Within the spectrum of hemifacial microsomia but more severe
b. Prominent frontal bossing, low hairline, mandibular and maxillary hypoplasia, facial muscle weakness, epibulbar
dermoids (ocular dermoid tumors), preauricular skin tags and ear pits, conductive hearing loss, and vertebral
abnormalities
3. Treatment: Similar to hemifacial microsomia

QUESTIONS YOU WILL BE ASKED


1. Virchow’s law.
Growth restriction occurs perpendicular to the affected suture, whereas compensatory skull growth occurs parallel to the
affected suture.
2. The difference between synostotic and deformational plagiocephaly.
Deformational plagiocephaly results from external pressure applied to the pliable fetal or infant skull versus craniosynostosis
which is due to premature fusion of cranial sutures and resultant compensatory growth according to properties of Virchow’s
law.
3. The most common craniofacial cleft.
Tessier cleft 7 resulting in ipsilateral microtia and macrostomia.
4. Characteristic associated findings in syndromic craniosynostosis.
See Section V and Figure 27-3.

THINGS TO DRAW
1. Cranial sutures, skull bones, and pathologic head shapes in craniosynostosis
2. Tessier clefts

Recommended Readings
Bradley JP, Gabbay JS, Taub PJ, et al. Monobloc advancement by distraction osteogenesis decreases morbidity and relapse. Plast Reconstr Surg. 2006;118(7):1585–
1597. PMID: 17102732.
Czerwinski M, Hopper RA, Gruss J, Fearon JA. Major morbidity and mortality rates in craniofacial surgery: an analysis of 8101 major procedures. Plast Reconstr Surg.
2010;126(1):181–186. PMID: 20220557.
Czerwinski M, Kolar JC, Fearon JA. Complex craniosynostosis. Plast Reconstr Surg. 2011;128(4): 955–961. PMID: 21681124.
Fearon JA, Ruotolo RA, Kolar JC. Single sutural craniosynostoses: surgical outcomes and long-term growth. Plast Reconstr Surg. 2009;123(2):635–642. PMID:
19182624.
Oh AK, Wong J, Ohta E, Rogers GF, Deutsch CK, Mulliken JB. Facial asymmetry in unilateral coronal synostosis: long-term results after fronto-orbital advancement.
Plast Reconstr Surg. 2008;121(2):545–562. PMID: 18300974.
Smartt JM Jr, Reid RR, Singh DJ, Bartlett SP. T rue lambdoid craniosynostosis: long-term results of surgical and conservative therapy. Plast Reconstr Surg.
2007;120(4):993–1003. PMID: 17805129.
Tessier P, Kawamoto H, Posnick J, Raulo Y, T ulasne JF, Wolfe SA. Taking calvarial grafts, either split in situ or splitting of the parietal bone flap ex vivo—tools and
techniques: V. A 9650-case experience in craniofacial and maxillofacial surgery. Plast Reconstr Surg. 2005;116(5 Suppl):54S–71S; discussion 92S–94S. PMID:
16217445.
Warren SM, Proctor MR, Bartlett SP, et al. Parameters of care for craniosynostosis: craniofacial and neurologic surgery perspectives. Plast Reconstr Surg.
2012;129(3):731–737. PMID: 22373978.
I. EMERGENCY DEPARTMENT (ED) EVALUATION
A. History
1. Mechanism of injury determines the degree of force
a. Interpersonal violence (usually low energy)
b. Motor vehicle accident (usually higher energy)
2. History, prior facial trauma
3. Time of injury
4. Loss of consciousness?
5. Subjective complaints: Diplopia, blindness, hearing loss, malocclusion, and rhinorrhea
6. Environmental considerations: Chemical exposure?
7. Past medical/surgical history, medications, smoking, and drug abuse
B. Physical exam
1. Trauma patients: ABCs (airway, breathing, circulation) must be first priority
a. *Most facial trauma patients need clinical/radiographic cervical spine (c-spine) evaluation and
management
b. *Over 10% of facial trauma patients have associated c-spine injury
2. Control hemorrhage—nasal packing, pressure dressing to lacerations
3. Adequate lighting, irrigation, and suction are required
4. Inspection: Lacerations, abrasions, burns, edema, symmetry, septal hematoma, and dental occlusion
5. Palpation
a. Skull, orbital rims, zygomatic arches, maxilla, and mandible
b. Assess for symmetry, step-offs, crepitus, and pain
6. Complete cranial nerve exam (prior to administration of local anesthetic) with emphasis on
a. Sensation: Light touch in three divisions of CN V—ophthalmic, maxillary, and mandibular
b. Motor: Test all CN VII branches (temporal, zygomatic, buccal, marginal mandibular, and cervical) and look for
asymmetry
7. Eyes
a. Test visual acuity with pocket card
b. Pupillary response to light
c. Swinging flashlight test to rule out afferent papillary defect (optic nerve injury)
d. Diplopia (horizontal versus vertical)
e. Extraocular movements
i. *Perform forced duction to rule out muscle entrapment if intubated/sedated and periorbital fractures
present
ii. Grasp the sclera (away from cornea) with fine forceps and move the globe into upward/downward/lateral gaze
positions to test for entrapment of extraocular muscles
f. Hyphema or globe injury
g. Enophthalmos
h. Eyelid position
i. Medial canthal tendon stability (versus telecanthus)

______________
*De note s common in-se rvice e xamination topics

8. Ears
a. Inspect external ear on all surfaces for lacerations, perichondral hematoma
b. Observe for Battle sign: Bruising of mastoid process indicative of skull base fracture
c. Otoscopy: Hemotympanum, cerebrospinal fluid (CSF) leak, perforation of tympanic membrane
d. *Hematoma on external ear must be evacuated and bolster placed
9. Nose
a. Assess contour of nasal bones
b. *Use nasal speculum for intranasal exam: Assess for lacerations, nasal obstruction, rule out septal hematoma
(can lead to septal necrosis if untreated)
10. Midface, cheek
a. *Lacerations should be examined for proximity to Stenson’s (parotid) duct (runs in middle third of a line
drawn from oral commissure to tragus)
b. Look for malar flattening and downsloping of palpebral fissure
c. Assess for midface mobility while stabilizing the skull
11. Mandible, oral cavity, occlusion
a. Assess occlusion
i. *Ask patient “Does your bite feel normal?”
ii. Inspect wear facets of teeth—these will intercuspate if occlusion is normal. This is very useful in unresponsive
patients.
iii. Anterior or posterior open bite, cross bite
b. Document loose/missing/broken teeth
c. Inspect oral lining for lacerations or ecchymosis
d. Measure incisal opening distance
e. Submucosal hematoma may indicate mandible fracture
f. Palpate temporomandibular joint (TMJ) in external auditory canal with opening and closing of mouth
g. Note oral hygiene and any carious teeth that may serve as source of infection (Table 28-1)
C. Diagnostic studies
1. Maxillofacial CT is the gold standard to evaluate for facial fractures
a. Coronal views
i. Accurate assessment of nasal bones
ii. Orbital walls and potential herniation of contents into maxillary sinus

b. Three-dimensional reformats are useful in planning complex panfacial fracture reconstruction


c. Herald findings of fracture
i. Osseous deformity
ii. Sinus opacification
iii. Pneumocephalus or soft tissue air/edema
2. Obtain Panorex in cases of mandible fracture (this requires a patient to sit up in the panoramic radiograph device and
therefore cannot be done in unresponsive patients)
3. Consider plain films, three views, to evaluate for missing mandibular segments (e.g., gunshot wounds); also useful
when Panorex not available
D. Soft-tissue injuries
1. Facial field blocks are useful for providing anesthesia in awake patients (see Chapter 10—Fig. 10.7)
a. Supraorbital, supratrochlear, and infratrochlear nerves
i. Forehead/anterior scalp/upper eyelid/glabella
ii. Insert needle in midpupillary line at supraorbital rim, advance medially to capture supratrochlear nerve
b. Infraorbital nerve
i. Lateral nose/upper lip/lower eyelid/medial cheek
ii. Insert needle into superior buccal sulcus above the canine tooth root at midpupillary line 6 to 10 mm below the
infraorbital rim
c. Mental nerve
i. Lower lip/chin
ii. *Insert needle into inferior buccal sulcus at second premolar
d. Cervical plexus, great auricular, transverse cervical nerves
i. Posterior auricle/mandibular angle/anterior neck
ii. *Both great auricular and transverse cervical nerves emerge at Erb’s point
a) 7 cm inferior to tragus
b) Posterior border of sternocleidomastoid (SCM) muscle
iii. Mark patient’s SCM when flexed, locate midpoint from clavicle to mastoid for injection
e. Auriculotemporal, great auricular, lesser occipital, Arnold’s nerve
i. Ear “ring block”
ii. Begin with needle at junction of lobule and cheek and proceed with four injections circumferentially
iii. Avoid superficial temporal artery
iv. Separate injection in external auditory canal for Arnold’s nerve (auricular branch of the vagus nerve, CN X)
2. Laceration repair
a. The face has a robust vascular supply; avoid excessive debridement
b. Repair in layers under minimal tension
c. Copious irrigation with normal saline, remove foreign bodies
d. Deep dermis: 5-0 interrupted buried absorbable sutures (e.g., vicryl and monocryl)
e. Skin: 5-0 or 6-0 interrupted or running permanent suture (e.g., nylon and prolene)
f. In young children, skin closure may be performed with 6-0 fast absorbing gut to eliminate the need for suture removal
g. Nonabsorbable sutures are removed in 5 to 7 days; delayed removal will result in suture tract epithelialization
h. Avoid undermining and/or local tissue rearrangement
i. Partial avulsions: Tissue present on small pedicles will usually survive
3. Scalp
a. Close with surgical staples or running locking absorbable suture (e.g., chromic gut)
b. Avulsions are indication for microvascular replantation
i. Scalp can tolerate 12 to 18 hours cold ischemia time
ii. Superficial temporal or occipital vessels can serve as recipient vessels during scalp replantation.
4. Eyebrows
a. Direction of hair growth helpful in realigning wound edges
b. Inspect within the wound for occult fracture
c. Avoid cautery: Cicatricial alopecia
d. *Temporal branch of facial nerve: Pitanguy’s line
i. 0.5 cm inferior to tragus to 1.5 cm superior to lateral margin of eyebrow
ii. Deep surface of superficial temporal fascia (i.e., temporal parietal fascia) with superficial temporal artery
e. Advance lateral brow if necessary to close, medial brow position more aesthetically important
5. Eyelids
a. Conjunctiva meets the skin at grey line on lid margin
b. Ptosis on exam may indicate levator injury
c. *Rounding and mobility of medial canthus may indicate nasoorbitoethmoid (NOE) fracture (telecanthus)
(normal intercanthal distance 32mm)
d. Epiphora (excessive tearing) indicates possible lacrimal canalicular injury
e. Repair techniques
i. Repair conjunctiva only if large defect present (e.g., 5-0 fast absorbing chromic)
ii. Repair tarsal plate (e.g., 5-0 Vicryl)
iii. Repair lid margin with vertical mattress at gray line using polyfilament (e.g., 6-0 Vicryl)
a) Eversion of closure prevents notching of lid margin
b) Avoids corneal abrasion from monofilament suture
c) May be removed in 5 to 7 days
iv. Keep all suture tails long, tied into an inferior suture knot away from globe
f. Lacrimal system injury
i. Canaliculus courses 2 mm perpendicular to lid margin then heads medially to lacrimal sac and nasolacrimal
apparatus
ii. *Drains into nose at inferior meatus
iii. Laceration to medial third of eyelid ⇒ suspect canaliculus injury
a) Exploration: Place lacrimal probe in punctum and pass it into canaliculus, look for probe within the wound
b) Place silastic lacrimal stent; “Crawford tubes” (±suture repair of duct)
c) Stent remains in place for 2 to 3 months
d) *Jones I and II tests may be used clinically
6. Cheek
a. Stenson duct penetrates buccinator to enter oral cavity opposite second molar; travels with buccal branches of
facial nerve
i. Probe intraoral papilla with 22G angiocath peripheral venous catheter and inject hydrogen peroxide: If duct is
injured, visualize gas bubbles in wound
ii. Repair duct to prevent sialocele, or leave drain
iii. *If sialocele develops, aspirate and apply pressure dressing
b. Nerve injury—can use nerve stimulator up to 48 to 72 hours later
i. Considerable crossover between zygomatic and buccal CN VII branches
ii. Does not require repair if medial to lateral canthus
7. Nose
a. Redundant arterial supply: Lateral nasal, external nasal, septal, and columellar arteries
b. Septum composed of septal cartilage, vomer bone, perpendicular plate of ethmoid, maxillary crest, and premaxilla
c. Septal hematoma
i. Evacuate with needle aspiration or blade to prevent necrosis and septal perforation
ii. Place running quilted 4-0 gut suture
d. Laceration repair
i. Mucosal lining: 4-0 chromic with knots in nasal cavity
ii. Cartilage: 5-0 clear nylon or monocryl
iii. Skin: 6-0 nylon in the skin
e. Avulsion injuries: Consider composite graft (replantation if possible)
i. 50% failure
ii. All grafted material must be within 5 mm of viable tissue
8. Ears
a. Arterial supply: Superficial temporal and postauricular arteries
b. Great auricular, auriculotemporal, Arnold, lesser occipital nerves provide sensation
c. Otohematoma
i. Evacuate with needle or blade to avoid “cauliflower ear”
ii. Compression dressing
a) Xeroform bolster mattressed with 3-0 through and through sutures
b) Remove in 1 week
d. Lacerations
i. May require figure-of-eight sutures in cartilage (clear nylon or absorbable monofilament)
ii. Evert skin margins in key locations (e.g., helix) with mattress sutures
e. Amputation
i. Partial amputation—suture repair
ii. Complete amputation—attempt replantation
iii. Consider leech therapy for venous congestion
iv. Consider dermabrasion of ear part and banking cartilage in dermal pocket
9. Mouth
a. Anatomic landmarks: Philtral columns, philtral dimple, Cupid bow, ver-million border, and white roll
b. Lacerations: Repair mucosa, orbicularis, and skin in layers. Mark white roll with methylene blue or marking pen
prior to administration of local anesthetic

II. FRACTURE EVALUATION AND MANAGEMENT


A. Mandible fractures
1. Anatomy (Fig. 28-1)
a. Mental nerve (CN V3 )
i. Exits skull base from foramen ovale
ii. Courses 2 mm below foramen
iii. *Exits mental foramen at second premolar
iv. *Nerve is closest to buccal cortex at third molar, farthest from buccal cortex at first molar
b. Muscles of mastication (CN V3 ) exert deforming forces of mandible
i. *Lateral pterygoid: Protracts (lowers) mandible
ii. Medial pterygoid: Closes mouth
iii. Temporalis: Elevates and retracts mandible
iv. Masseter: Elevates mandible
v. Geniohyoid, genioglossus, mylohyoid, digastric muscles: Depress mandible
2. The mandible is like a pretzel: Difficult to break in only one location; look for second fracture
3. Classification of fracture—location on mandible, simple versus comminuted, open versus closed, and
intracapsular/extracapsular
4. Teeth in line of fracture should be retained if roots are not fractured
5. MMF (maxillomandibular fixation; also called intermaxillary fixation, or IMF) may be used as a single modality
(controversial) for 4 to 6 weeks
6. Principles of ORIF (open reduction and internal fixation)
a. Indications: Displaced fracture with abnormal occlusion
b. MMF to restore occlusion

Figure 28-1. Mandible anatomy. (Asset provided by Anatomical Chart Co., 2013.)

c. Subperiosteal dissection to expose fracture line


d. Reduction of fracture fragments
e. Rigid fixation using plates/screws, 2.0 mm plating systems
f. Early, active mobility
g. Tension band plate placed along alveolar border
h. Large reconstruction plate along inferior border
7. Fracture subtypes
a. Symphyseal/parasymphyseal fractures. Miniplate fixation with at least two points of fixation
b. Body fractures. Miniplate fixation
c. Angle fractures. Highest complication rate
d. Coronoid fractures-MMF for 2 weeks usually enough
e. Condylar and subcondylar fractures
i. Intracapsular
a) Condylar fractures (head and upper neck)
b) Closed reduction and limited (2 weeks) MMF with early controlled mobilization; rarely ORIF
c) *Open treatment warranted if: (1) Cannot reduce fracture and it precludes ranging the mandible, (2) a
foreign body is present within the TMJ, (3) the condyle has displaced into the middle cranial fossa, and (4)
bilateral condyle fractures with midface fractures to restore vertical height
ii. Extracapsular
a) Subcondylar fractures
b) IMF × 4 to 6 weeks, weekly observation of occlusion after release
f. Pediatric mandible fractures
i. *Avoid immobilization; early active therapy; growth potential allows improvement of occlusion with
time
ii. May require MMF
iii. In the absence of permanent dentition
a) Piriform drop wires
b) Circum-mandibular wires
g. Edentulous mandible
i. Closed fractures with minimal displacement: No dentures, soft diet
ii. Open fractures or those with displacement: ORIF with load-bearing plate
h. Dislocations
i. Anterior displacement of condyle from glenoid fossa
ii. Closed reduction necessary
a) Conscious sedation
b) Intraoral downward and posterior pressure at ramus
8. Indications for tooth removal
a. Grossly mobile
b. Severe periodontal disease
c. Root fracture
d. Exposed apices
9. Common complications
a. Malocclusion/malunion/nonunion
b. Increased facial width, rotation of mandible
c. TMJ ankylosis: Stiffness, pain, limited range of motion
d. Infection: Often treated with I&D, hardware removal generally not required
B. Zygoma fractures
1. Anatomy
a. Zygoma has a quadrilateral shape: Articulates with maxilla, sphenoid, temporal, and frontal bones; fractures are
therefore “tetrapod fractures”
b. Muscle attachments: Masseter, temporalis, zygomaticus major and minor
2. Clinical presentation
a. *Flattening of malar eminence with downslanting palpebral fissure: Lateral canthus attaches to zygoma via
Whitnall tubercle
b. Zygomatic arch fractures may limit the motion of coronoid, resulting in trismus
c. Enophthalmos
d. Infraorbital paresthesia
3. ORIF: Required to restore facial width, malar projection, and orbital dystopia
a. Approaches
i. Upper blepharoplasty incision: Access to zygomaticofrontal junction
ii. Coronal incision: To expose entire arch and lateral orbital rim
iii. Gillies approach
a) Temporal incision behind hair line
b) *Dissect deep to temporalis muscle fascia
c) Reduce posteriorly displaced arch fracture with outward force
iv. Transconjunctival incision: Access to zygomaticomaxillary junction (and orbital floor)
v. Intraoral incision: Dingman elevator placed under arch with outward force
b. Fixation: 1.5- or 2.0-mm plating systems
c. Postoperative arch splint: May wrap tongue depressor in silk tape and bend into bridge shape, secure to face with
tape as buttress to prevent infracturing during sleep (not needed when plated)
d. Zygomaticosphenoid articulation is the most important to assess reduction
C. Orbital fractures
1. Anatomy (Fig. 28-2)
a. Orbit is constructed of seven bones—maxilla, zygoma, sphenoid, frontal, palatine, lacrimal, and ethmoid
b. *Conical/pyramid shape: Optic nerve is ~4 cm posterior to orbital rim
c. Thinnest region is medial wall (lamina papyracea)
2. All orbital fractures require consultation with ophthalmologist to evaluate for ocular trauma
3. Fractures most common in orbital floor and medial wall (lamina papyracea of ethmoid)

Figure 28-2. Skeletal orbital anatomy and the relationship of the superior and inferior orbital fissures and optic foramen. (From Moore KL, Dalley AF II. Clinical
Oriented Anatomy. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins; 1999, with permission.)

4. Dystopia occurs if loss of bony support


5. Enophthalmos
a. Fractures of orbit result in increased intraorbital volume and disrupt ligamentous support of globe
b. During healing, periorbital takes on shape with smaller volume
6. Clinical presentation
a. Periorbital edema
b. Periorbital ecchymosis
c. Diplopia
d. Infraorbtial nerve paresthesia
e. Enophthalmos
f. Orbital rim step-off
g. Limited globe excursion from edema or entrapment
7. Indication for ORIF
a. Persistent diplopia (>2 weeks)
b. Fractures that involve >50% orbital floor or >2 cm2
c. Clinically significant enophthalmos
d. *Entrapment of extraocular muscles (requires emergent intervention, i.e., less than 24 hours, to release
ischemic muscle). Entrapment is determined by assessing extraocular movements or by forced duction testing (see
above, under ED Evaluation and Physical Examination) if unconscious.
8. ORIF
a. Subciliary, transconjunctival, inferior orbital rim incisions
b. *Transconjunctival approach is associated with lowest rate of postoperative ectropion
c. Medpor (porous polyethylene) implant or cranial bone grafts can be used to reconstruct the orbital floor: Secured in
place with screws at infraorbital rim
d. Young children may present with a “trapdoor” floor fracture in which there is no defect but the fracture has
entrapped the extraocular muscle (usually the inferior rectus muscle). The muscle can be released and the orbital
floor usually needs no implant or reconstruction if it feels stable.
9. Associated potential ophthalmic consequences
a. Corneal abrasion
b. Hyphema: Blood in anterior chamber
c. Sympathetic ophthalmia
d. Traumatic optic neuropathy: Traumatic loss of vision
i. Requires surgical decompression, and high-dose steroids
e. *Superior orbital fissure syndrome
i. Effects oculomotor, trochlear, abducens, and trigeminal (lacrimal, frontal, and nasociliary branches)
nerves and ophthalmic vein
ii. Signs
a) Ptosis
b) Proptosis
c) Ophthalmoplegia
d) Numbness in VN V1
e) Dilation and fixation of ipsilateral pupil
f. *Orbital apex syndrome: Same as superior orbital fissure syndrome but with loss of vision due to injury to
optic nerve
g. Traumatic carotid cavernous sinus fistula
i. Proptosis
ii. Ocular bruit
iii. Ophthalmoplegia of CN III, IV, or VI
iv. Treatment: Surgical ligation of carotid artery or coils to block off fistula
D. Nasal bone fractures
1. Nasal anatomy
a. Upper one-third of the nose: Paired nasal bones
i. Fractures common in thinner lower halves of paired nasal bones
ii. Younger patients experience fracture–dislocations of larger segments
iii. Older patients develop comminuted patterns
b. Lower two-thirds of the nose: Paired upper lateral cartilage, lower lateral cartilage
c. Septum consists of quadrangular cartilage, vomer, perpendicular
2. Treatment goals
a. Restoration of function and appearance
b. Wait 6 months before considering revision rhinoplasty or secondary closed reduction plate of ethmoid bone
c. Acutely before edema begins (uncommon) or after swelling resolves (3 to 5 days)
d. Closed reduction should be accomplished within 2 weeks of injury to avoid osteotomies
3. Principles and technique
a. Look for septal hematoma
b. Do not misdiagnose NOE for simple fx as NOE is hard to fix
c. Usually treat closed except with complex facial fractures, inability to obtain good closed reduction, severe
comminution
d. External nose anesthetized by regional block 0.5% lidocaine with 1:200,000 epinephrine
e. Internal nose anesthetized by afrin-soaked pledgets
f. Reduce bridge with elevator and septum and Asch forceps or butter knife
g. Nasal bone must be mobilized before reduction
h. External thermoplast splint and internal nasal splints placed after reduction
4. Complications
a. Subperichondral fibrosis with partial obstruction
b. Synechiae
c. Obstruction of the nasal vestibule from malunited fractures or scar contractures from loss of vestibular lining
d. Osteitis
e. Malunion of nasal fractures with residual deviation
E. NOE fractures
1. Fractures of nasal bones, frontal processes of maxilla, lacrimal bone, and ethmoid bone
2. Markowitz classification: Based on central fragment with medial canthal tendon
a. Type I: Single, noncomminuted, central fragment without medial canthal tendon disruption
b. Type II: Comminuted central fragment without medial canthal disruption
c. Type III: Severely comminuted central fragment with disruption of medial canthal tendon
3. Clinical presentation
a. *Telecanthus (not always seen acutely): Normal intercanthal distance is 30 to 34 mm
b. Foreshortened and depressed nose
c. Lack of nasal support on palpation
d. Subconjunctival hemorrhage
e. CSF rhinorrhea
f. Mobility of the medial canthus on bimanual exam
4. *Commonly includes medial canthal ligament-bearing bone
a. Fracture line through anterior and posterior lacrimal crest
b. Leads to traumatic telecanthus
c. Possible damage to nasolacrimal system, leading to epiphora
5. Septal cartilage fractures: Progressive deviation from warping forces due to perichondrium
6. Treatment
a. Principles
i. Rule out brain injury (frontal lobes, dural tears, and bone fragments in the brain) and coordinate with neurosurgery
ii. Early intervention (very difficult to fix if done as a late reconstruction
iii. Wide exposure; reduce and stabilize anterior orbital rim; restore internal orbital architecture with bone graft;
reconstruct glabella, upper nasal region, medial canthi; and release soft tissue
b. Exposure
i. Usually required two to three separate incisions
ii. Nasofrontal area: Through laceration, midline nasal, or coronal incision (best exposure)
iii. Subciliary or transconjunctival: with lateral canthotomy
iv. Upper buccal sulcus: May be required to obtain adequate reduction
c. Technique
i. Subperiosteal dissection to inferior orbital rim and floor
ii. Asch forceps used intranasally to elevate and reduce nasal fragments
iii. Do not detach canthal ligament from bone fragment if avulsed
iv. Preserve medial canthal ligament attachments to the bone
v. Preserve lacrimal sac and nasolacrimal duct attachment to the bone
vi. Isolate segments containing canthal ligament, place in perfect anatomic reduction, and stabilize with rigid fixation
vii. Preserve and attach all bone fragments
viii. Reduction, rigid fixation
a. Plates/screws if canthal-bearing segment is large enough
b. If canthus is avulsed from bone, reposition using transnasal wires
c. *Vector of wire fixation: Posterior and superior
ix. Bone graft often needed for medial orbital wall and floor and for restoration of nasal dorsum height and contour
(cantilever cranial bone graft or rib graft)
x. External splinting 2 weeks
F. Frontal bone/sinus fractures
1. Anatomy
a. Thick anterior table, thin floor (orbital roof), and thinner posterior table
b. Nasofrontal duct is posterior medial in location and runs through anterior ethmoid bone
c. Drains into middle meatus
d. *Not present at birth, begins to develop at 2 years old, and does not reach adult size until 12 years old
2. Fracture classification
a. Anterior table
b. Posterior table
c. Nasofrontal duct involvement
3. *Forces of 800 to 2,200 lb are required for frontal sinus fractures, 2 to 3× greater than any other facial bone
4. Frequently associated with NOE and midface fractures
5. Clinical presentation
a. Palpable deformity to frontal bone
b. CSF rhinorrhea
c. Paresthesia in pattern of supraorbital and supratrochlear nerves
d. Inferior globe displacement of orbital roof
6. Complications
a. Mucocele; pyomucocele
b. Osteomyelitis
c. Infection of orbital contents
d. CSF rhinorrhea
i. Halo test/ring sign: Fluid is placed on gauze and concentric rings of blood and CSF form, indicating CSF leak
ii. Fluid can be sent for beta transferrin level to confirm leak
7. Indications for operative management
a. Displaced anterior table (leads to contour deformity)
b. Nasofrontal duct involvement or obstruction (leads to mucocele)
c. Depressed posterior table
8. Treatment goals
a. Restoration of contour
b. Isolation of cranial cavity from upper airway
c. Construction of safe sinus
9. *Operative management
a. Displaced anterior table
i. ORIF with low-profile miniplates
ii. If comminuted, IO wiring may be needed
iii. Nasofrontal duct obstruction or posterior table displacement with minimal or no CSF leak. Obliteration of sinus
with bone, fat grafts, or pericranial flaps after exenteration of sinus mucosa
b. Posterior table fracture with CSF leak: Cranialization
i. Exenterate sinus mucosa
ii. Remove posterior table allowing the brain to fill potential space
c. Nasofrontal duct obstruction can result in mucopyocele. To test for patency: Instill methylene blue into sinus and
place cotton tip applicator (i.e., Q-Tip) endonasally for confirmation of flow (Table 28-2)
G. Maxillary fractures
1. Anatomy
a. Four processes: Frontal, zygomatic, palatine, and alveolar
b. Contains maxillary sinus
c. Muscle attachments include facial expression muscles anteriorly and pterygoid muscles posteriorly
d. Three major buttresses that provide strength (Fig. 28-3)
i. Nasomaxillary
ii. Zygomatic
iii. Pterygomaxillary
2. *Le Fort classification (Fig. 28-4)
a. Alternating thick buttresses and thinner segments create distinct fracture patterns
b. Usually involve pterygoid plates
c. Le Fort I: Transverse
i. Fracture at the level of tooth apices above the palate and alveolus
ii. Separates tooth-bearing maxilla from midface
iii. Extends from pyriform aperture posteriorly through nasal septum, anterior maxillary wall, lateral nasal wall, and
pterygoid plates
d. Le Fort II: Pyramidal
i. Fracture crosses nasal bones along zygomaticomaxillary suture
ii. May involve frontal sinus
iii. Upper jaw and nasal bones mobile as single unit
e. Le Fort III: Craniofacial disjunction
i. May be minimally displaced with subtle occlusion problems
ii. Entire midface is mobile and detached from cranial base
iii. Fracture though pterygoid plates at a high level
iv. Simultaneous mobility of maxilla and nasofrontal and zygomaticofrontal regions
3. Vertical or sagittal fractures
a. Fracture sections maxilla in AP plane
b. Split palate, less common than Le Fort
Figure 28-3. Vertical and transverse buttresses of the facial skeleton. (From Mulholland MW, ed. Greenfield’s Surgery. 5th ed. Philadelphia, PA: Lippincott Williams
& Wilkins; 2011.)

Figure 28-4. Le Fort fracture patterns. (From T asman W, Jaeger EA. Duane’s Ophthalmology. 2006 ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005.)

4. Initial management
a. ABCs: Midfacial fractures are associated with high impact injury and concomitant C-spine fracture (10%)
b. IMF reduces fracture and decreases bleeding
5. Treatment
a. Alveolar fractures: Apply arch bars, place segment in occlusion, place IMF wires, 2-0 plates to stabilize fracture
b. Le Fort fractures: Primary bone grafts and rigid fixation
i. IMF 4 to 6 weeks
ii. Ensure proper reduction of nasomaxillary and zygomaxillary buttresses
c. Surgical steps
i. MMF to reestablish proper occlusal relations. This will usually establish the known starting point, mandible to
crania base (may be difficult in the presence of split palate, alveolar, or mandible fx).
ii. Expose widely. May require multiple incisions—coronal, upper buccal sulcus, transconj, depending on the location
of fractures.
iii. Reduce each segment anatomically starting from mandible → maxilla → zygoma → NOE, etc.
iv. Stabilize with mini-plates. Le Fort II must stabilize nasofrontal jx and infraorbital rims; Le Fort III must stabilize
zygomaticofrontal suture.
v. Primary bone grafting utilized in the acute setting. Bridge gaps >0.5 cm of maxillary buttresses, >1.5 cm of antral
wall.
vi. Soft tissue suspension of check to infraorbital rim
vii. Immobilization in MMF is not necessary for the healing of Le Fort fx if rigid fixation is utilized in the fx repair
viii. For Le Fort fx without mobility (<10%), place in MMF with elastics. If occlusion is not restored in 3 days do
ORIF, otherwise keep in MMF for 6 weeks with soft diet.
ix. If the patient is allowed to return to early fx, soft foods only as true rigid fixation in the midface is not completely
attained due to the thin bones and corresponding thin plates and screws
x. If the mandible is fractured at the condyle—cannot rely on mandible to establish proper facial height. ORIF
midface first and star with the zygoma then place the patient in MMF and treat the mandible as indicated
xi. If the palate is fractured it may be helpful to first wire the posterior aspect of the palate for stability before MMF
or any midfacial plating is undertaken
xii. Most common complication of Le Fort is reduced facial height and projection
f. Common inadequate fixation sequelae: Enophthalmos, malocclusion, increased facial width, soft-tissue descent,
facial diastasis, and fat atrophy
g. Complications: Hemorrhage, airway compromise, pneumocephalus, open bite, nonunion, and malunion
H. Temporal bone trauma
1. Clinical signs
a. Facial palsy
b. Bruising over mastoid (Battle)
c. Hemotympanum
I. Palate fractures
1. Indications for surgery
a. Anterior–posterior-oriented fractures with large individual segments and no comminution
b. Palatal splints are used for complex fractures to provide the best vault stabilization
2. Surgical approach
a. Avoid devascularizing the buccal, gingival, or palatal mucosa during fracture exposure
b. Full open reduction must include reduction and stabilization of the palatal vault, dental arch (alveolus and pyriform
aperture), and the four anterior vertical buttresses of the maxilla
c. Place the patient in MMF for 2 to 6 weeks
d. Splints only to supplement fixation

QUESTIONS YOU WILL BE ASKED


1. The bones comprising the orbit
Maxilla, zygoma, sphenoid, palatine, ethmoid, lacrimal, and frontal (see Fig. 28-2).
2. Facial nerve branches
(“two zebras bit my cat”) temporal, zygomatic, buccal, marginal mandibular, and cervical.
3. Patterns of Le Fort fractures
See Figure 28-4. Le Fort I is horizontal maxillary fracture. Le Fort II is pyramidal maxillary fracture. Le Fort III is craniofacial
disjunction. All involve pterygoid plates.
4. The ZMC “tetrapod”
The zygoma has a quadrilateral shape. It articulates with maxilla, frontal, sphenoid, and temporal bones.
5. The facial buttresses and their importance
See Figure 28-3. Four transverse and four vertical paired structural units of thicker bone lend strength and stability and project
the soft-tissue envelope of face.
6. How to diagnose a CSF leak?
Send fluid for β-transferrin.

Recommended Readings
Fraioli RE, Branstetter BF 4th, Deleyiannis FW. Facial fractures: beyond Le Fort. Otolaryngol Clin North Am. 2008;41(1):51-76, vi. PMID: 18261526.
Haug RH, Buchbinder D. Incisions for access to craniomaxillofacial fractures. Atlas Oral Maxillofac Surg Clin North Am. 1993;1(2):1-29. PMID: 8118664.
Sargent LA. Nasoethmoid orbital fractures: diagnosis and treatment. Plast Reconstr Surg. 2007;120(7 Suppl 2):16S-31S. PMID: 18090726.
Sharabi SE, Koshy JC, T hornton JF, Hollier LH Jr. Facial fractures. Plast Reconstr Surg. 2011;127(2):25e-34e. PMID: 21285753.
Yavuzer R, Sari A, Kelly CP, et al. Management of frontal sinus fractures. Plast Reconstr Surg. 2005;115(6):79e-93e; discussion 94e-95e. PMID: 15861045.
I. OVERVIEW
A. From Greek-Ortho: “Straight” or “correct” + Gnath: “jaw”
B. Goals of treatment include restoration of form and function
1. Restoration of ideal facial proportions
2. Restoration of functional occlusion for mastication

II. DENTITION
A. Pediatric: Primary or deciduous teeth
1. Eruption sequence (months)
a. *Incisors: 6 months; first teeth
b. First molars: 12 months
c. Canines: 16 months
d. Second molars: 20 months
2. Nomenclature for the 20 primary teeth
a. Letter system: A–P
b. Mnemonic: All Just Kids Teeth
i. A, right maxillary second molar
ii. J, left maxillary second molar
iii. K, left mandibular second molar
iv. T, right mandibular second molar
B. Mixed dentition: When both primary and secondary teeth are present; age 6 to 9 years
C. Adult: Secondary, permanent
1. Eruption sequence (years)
a. *First molars: 6 to 7; first adult teeth
b. Incisors: 6 to 9
c. Canines: 9 to 10
d. First premolars: 10 to 12
e. Second premolars: 11 to 12
f. Second molars: 11 to 13
g. Third molars: 17 to 21; “wisdom” teeth
2. Numbering (international standard): 1 to 32 (Fig. 29-1A)
a. 1, right maxillary third molar
b. 17, left mandibular third molar

III. DENTAL ANATOMY


A. Crown: Above the gingiva
B. Root: Within the bone
C. Cusp: Protruding portion of occlusal surface
D. Groove: Intruding portion of occlusal surface

IV. TERMINOLOGY
A. Mesial: Toward midline (e.g., incisors are mesial to molars)
B. Distal: Away from midline
C. Buccal: Toward the cheek
______________
*De note s common in-se rvice e xamination topics

Figure 29-1. T eeth (A) and Angle classification of occlusion (B).

D. Lingual: Toward the tongue


E. Overbite: Vertical relationship of the maxillary and mandibular tooth apices
F. Overjet: Horizontal relationship of the maxillary and mandibular tooth apices
G. Proclination: Angulation of apex toward the lips
H. Retroclination: Angulation of apex toward the tongue
I. Apertognathia: Open bite, negative overbite
J. Incisal show: Amount of vertical show of maxillary central incisor in repose
K. Centric occlusion: Maximal intercuspation of teeth
L. Centric relation: Mandibular condyles fully seated in glenoid fossae
M. Open bite: Part of the dentition does not occlude (can be anywhere)
N. Deep bite: A pronounced overbite
O. Crossbite: Can be buccal, neutral (normal), or lingual. Often caused by tilting of the maxillary teeth.

V. *ANGLE CLASSIFICATION (EDWARD HARTLEY ANGLE, “FATHER OF MODERN ORTHODONTICS”)


A. Based on the relationship of maxillary first molar (Fig. 29-1B)
B. Class I: Mesial buccal cusp of maxillary first molar in buccal grove of mandibular first molar
C. Class II: Mesial buccal cusp of maxillary first molar is mesial to buccal grove of mandibular first molar
1. Division 1: Excessive overjet with normal angulation of maxillary incisor
2. Division 2: Retroclination of maxillary incisors
D. Class III: Mesial buccal cusp of maxillary first molar is distal to buccal grove of mandibular first molar

VI. ORTHOGNATHIC SURGERY EVALUATION


A. Close coordination with orthodontist
B. Complete medical and dental history
1. Functional problems: Temporomandibular joint (TMJ) derangement, obstructive sleep apnea (OSA), masticatory
difficulty, history of cleft lip/palate
2. Aesthetic concerns
C. Oral exam
1. Occlusion: Number of dental contacts; Angle classification
a. Curve of Spee: AP curvature of occlusal plane
b. Curve of Wilson: Lateral curvature of occlusal plane
2. Midline: Coincidence (alignment) of maxillary and mandibular central incisors
3. Cant: Discrepancy of occlusal plane from horizontal
4. *Ideal incisal show
a. 2 to 4 mm in women
b. 0 to 2 mm in men
5. Restorations and overall oral hygiene health
6. TMJ: Crepitus, subluxation, and pain
D. Aesthetic evaluation
1. Neoclassical canon (see Rhinoplasty, chapter 30)
a. Measure horizontal thirds and vertical fifths
b. Assess nose–lip–chin relationship
2. Determine facial symmetry
E. Radiographic (cephalometric) evaluation
1. PA and lateral cephalogram ± orthopantomogram (Panorex)
2. Determine convexity/concavity
3. Facial divergence
a. Anteriorly divergent: Soft-tissue pogonion anterior to glabella
b. Posteriorly divergent: Soft-tissue pogonion posterior to glabella
4. *Key anatomic points on lateral cephalogram (Fig. 29-2)
a. Sella: Midpoint of the sella turcica of sphenoid bone
b. Nasion: Most concave point on the nasal bone
c. A point: Most concave point on the maxilla
d. B point: Most concave point on the mandible
c. Normative values (differ based on race/ethnicity, sex)
i. SNA = 82
II. SNB = 80
F. Treatment planning
1. Expansion of the soft–tissue envelope with anterior skeletal movement is generally preferred to the opposite
a. Anterior movements produce a more youthful, rather than aged, appearance
b. Consider but “ignore” normative angles
2. “Decompensate” occlusion
a. Orthodontic correction of proclined/retroclined teeth in preparation for anticipated postoperative occlusion
b. Worsens preoperative occlusion
Figure 29-2. Standard lateral cephalometric tracing with landmarks. FH, Frankfort Horizontal; MP, Mandibular plane; Po, Pogonion; S, Sella; Ba, Basion; A, articulare;
Ptm, Pterygomaxillary fissure; PNS, Posterior nasal spine; PO, Porion; ANS, Anterior nasal spine; OP, Occlusal plane; Or, Orbitale; Pog, Pogonion; Go, Gonion; Me,
Menton; Gn, Gnathion; A, Point A (most posterior point of maxilla cephalad to teeth); B, Point B (most posterior point of mandible caudal to teeth)

3. Virtual surgery can be helpful in preoperative planning


a. Two-dimensional software (e.g., Dolphin)
b. Predicts soft tissue response to skeletal movement
c. Estimates postoperative SNA/SNB angles
d. Three-dimensional treatment planning is also used (e.g., Medical Modeling)
4. Casts, model surgery, and occlusal splints
a. Dental impressions followed by plaster casts
b. Casts enable determination of maximal intercuspation: Centric occlusion
c. Casts facilitate fabrication of occlusal splint to guide skeletal segments into position following osteotomy
i. For “two-piece” Le Fort I cases (i.e., maxillary arch must be widened with sagittal osteotomy), a splint is required
to maintain desired palatal width
ii. For “two-jaw” or “double-jaw” cases (i.e., maxillary and mandibular osteotomies), two splints are required:
Intermediate and final
d. In “double-jaw” cases, facebow transfer is required to establish the relationship of the maxilla to the skull base
i. Bite registration needed to then relate mandibular cast to maxillary cast on articulator
ii. Maxillary cast osteotomy (model surgery) performed on articulator to fashion intermediate splint
iii. Final splint fabricated on separate models mounted on Galetti articulator
5. Arch bars or braces with brackets required

VII. DIAGNOSIS AND TREATMENT


A. *Vertical maxillary excess
1. Long face/“gummy smile” with excess gingival show
2. >4 mm incisor show
3. Mentalis strain
4. Flattened midface
5. Class II malocclusion most common, but can have any occlusion
6. SNA and SNB are decreased; ANB increased
7. Etiology: Open-mouthed breathing–nasal airway obstruction, myotonic dystrophy, adenoid hypertrophy, and familial
8. Treatment: Le Fort I impaction, possible mandibular advancement. With maxillary impaction, mandible will autorotate
into occlusion with maxillary dentition
a. This will improve SNB angle without mandibular osteotomy
b. Concomitant genioplasty sometimes needed to correct relative chin retrusion or midline menton discrepancy
B. Vertical maxillary deficiency
1. Short face: See very little maxillary dentition in repose and with smiling
2. No incisor show
3. Aged, edentulous appearance
4. Prominent chin with jowling
5. Class II malocclusion
6. Increased SNA and SNB angles
7. Treatment: Downfracture Le Fort I with bone grafting, possible mandibular advancement
8. Orthodontics: Curve of Spee (vertical wave in occlusal plane) is corrected postsurgically
C. Maxillary retrusion/midface hypoplasia
1. Flat or dish face
2. Depressed nasal tip and wide alar base
3. Negative overjet
4. Short upper lip
5. Class III malocclusion
6. Decreased SNA; normal to larger SNB; negative ANB
7. Etiology: Often history of cleft lip ± palate, CPAP (continuous positive airway pressure) during childhood
8. Treatment: Maxillary advancement
a. High-winged Le Fort I
i. Improves malar position with one operation
ii. Obviates need for implants or bone grafts
b. Le Fort I via distraction osteogenesis
i. Used in large advancements (>10 mm)
ii. Requires halo mounted to cranium during initiation, activation, and consolidation phases
iii. Unable to precisely establish final occlusion
c. *Le Fort I advancement changes the nasal appearance
i. Widened alar base
ii. Increased tip projection
iii. Increased nasolabial angled.
iii. Narrowing of upper lip show (smaller vermillion)
d. Soft tissue of upper lip moves 0.5 to 0.9 compared with the bone
D. Retrognathia
1. Decreased mandibular projection
2. Obtuse cervicomental angle
3. May have excessive eversion of lower lip
4. Redundant submental soft tissue
5. Class II malocclusion
6. Decreased SNB angle
7. Positive overjet
8. Orthodontic presurgical management seeks to eliminate crowding (limits the amount by which the mandible can be
advanced)
9. Etiology: May have history of Pierre Robin sequence
10. Treatment: Bilateral sagittal split osteotomy (BSSO), possible genioplasty
E. Prognathia
1. Prominence mandible with apparent midface retrusion
2. Mandibular over-rotation
3. Class III malocclusion
4. Increased SNB angle
5. Negative overjet
6. Treatment
a. Consider maxillary advancement only
b. Setback mandible only in severe cases
i. BSSO
ii. Intraoral vertical ramus osteotomy (IVRO)
a) If setback is >10 mm
b) Requires postoperative maxillomandibular fixation (MMF)
F. OSA
1. With severe OSA not amenable to CPAP, “bi-max” advancement is considered
2. Advancement of maxillomandibular skeleton improves airway patency

VIII. OPERATIVE TECHNIQUES


A. Anesthetic considerations
1. Hypotensive anesthesia, and
2. Reverse Trendelenburg positioning (head up) reduces bleeding intraoperatively
B. Le Fort I osteotomy (Fig. 29-3)
1. Upper buccal sulcus incision
2. Leave 2- to 3-mm cuff of tissue on gingiva for closure
3. Avoid parotid papilla
4. Identify infraorbital nerve in midpupillary line
5. Dissect along buttresses in subperiosteal plane
6. Elevate mucosa from nasal floor, septum, and sidewalls
7. Buttress osteotomies
a. Nasomaxillary: Reciprocating saw directed from piriform aperture medial to lateral in horizontal plane
b. Zygomaticomaxillary: Reciprocating saw directed from lateral to medial in horizontal plane
c. Pterygomaxillary: Curved (e.g., Kawamoto) osteotome placed behind maxillary tuberosity into pterygomaxillary
fissure
d. Nasal septum divided using double-ball, guarded osteotome
e. Check lip–tooth relationship with acrylic splint in place
f. Plate fixation at piriform ± maxillary buttress
g. V-Y vestibular closure to prevent excess nasal widening, thinning of upper lip, and downturning of the corner of the
mouth
h. Check occlusion and revise hardware if incorrect
C. Bilateral sagittal split osteotomy (BSSO) (Fig. 29-4)
1. Requires removal of third molars ~6 months preoperatively
2. Intraoral incision over ascending ramus and external oblique ridge
3. Subperiosteal dissection on medial surface of ramus
a. Above the level of occlusal plane at lingula
b. Point where inferior alveolar nerve enters the mandible
4. Step-wise osteotomy in sagittal plane
5. Segments mandible into three segments
a. Proximal (two segments, bilateral): Contains ramus and condyle
b. Distal (one segment, central): Contains body, both branches of inferior alveolar nerve
6. Acrylic splint guides the distal segment into occlusion
Figure 29-3. Versatility of the Le Fort I osteotomy. T he LeFort osteotomy can be varied to position portions of the maxilla in various ways. A: Inferior displacement
(with bone graft) to increase vertical length. B: Impaction to reduce maxillary height. C: Anterior movement of the maxilla is possible. D: T he surgeon may adjust the
width of the maxilla as needed. E: Posterior movement of the maxilla is possible as well.

7. Transbuccal trochar is used to assist in bicortical screw fixation of both mandibular segments
8. Seat condyles in glenoid fossa (centric relation) during fixation
9. Check occlusion on release of MMF and revise hardware if incorrect
D. Intraoral vertical ramus osteotomy (IVRO)
1. Intraoral incision over ascending ramus and external oblique ridge
2. Subperiosteal dissection on lateral surface of ramus
a. Posterior to entrance of inferior alveolar nerve
b. Splits mandible in coronal plane between condyle and coronoid (sigmoid notch)
c. Internal maxillary artery traverses this bony interval
Figure 29-4. T he sagittal split osteotomy. It may be used to move the anterior mandible into a more anterior position (A) or, more rarely, into a more posterior
position (B).

3. Less favored technique of mandibular osteotomy


4. Used when large mandibular setback is required (i.e., Class III malocclusion)
5. No osseous fixation employed; requires MMF postoperatively
E. Genioplasty
1. Lower buccal sulcus incision
2. Leave the cuff of mucosa and mentalis muscle for two-layer closure
3. Subperiosteal dissection centrally and along inferior mandibular border to reveal mental nerves
a. Located between first and second premolars
b. *May course ~2 mm beneath the mental foramen before exiting
4. Transverse osteotomy with sagittal saw
5. Measured step plates may be used to achieve fixation at desired location
F. “Double-jaw” surgery
1. Le Fort I
2. BSSO or IVRO
3. Performed in series, beginning with Le Fort I osteotomy
4. Intermediate and final occlusal splints used to establish occlusion

IX. POSTOPERATIVE CARE


A. Use of elastic bands
1. Temporary elastics used to secure desired occlusion during fixation
2. Often removed prior to extubation
3. May be left in place as “guiding elastics”
a. Class II elastics
i. Used to “correct” a class II malocclusion
ii. Vector from anterior maxilla to posterior mandible
b. Class III elastics
i. Used to “correct” a class III malocclusion
ii. Vector from anterior mandible to posterior maxilla
B. MMF
1. Used in cases of suboptimal fixation or in large/unstable skeletal movements
2. May be kept in place for several months
3. Wire cutters required at bedside in cases of airway compromise and/or emesis
C. Steroid (fluocinolone) cream used for labial swelling
D. Peridex mouth rinses
E. Soft diet
F. Elevate head of bed and employ cool compresses

X. COMPLICATIONS
A. Relapse
1. Surgical: Loss of plate fixation (malunion)
2. Dental: Malpositioned teeth; requires appropriate decompensation
3. Condylar
a. Resorption of bone at condyle (progressive condylar resorption)
b. Related to residual apertognathia and unfavorable TMJ dynamics
4. Soft tissue: Recoil forces from “Moss’ functional matrix”
B. *Paresthesia
1. Risk of inferior alveolar nerve injury in BSSO is 10%
2. About 90% of patients have temporary postoperative symptoms
C. Infection: May require abscess drainage, but not removal of hardware in most cases
D. Hemorrhage
1. Le Fort osteotomy may damage internal maxillary artery branches and pterygoid venous plexus during
pterygomaxillary disjunction
a. Maintain subperiosteal dissection
b. Ensure osteotome placement in pterygopalatine fossa
2. Use hypotensive anesthesia (SBP ~80 mmHg) and reverse Trendelenburg position
E. Ischemia
1. Rare occurrence in Le Fort I advancement, presents as dusky, violaceous mucosal appearance
2. More common in
a. Large anterior movements
b. Cases of cleft lip and palate, and/or
c. Two-piece movements with osseous discontinuity
3. Blood supply to Le Fort I segment
a. Interruption of descending palatine a. after osteotomy
b. Maintained on ascending palatine branch of facial a
c. Anterior branch of ascending pharyngeal a., through mucosal attachments

QUESTIONS YOU WILL BE ASKED


1. The location of the mental and infraorbital foramina and nerves
a. Mental n.: Between first and second mandibular premolars
b. Infraorbital n.: ~1 cm below rim in midpupillary line
2. The course of the inferior alveolar nerve within the mandible
a. Enters mandibular foramen at lingula on medial surface of ramus
b. Moves from medial to lateral cortex distally
c. Curves below mental foramen prior to exiting
3. Characteristic nasolabial changes following Le Fort I advancement
a. Alar widening
b. Increased tip projection
c. Vertical lip shortening
4. The difference between centric occlusion and centric relation
a. Centric occlusion: Maximal intercuspation of the teeth in wear facets
b. Centric relation: Normal resting relationship of mandibular condyle in glenoid fossa
c. CO-CR shift
i. Sacrifice of centric relation in order to obtain occlusion and increase mandibular projection
ii. Common in class III malocclusion

Recommended Readings
1. Legan HL, Burstone CJ. Soft tissue cephalometric analysis for orthognathic surgery. J Oral Surg. 1980;38(10):744-751. PMID: 6932485.
2. Panula K, Finne K, Oikarinen K. Incidence of complications and problems related to orthognathic surgery: a review of 655 patients. J Oral Maxillofac Surg.
2001;59(10):1128-1136; discussion 1137. PMID: 11573165.
3. Proffit WR, T urvey T A, Phillips C. Orthognathic surgery: a hierarchy of stability. Int J Adult Orthodon Orthognath Surg. 1996;11(3):191-204. PMID: 9456622.
I. NASAL ANATOMY (FIG. 30-1)
A. Skin: The thickness of nasal skin is a crucial consideration during preoperative analysis
1. Thickness varies between ethnic populations
2. Thin skin will readily reveal the underlying structural irregularities and is less forgiving to extensive dissection.
3. Thick skin will require more significant cartilage/bone manipulation to achieve the desired aesthetic changes.
4. The skin of the lower third of the nose is almost twice the average thickness of the skin of the upper two-thirds. In
addition, the lower skin is much less mobile and contains more sebaceous glands.
5. The external appearance of the nose is a balance between the skin layer and the osseocartilaginous framework.
6. Patients with thicker nasal skin are more prone to postoperative edema and scar formation, which results in a longer
recovery period.
7. The unique skin-to-skin relationship at the soft triangle predisposes to notching after incisions are made in this
delicate region.
B. Muscle
1. There are four groups of paired nasal muscles that are part of the superficial musculoaponeurotic system (SMAS)
of the face
2. The blood vessels and nerves run on the undersurface of the nasal SMAS. Therefore, the proper plane of
dissection is within a relatively avascular plane deep to the SMAS layer and just superficial to the periosteum and
perichondrium.
3. Elevators shorten the nose and dilate the nostrils: Procerus, levator labii superioris alaeque nasi (opens external valve),
and anomalous nasi.
4. Depressors lengthen the nose and dilate the nostrils: The alar portion of the nasalis muscle (dilator naris posterior) and
depressor septi (can be hyperactive causing decreased tip projection when smiling).
5. The minor dilator is the dilator nasalis anterior.
6. Compressors lengthen the nose and narrow the nostrils: The transverse portion of the nasalis muscle and compressor
narium minor.
C. Blood supply: A rich vascular network is comprised of branches of the ophthalmic, internal maxillary, and facial arteries.
Venous drainage accompanies the arterial supply.
1. The dorsal nasal artery (branch of ophthalmic) perforates the orbital septum superior to the medial canthal ligament
and courses inferiorly along the nasal sidewall.
2. The facial artery bifurcates into the angular artery and the superior labial artery. The latter supplies the nostril sill
and the columella, via the columellar artery.
3. The nasal tip receives blood from the columellar artery, the external nasal branch of the anterior ethmoidal artery,
and the lateral nasal artery (branch of angular)

______________
*De note s common in-se rvice e xamination topics
Figure 30-1. Frontal (above) and lateral (below) views of the anatomy of the external portions of the nose.

4. *With a transcolumellar incision, the columellar branch is divided and blood supply is largely dependent on
the lateral nasal artery, which runs 2 mm superior to the alar groove. Therefore, alar base excision should be
performed conservatively in these instances.
D. Innervation: Motor innervation is from the zygomatic and buccal branches of the facial nerve. Sensation to the external
nose is through divisions of CN V.
1. The radix, the upper dorsum, and upper nasal side walls are supplied by supratrochlear and infratrochlear
branches of the ophthalmic nerve
2. *The external nasal branch of the anterior ethmoid nerve (V1), which emerges between the nasal bones and
the upper lateral cartilages (ULCs), supplies sensation to the distal dorsum and the nasal tip.
3. Sensation to the lower half of the nasal sidewall, columella, and ala is supplied by the infraorbital branches of the
maxillary nerve.
E. Osseocartilaginous framework
1. Bony vault
a. Comprised of the paired nasal bones and the ascending frontal process of the maxilla.
b. Upper one-third to one-half of the nose
2. ULC
a. The cartilaginous vault (or midvault) is comprised of the ULCs and the cartilaginous septum. This vault is actually
one single anatomic entity, which during dorsal reduction is separated into three separate units.
b. At the “keystone” area, the nasal bones broadly overlap the cephalic aspect of the ULCs by about 8 to 10 mm in
the midline
c. At the caudal end of the midvault, *the relationship between the ULC and septum forms the internal nasal
valve, which ideally is 10 to 15 degrees (Fig. 30-2)
d. There is a contiguous perichondrial lining from the undersurface of the ULCs to the septum. During component
dorsal hump reduction, this lining must first be released from the apex of the cartilaginous vault, creating a
“submucosal tunnel” prior to dorsal cartilage resection.
e. Maneuvers that disrupt the smooth dorsal aesthetic lines of the dorsum (e.g., over-resection of the dorsal
cartilage or overly narrowed mid-vault after osteotomies) may result in an “inverted-V” deformity
3. Lower lateral cartilage (LLC): Also known as the alar cartilages, the paired LLCs may be viewed as a tripod which
supports the nasal tip.
a. Each LLC is subdivided into the medial crus, the middle crus, and the lateral crus. The cephalic edge of the domal
segment of the middle crus creates the important “tip-defining point” or pronasale.

Figure 30-2. T he internal nasal valve.

b. The junction between the lateral crus of the LLC and the caudal edge of the ULC is known as the “scroll area.”
At this location, the ULC edge is rolled deep to the more superficial LLC edge.
c. The lateral crus does not extend to the pyriform aperture. Instead, the patency of the posterior aspect of the ala
depends on dense fibrofatty connective tissue and accessory cartilages. These structures contribute to the arch of
the vestibule and provide support for the external nasal valve.
4. Septum
a. The cartilaginous component is the quadrangular cartilage.
b. This articulates with the posterior bony septum, consists of the perpendicular plate of the ethmoid bone, the vomer,
the nasal crest of the maxilla, and the nasal crest of the palatine bone.

II. GOALS AND PATIENT SELECTION


A. Patients seek rhinoplasty for cosmetic and/or functional reasons.
1. In addition to the patient’s concerns about the nose, the surgeon should also respect nasofacial balance, gender-
specific characteristics, and ethnic congruence.
2. In cosmetic patients without nasal obstruction, an important goal is to preserve the nasal airway.
B. Selection of appropriate patients is key to good outcomes
1. Ask the patient specifically what they dislike about their nose and commit to a set of aesthetic/functional goals. Then
examine the patient to determine if those goals can be achieved.
2. Be wary of patients with uncorrectable problems, unrealistic expectations, or unhealthy motivating factors. Poor patient
satisfaction after rhinoplasty is often due to emotion dissatisfaction and not technical failure.
3. The acronym SIMON represents some red flags: Single, immature, male, overly expectant, and narcissistic.
4. Body dysmorphic disorder (BDD)
a. Somatoform disorder marked by excessive preoccupation with a trivial or perceived defect in physical appearance
which causes significant psychological or social impairment
b. Look for compulsive behaviors, intrusive thoughts, camouflaging, and inability to maintain relationships or employment
c. *Affects 7% to 15% of all plastic surgery patients (general population 1% to 2%). Most common sites of
patient concern: Skin, hair, and nose.
d. BDD is a contraindication for surgery. Refer the patient to the psychiatrist.

III. PREOPERATIVE ASSESSMENT (TABLE 30-1)


A. Nasal evaluation: A patient’s nasal history must be elicited in detail, as certain medical conditions, trauma, allergies,
sinusitis, medications, or previous interventions may affect the final outcome.
1. Nasal obstruction: Alteration in normal aerodynamic flow from increased resistance due to medical or anatomic
reasons. Diagnosis is made by history and rhinoscopic examination.
a. *The Cottle maneuver: Lateral cheek traction by the examiner opens a narrow internal valve and results
in clinically noticeable improvement in airflow.
b. Inferior turbinate hypertrophy: Compensatory enlargement occurs on the side opposite of septal deviation.
Combined with the internal valve, the anterior aspect of the inferior turbinate can account for up to two-thirds of
upper airway resistance.
2. Inquire about medications (especially antihypertensives), smoking, drug abuse, previous nasal trauma, and sinus or
nasal surgeries.
3. Document allergic disorders and symptoms: Hay fever, asthma, vasomotor rhinitis, sinusitis, nasal stuffiness, dry
raw pharynx, postnasal drip, and alterations in taste or smell
4. Previous operative notes may be helpful if the patient has had prior rhinoplasty.
B. Nasal analysis
1. Nasal analysis begins with facial analysis.
a. The ideal face is divided into equal vertical fifths and horizontal thirds.
b. Preexisting asymmetries and the appearance of the patient’s maxilla and mandible should be noted prior to surgery.
b. Look for underlying craniofacial diagnoses such as vertical maxillary excess or malocclusion, which may necessitate
intervention prior to rhinoplasty.
c. It is more important for a nose to be in harmony with the rest of the patient’s face than to achieve ideal relationships
within the nose itself.
2. Radix: The area where the nose meets the brow is called the radix.
a. The nasion is at the deepest point of the radix and is the apex of the *nasofrontal angle (ideal = 134
degree for women, 130 degree for men).
b. Because the position of the nasion affects the appearance of the rest of the nose, its location is extremely important
and setting the nasion is often the first step in planning a rhinoplasty.
c. The vertical level (aka takeoff) of the nasion on profile is critical. A low nasion will give the appearance of a heavier
nose, whereas a high nasion will give the appearance of a smaller nose. The nasion should ideally be located at the
level of the supratarsal fold or 6 mm above the medial canthus.
d. The projection is measured from a vertical plane tangent to the cornea. Normal projection is 10 to 14 mm.
3. Dorsum: The ideal dorsum on frontal view is outlined by the dorsal aesthetic lines which begin at the medial brow and
end at the tip-defining points of the nasal lobule.
a. On lateral view, the dorsal line is drawn from the nasion to the tip-defining point. For women, the ideal line is slightly
concave and for men, slightly convex.
b. The nasofacial angle (ideal = 34 degrees for women, 36 degrees for men) is created from a vertical line through
the nasion and the dorsal line
c. The width of the nasal bony base should be about 80% of the alar base on frontal view.
d. The distance between the anterior septal