DERMATOLOGY

Requisites in
ERRNVPHGLFRVRUJ

Dermatologic
Surgery
Edited by
Allison T Vidimos,
RPh, MD, FAAD, FACMS
Chair, Department of Dermatology
Cleveland Clinic Foundation
Cleveland, OH, USA

Christie T Ammirati,
MD, FAAD, FACMS
Associate Professor,
Department of Dermatology
Penn State Milton S. Hershey Medical Center
Hershey, PA, USA

Christine Poblete-Lopez,
MD, FAAD, FACMS
Associate Staff,
Department of Dermatology
Cleveland Clinic Foundation
Cleveland, OH, USA Series editor
DIRK M
ELSTON
Edinburgh London New York Oxford Philadelphia St Louis Sydney Toronto 2009
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First published 2009

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 Acknowledgments
We would like to thank our mentors and teachers
who have taught us the art and science of
dermatologic surgery, our residents, fellows and
medical students who have given us the privilege
and pleasure of teaching them, and our patients
who put their trust in us and challenge us to be
Dermatologic surgery dedications
This text is dedicated to my parents Al and
Audrey Vidimos, my brothers Scott, David and
Dan, my husband Todd Stultz, and daughters
Katherine and Kristen for their love, support,
encouragement, and inspiration.
Allison T Vidimos
This text is dedicated to my children Emma and
Nicholas and my parents Bob and Bee Travelute,
who inspired me to always reach higher, and to
my husband Chris, who held the ladder so I could
climb.
Christie T Ammirati
better physicians every day. Special thanks go
to the the art and photography departments at
Cleveland Clinic, especially Joe Pangrace, Bill
Garriott, Beth Halasz, and our dermatology
department photographer, Flora Williams.
This text is dedicated to my husband, Seevee,
who has given me unconditional love and the
support to pursue what I truly enjoy, most evident
in this endeavor; to my children, Veto, Samee,
and Neo, who are the source of my strength
and inspiration; to my parents, who taught me
the value of education; to all my mentors, from
whom I learned the art of surgical technique; and
to all the residents and fellows to whom I’ve tried
to teach the importance of this art.
Christine Poblete-Lopez

Erin J. Allen, md
Providence Dermatologic Surgery
Portland, OR
Christie T. Ammirati, md
Associate Professor of Dermatology
Department of Dermatology
Penn State Milton S. Hershey Medical Center
Hershey, PA
Philip L. Bailin, md
Program Director, Dermatologic Surgery
and Cutaneous Oncology
Department of Dermatology
Cleveland Clinic Foundation
Cleveland, OH
Ashish C. Bhatia, md
Department of Dermatology and
Dermatologic Surgery
DuPage Medical Group,
Naperville, IL
Assistant Professor of Clinical Dermatology
Department of Dermatology
Northwestern University – Feinberg School
of Medicine
Chicago, IL
Elizabeth Magill Billingsley, md
Associate Professor of Dermatology
Department of Dermatology
Penn State Milton S. Hershey Medical Center
Hershey, PA
Lisa B. Campbell, md
Chief of Dermatology and Dermatologic
Surgery
Geisinger Health System Western Region
Geisinger Medical Group
State College, PA
T. Minsue Chen, md
Fellow, Mohs Research in Advanced
Dermatologic Surgery Education
Mohs and Dermasurgery Unit
Department of Dermatology
University of Texas, M. D. Anderson Cancer
Center
Houston, TX
Contributors
Theresa Dressler Conologue, do
Director, Cosmetic Dermatology Service
Geisinger Medical Center
Danville, PA
Daihung Vu do, md
Instructor in Dermatology
Associate Director of Dermatologic Surgery
Department of Dermatology
Beth Israel Deaconess Medical Center
Boston, MA
John Ebner, do
Department of Dermatology
Cleveland Clinic Foundation
Cleveland, OH
Gregory J. Fulchiero Jr, md, MSBioEng
Dermatologic Surgery and Cutaneous
Oncology
Department of Dermatology
UT Southwestern Medical Center
Dallas, TX
Christopher Charles Gasbarre, DO
Department of Dermatology
Cleveland Clinic Foundation
Cleveland, OH
Lisa M. Grandinetti, md
Department of Dermatology
Cleveland Clinic Foundation
Cleveland, OH
Joseph F. Greco, md
Clinical Instructor
UCLA Division of Dermatology
Department of Medicine
David Geffen School of Medicine at UCLA
Los Angeles, CA
viii Contributors

Christine M. Hayes, md Christine Poblete-Lopez, md

Associate Professor of Dermatology Associate Program Director
Department of Dermatology Department of Dermatology
Boston University School of Medicine Cleveland Clinic Foundation
Boston, MA Cleveland, OH

Christopher Riddell Jones, md Matthew R. Ricks, md

Department of Dermatology LtCol, USAF, MC, SFS
Penn State Milton S. Hershey Medical Center Chief of Mohs Surgery
Hershey, PA Wilford Hall Medical Center
Lackland AFB, TX
Ken K. Lee, md
Director of Dermatologic and Laser Surgery Christopher B. Skvarka, md
Associate Professor of Dermatology, Surgery, Department of Dermatology
Otolarynogology – Head and Neck Surgery Hahnemann Hospital
Oregon Health and Science University Drexel University College of Medicine
Portland, OR Philadelphia, PA

Victor J. Marks, md Aashish Taneja, md

Department of Dermatology Department of Dermatology
Geisinger Medical Center Wayne State University
Danville, PA Dearborn, MI

Edward V. Maytin, md, PhD Leonid Benjamin Trost, md

Staff, Dermatology Department of Dermatology
Cleveland Clinic Foundation Cleveland Clinic Foundation
Assistant Professor of Molecular Medicine Cleveland, OH
Cleveland Clinic Lerner College of Medicine
of Case Western Reserve University Allison T. Vidimos, RPh, md
Cleveland, OH Chair, Dermatology
Cleveland Clinic Foundation
Susan Teri McGillis, md Cleveland, OH
Director, Dermasurgery Center
Lancaster, PA Paula S. Vogel, md
Col (Ret), USA, MC
Jon G. Meine, md Mohs Surgeon
Staff, Department of Dermatology, Section Dermatology Associates
of Dermatologic Surgery and Cutaneous San Antonio, TX
Oncology
Cleveland Clinic Foundation Rungsima Wanitphakdeedecha, md
Cleveland, OH Department of Dermatology
Faculty of Medicine Siriraj Hospital
Allison Jo Moosally, md Mahidol University
Clinical Associate Staff Bangkok, Thailand
Department of Dermatology
Cleveland Clinic Foundation Andrea Willey, md
Cleveland, OH Assistant Clinical Professor
Department of Dermatology
Tri H. Nguyen, md University of California, Davis
Director of Mohs/Dermatologic Surgery Davis, CA
Associate Professor
Mohs and Dermasurgery Unit Brittany Wilson, md
Department of Dermatology Department of Dermatology
University of Texas, M. D. Anderson Cancer Oregon Health and Science University
Center Portland, OR
Houston, TX
 Contributors ix

Oliver J. Wisco, do Summer R. Youker, md

Maj, USAF, MC, FS Assistant Professor of Dermatology
Department of Dermatology Saint Louis University
Wilford Hall Medical Center St Louis, MO
Lackland AFB, TX

Justin G. Woodhouse, md
University Dermatologists, Inc.
South Euclid, OH
Also in the series
Requisites in

Dermatology
Series Editor: Dirk M Elston

Dermatopathology
Dirk M Elston and Tammie Ferringer

Cosmetic Dermatology
Murad Alam, Hayes B Gladstone,
and Rebecca C Tung

Pediatric Dermatology
Howard B Pride, Albert C Yan,
and Andrea L Zaenglein

Dermatologic Surgery
Allison T Vidimos, Christie T Ammirati,
and Christine Poblete-Lopez

General Dermatology
Kathryn Schwarzenberger, Andrew E Werchniak,
and Christine J Ko

The Requisites in Dermatology series of textbooks
is designed around the principle that learning
and retention are best accomplished when
the forest is clearly delineated from the trees.
Topics are presented with an emphasis on the
key points essential for residents and practicing
clinicians. Each text is designed to stand alone as
a reference or to be used as part of an integrated
teaching curriculum. Many gifted physicians
Series foreword
have contributed their time and energy to create
the sort of texts we wish we had had during our
own training and each of the texts in the series
is accompanied by an innovative on-line module.
Each on-line module is designed to complement
the text, providing lecture material not possible
in print format, including video and lectures with
voice-over. These books have been a labor of love
for all involved. We hope you enjoy them.
Series dedication
This series of textbooks is dedicated to my wife
Kathy and my children, Carly and Nate. Thank
you for your love, support and inspiration. It is
also dedicated to the residents and fellows it has
been my privilege to teach and to the patients
who have taught me so much.
Dirk M Elston

This text is designed to cover the essentials of
dermatologic surgery in a style that is straight
forward and easily understood. Each topic is
presented as a concise, yet thorough, review,
and each chapter is paired with an on-line
Volume preface
lecture. In this manner, the text acts as an over­
view for students learning the surgical aspects
of dermatology, a focused study guide for
dermatology residents, and a ready reference for
those in practice.
 Acknowledgments
We would like to thank our mentors and teachers
who have taught us the art and science of
dermatologic surgery, our residents, fellows and
medical students who have given us the privilege
and pleasure of teaching them, and our patients
who put their trust in us and challenge us to be
Dermatologic surgery dedications
This text is dedicated to my parents Al and
Audrey Vidimos, my brothers Scott, David and
Dan, my husband Todd Stultz, and daughters
Katherine and Kristen for their love, support,
encouragement, and inspiration.
Allison T Vidimos
This text is dedicated to my children Emma and
Nicholas and my parents Bob and Bee Travelute,
who inspired me to always reach higher, and to
my husband Chris, who held the ladder so I could
climb.
Christie T Ammirati
better physicians every day. Special thanks go
to the the art and photography departments at
Cleveland Clinic, especially Joe Pangrace, Bill
Garriott, Beth Halasz, and our dermatology
department photographer, Flora Williams.
This text is dedicated to my husband, Seevee,
who has given me unconditional love and the
support to pursue what I truly enjoy, most evident
in this endeavor; to my children, Veto, Samee,
and Neo, who are the source of my strength
and inspiration; to my parents, who taught me
the value of education; to all my mentors, from
whom I learned the art of surgical technique; and
to all the residents and fellows to whom I’ve tried
to teach the importance of this art.
Christine Poblete-Lopez

Surgical anatomy of the
head and neck
Joseph F. Greco and Christopher B. Skvarka
The essentials of dermatologic surgery must be
founded on a fundamental and thorough under­
standing of the head and neck anatomy.This ­chapter
begins with an outline of important topographic
landmarks and cosmetic units before focusing on
the musculature, nerve anatomy, vasculature, and
lymphatics of the head and neck. Special anato­
mic structures and regions such as the parotid
gland and scalp are addressed as well. Emphasis
has been placed on the boundaries of anatomic
regions and danger zones as well as the spacial
relationships among clinically relevent structures.
Topographical landmarks
Key Points
• The bony and muscular landmarks of the head
and neck aid in locating underlying structures.
• The supraorbital, infraorbital, and mental
foramina lie on the midpupillary line.
• The masseter muscle aids in locating the facial
artery and Stenson’s duct (parotid duct).
• The sternocleidomastoid muscle divides the neck
into anterior2 and posterior triangles.
The important topographical landmarks of the
head and neck are formed primarily by underlying
bones and musculature, but superficial accepted
divisions are also made. These landmarks and
divisions are important cosmetically and are used
in communication by the cutaneous surgeon.
The scalp is divided into four areas – frontal,
parietal, temporal, and occipital. The frontal scalp
extends from the forehead to the vertex and is
bordered by the parietal and temporal regions.
The occipital scalp is located at the inferior por­
tion of the scalp, and overlies the occipital bone.
The forehead meets the frontal scalp and extends
down to the eyebrows and glabella. The glabella
lies between the eyebrows superior to the nasal
root. Vertical furrows (glabellar lines) are accen­
tuated over this region when frowning.
The frontal, maxillary, zygomatic, temporal,
and mandibular bones all form prominent bony
surface markers – the orbital rims, zygomatic
ERRNVPHGLFRVRUJ
1
Chapter
Table 1-1  The orbital rim
Border Bones
Superior Frontal bone
Lateral Frontal process of zygomatic bone
Inferior Zygomatic bone laterally and maxillary bone
medially
Medial Frontal bone superiorly and maxilla inferiorly
arch, mastoid process, and mental protuberance.
The orbital rim is formed by contributions from
the frontal, zygomatic, and maxillary bones (­Table
1). Of note, the medial canthal ligaments are
1-�
easily palpated at the medial rim.
Immediately above the superior orbital rim
lies the first of the three major foramina that can
be found along a vertical, midpupillary line imag­
ined approximately 2.5 cm lateral to the midline
(Fig. 1-1). The supraorbital, along with the
­infraorbital and mental foramina will be discussed
further in the sensory innervation of the head and
neck section.
The prominence of the cheek or “cheekbone” is
formed by the malar eminence of the ­zygoma­tic
bone. The buccal fat pad fills the area beneath
this eminence and gives fullness to the cheek. The
zygomatic arch extends from the malar eminence
towards the external acoustic meatus and is formed
by the temporal process of the zygomatic bone
and the zygomatic process of the temporal bone.
The zygomatic arch also divides the temporal fossa
superiorly from the infratemporal fossa inferiorly.
The temple is a well defined danger zone where
the temporal branch of the facial nerve and the
superficial temporal artery and vein lie vulnerable
to injury (Table 1-� 2). The danger zones and areas
of susceptibility to injury are characterized later
in this chapter.
The auricle is the entire visible portion of the
external ear with many named processes (Fig. 1-2).
The rim of the auricle is known as the helix, which
runs with a paired prominence, the anti­helix. The
antihelix runs anterior to the helix and divides
 Dermatologic Surgery

Frontal bone Parietal bone

Midpupillary line
Supraorbital foramen
2.5cm

Temporal bone
Nasal bone
Infraorbital foramen

Mastoid process

Zygomatic arch
Maxillary bone
Ramus of mandible

Angle of mandible

Body of mandible

Mental foramen
Figure 1-1  Bony landmarks of the skull and foramina

into two crura. Between these crura, the named
triangular fossa appears. The curved depression
between the helix and antihelix is referred to as
the scapha. Inferior to the antihelix lies a deep
cavity known as the concha. Anterior to the con­
cha, the tragus arises as an eminence in front of
the external acoustic meatus. ­Opposite from the
tragus (separated by the intertragic notch) is a
small tubercle called the antitragus.
Behind the ear lies the mastoid process of the
temporal bone. It is a bony prominence that, after
adolescence, protects the facial nerve as it exits
the stylomastoid foramen.  Anterior to the ear lies
the condyle of the mandibular ramus, which can
be palpated as the mouth opens and closes. The
angle of the jaw and prominence of the chin are
formed by the mandibular angle and mental pro­
tuberance, respectively.
The masseter muscle attaches to the ­zygomatic
arch and inserts on the ramus of the mandible.
It can be palpated most easily while the teeth
Table 1-2  Borders of the temple
Border
Inferior Zygomatic arch
Anterior Tail of the eyebrow
Superior Coronal suture line
Posterior Temporal hairline
are clenched. The facial artery may be found and
palpated near the antero-inferior border of the
masseter.
The nasal bones, alar cartilages, and anterior
nasal spine of the maxilla form the palpable bor­
ders of the nose. The nasal bones form the supe­
rior root of the nose and the anterior nasal spine
can be palpated at the root of the columella.
The labial area is bordered by the nose, medial
cheek, and mental chin. This area is separated from
the cheek by the melolabial crease. The upper lip

ERRNVPHGLFRVRUJ
 1

Chapter
Surgical anatomy of the head and neck 

ah antihelix hr helical root/crus

at antitragus in intertragic notch
atn auriculotemporal nerve l lobule
c conchal bowl sf scaphoid fossa
cav cavum of conchal bowl sta superficial temporal artery
cym cymba of conchal bowl stv superficial temporal vein
ea external auditory meatus tf triangular fossa
h helix tr tragus

Figure 1-2  Anatomy of the ear, superficial temporal artery, and auriculotemporal nerve

is divided in half by the philtrum. The philtrum is
a central linear depression bordered by two verti­
cal columns extending from the columella to the
vermillion border of the upper lip. At this inferior
border, the columns help to create a contoured
double curve, resembling Cupid’s bow.
Continuing inferiorly, the most important
­superficial landmark of the neck is the sternoclei­
domastoid muscle. When contracted, it is easily
palpated. See Table 1-� 3 for a discussion of the
sternocleidomastoid muscle. This muscle divides
the neck into anterior and posterior triangles (see
Table 1-�4 for information on the anterior ­triangle
and Table 1-15 for the posterior triangle). The
­anterior triangle can be subdivided into the muscu­
lar, carotid, digastric, and submental triangles.
Of note, the spinal accessory nerve is suscep­
tible to injury in the posterior triangle. Injury
­results in paralysis of the sternocleidomastoid and
trapezius muscles.

ERRNVPHGLFRVRUJ
 Dermatologic Surgery
Table 1-3  The sternocleidomastoid muscle
Origin Two heads – medial head attaches to the
sternum; lateral head attaches to the medial
third of the clavicle
Insertion Mastoid process of the temporal bone and
lateral portion of the superior nuchal line
Innervation Accessory nerve (cranial nerve XI)
Action Acting alone, a single sternocleidomastoid
muscle turns the head towards the ipsilateral
shoulder in an upward glance; in tandem, both
sternocleidomastoid muscles draw the head
forward
Comments The two originating heads of each
sternocleidomastoid muscle form a depression
referred to as the lesser supraclavicular fossa;
torticollis is due to the permanent contracture
of the sternocleidomastoid
Parotid gland and duct
Key Points
• The parotid glands are the largest paired salivary
glands.
• The facial nerve pierces the parotid gland soon
after leaving the stylomastoid foramen.
• The parotid duct may be palpated as it courses
over the masseter muscle.
The parotid gland is an anatomic landmark
deserving of special consideration. It is a ­triangular-
shaped salivary gland nestled anterior to the auri­
cle within the borders of the zygomatic arch and
mandible (Fig. 1-� 3, Table 1-�
5). It is anchored into
place by a fibrous fascial capsule contiguous with
the deep facia of the neck. The substance of the
gland houses and protects the facial nerve as it
branches into a superior temporofacial and infe­
rior cervicofacial division. The five well known
branches of the facial nerve originate from these
divisions prior to exiting the different poles of the
parotid gland (Table 1-� 6).
The parotid duct emerges from the gland at
its upper anterior pole and courses over the mas­
seter muscle and buccal fatpad (Fig. 1-� 4). Here
it turns medially to pierce the buccinator muscle
and ­ enters the oral mucosa opposite the second
upper molar (Fig. 1-� 5). The duct runs approxi­
mately one fingerbreadth inferior to the zygomatic
arch, between the transverse facial artery and
buccal branch of the facial nerve. With the jaw
clenched, the parotid duct may be palpated as a
firm cord along the middle third of a line drawn
from the earlobe to a point between the oral com­
missure and the nasal ala as it runs atop the mas­
seter. The duct is most vulnerable in this ­location
ERRNVPHGLFRVRUJ
Table 1-4  The anterior triangle
Boundary
Anterior Median line of neck
Posterior Anterior border of sternocleidomastoid
muscle
Superior (base) Inferior border of mandible
Roof Skin, SMAS, platysma, and deep fascia
of neck
Floor Inferior and middle pharyngeal constric­
tors; thyrohyoid and hyoglossus muscles
(carotid triangle); mylo­hyoid and
hyoglossus muscles (digastric triangle),
mylohyoid muscle (submental triangle)
during surgical procedures. ­Transection will result
in extravasation of a clear watery fluid. If left
­unrepaired, an external fistula may develop.
Thin watery saliva and thicker mucous of the
parotid gland mediated by sympathetic and para­
sympathetic fibers respectively. Cutaneous sen­
sory innervation over the parotid gland is carried
by the auriculotemporal nerve. Vascular supply
and lymphatic drainage of the parotid area are
des­cribed elsewhere in this chapter.
Contour lines and cosmetic
units
Key Points
• Contour lines separate the face into anatomic
subunits.
• Regional variablility in skin structure impacts the
dermatologic surgeon’s choice of repair.
• Free margins are a type of contour line.
Contour lines are the natural lines of demarcation
that divide the face into several cosmetic units,
such as the forehead and nose (Table 1-� 7). Gen­
erally speaking, the skin texture and color is con­
sistent within each cosmetic unit and may vary
considerably among them. This is due in part to
the differences in the density of sebaceous glands,
terminal hair follicles, thickness and elasticity of
the skin. The highly thick and sebaceous skin of
the nose, for example, lies in stark contrast to the
neighboring thin and highly lax skin of the eyelid.
Defects in one cosmetic unit are therefore best
repaired with skin of that same cosmetic unit. The
dermatologic surgeon must consider this regional
variability during reconstructive surgery. Surgical
incisions may be placed so that the final scar lies
along or parallel to contour lines. Incisions that
violate this principle by crossing the demarca­
tion lines may distort anatomic units and result in
highly perceptible scarring.
 1

Chapter
Surgical anatomy of the head and neck 

bfp buccal fat pad orb or orbicularis oris

fa facial artery pd parotid duct
fv facial vein scm sternocleidomastoid muscle
ma masseter muscle sta superficial temporal artery
orb oc orbicularis oculi tfa transverse facial arter
zm zygomaticus major

Figure 1-3  Anatomy of the parotid gland and related structures

Table 1-5  Borders of the parotid gland Table 1-6  Facial nerve branches and the parotid gland
Superior Posterior two thirds of zygomatic arch Exiting pole of the
Facial nerve branch parotid
Posterior Posterior border of mandibular ramus
Temporal (temporofacial division) Superior
Inferior Angle of mandible
Zygomatic (temporofacial division) Anterosuperior
Anterior Highly variable
Buccal (temporofacial division) Anterior
Floor Posterior half of masseter
Marginal mandibular Anteroinferior
Roof Integument, parotid fascia
(cervicofacial division)
Cervical (cervicofacial division) Inferior

Free margins are a unique type of anatomic

unit characterized by skin edges that are ­separated
from neighboring tissue by an open cavity. Exam­
ples include the lips, eyelids, helical rims, nasal
alae, and columella. Defects and repairs in close
proximity to free margins may have tension forces
that push or pull on the margin. Distortion may
result in both aesthetic and functional impairment
such as eversion of the eyelid (ectropion) or lip
(eclabion).
Cosmetic units may be further divided into
subunits for anatomic classification. This permits
more precise localization of cutaneous neoplasms
especially in patients presenting with numerous
lesions.

ERRNVPHGLFRVRUJ
 Dermatologic Surgery

b buccal branch (VII) pd parotid duct

bfp buccal fat pad pg parotid gland
bz buccal/zygomatic nerve anastomoses t temporal branch (VII)
fa facial artery tfa transverse facial artery
fv facial vein z zygomatic branch (VII)
orb oc orbicularis oculi zm zygomaticus major

Figure 1-4  Anatomy of the parotid duct and facial nerve

The superficial The superficial musculoaponeurotic system

musculoaponeurotic system
(SMAS)
Key Points
• The fibromuscular layer is composed of the
muscles of facial expression and enveloping fascia.
• Muscular contraction is transmitted evenly to the
skin and adjacent muscles via this system.
• The SMAS permits complex facial movements
and contributes to the symmetry of the face.
• It provides an anatomic plane for dissection and
protection to neurovascular structures.
• It acts a barrier to infection.
(SMAS) lies just deep to the subcutaneous fat and
contains two layers of fascia that split to envelop
the muscles of facial expression. The breadth of
the SMAS is described in Table 1-� 8. In addition
to these musculofascial connections, the SMAS
bonds to the skin via fibrous strands. Collectively,
this system augments and harmonizes facial
movements, while acting as a screen to prevent
the spread of infection from superficial to deep
regions (Fig. 1-�
6).
Knowledge of the SMAS aids the cutaneous
surgeon in predicting the location of major neuro­
vascular structures. Arteries and sensory nerves of
the face are found within the subcutaneous fat or

ERRNVPHGLFRVRUJ
 1

Chapter
Surgical anatomy of the head and neck 

an facial nerve anastomoses fv facial vein

b buccinator muscle m masseter muscle
bfp buccal fat pad pd parotid duct
dao depressor anguli oris pg parotid gland
fa facial artery
* parotid duct piercing buccinator muscle
* marginal mandibular nerve traveling with facial artery
Figure 1-5  Parotid duct as it pierces the buccinator muscle

Table 1-7  Cosmetic units and contour lines
of the face
Contour line
�  Nasolabial fold
�  Nasofacial sulcus
�  Mentolabial crease
�  Preauricular sulcus
�  Eyelid margins
�  Philtral columns/crest
�  Alar contours
�  Vermillion border
�  Eyebrows
�  Hairline
at the SMAS–subcutaneous fat junction. All mo­
tor nerves course below the SMAS. A sub-SMAS
Cosmetic unit dissecting plane is attractive owing to its ­relatively
avascular nature. However, the risk to the motor
�  Forehead
nerves precludes use of the sub-SMAS plane in
�  Nose most locations. The subcutaneous fat superficial
�  Cheek to the SMAS is therefore the ideal dissecting
plane. An exception occurs over the pre-parotid
�  Eye
cheek where the motor fibers of the facial nerve
�  Lip lie protected within the substance of the parotid
�  Chin gland.
Of note, the temporal branch of the facial
�  Ear
nerve lies just deep to the thin superficial tem­
poral ­fascia on the medial temple. On the lateral
temple, the auriculotemporal nerve and ­superficial
temporal vessels are located in the subcutaneous
fat above the superficial temporal fascia.

ERRNVPHGLFRVRUJ
 Dermatologic Surgery

Table 1-8  SMAS relationships Skin tension lines of the face

Region SMAS attachment site (STLs)
Posterior Inserts onto the mastoid process and fascia
(occiput) of sternocleidomastoid muscle; envelops
Key Points
occipitalis • Skin tension lines are the distinctive furrowed or
wrinkled lines on the face.
Superior Forms the galea aponeurotica to unite the • Dynamic and relaxed STLs lie perpendicular to
(scalp) occipitofrontalis muscle; lacks muscle fibers the action of underlying muscle fibers.
Forehead Envelops frontalis muscle • Lines become more visible and deeper with age
and sun damage.
Temporal Continuous with the superficial temporal fascia
• Knowledge of the skin tension lines is required
scalp
for successful cutaneous surgery and proper use
Zygomatic SMAS is discontinuous above and below of cosmetic injectables.
arch this insertion point; the actions of the upper
and lower muscles of facial expression are Tension, created by the intermittent contraction
functionally separated here of the muscles of facial expression, is transmit­
Cheek Deep leaflet of the SMAS fuses with the parotid ted by fibrous strands from the SMAS to the skin.
and masseteric fascia; envelops muscles of The elasticity of the skin with youth opposes this
facial expression tension and maintains a smooth appearance. With
Anterior Continuous with the superficial cervical fascia; age, the elastic fibers decrease in their ability to
(neck) envelops platysma resist tension, and collagen fibers elongate, decrease
Midfacial Devoid in areas; not well delineated in size, and become cross-linked. With damaged
region collagen and elastin, linear wrinkles form along
the attachments of the SMAS to the skin.

* SMAS fibers connecting the underlying temporalis muscle to the skin

Figure 1-6  Superficial musculoaponeurotic system (SMAS)

ERRNVPHGLFRVRUJ

Surgical anatomy of the head and neck
Figure 1-7  Skin tension lines
Generally these wrinkles, termed skin tension
lines (STLs), run perpendicular to the underlying
muscle fibers (Fig. 1-� 7). For example, the STLs of
the forehead are horizontal because the frontalis
muscle contracts vertically. The skin tension lines
of the lateral periocular skin (crow’s feet) radiate
away from the lateral canthus, as the fibers of the
orbicularis oculi circumferentially wrap from the
superior to inferior eyelid. The horizontal wrinkles
of the upper eyelid, which at first seem to contra­
dict this principle, lie perpendicular to the axis of
the underlying levator palpebrae superioris.
Surgical planning must include a thorough
knowledge of the STLs. The reconstruction of sur­
gical defects should be designed to minimize per­
ceptible scarring. One such way is to align the long
axis of a repair within or parallel to the STLs. This
places the scar under the least amount of tension,
allowing the scar to fall within a natural wrinkle.
Wounds close more easily in this orientation, as
the skin is approximately three times more disten­
sible perpendicular to the STLs than parallel.
In elderly patients with severe sun damage,
the relaxed STLs will be obvious to any observer.
However, certain techniques may be utilized to
accentuate these lines where the static wrinkles
ERRNVPHGLFRVRUJ
1
Chapter

may not be so noticeable. Furrows can be accen­
tuated by asking patients to perform exaggerated
facial expressions, such as smiling, frowning,
puckering lips, or whistling. Active manipulation
of the skin by a gentle pinch or massage may also
reproduce the natural folds and tension lines.
STLs may be softened or eliminated by cos­
metic injectable treatments. Injectable botulinum
toxin targets the dynamic STLs and moderately
fine relaxed STLs by blunting the actions of
the underlying musculature. However, deeper
­relaxed STLs, accentuated by the gravitational
pull of sun-damaged skin, are better treated by
injectable fillers, which replace volume loss.
The facial nerve and muscles
of facial expression
Key Points
• The muscles of facial expression develop from
the second embryonic arch.
• They contribute to the relaxed skin tension lines
of the face.
• They are innervated by the seventh cranial nerve –
the facial nerve.
10 Dermatologic Surgery
Temporal branches
Zygomatic branch
Parotid duct
Buccal branches
Facial artery
Masseter muscle
Marginal mandibular branches
Figure 1-8  Illustration of the facial nerve
The facial nerve, or cranial nerve VII, exits the
skull at the stylomastoid foramen and proceeds
to innervate the muscles of facial expression
(Fig. 1-�
8). Immediately after exiting the foramen,
the posterior auricular branch breaks off the main
trunk to innervate the occipitalis and ­postauricular
muscles. The remainder of the nerve pierces the
parotid gland and departs as five branches –
temporal, zygomatic, buccal, marginal mandi­
bular, and cervical (Fig. 1-�
9). Each branch of the
nerve is discussed separately. Table 1-� 9 highlights
the muscles innervated by each branch.
During surgical procedures injury to a single
branch of the facial nerve is more likely to occur
than injury to the main trunk. Conflicting ­reports
exist on the most common branch injured, as
ERRNVPHGLFRVRUJ
Zygomatic arch
Superficial temporal artery
Stylomastoid foramen
Facial nerve (CN-VII):
main trunk
Temporofacial division of VII
Cervicofacial division of VII
Parotid gland
Cervical branch
the temporal, buccal, and marginal mandibular
branches have all been implicated in different
series. Permanent injury to one of the branches
of the facial nerve is reported as 0.4–2.6%, with
equal rates for subcutaneous and sub-SMAS
­procedures.
The temporal branch is particularly vulnerable
to damage on the lateral face after exiting the
­superior pole of the parotid gland (Table 1-10, Fig.
1-10). This branch runs deep to the skin, subcu­
taneous tissue and a thin layer of fascia along its
course to the frontails and orbicularis oculi mus­
cles. To prevent damage to this nerve, the surgeon
should only dissect down to the superficial fat in
this area. Table 1-10 highlights other areas where
the facial nerve is susceptible to injury.

b buccal branch
bz buccal/zygomatic anastomoses
c cervical branch
fa facial artery
dotted line damaged nerves anterior to it likely result in full recovery while
damaged nerves posterior to it likely result in permanent paralysis
dotted circle danger zone for fa and mm
Figure 1-9  Anatomy of the facial nerve
The zygomatic branch exits the anterosuperior
border of the parotid gland and divides into ­upper
and lower rami (see Figs 1-4 & 1-9). Branches of
the lower ramus lie on the parotid duct. Injury
to the zygomatic branch results in difficult clos­
ing the ipsilateral lower eyelid and can affect the
nasal muscles and lip ­elevators.
The buccal branch exits the anterior border of
the parotid gland before coursing anteriorly over
the masseter muscle and buccal fat pad. This
­division runs parallel to the parotid duct prior to
delivering extensive rami to the mid-facial region
(see Figs 1-4 & 1-9). Damage to this branch may
lead to the accumulation of food between the
teeth and buccal mucosa while chewing, as well
as drooling, impaired lip pursing, and impaired
smiling. Injury to the zygomatic or buccal branch­
es is often temporary because of the high degree
of anastamoses between the two branches. Some
70–90% of ­patients have these anastomoses.
ERRNVPHGLFRVRUJ
1
Chapter
Surgical anatomy of the head and neck 11
mm marginal mandibular branch
t temporal branch
z zygomatic branch
The marginal mandibular branch exits the infe­
rior pole of the parotid gland and travels along the
lower angle of the mandible anterior to the facial
artery (see Fig. 1-�
9). Ramification occurs distally,
near the muscles of the lower lip. This renders the
nerve vulnerable in its more proximal subplatys­
mal location near the anterior insertion point of
the masseter muscle on the mandible. With injury
to this nerve, the lower lip becomes impaired in
its downward movement, which can lead to an
asymmetric smile.
The cervical branch of the facial nerve exits
the inferior pole of the parotid gland and ­descends
toward the submandibular triangle before ram­
ifying extensively to innervate the platysma (see
Fig. 1-� 9). Injury to this branch rarely causes
­noticeable damage.
The extensive anastomotic network of the
facial nerve, particularly via the zygomatic and
buccal branches, may be predicted by dropping
12 Dermatologic Surgery
Table 1-9  Muscles innervated by the facial nerve
Muscle innervated
Branch of facial nerve by branch
Temporal Frontalis
Corrugator supercilii
Orbicularis oculi (upper
portion)
Auricular
Zygomatic Orbicularis oculi (lower
portion)
Nasalis (alar portion)
Procerus
Buccinator
Buccal Buccinator
Depressor septi nasi
Nasalis (transverse portion)
Zygomaticus major and
minor
Levator labii superioris
Levator anguli oris
Risorius
Orbicularis oris (upper
portion)
Marginal mandibular Orbicularis oris (lower
portion)
Depressor anguli oris
Depressor labii inferioris
Mentalis
Cervical Platysma
an imaginary vertical line down from the lat­
eral canthus. Branches anterior to this line have
­extensive anastomoses, and injured nerves in this
“safe zone” will likely recover. Damage posterior
to this line, however, often results in permanent
paralysis of the target musculature.
Table 1-11 discusses each muscle of facial
­expression separately. See Figures 1-11 through
1-13 for the muscular anatomy of the face. With
the exception of the buccinator, the muscles
of ­ facial expression receive motor innervation
from their deep surface and thus protect their
­terminal branches (Fig. 1-14). Of note, the ­levator
­palpebrae superioris muscle elevates the upper
­eyelid under the direction of the ­ oculomotor
nerve ­ (cranial nerve III) rather than the facial
ERRNVPHGLFRVRUJ
Table 1-10  Areas of the facial nerve susceptible to injury
Branch of facial
nerve Danger zone description
Facial nerve Behind the earlobe in children, the
trunk as it exits facial nerve trunk is vulnerable to injury.
the stylomastoid In adults, the trunk is protected by the
foramen mastoid process
Facial nerve in Vulnerable to injury if the procedure
the parotid gland breaches the fascia of the parotid gland
Temporal branch  Located between an imaginary line
drawn between the earlobe and the
lateral eyebrow and a second line drawn
between the earlobe and the most
superior forehead crease. It lies in its
most superficial position as it crosses
the zygomatic arch. The facial nerve
likely has multiple rami at this point
Buccal branch Lying superficial to the masseter muscle,
but deep to SMAS, this section is
vulnerable at its branching points, 2 cm
anterior to its exit of the parotid gland
and under the modiolus (see below)
Marginal This branch lies just below the fascia of
mandibular the SMAS anterior to the facial vein and
artery as it crosses the inferior edge of
the mandible near the insertion point of
the masseter
nerve (Fig. 1-15). See ­ Boxes 1-1 through 1-3 for
the other functions of the facial nerve.
Sensory innervation of the
head and neck
The trigeminal nerve
Key Points
• The trigeminal nerve, cranial nerve V, is the
largest of the 12 cranial nerves.
• The three main branches are the ophthalmic (V1),
maxillary (V2), and mandibular (V3).
• The trigeminal nerve provides the primary
sensory innervation to the face.
• It also provides motor innervation to the muscles
of mastication.
• Effective anesthesia via nerve blocks can be placed
by the cutaneous surgeon with an understanding
of the anatomy of the trigeminal nerve.
The trigeminal nerve, the largest of the cranial
nerves, is the fundamental provider of sensory
­innervation to the face, supplying structures de­
rived from the first branchial arch. Three branches
 1

Chapter
Surgical anatomy of the head and neck 13

The danger zone is predicted by drawing an imaginary line between the earlobe and the lateral
eyebrow and a second line drawn between the earlobe and the most superior forehead crease.
The temporal branch of the facial nerve is vulnerable to injury as it courses over the zygomatic
arch within this zone.

Figure 1-10  The facial nerve: danger zone

Table 1-11  The muscles of facial expression

Muscle Contraction Origin Insertion Comments
Frontalis Raises eyebrows and Galea aponeurosis Fibers intertwine with Part of the epicranius;
wrinkles forehead; procerus, orbicularis the fibers of the
allows skin to slide oculi, and corrugator frontalis are vertically
over scalp supercilii muscles oriented. The horizontal
forehead skin tension
lines are created by this
muscle. If denervated,
the eyebrow droops
and skin tension lines
relax on the damaged
side
Corrugator supercilii Draws eyebrows Nasal bone Skin above middle Creates the vertical
medially and downward eyebrow glabellar frown lines
with the medial portion
of the orbicularis
oculi and depressor
supercilii
Orbicularis oculi Eyelid closure Medial canthal tendon Eyelid skin and Contraction forms folds
and upper eyelid and nasal portion of surrounding that radiate from the
depression; aids in tear frontal bone musculature; lateral lateral canthus (“crow’s
excretion portion of orbicularis feet”)
oculi is uninterrupted at
the lateral canthus

ERRNVPHGLFRVRUJ
14 Dermatologic Surgery

Table 1-11  The muscles of facial expression—cont’d

Muscle Contraction Origin Insertion Comments
Nasalis Compresses and Maxilla lateral to nasal Nasal aponeurosis Major muscle of the
widens nasal aperture notch nose
(“flares nostrils”) with
deep inspiration
Levator labii Elevates ala and upper Superiorly at maxilla Alar cartilage and
superioris alaque nasi lip upper lip
Procerus Draws down medial Nasal bones and Skin between eyebrows Temporary paralysis
angle of eyebrow and cartilage of this muscle helps
produces horizontal to reduce “bunny
wrinkles over nasal lines”; continuous with
bridge frontalis muscle
Buccinator Compresses cheek Maxilla and mandible Submucosa of cheek Muscular wall of cheek;
against teeth and orbicularis oris if denervated, food
accumulates between
teeth and cheek while
chewing. Pierced by
parotid duct as it enters
the mouth; receives
motor innervation from
its superficial surface
Zygomaticus major Upper lip elevator; Zygomatic bone Upper lip, angle of Important for smiling
draws angle of mouth mouth and laughing
upward
Zygomaticus minor Upper lip elevator Zygomatic bone Orbicularis oris muscle Deepens nasolabial
sulcus during sadness
Levator labii Elevates and everts Maxilla and zygomatic Upper lip Provides a protective
superioris upper lip bone roof over the
infraorbital foramen
Levator anguli oris Raises angle of mouth Maxilla Angle of mouth Contributes to depth of
nasolabial furrow
Risorius Draws corner of mouth Zygomatic arch and Angle of mouth/ Important for the smile
laterally parotid fascia modiolus
Orbicularis oris Sphincter muscle Maxilla, mandible, and Lips and vermillion Modiolus contributes
of lips for closing, modiolus (1 cm lateral border to cheek dimples
pursing, protruding, or to corner of lips; fibers
inflecting (prevents lip from orbicularis oris,
protrusion) lip elevators, and lip
depressors converge to
form a compact, mobile,
fibromuscular mass
called the modiolus)
Depressor anguli oris Pulls angle of mouth Mandible Angle of mouth
downward and laterally
Depressor labii Draws lower lips Mandible and mental Skin and mucosa of Contributes to
inferioris downward as to convey foramen lower lip expression of irony,
impatience, and may sorrow, melancholy,
assist with eversion and doubt
Mentalis Raises skin of chin Mandible Skin of chin A wide space between
and everts lower lip the two mentalis
to express doubt or muscles can create a
to pout chin dimple
Platysma Depresses and wrinkles Mandible Skin of neck and chest Most superficial
skin of lower face and muscle of neck;
neck overlies facial artery
and vein, as well as
marginal mandibular
and cervical branches
of facial nerve

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Chapter
Surgical anatomy of the head and neck 15

Anterior auricular Superior auricular

Frontal belly of
occipitofrontalis

Orbicularis oculi
Corrugator supercilii
Procerus

Nasalis

Levator labii
superioris
alaeque nasi
Levator labii
superioris

Zygomaticus minor
Zygomaticus major Occipital
belly of
Modiolus occipitofrontalis

Orbicularis oris
Depressor labii
inferioris
Mentalis
Posterior auricular
Depressor anguli oris
Risorius
Buccinator
Platysma

Figure 1-11  Muscles of facial expression

ERRNVPHGLFRVRUJ
16 Dermatologic Surgery

an levator labii superioris alequae nasi (alar & labial)

fa facial artery
fv facial vein
lao levator anguli oris
lls levator labii superioris
orb orbicularis oculi
z zygomaticus minor
zma zygomaticus major

Figure 1-12  The cheek: anatomy of the infraorbital muscles

of the trigeminal nerve, the ophthalmic (V1),
maxillary (V2), and mandibular (V3), carry sensa­
tion from distinct regions of the face (Fig. 1-16).
The regions are located anterior to an angled
coronal plane located at the vertex of the skull.
Each main branch divides into smaller cutaneous
branches either before or after emerging from the
skull via bony foramina (the significant branches
are listed in Table 1-12).
The ophthalmic nerve (V1) is the smallest and
uppermost division, and further subdivides into
the nasociliary, frontal, and lacrimal nerves. The
nasociliary nerve is the progenitor to the exter­
nal nasal branch of the anterior ethmoidal nerve
(which innervates the tip of the nose) and the
ciliary nerve (which innervates the cornea). Her­
petic invasion of the ophthalmic division present­
ing with blistering on the nasal tip (Hutchinson’s
sign) should alert the doctor to potential corneal
involvement. Zoster involvement of the external
nasal nerve in one series indicated a 76% chance
of ocular involvement – double the chance if no
lesions were present at the nasal tip.
The frontal branch of the ophthalmic nerve
gives rise to the supratrochlear and supraorbital
nerves (Fig. 1-17). The supratrochlear nerve is
the smaller of the two branches and runs 1 cm
lateral to the midline, lying in the supratrochlear

ERRNVPHGLFRVRUJ

Surgical anatomy of the head and neck
provides motor fibers to the muscles of masti­
cation (Box 1-�
­auri­culotemporal, buccal, and inferior alveolar
dao depressor anguli inferioris
dli depressor labii inferioris
lao levator anguli oris
lls levator labii superioris
m modiolus
oo orbicularis oris
r risorius
zm zygomaticus major
Figure 1-13  Modiolus, elevators, and depressors
notch of the orbital rim. The supraorbital nerve
lies 2.5 cm lateral to the midline and exits via the
supraorbital foramen. It is the largest extracranial
branch of the ophthalmic nerve. Both branches of
the frontal nerve initially run deep to the frontalis
muscle. At the mid-forehead, the medial branch
of the supraorbital nerve penetrates the frontalis
to run superficial to it.
The maxillary branch (V2) divides into the
infraorbital, zygomaticofacial, and zygomatico­
temporal branches. Of note, the infraorbital nerve
exits via the infraorbital foramen of the maxilla
(discussed below) and lies between the superior
heads of the levator labii superioris and levator
anguli oris (Fig. 1-18). The infraorbital division
innervates the medial cheek, upper lip, lower eye­
lid, lateral portion of the nose, and ­nasal ala.
Two divisions (ophthalmic [V1] and maxil­
lary [V2]) of the trigeminal nerve provide sensory
fibers to the nose (Table 1-13). In the ­trigeminal
trophic syndrome, injury to the maxillary division
ERRNVPHGLFRVRUJ
1
Chapter
17
(V2) results in a characteristic anesthetic
­ lceration of the nasal ala or alar crease. This der­
u
matomal insult of the trigeminal nerve may occur
after surgical damage to the gasserian ganglion
or during postencephalitic states. The nasal tip is
spared in this syndrome, as it is innervated by the
ophthalmic division (V1).
The mandibular branch (V3) is the largest
division of the trigeminal nerve. In addition to
the sensory functions listed in Table 1-14, it also
4). Its main branches include the
nerves. The auriculotemporal nerve emerges on
the face anterior to the tragus and crosses the
root of the zygoma to accompany the superfi­
cial temporal artery and vein to the scalp (see
2). The ­buccal nerve runs deep to the pa­
Fig. 1-�
rotid gland where it divides into many rami to
innervate the skin over the buccinator muscle.
The terminal division of the inferior alveolar
branch is the mental nerve, which exits to the
skin at the mental foramen of the mandible (Fig.
1-19). See Table 1-14 for the cutaneous areas
innervated by the branches of all three divisions
mentioned.
The trigeminal nerve also supplies postgangli­
onic parasympathetic fibers to the lacrimal and
parotid glands. Frey’s syndrome, also known as
auriculotemporal syndrome, is characterized by
pain, hyperhidrosis, and vasodilatation of the
cheek when eating (gustatory sweating). This syn­
drome usually occurs after parotid gland surgery
with injury to the auriculotemporal nerve. Para­
sympathetic fibers of the auriculotemporal nerve,
normally carrying salivary stimuli, incorrectly
reinnervate the sweat glands and blood vessels of
the cheek. Subsequent gustatory stimuli precipi­
tate the above clinical features.
The exit points, or bony foramina, of the
­supraorbital, infraorbital, and mental nerves are
found in a vertically oriented, midpupillary line,
2.5 cm lateral to the midline. This vertical line
exists because of the predetermined embryol­
ogy of each branch. The supraorbital foramen lies
slightly superior to the superior orbital rim. The
infraorbital foramen lies 1 cm inferior to the infe­
rior orbital rim along the backslope of the maxil­
lary bone. The mental foramen is located on the
lateral surface of the mandible toward the inferior
edge of the ramus in the same midpupillary line
as the above. Know­ledge of these foramina ­allows
the clinician to place anesthesia for ­ effective
nerve blocks.
18 Dermatologic Surgery

Shows the undersurface of the orbicularis oculi receiving terminal nerve fibers of the
zygomatic branch of the facial nerve.

Figure 1-14  Orbicularis oculi muscle and the zygomatic branch of the facial nerve

The supraorbital and supratrochlear nerve
block can be achieved with anesthetic placed
slightly superior to the superior orbital rim,
0.5–2.5 cm lateral to the midline. Anesthetic
should be infiltrated deeply as both of these
nerves lie underneath the frontalis and corruga­
tor ­ supercilii muscles at this location. Blocking
the nerves will provide adequate anesthesia to
the ipsilateral forehead and frontal scalp. Care
should be taken to avoid intraneural injection for
all nerve blocks. Severe pain on injection reported
by the patient may indicate an intraneural loca­
tion. This can be corrected by slightly retracting
the needle.
Intraoral and percutaneous approaches can
be used for the infraorbital nerve block. For the
intraoral route, the needle is inserted into the
superior labial sulcus with the surgeon’s thumb
and index finger grasping the upper lip. The
needle is aimed toward the surgeon’s fourth
finger overlying the infraorbital foramen (1 cm
below the infraorbital rim). Some 1.0–1.5 mL
of anesthetic can be injected in this location.
The intraoral block offers less pain to the ­patient
than the percutaneous route, and allows the
needle to enter the tissue in the same plane as
the ­ infraorbital nerve. For the percutaneous
­approach, the needle is aimed deeply toward

ERRNVPHGLFRVRUJ
 1

Chapter
Surgical anatomy of the head and neck 19

aa angular artery soa supraorbital artery

dna dorsal nasal artery sof supraorbital foramen
mcl medial canthal ligament son supraorbital nerve

Figure 1-15  Levator palpebrae superioris (LPS)

B ox 1 - 1 B ox 1 - 2
Other muscles innervated by branches Areas innervated by sensory fibers
of the facial nerve of the facial nerve

• Stapedius • External auditory meatus

• Posterior belly of the digastric • Soft palate
• Stylohyoid • Pharynx
• Taste sensation to the anterior two thirds of the tongue via the
chorda tympani branch
B ox 1 - 3
Glands innervated by the facial nerve
with parasympathetic fibers

• Submaxillary
• Submandibular
• Lacrimal

ERRNVPHGLFRVRUJ
20 Dermatologic Surgery

From ophthalmic division Medial branches of

of trigeminal nerve [V1] dorsal rami of cervical
Supraorbital nerve spinal nerves
Greater occipital nerve
Supratrochlear nerve (C2)
Third occipital nerve
(C3)
Infratrochlear nerve
From fourth, fifth, sixth,
External nasal nerve seventh and eighth
cervical nerves

Branches from
From maxillary division cervical plexus
of trigeminal nerve [V2] Lesser occipital nerve
Infraorbital nerve (C2,3)

Zygomaticofacial Great auricular nerve

nerve (C2,3)
Zygomaticotemporal Transverse cervical
nerves nerve (C2,3)
Marginal mandibular branch Supraclavicular nerves
of facial nerve (C3,4)
From mandibular division
of trigeminal nerve [V3]
Mental nerve
Buccal nerve
Auriculotemporal
nerve

Figure 1-16  Trigeminal nerve

the same foramen through the skin of the cheek.

Table 1-12  Divisions and branches of the trigeminal
nerve The anesthetic is injected slightly superficial to the
­foramen. This block will provide anesthesia to the
Major branch of Main cutaneous sensory upper lip and areas summarized in Table 1-14.
trigeminal nerve branches
The mental block can also be performed
Ophthalmic (V1) Nasociliary ­using intraoral and percutaneous approaches. For
Frontal the intraoral approach, the needle is advanced
in the inferior labial sulcus between the lower
Lacrimal first and second premolars towards the fourth
Maxillary (V2) Infraorbital ­finger resting on the mental foramen. During this
Zygomaticofacial ­insertion, the surgeon’s thumb and index finger
grasp the lower lip. Some 0.5–1 mL of anesthetic
Zygomaticotemporal is ­ required for the mental block, producing
Mandibular (V3) Auriculotemporal ­anesthesia of the ipsilateral chin and lower lip.
Buccal
Inferior alveolar

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 1

Chapter
Surgical anatomy of the head and neck 21

aa angular artery pro procerus

av angular vein soa supraorbital artery (red)
dna dorsal nasal artery son supraorbital nerve (green)
fro frontalis sta supratrochlear artery
mcl medial canthal ligament stn supratrochlear nerve (yellow)

Figure 1-17  Medial forehead: supraorbital and supratrochlear neurovascular structures

The cervical nerves and the
posterior triangle of the neck
Key Points
• Peripheral nerves of the cervical plexus include
the great auricular, lesser occipital, transverse
cervical, and supraclavicular nerve.
• A superficial neural-rich zone may be identified
within the posterior triangle. Nerves lying within
this zone are susceptible to injury during minor
surgical procedures.
• These nerves are responsible for the sensory
innervation of the neck, posterior scalp, a portion
of the ear, and skin over the clavicle.
The posterior triangle of the neck has definable
boundaries and contains critical motor and sen­
sory nerves (Table 1-15). Cutaneous branches of
the cervical plexus, along with the spinal acces­
sory nerve, course through the posterior triangle
of the neck in a region worthy of anatomic dis­
tinction. Using an imaginary line drawn from the
angle of the jaw to the mastoid process, it may be
localized approximately 6 cm inferior to the mid­
point of this line at the posterior border of the
sternocleidomastoid muscle (Figs 1-20 & 1-21).
This neural-rich zone sits approximately at the
level of the hyoid bone or the third cervical ver­
tebra. Alternatively, the region may be identified
roughly as an area near the junction of the ­upper
and middle thirds of the sternocleidomastoid
muscle along its posterior border.
Interestingly, this neural-rich zone has often
and erroneously received distinction as “Erb’s
point.” Dr Wilhelm Heinrich Erb (1840–1921),
a renowned German physician known widely
for his prolific contributions to the field of neuro­
logy, described and illustrated an area on the side
of the neck “from a circumscribed point, about
two to three centimeters above the ­ clavicle,
somewhat outside of the posterior border of the
sternomastoid and immediately in front of the
transverse process of the sixth cervical vertebra.”
He termed this point “Erb’s point” or the “supra­
clavicular point.” Erb noted that at this point,

ERRNVPHGLFRVRUJ
22 Dermatologic Surgery
a infraorbital artery
lao levator anguli oris
lls levator labii superioris (reflected)
Figure 1-18  Infraorbital foramen and related structures
Table 1-13  Nerves that innervate the nose
Infraorbital nerve (V2) Mid-lower sidewall, ala
External nasal branch Nasal tip
of anterior ethmoidal
nerve (V1)
Supratrochlear nerve (V1) Root, bridge, upper sidewall
Infratrochlear nerve (V1) Bridge, upper sidewall
“­ simultaneous contraction may be produced in
the deltoid, biceps, brachialis anticus, and supi­
nator longus muscles” through transcutaneous
electrical stimulation. The neural-rich zone of
the cervical plexus within the posterior triangle
­(approximately at the level of the third cervical
vertebra) thus lies superior to Erb’s point found
just above the clavicle (approximately at the level
of the sixth cervical vertebra). We shall refer to
the former as “pseudo-Erb’s point.” One motor
and four sensory nerves of the cervical plexus
emerge approximately 2 cm above or below
­pseudo-Erb’s point along their course in and out
of the posterior triangle.
The spinal accessory nerve (Table 1-16) is a
cranial motor nerve that courses ­posteroinferiorly
ERRNVPHGLFRVRUJ
n infraorbital nerve
z zygomaticus minor
zma zygomaticus major
through the posterior triangle of the neck. ­Lying
deep only to the skin and superficial cervical
­fascia, the nerve is vulnerable to injury during
routine surgical procedures such as the punch
biopsy.
The cervical plexus lies deep to the sternoclei­
domastoid muscle. It is assembled from the ven­
tral rami of the first four cervical nerves. The most
prominent peripheral branches that arise from
this plexus are derived from the second through
fourth (C2–C4) cervical nerves (Table 1-17).
The lesser occipital nerve (C2) emerges from
behind the sternocleidomastoid muscle and runs
parallel to its posterior edge to innervate the neck,
mastoid area, and scalp posterior to the ear. The
great auricular nerves (C2 and C3) passes around
the posterior border of the sternocleidomastoid
muscle and ascends vertically towards the ­parotid
gland and earlobe (Fig. 1-22). The external
­jugular vein runs in close approximation to the
great ­auricular nerves as they cross the superficial
border of the sternocleidomastoid.
The transverse cervical nerves (C2 and C3)
sharply curve anteromedially upon exiting the
posterior triangle, running between the ­ external
jugular vein and the sternocleidomastoid ­muscle.
 1

Chapter
Surgical anatomy of the head and neck 23

Table 1-14  Regional sensory innervation B ox 1 - 4

of the trigeminal nerve
Muscles of mastication innervated
Ophthalmic (V1) by the trigeminal nerve
Nasociliary Root of nose, medial
canthus, dorsum of nose, • Masseter
nasal tip, columella, a • Temporalis
portion of upper eyelid, and
• Medial pterygoid
cornea
• Lateral pterygoid
Frontal (supratrochlear and Medial upper eyelid and
supraorbital branches) conjunctiva, forehead, and • Tensor veli palatini
frontal scalp
• Lylohyoid
Lacrimal Lateral upper eyelid
• Anterior belly digastric
Maxillary (V2)
• Tensor tympani
Infraorbital Lower eyelid, medial cheek,
lateral portion of nose, nasal
ala, and upper lip
Zygomaticofacial Malar eminence Sensory innervation of the ear
Zygomaticotemporal Medial temple and
supratemporal scalp Key Points
Superior alveolar and Upper teeth and • See Figure 1-�2 for anatomic terms used to
palatine gingiva, palate, and nasal describe the features of the ear.
mucosa • The innervation of the ear is supplied by
the auriculotemporal nerve (a branch of the
Mandibular (V3) trigeminal nerve), great auricular nerve, and
Auriculotemporal Lateral ear including lesser occipital nerve (the latter two are branches
tragus, lateral temple, of the cervical plexus) (Table 1-18).
temporoparietal scalp,
and temporomandibular
joint The ear can be described with a cranial surface
(medial or closest to the scalp) and a lateral sur­
Buccal Cheek, buccal mucosa, and face (visible surface in anatomic position). The
gingiva
auricle is the entire visible part of the external
Inferior alveolar Mandibular teeth; lower ear. It is divided into cartilaginous and noncarti­
lip and chin (via mental laginous (lobule) domains.
nerve) The great auricular nerve supplies the anterior
Lingual Anterior two thirds of and posterior portions of the ear lobule, inferior
the tongue, floor cranial surface, and posterior portion of the lateral
of the mouth, and lower surface (portions of the helix and antihelix). The
gingiva lesser occipital nerve innervates the upper portion
of the cranial surface. The auriculotemporal nerve
supplies the majority of the lateral portion of the
ear including the tragus and crus of the helix.
Neither the great auricular nerve nor the The conchal bowl is variably innervated by
­transverse cervical nerve supplies the skin of the branches of the vagus and facial nerves.
­posterior triangle, as they leave the region ­quickly.
The fourth branch of the cervical plexus, the
­supraclavicular nerve (C3 and C4), emerges from Arterial and venous supply
pseudo-Erb’s point to innervate the skin of the of the face
lower neck, clavicle, shoulder, and upper chest.
For completeness, the posterior midline scalp is Key Points
innervated by the greater occipital nerve (C2) and • The facial blood supply is derived from the
the third occipital nerve (C3). Neither develops external and internal carotid arterial systems.
from the cervical plexus. The platysma muscle • The facial artery runs with the marginal mandibular
overlies and grants protection only to structures branch of the facial nerve near the masseter.
at the inferomedial border of the posterior tri­ • Most central facial blood vessels anastomose with
angle, such as the external jugular vein and the their contralateral counterpart along the midline.
• Dermatologists should be aware of multiple
transverse cervical nerve. It is not a ­reliable struc­
danger zones along the superficial face where
ture that protects the major motor and sensory named arteries may be injured during surgery.
nerves of this region.

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24 Dermatologic Surgery

dao depressor anguli oris ma mental artery

dli depressor labii inferioris (transected) mf mental foramen
fa facial artery mn mental nerve
ila inferior labial artery orb orbicularis oris
m mentalis

Figure 1-19  Mental foramen and related structures

Table 1-15  The posterior triangle The superficial arterial supply of the face encom­
passes a vast network of vessels derived from both
Boundary
the external and internal carotid vascular systems
Anterior Posterior border of sternocleidomastoid (Fig. 1-23, Table 1-19). The dual contribution and
muscle intricate anastomoses among each system create
Posterior Anterior border of trapezius muscle a redundant blood supply that bathes the skin
Inferior (base) Middle third of clavicle and underlying structures richly with oxygen and
­essential nutrients.
Roof Skin, SMAS, platysma (variable), deep The premiere facial branch of the external
fascia of neck (variable)
­carotid system is the facial artery. This ­principal
Floor Splenius capitis, levator scapulae, and ­vessel carves a tortuous path throughout its course
scalene muscles over the superficial face, delivering ­ multiple
Contents branches as described in Table 1-20. The facial
­artery debuts on the superficial face at the anteroin­
Motor nerves Spinal accessory (cranial nerve XI)
ferior angle of the masseter muscle over the body
Sensory nerves Lesser occipital (C2), great auricular of the mandible (see Fig. 1-� 9). Here the marginal
(C2,C3), transverse cervical (C2,C3), mandibular branch of the facial nerve may be
supraclavicular (C3,C4) found along with the facial artery. This ­potential

ERRNVPHGLFRVRUJ

Surgical anatomy of the head and neck
Transverse cervical nerve
Sternocleidomastoid muscle
Clavicle
Supraclavicular nerves
Figure 1-20  Illustration of the posterior triangle of the neck
danger zone is protected by the ­ overlying skin,
subcutaneous tissue, SMAS, and platysma. Along
its course, the facial artery runs deep to the riso­
rius and zygomaticus muscles, anterior to the
buccinator, and variably anterior or posterior to
the levator labii superioris. After the lateral nasal
branch splits from the facial ­artery near the nasal
ala, the terminal facial artery is known as the
angular artery (Fig. 1-24).
After the facial artery branches off, the external
carotid artery divides into two terminal branches –
the maxillary artery and the ­superficial ­temporal
artery. The internal maxillary artery runs a deep
course within the head. It contains four pertinent
branches that supply blood to the ­superficial face
(Table 1-21).
The superficial temporal artery (STA) arises
within the parotid gland and ascends superiorly
over the posterior aspect of the zygomatic proc­
ess. It terminates by bifurcating into two divisions,
both of which enter the temporal fossa (Table
1-22). The STA courses along with, and anterior
to, the auriculotemporal nerve (see Fig. 1-� 2).
The internal carotid system contributes to the
arterial supply of the superficial face through its
ophthalmic arterial branches (see Fig. 1-17, Table
1-23). The internal and external carotid systems
ERRNVPHGLFRVRUJ
1
Chapter
25
Lesser occipital nerve
Great auricular nerve
Spinal accessory nerve [XI]
Trapezius muscle
unite superior to the medial canthal ligament
where the dorsal nasal and angular artery anas­
tomose. Table 1-24 reviews the regional blood
­supply of the face.
Peripheral pulses may be palpated over cer­
tain anatomical regions of the face (Table 1-25).
The superficial location of the vessels in these
areas renders them susceptible to trauma dur­
ing surgical procedures. Physicians should always
­recognize these “danger zones” prior to any surgi­
cal procedure in the area.
Venous supply of the face
Key Points
• Veins of the face run parallel to the arteries.
• Superficial regions of the face drain to the internal
jugular venous system.
• Deep regions of the face drain to the external
jugular venous system.
Figure 1-23 and Table 1-26 review the veins
of the face. The supratrochlear and supraor­
bital veins unite to form the facial vein near the
­medial canthus. The facial vein runs posteroinfe­
riorly and merges with the anterior branch of the
­retromandibular vein inferior to the mandible.
26 Dermatologic Surgery

ga great auricular nerve scm sternocleidomastoid muscle

lo lesser occipital nerve tc transverse cervical nerve
san spinal accessory nerve tpz trapezius muscle
sc supraclavicular nerve

Figure 1-21  Anatomy of the posterior triangle of the neck (Erb’s point)

Within the parotid gland, the superficial tem­

Table 1-16  Spinal accessory nerve
Innervation Trapezius and sternocleidomastoid (SCM)
muscles
Course Travels along a line connecting
junction of upper and middle third of
sternocleidomastoid to junction of middle
and lower third of trapezius
Damage Drooping of ipsilateral shoulder or
“winged scapula” (trapezius)
Inability to raise and retract ipsilateral
shoulder (trapezius)
Weakness in turning head to contralateral
side against resistance (SCM)
As the facial vein drains the majority of the face,
it travels posteriorly and superficial to the facial
artery. The facial vein terminally drains into the
internal jugular vein.
poral and maxillary veins unite to form the retro­
mandibular vein, which then descends between
the external carotid artery and the deeper
­positioned facial nerve. The retromandibular vein
bifurcates into an anterior branch (above) and
a posterior branch. The posterior limb coalesces
with the posterior auricular vein to form the
­external jugular vein.
Veins of the face do not contain valves and are
subject to potential retrograde flow. The superior
ophthalmic vein is contiguous proximally with the
cavernous venous sinus of the dura mater covering
the brain. Distally, the superior ophthalmic vein
connects with the angular vein. Superficial midfa­
cial thrombophlebitis with involvement of the fa­
cial vein may result in retrograde flow of bacteria
to the dural venous system. Care must be taken to
avoid squeezing large pustules or ­furuncles of the
midfacial region to avoid seeding the blood and
dura with bacteria, given the above anatomy.

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Chapter
Surgical anatomy of the head and neck 27

Table 1-17  Sensory nerves of the cervical plexus and ­superolateral arms respectively. The internal
jugular chain is the major collecting system of the
Spinal Cutaneous area head and neck. See Table 1-30 for the areas that
Nerve rami supplied
drain to each chain.
Great auricular C2 and C3 Lateral neck, angle of jaw,
skin over parotid gland,
anterior and posterior ear
The anatomy of the scalp
lobule, inferior cranial Key Points
surface of ear, and
posterior portion of lateral • The scalp is the soft tissue that covers the
surface of ear cranium and is made up of five layers.
• The forehead and temple are components of the
Lesser C2 Neck, mastoid area, and scalp, embryologically speaking.
occipital scalp posterior to the ear; • Regions of the scalp include: frontal, temporal,
superior portion of cranial parietal, occipital, vertex, and crown.
ear • The vertex lies at top of the scalp anterior to the
Transverse C2 and C3 Anterior neck crown.
cervical • The galea aponeurotica is a component of the
superficial musculoaponeurotic system (SMAS).
Supraclavicular C3 and C4 Lower neck, clavicle, and • Infection of the scalp can spread to the meninges
shoulder via emissary veins.

The lymphatic system
of the head and neck
Key Points
• Lymphatic drainage flows in an inferior and
diagonal direction away from the head towards
the deep lymph nodes in the neck.
• Flow is superficial to deep.
• Lymphatic vessels contain valves.
• The superficial collecting nodes drain to the deep
cervical nodes.
Knowledge of the lymphatic drainage of the
head and neck is essential for evaluation of
­malignancy and infection of the skin (Fig. 1-27).
The lymphatic system begins with fine lymphatic
capillaries in the superficial dermis that con­
nect with larger lymphatic vessels deeper in the
skin. Unidirectional flow into lymph nodes and
­lymphatic chains ultimately returns fluid to the
venous circulation at the junction of the internal
jugular and subclavian veins via the thoracic and
right lymphatic duct. The clinically important
lymph nodes of the head and neck are listed in
Table 1-27.
The lymphatic drainage of the scalp and face
­follows a predictable pattern (Table 1-28), ­although
the drainage can be variable for each patient.
The above groups of superficial collecting
lymph nodes ultimately drain to the superficial
and deep lateral cervical nodes. The superficial
lateral cervical nodes lie above the sternocleido­
mastoid muscle and are associated with the
­external jugular vein. The deep lateral cervical
nodes run below the sternocleidomastoid muscle
with the internal jugular vein. The deep cervical
nodes form a triangular pattern with the spinal
accessory, transverse cervical, and internal jugular
chains forming the superomedial, inferior base,
The layers of the scalp are summarized in Box 1-� 5
and Figure 1-28 using the mnemonic SCALP. Its
borders are delineated in Table 1-31.
The skin of the scalp contains many hair follicles
and sebaceous glands that slice into the subcutane­
ous fat. A rich network of nerves and blood vessels
traverses the connective tissue layer. This second
layer also contains thick fibrous bands (retinacula)
that connect the skin to the galea aponeurotica
and form the support network for the blood ves­
sels. When these vessels are cut, the thick bands
hold the vessels open allowing the scalp to bleed
profusely. Consequently, under­mining in this
plane is suboptimal due to decreased visualization
from excessive bleeding and significant resistance
to movement from retinacular attachments.
The third layer of the scalp, the galea aponeu­
rotica, contains two layers of fascia that encase and
unite the bellies of the occipitofrontalis muscle
through an intervening inelastic fascial membrane.
The galea is the strongest layer of the scalp, and
wounds superficial to it do not spread. Together
with the skin, it functions as a unit that can move
freely over the deeper layers. As the frontalis
and occipitalis muscles pull the scalp in opposite
­directions, incisions that interrupt the galea in a
coronal plane increase the mobility of this inelas­
tic membrane. Cutaneous surgeons may exploit
this tendency by making a small coronal incision,
or galeotomy, anterior or posterior to wound edges
to relax tension forces and permit easier closures.
The loose areolar tissue of the scalp attaches
the galea aponeurotica to the periosteum. This
relatively avascular layer provides the optimum
site for undermining in the scalp. Although the
looseness of this space permits mobility of the
skin and galea, it creates a potential space where
large amounts of blood can collect after trauma
or surgery. Posterior and posterolateral bony

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28 Dermatologic Surgery

ejv external jugular vein pg parotid gland

ga great auricular nerve scm sternocleidomastoid muscle
l ear lobule

Figure 1-22  Great auricular nerve and external jugular vein

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Chapter
Surgical anatomy of the head and neck 29

Table 1-18  Sensory innervation of the ear no bony insertions exist over the anterior bound­
ary, infection or blood from the scalp may track
Nerve Anatomic location into the eyelids and root of the nose. Infection
Great auricular Majority of anterior and posterior in loose areolar tissue can also spread to the
auricle: helix, antihelix, antitragus, ­meninges via emissary veins that pass directly to
entire lobule the dura (see below).
Auriculotemporal Anterocranial auricle above external The final and deepest layer, the periosteum, is
auditory meatus: tragus, anterior adherent to the bones of the cranium by connec­
crus and rim of helix, anterior half of tive tissue fibers known as Sharpey’s fibers.
external auditory canal The muscles of the scalp are summarized in
Lesser occipital Small segment of posterior auricle Table 1-33.
and pre-mastoid skin The sensory innervation of the scalp is provid­
Facial, vagus Posterior half of external auditory
ed by six nerves, summarized in Table 1-34. When
(cranial canal, skin of concha, antihelix, anesthetizing the scalp, the anesthetic should be
nerve X), and tragus, and antitragus, posterior placed superficial to the galea aponeurotica, as
glossopharyngeal auricle–mastoid junction branches from these six nerves run in the connec­
(cranial nerve IX) tive tissue layer.
nerves The arteries that supply the scalp navigate the
connective tissue layer. They are derived from
both the internal and external carotid arteries
i­nsertions of the scalp prevent the spread of ­fluid (Table 1-35). Rich bilateral anastomoses, in
or infection to the neck (Table 1-32). Lateral addi­tion to the aforementioned retinacular
spread is contained at the zygomatic arch, the attachments, explain why ligation of one end of a
­insertion site for the temporal fascia. However, as transected artery is insufficient to stop bleeding.

Supratrochlear
artery and vein
Supraorbital
artery and vein
Angular artery
and vein

Lateral nasal
artery and vein
Posterior auricular
vein
Superficial temporal Posterior auricular
artery and vein artery
Occipital vein
Transverse facial
artery and vein
Occipital artery
Superior labial artery
Inferior labial artery
External jugular
Marginal mandibular vein
nerve
Facial artery and vein Internal jugular
vein
External carotid artery
Figure 1-23  Arterial and venous supply of the face

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30 Dermatologic Surgery

Table 1-19  Pertinent facial arterial supply

Branches of external carotid artery (ECA) system Branches of internal carotid artery (ICA) system
Facial artery Ophthalmic artery branches
Internal maxillary artery
Superficial temporal artery

Table 1-20  Facial artery branches (external carotid system)

Branch Origin Course Comments Supplies
Inferior labial Inferior to oral Runs anterosuperior Sandwiched between Labial glands, muscles,
(Fig. 1-25) commissure deep to depressor orbicularis oris and skin, and mucosa of
anguli oris before mucous membrane lower lip
penetrating orbicularis as it travels along the
oris margin of the lower lip
Superior labial Just superior to inferior Runs deep to depressor Has a septal branch Labial glands, muscles,
(Fig. 1-26) labial artery anguli oris before that runs superiorly skin, and mucosa of
penetrating orbicularis along columella to upper lip, nasal septum
oris; sandwiched nasal tip and an alar and alae
between orbicularis branch that runs
oris and mucous superiorly towards
membrane as it travels nasal ala
along margin of upper
lip
Lateral nasal Near superior alar Runs medially towards Has extensive Skin of nasal alae,
groove dorsum of nose anastomotic branches soft triangle, dorsum,
with septal, alar, dorsal and tip
nasal, and contralateral
lateral nasal arteries
Angular Terminal branch of Towards medial canthal Anastomoses with Skin of cheek, elevators
facial artery after lateral ligament along nasal dorsal nasal artery of upper lip, orbicularis
nasal branch departs sidewall superior to medial oculi, and nasal
canthal ligament sidewall

The veins of the scalp accompany the arter­
ies and are similarly named. They anastomose
with the diploic veins of the cranial bones and
­intracranial dural sinuses via emissary veins which
lack valves. Subsequently, infection from the scalp
can spread in a retrograde flow to the meninges
via these valveless veins.
Skin cancer on the scalp can metastasize to
the lymph nodes of the head and neck. The scalp
anterior to the ears drains to the parotid, sub­
mandibular, and deep cervical lymph nodes. The
posterior scalp is drained by the occipital and pos­
terior auricular lymph nodes.

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Chapter
Surgical anatomy of the head and neck 31

aa angular artery
fa facial artery
ln lateral nasal branch (facial artery)

Figure 1-24  Facial artery with angular artery

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32 Dermatologic Surgery

dao depressor anguli oris m mentalis

dli depressor labii inferioris (reflected) mf mental foramen
fa facial artery orb orbicularis oris
ila inferior labial artery

Figure 1-25  Inferior labial artery and related structures of the lower lip and chin

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Chapter
Surgical anatomy of the head and neck 33

a superior labial artery (SLA) f levator labii superioris

b septal branch of SLA g levator anguli oris
c alar branches of SLA h zygomaticus minor
d,e levator labii superioris alequae nasi i zygomaticus major
alar and labial branches

Figure 1-26  Superior labial artery and related structures of the upper lip and cheek

ERRNVPHGLFRVRUJ
34 Dermatologic Surgery

Table 1-21  Pertinent internal maxillary artery branches (ECA system)

Branch Description
Inferior alveolar (see Fig. Origin on face: exits mental foramen as mental artery
1-19)
Supplies: skin and muscles of the chin
Masseteric Course: along posterior surface of masseter
Buccal Course: along anterior surface of buccinator
Infraorbital (see Fig. 1-18) Origin on face: exits infraorbital foramen along with infraorbital nerve
Comments: emerges deep to levator labii superioris
Supplies: skin and muscles of cheek with extensive branching superiorly, medially, inferiorly,
and laterally

Table 1-22  Superficial temporal artery branches (ECA system)

Branch Description
Transverse facial Origin: within parotid gland
(see Figs 1-3 & 1-4)
Course: traverses across face between inferior border of zygomatic arch (one fingerbreadth below)
and parotid duct
Comments: lies on masseter muscle; often travels with zygomatic or buccal branches of cranial
nerve VII
Supplies: parotid gland and duct, masseter, and skin of cheek
Frontal branch Course: terminal division running anterosuperiorly
Supplies: skin, muscles, and periosteum of frontal forehead
Parietal branch Course: terminal division running posterosuperiorly
Supplies: skin, muscles, and periosteum of parietal forehead

Table 1-23  Ophthalmic artery branches (ICA system)

Branch Description
Dorsal nasal Origin: terminal branch of ophthalmic artery
Course: exits orbit superior to medial canthal ligament before anastomosing with angular artery
Comments: two terminal branches exist, one runs medially across nasal root and the other inferiorly along
dorsum of nose
Supplies: nasal root, dorsum, and tip
Supratrochlear Origin: terminal branch of ophthalmic artery
Course: superomedially along mid-forehead
Comments: arterial base of paramedian forehead axial pattern flap; travels with supratrochlear nerve
Supplies: mid-forehead and anterior scalp
Supraorbital Origin: exits supraorbital foramen along with supraorbital nerve
Course: superficial and deep branches run superolaterally along forehead
Supplies: mid and lateral forehead, anterior scalp
Lacrimal Course: with lacrimal nerve, runs towards the lacrimal gland, eyelids, and conjunctiva

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Chapter
Surgical anatomy of the head and neck 35

Table 1-24  Regional blood supply

Region supplied Artery of ECA system Artery of ICA system
Scalp and forehead Superficial temporal Supraorbital
Posterior auricular Supratrochlear
Occipital
Eyelid and periorbital Frontal branch of STA Lacrimal
Transverse facial Supraorbital
Infraorbital Supratrochlear
Zygomatico-orbital
External nose Lateral nasal Dorsal nasal
Superior labial (septal/alar)
Cheek Transverse facial
Infraorbital
Buccal
Facial and angular
Lips and oral cavity Superior labial
Inferior labial
Buccal
Inferior alveolar (mental)
Ear Superficial temporal (supplies anterior auricle
and external auditory meatus)
Occipital (supplies posterior auricle)
Posterior auricular (supplies posterior auricle)

Table 1-25  Arterial pulses and danger zones of the face

Facial artery With the jaw firmly clenched, the artery may be palpated at the anteroinferior border of the masseter
muscle as this muscle inserts on the body of the mandible
Facial artery Grasp the cheek between the first and second fingers about one fingerbreadth lateral to the oral commissure
Angular artery Palpated just inside the medial canthus against the nasal sidewall, also along the naso–cheek junction
as it ascends to the medial canthus
Superficial temporal artery Palpate the root of the zygomatic process at its superior border just anterior to the tragus

Table 1-26  Veins of the face

External jugular vein tributaries Internal jugular vein tributaries
Superficial temporal vein Supraorbital and supratrochlear veins
Maxillary vein Ophthalmic vein
Retromandibular vein Infraorbital vein
Posterior auricular vein Lateral nasal vein
Transverse facial Labial vein
Facial vein
Transverse facial

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36 Dermatologic Surgery

Direction of
Preauricular/ lymph flow
parotid nodes

Occipital nodes

Postauricular nodes

Jugulodigastric node

Submental nodes

Deep cervical nodes

Submandibular nodes

Omohyoid muscle
Internal jugular vein
Jugulo-omohyoid node

External jugular vein

Figure 1-27  Lymphatics of the head and neck

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Chapter
Surgical anatomy of the head and neck 37

Table 1-27  Lymph nodes of the head and neck

Nodes Location
Occipital Apex of posterior triangle near insertion of trapezius and sternocleidomastoid muscles
Postauricular On mastoid insertion of sternocleidomastoid muscle
Preauricular Superficial to parotid gland immediately anterior to tragus
Parotid Clustered within and around parotid gland
Facial See Table 1-29: Facial group of lymph nodes
Submandibular Inferior to lower edge of mandible near submandibular salivary glands and facial vein
Submental In submental triangle (formed by hyoid bone, anterior digastric muscles, and mandible)
Internal jugular chain Runs along with internal jugular vein deep to sternocleidomastoid muscle
Spinal accessory chain Runs along with 11th cranial nerve deep to sternocleidomastoid muscle
Transverse cervical chain Extends from inferior edge of spinal accessory chain to junction of internal jugular and subclavian veins

Table 1-28  Superficial collecting nodes

Area of skin Lymph nodes draining the area
Scalp posterior to vertex Postauricular and occipital nodes
Ear lobule Superficial lateral cervical nodes
Lateral ear superior to lobule Preauricular node
Cranial ear superior to lobule Postauricular node
Anterior scalp, forehead, temple, lateral eyelids, nasal root, lateral cheek, Parotid nodes
external acoustic meatus, superior ear, parotid gland, and buccal mucosa
Medial cheek, medial canthus, medial eyelids, central face, nose, upper lip, Facial group of lymph nodes (Table 1-29) and
and lateral lower lip submandibular nodes
Chin, medial lower lip, anterior third of tongue, and buccal floor Submental nodes

Table 1-29  Facial group of lymph nodes

Nodes Location
Mandibular Along external surface of mandible adjacent to facial artery and anterior to masseter muscle
Buccinator Superficial to buccinator muscle or within buccal fat pad
Infraorbital Along nasolabial fold
Malar Superficial to malar eminence, lateral to eye

Table 1-30  Deep lateral cervical nodes

Nodes/area draining to each
Chain chain
Spinal accessory Occipital, postauricular, and
suprascapular nodes
B ox 1 - 5
Transverse cervical Spinal accessory chain, subclavian
nodes, and lymphatic vessels from Layers of the scalp
upper chest
Skin (epidermis and dermis)
Internal jugular Submental, submandibular, parotid,
preauricular and postauricular Connective tissue (subcutaneous fat)
lymph nodes; ears, tongue, nasal Aponeurosis (galea aponeurotica)
pharyngeal area, paranasal sinuses,
Loose areolar tissue (subgaleal space)
teeth, palate, larynx, pharynx, and
vocal cords; spinal accessory and Pericranium (periosteum)
transverse cervical chains

ERRNVPHGLFRVRUJ
38 Dermatologic Surgery

Skin; Connective Tissue; Aponeurosis (galea); Loose Alveolar Tissue; Pericranium

Figure 1-28  Layers of the scalp

Table 1-31  Borders of the scalp Table 1-33  Muscles of the scalp
Anterior Supraorbital ridges Frontalis Occipitalis
Posterior Base of occipital bone Origin Galea Superior nuchal
Lateral Frontal process of zygomatic bone, aponeurotica line of occipital
zygomatic arch, external acoustic bone
meatus, mastoid process, and superior Insertion Skin and Galea
nuchal line of occipital bone muscular fascia of aponeurotica
upper eyelids
Innervation Temporal branch Posterior auricular
Table 1-32  Boundaries of the loose alveolar space
of facial nerve branch of facial
Posterior Superior nuchal line of occipital bone nerve
Posterolateral Mastoid process of temporal bone Action Raises eyebrows; Not under
allows skin to voluntary control;
Lateral Temporal fascia
slide over bones allows skin to
Anterior Frontalis muscle insertion points on skin of cranium slide over bones
and subcutaneous connective tissue of cranium

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 1

Chapter
Surgical anatomy of the head and neck 39

Table 1-34  Nerves of the scalp

Origin Scalp area innervated

Supratrochlear nerve
Supraorbital nerve
Zygomaticotemporal nerve
Auriculotemporal nerve
Lesser occipital nerve
Greater occipital nerve
Ophthalmic division of trigeminal nerve Frontal scalp up to vertex in medial plane
Ophthalmic division of trigeminal nerve Frontal scalp up to vertex lateral to supratrochlear
nerve
Maxillary division of trigeminal nerve Scalp nearest temple
Mandibular division of trigeminal nerve Temporal region of scalp
Cervical plexus (C2) Lateral occipital region
Dorsal ramus of second cervical nerve (C2) Medial posterior scalp from occipital region to vertex

Table 1-35  Arterial supply of the scalp

Proximal artery Distal branch Region supplied
Internal carotid Supratrochlear artery Medial forehead; crown and vertex (minor)
Supraorbital artery
External carotid Superficial temporal artery Lateral forehead, occiput, temporoparietal scalp,
crown and vertex (major)
Posterior auricular artery
Occipital artery

Further reading
Asarch RG. A review of the lymphatic drain­
age of the head and neck: use in evaluation of
potential metastases. J Dermatol Surg Oncol
1982;8(10):869–872.
Baker DC, Conley J. Avoiding facial nerve injuries in
rhytidectomy. Anatomical variations and pitfalls.
Plast Reconstr Surg 1979;64(6):781–795.
Bennett RG. Fundamentals of Cutaneous Surgery.
Washington, DC: CV Mosby, 1988.
Breisch EA, Greenway HT. Cutaneous Surgical Anat­
omy of the Head and Neck. New York: Churchill
Livingstone, 1992.
Carlson KC, Roenigk RK. Know your anatomy:
perineural involvement of basal and squamous cell
carcinoma on the face. J Dermatol Surg Oncol
1990;16(9):827–833.
Erb W. Handbook of Electro-Therapies (Translated by
Putzel L.) William Wood and Company. New York.
1883; 122-124. Accessed online at: http://books.
google.com/books?q=handbook+of+electro+  and abnormal CT appearance. Radiology
therapeutics
Gosain AK. Surgical anatomy of the facial nerve. Clin
Plast Surg 1995;22(2):241–251.
Harding SP, Lipton JR, Wells JC. Natural history of
herpes zoster ophthalmicus: predictors of post­
herpetic neuralgia and ocular involvement. Br J
Ophthalmol 1987;71(5):353–358.
Moore KL, ed. Clinically Oriented Anatomy, 3rd edn.
Baltimore: Williams & Wilkins, 1992.
Reich SG, Grill SE. Gustatory sweating: Frey syn­
drome. Neurology 2005;65(11):E24.
Robinson JK, Anderson ER. Skin structure and surgi­
cal anatomy. In: Robinson JK, Hanke CW, Sen­
gelmann RD, Siegel DM, eds. Surgery of the Skin:
Procedural Dermatology. Philadelphia: Elsevier
Mosby, 2005.
Robinson JK, Hanke W, Sengelmann RD, Siegel DM.
Surgery of the Skin: Procedural Dermatology.
St Louis: Elsevier Mosby, 2005.
Salasche SJ, Berstein G, Senkarik M. Surgical Anato­
my of the Skin. Norwalk: Appleton & Lange, 1988.
Scarborough D, Bisaccia E, Schuen W, Swensen R.
Anesthesia for the dermatologic surgeon. Int J
Dermatol 1989;28(10):629–637.
Standring S, Healy J, Johnson D, Williams A. Gray’s
Anatomy: The Anatomical Basis of Clinical Prac­
tice. New York: Elsevier Churchill Livingstone,
2005.
Tart RP, Mukherji SK, Avino AJ, Stringer SP,
­Mancuso AA. Facial lymph nodes: normal
1993;188(3):695–700.
Tolhurst DE, Carstens MH, Greco RJ, Hurwitz DJ.
The surgical anatomy of the scalp. Plast Reconstr
Surg 1991;87(4):603–614.
Tubbs RS, Loukas M, Salter EG, Oakes WJ. Wilhelm
Erb and Erb’s Point. Clin Anat. 2007;20:486–488.

ERRNVPHGLFRVRUJ

Antisepsis
Gregory J. Fulchiero Jr, Christopher Riddell Jones,
and Christie T. Ammirati
Key Points
• Most surgical site infections are the result of
wound contamination at the time of surgery.
• Four potential sources of infection are: the
patient, surgical personnel, the surgical
environment, and surgical instruments (including
suture).
• Surgical site infections are defined as any
surgical wound that produces pus within 30 days
of the procedure.
• Staphylococcus aureus is the most frequent
cause of wound infections in dermatologic
surgery.
• The surgeon’s hands should be washed before
donning gloves and after their removal.
• Alcohol-containing preparations are flammable
and must be allowed to dry completely before
electrocautery or lasers are used.
• Povidone–iodine has broad-spectrum activity
but must remain on the skin to have a prolonged
effect.
• Chlorhexidine gluconate has sustained broad-
spectrum activity but is toxic to the cornea and
the middle/inner ear.
• Shaving hair at the surgical site causes
microabrasions that increase the risk of infection.
When possible, hair should be left in place or
clipped with scissors prior to establishing a sterile
field.
• Good surgical technique avoids compromising
the environment of the surgical wound and
decreases the risk of infection. This includes:
establishing and maintaining a sterile field,
atraumatic handling of tissue, effective
hemostasis with minimal electrocautery, and
limiting the amount of implanted material within
the wound.
• There is debate over the influence of surgical
attire (scrub suit, facemask, disposable booties,
surgical cap) on wound infection rate.
Clinical overview
Surgical wound infections are relatively rare in
dermatologic surgery (incidence <2%), and most
are thought to arise from contamination that
ERRNVPHGLFRVRUJ
2
Chapter
occurs at the time of surgery (Box 2-1). Good
surgical technique avoids compromising the envi-
ronment of the surgical wound and decreases the
risk of infection (Box 2-2). Any abrupt increase in
wound infection rate should be investigated. Of-
ten it can be traced to inconsistencies in aseptic
technique that are easily remedied (Box 2-3).
Flora
There are two types of cutaneous bacterial flora,
normal and transient. Normal or resident flora
are organisms that inhabit the skin surface and
­adnexal structures. They are usually not consi­
dered pathogenic but in some instances may cause
wound infections (Table 2-1). Transient flora are
acquired through contact with people, objects,
or the environment, and are the major source
of wound infection in dermatologic surgery. Un-
like normal flora, which can be embedded within
adne­xal structures and beyond the reach of a sur-
gical scrub, transient flora are loosely attached to
the skin surface and can be removed by washing
the skin surface.
Surgical site infection
Surgical site infections are defined as any surgi-
cal wound that produces pus within 30 days of
the procedure. A number of objective and sub-
jective criteria for infection have been proposed
(Table 2-2).
Classification of wounds
The Centers for Disease Control have classified
surgical wounds into four categories, which corres­
pond to their risk of surgical site infection: clean
(class I), clean-contaminated (class II), contaminated
(class III), and dirty-infected (class IV) (Table 2-3).
Each category carries an increasingly greater
­incidence of postoperative wound infection. This
classification allows the surgeon to quantify the
42 Dermatologic Surgery

B ox 2 - 1 Table 2-1  Common bacterial skin flora

Potential sources of surgical site Resident flora Transient flora

contamination Coagulase-negative Staphylococcus aureus
staphylococci (>90% of
• Patient’s endogenous flora resident aerobes are
• Surgical personnel S. epidermidis)
• Surgical environment Anaerobic diphtheroids Coagulase-negative
(P. acnes) staphylococci
• Surgical instruments and suture
Gram-negative organisms Enterococcus spp.
(Enterobacter, Klebsiella,
Escherichia coli
E. coli, and Proteus spp.)
B ox 2 - 2 Group A streptococci

Good surgical technique Pseudomonas aeruginosa

Enterobacteriaceae (Serratia
• Establishing and maintaining a sterile field spp., Klebsiella spp.)
• Atraumatic handling of tissue
• Effective hemostasis with minimal electrocautery
• Limited amount of implanted suture material
Table 2-2  Characteristics of surgical site infection
Objective criteria Subjective criteria
B ox 2 - 3 Purulent wound drainage Erythema
Frequent causes of abrupt increase Positive wound culture Induration
in wound infection rate
>105 organisms per gram Warmth
• Not washing hands before and after each patient contact of tissue
Tenderness
• Failure to perform an adequate surgical scrub Opening of incision
• Poor surgical technique postoperatively for any reason

• Inadequate cleanliness of the surgical environment Infection as deemed by clinical

assessment of the surgeon
• Bacterial colonization of a member of the surgical team

likelihood of developing an infection for each
procedure based on the status of the surgical site
and the anatomic location (Fig. 2-1). Dermato-
logic surgery, in general, carries a low infection
rate but surgical wounds of the groin, axilla,
mouth, ear, and below the knee may be at a high-
er risk of postoperative infection (exceeding 5%)
(Fig. 2-2).
Risk factors
Certain patient risk factors and comorbidities
are known to increase the risk of surgical site
infection and may warrant the use of prophyl­
actic antibiotics (Box 2-4). A history of pre-
vious wound infection may indicate that the
patient has chronic bacterial colonization, most
frequently with S. aureus, and is at increased
risk for subsequent wound infections. Reduced
perfusion of the wound bed by either endoge­
nous vascular insufficiency or nicotine-induced
vasoconstriction increases the risk of necro-
sis, dehiscence, and wound infection. ­ Patients
with poorly controlled diabetes mellitus are
at ­ increased risk for Pseudomonas sp. coloniza-
tion of the ear canal and may be predisposed
to infection after auricular surgery, particularly
of the conchal bowl. Severe malnutrition and
chronic alcoholism are considered immunocom-
promised states and associated with increased
risk of wound infection. Chronic corticosteroid
usage, chemotherapy, neutropenia (granulocyte
count <1000/mm3), and organ transplant pa-
tients on chronic immunosuppressive medica-
tions have been associated with an increased
risk of infection in general surgery but rarely in
dermatologic surgery.
Most studies concerning immunosuppression
and the risk for surgical site infection after derma-
tologic surgery have focused on organ transplant
recipients. The vast majority of these reports do
not support the use of prophylactic antibiotics
for uncomplicated dermatologic surgery in these
patients. The effect of HIV-induced immuno-
suppression on surgical site infection remains to
be fully defined. Even when controlled for CD4
count, there are conflicting data and further
­studies are needed.

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 2

Chapter
Antisepsis 43

Table 2-3  Classification of surgical wounds

Classification Description of wound Infection risk
Class I: Clean Uninfected operative wound <2%
No acute inflammation
Primary closure
No break in aseptic technique
Example: routine excision on noninflamed skin under aseptic conditions
Class II: Clean- Elective entry into axillary, inguinal, or mucosal regions <10%
contaminated
Minor break in asepsis
Examples: mucosal biopsy; suture briefly touches nonsterile surface
Class III: Inflammation without purulent drainage ≈20%
Contaminated
Penetrating traumatic wounds <4 h previously
Major break in aseptic technique
Examples: excision of ulcerated, inflamed basal cell carcinoma; surgeon (without
facemask) sneezes onto surgical field
Class IV: Dirty- Purulent inflammation (pus) ≈40%
infected
Devitalized or necrotic tissue
Penetrating traumatic wounds >4 h, or foreign bodies
Example: excision of purulent hidradenitis suppurativa nodule

Figure 2-1  Example of a class IV wound. This inflamed,

purulent cyst carries a significant risk of infection if excised
and sutured in its present state. The appropriate course
would be to incise and drain the lesion then prescribe
antibiotics as indicated by culture and clinical impression.
Once the infection has resolved, it can be excised
electively with minimal risk for surgical site infection

Differential diagnosis Figure 2-2  Wound infection of the lower extremity

The differential diagnosis of wound infection var­
ies, based on the length of time after surgery, clini­
cal picture of the wound, and the complaints of
the patient (Table 2-4). Normal postoperative se-
quelae that must be differentiated from infection
include incisional discomfort and swelling secon­
dary to anesthesia or postoperative edema. A
­suture abscess, which may suppurate but resolves
with removal of the suture, is not considered to be
a wound infection (Fig. 2-3). ­Postoperative ­patient
application of hydrogen peroxide, ­alcohol, or topi­
cal antibiotics may cause an irritant or ­ allergic
­contact dermatitis that can mimic a wound
­infection (Fig. 2-4).
Antiseptic scrubs
There are several effective antiseptic agents that
can be used to cleanse the skin prior to surgery.
The most common are povidone–iodine and

ERRNVPHGLFRVRUJ
44 Dermatologic Surgery

B ox 2 - 4
Patient comorbid risk factors for surgical
site infection

• History of previous wound infection

• Tobacco use within past 30 days
• Vascular insufficiency
• Diabetes mellitus
• Malnutrition
• Alcohol abuse
• Intravenous drug abuse
Figure 2-3  Suture abscess. Six weeks after undergoing
• Chemotherapy Mohs micrographic surgery for a basal cell carcinoma with
advancement flap repair, this patient developed a tender
• Neutropeniaa
papule within the suture line. It resolved with expression of
• Immunosuppressionb the underlying suture
• Organ transplant recipientsb
• HIV/AIDSb

aGranulocyte count <1000/mm3

bRelative risk factor

Table 2-4  Differential diagnosis of surgical site

infection
Clinical
Etiology symptoms Time course
Hematoma Ecchymosis Immediate to 48 h
Hemorrhagic
bullae
Progressive
Figure 2-4  Contact dermatitis secondary to bacitracin
painful swelling
may mimic a wound infection
Seroma Swelling 12–72 h
Erythema
Chlorhexidine has broad antimicrobial acti­vity
Irritant or Pruritus 12–72 h and is able to bind to the stratum corneum. It
allergic contact
Erythema maintains residual activity for more than 6 h, even
dermatitis
Papules, vesicles when wiped from the surgical field. A significant
concern with chlorhexidine is its risk for corneal
Bacterial Erythema without Days to weeks ulceration if allowed to come in contact with the
colonization purulence
eye, and potential middle ear toxicity via a perfo-
Exudate rated tympanic membrane.
Delayed healing Isopropyl- and ethanol-based alcohol prepa-
rations are gaining popularity. They have an im-
Suture reaction Sterile pustule Weeks to months
mediate effect and broad spectrum of activity. As
(suture abscess)
Extruding suture they work by desiccating microorganisms, they
material must be allowed to dry before their effect is com-
plete. They do not have detergent properties and
chlorhexidine gluconate with or without alcohol should be used only after visible debris has been
(Table 2-5). cleansed from the surface. As the use of alcohol-
Povidone–iodine has broad-spectrum acti­vity based preparations increases, it is also important
within minutes but must be left on the skin to to keep in mind that alcohol is highly flammable
remain effective. It is safe for use around the and must be allowed to dry completely before us-
eyes and mucous membranes, but its drawbacks ing cautery or lasers. Once evaporated, alcohol has
­include rapid inactivation by blood or sputum, minimal residual activity and it is ­recommended
the ability to stain fabric, and risk of neonatal that the agent be combined with other antisep-
hypo­thyroidism with prolonged maternal use. tics, such as chlorhexidine.

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 2

Chapter
Antisepsis 45

Table 2-5  Antiseptic agents commonly used for dermatologic surgery

Agent Activity Onset Duration Comments
Isopropyl and ethyl Gram (+) Very fast Minimal Flammable
alcohols
Gram (−) Poor cleanser
Mycobacteria Use liberally and allow
to dry for efficacy
Fungi Irritating near mucous
membranes
Enveloped viruses
Chlorhexidine Gram (+) Fast Prolonged (additive Keratitis
gluconate with successive
Gram (−) Ototoxicity
applications)
Fungi Poor activity on spores,
mycobacteria
Enveloped viruses
Povidone–iodine Gram (+) Fast Intermediate (minimal Potential risk
if wiped from the of neonatal
surgical site) hypothyroidism
Gram (−) Rapidly inactivated by
blood or sputum
Mycobacteria
Fungi
Enveloped viruses
Para- Gram (+) Moderate Intermediate Poor pseudomonal
chlorometaxylenol coverage as a single
(PCMX) agent
Moderately Gram (−) Activity enhanced with
preparations containing
Mycobacteria
an EDTA chelator
Fungi
Enveloped viruses
(less activity on above
organisms compared
with chlorhexidine
gluconate)

Another common antiseptic preparation is
para-chlorometaxylenol (PCMX), or chloroxyle-
nol. PCMX has effective Gram-positive bacterial
coverage but poor activity against Gram-negative
organisms, such as P. aeruginosa. Some commercial
PCMX preparations have added a chelator, such
as ethylene diamine tetra-acetic acid (EDTA),
to markedly increase the formulation’s anti-
­Pseudomonas activity. Although PCMX has re-
sidual activity for several hours, it is somewhat
less durable than chlorhexidine. The antiseptic
hexachlorophene (pHisoHex®) has been banned
from use in newborns and pregnant women as it
has been shown to be neurotoxic to neonates if
absorbed through the skin.
scrub is to remove transient flora and soil from
the fingernails and skin. Its efficacy is dependent
on the duration, technique, and agent chosen. If
done properly, a hand scrub can reduce the bacte-
rial load by 90–99%. The majority of hand flora
are located under and around the fingernails, and
these areas should receive close attention during
the hand scrub. Most studies have found that,
­regardless of the agent used, the first scrub of the
day should be at least 2 min. The most common
agents are chlorhexidine, povidone–iodine, and
alcohol preparations. One limitation of alcohol
rubs is that they do not have detergent qualities
and should be used only after the skin has been
cleansed of all visible debris.

Hand scrub Surgical site preparation

The surgeon’s hands and forearms represent a sig- The goal of the surgical site scrub is to decrease
nificant potential source of wound contamination the risk of wound infection by removing debris
and should be scrubbed prior to donning gloves and transient organisms from the operative field.
and after their removal. The goal of the hand The ideal length of surgical site preparation has

ERRNVPHGLFRVRUJ
46 Dermatologic Surgery
not been determined with certainty, but the ma-
jority of studies support a 1–2-min scrub. The
most favored technique employs three succes-
sive scrubs with a fresh sponge or gauze, starting
at the center of the surgical site and progressing
outward in concentric circles. A sufficient area
should be included in the scrub so that, once
draped, a ­sterile field can be maintained. Common
­antiseptics used for this purpose are chlorhexi-
dine gluconate, povidone–iodine, and PCMX. On
the evening before surgery, a preoperative shower
with chlorhexidine or benzoyl peroxide has been
shown to decrease surgical site infections with
S. aureus and may be considered for large surgical
fields such as liposuction.
Sterile field
A sterile field limits contamination during surgery
and aims to maintain the low microbial counts of
the surgical site achieved after antiseptic scrub-
bing. Disposable, impermeable sterile drapes and
reusable, tightly woven cotton drapes are the types
most commonly used in dermatologic surgery.
Disposable impermeable drapes are ­inexpensive,
but they may allow blood and ­ fluids to pool on
them, and their stiffness can cause them to shift
easily during surgery. Cotton ­ surgical drapes
are more pliable, and this allows them to be
shaped to fit the surgical site. They are arguably
more comfortable for the patient, but may wick
bacteria into the surgical field if saturated.
Breaks in sterile field
A break in the sterile field can include any
number of scenarios (i.e. patient touches surgi-
cal site, nonsterile instrument placed onto field,
or suture-tail touching nonsterile surface). When
a break in the sterile field occurs, the surgical
wound is likely to be upgraded (see Table 2-3),
corresponding to a higher risk of postoperative
infection. This may influence the decision to re-
scrub the sterile field, replace the drapes, change
gloves, or replace contaminated suture. Depend-
ing on the degree of contamination, the surgeon
may also decide to place the patient on prophyl­
actic antibiotics.
Surgical attire
The image of the surgeon in scrub suit, surgical
cap, and facemask is well known to us all. Al-
though this attire is familiar and at times expected
by patients, it has not been proven to affect the
incidence of surgical site infection. In fact, there
are no scientific data that prove wearing scrub
suits, rather than street clothes, affects the inci-
dence of surgical site infection. Polyester/cotton
scrub suits serve to maintain the overall hygiene
ERRNVPHGLFRVRUJ
of the ­surgical atmosphere and have a moderate
role as personal protective gear. However, they can
harbor pathogenic bacteria and fungi, which can
survive on these materials for extended periods,
particularly if allowed to become saturated. They
should be changed immediately if visibly contam-
inated and, regardless of their state, laundered on
a daily basis. This is particularly true for white lab
coats, which are frequently hung on hooks and
worn for several days without laundering.
The role of facemasks with eye shields as
­personal protective gear is undisputed, but their
value in reducing surgical site infections remains
debatable. It has been argued that facemasks may
abrade the skin and increase the risk for contami-
nating the surgical field with desquamated skin
cells. Alternatively, studies have shown a relation-
ship between bacterial contamination of the sur-
gical field and the volume at which the surgeon
speaks. Speaking even briefly in a loud tone can
aerosolize significantly more bacteria (up to 1 m
away) than speaking in a normal tone for up to
30 min. In this respect, a properly fitted mask may
play a role in decreasing wound contamination,
especially when coughing or sneezing (which can
propel bacteria up to 3 m away). When worn,
facemasks should be discarded and replaced after
every surgical procedure as they rapidly become
saturated with the surgeon’s expired flora. Bouf-
fant hair covers that enclose all of the scalp hair,
as opposed to small surgical caps that cover only
the top of the head, may decrease the incidence
of surgical site infections. Outbreaks of infection
have been traced to S. aureus and group A Strep-
tococcus bacteria from the scalp and hair of both
surgical personnel and the patient. There is no evi-
dence supporting a correlation between disposable
shoe covers and surgical site infection. However,
in procedures known to be associated with fluid
transfer (i.e. liposuction), they may serve to limit
contamination of the surgeon’s shoes.
Patient preparation and hair
removal
Several studies have shown a clear ­ correlation
bet­ween wound infection and hair remo­
val by shaving (incidence 2.3–7.1%). This is
­particularly true when the surgical site is shaved
more than 24 h before the procedure (incidence
up to 20%). This increased risk is attributed to
microabrasions in the skin caused by shaving, as
abrasions encourage higher levels of resident and
transient flora. If hair must be removed from the
surgical field, it is best to clip it with scissors or
electric shears prior to establishing a sterile field,
as this is associated with only a modest increase
in risk for wound infection (1.7% versus a con-
trol of 0.9% in one study). When possible, the
 2

Chapter
Antisepsis 47

patient’s hair should be left intact. If the hair is Pearls

interfering with surgery, it can be held out of the
surgical field with sterile clips or water-soluble
lubricating jelly.
Instrument sterilization
Sterilization refers to a physical (heat, pressure,
or steam) or chemical (gas vapor or disinfectant)
process that completely destroys and removes
all viable microorganisms from a surgical instru-
ment. Many processes combine both physical
and chemical aspects to achieve sterilization
(Table 2-6). Several methods are available that
can be performed in an office-based setting,
whereas others are more practical for a hospital
(industrial setting). The most common method
used in office settings is steam under pressure,
or autoclave. A drawback to steam sterilization
is that it may dull the sharp cutting surfaces of
high-grade carbon steel instruments (hair trans-
plant punches, super-cut scissors) with repeated
processing. Immersion sterilization in a liquid
disinfectant is less practical because instruments
cannot be wrapped for storage and must be used
immediately.
• Increases in wound infections may be traced
frequently to routine breaks or inconsistencies
in aseptic technique by the surgeon (handwash-
ing) and staff (lack of adequate patient scrub),
or bacterial colonization of a member of
the surgical team.
• Good surgical technique avoids compromising
the environment of the surgical wound
and decreases the risk of infection. This
includes: establishing and maintaining a sterile
field, atraumatic handling of tissue, effective
hemostasis with minimal electrocautery, and
limiting the amount of implanted material within
the wound.
• Postoperative patient application of hydrogen
peroxide, topical antibiotics, or alcohol may
irritate the wound and mimic infection.

Table 2-6  Instrument sterilization techniques

Technique Materials Protocol Application Comments
Steam under pressure High-pressure 15–30 min (complete Office setting (many Most efficient and
(autoclave) distilled water (15– heating and drying liquids, glass, metal, economical
20 psi)121°C (250°F) phases total 50 min) paper, cotton) May dull edges on
carbon steel
Not for certain plastics
or oils
Heated chemical Alcohol and 15–20 min (shorter Hospital setting Can be used on
vapor formaldehyde heating time than sharp instruments
Low humidity an autoclave and no Requires protective
drying phase) gear, ventilation, safety
monitoring
Dry heat Temperatures of 121– 20–30 min (requires Office or hospital Does not dull, corrode,
204°C (250–400°F) heating time and cool setting or rust instruments
No humidity down phase) Risk of burn injury to
personnel
Gas sterilization Ethylene oxide or Long process (requires Hospital setting Good for heat- and
formaldehyde complete gas venting moisture-sensitive
Highly toxic and phase) tools
carcinogenic Extensive venting
systems needed
Chemical immersion Glutaraldehyde or 6–12 h (tools must Hospital setting Instruments cannot be
formaldehyde (liquid be rinsed, dried, and wrapped for storage 2%
solutions) used immediately for glutaraldehyde most
sterility) common (not reliably
sporicidal)
Ortho-pthalaldehyde Faster (10–15 min; Office or hospital Superior mycobacterial
(OPA – new liquid nonirritating; tools setting and sporicidal activity
sterilant FDA approved must be rinsed, dried but may stain skin gray
for use in 1999) and used immediately)

ERRNVPHGLFRVRUJ
48 Dermatologic Surgery
Further reading
Dixon AJ, Dixon MP, Askew DA, et al. Prospective
study of wound infections in dermatologic surgery
in the absence of prophylactic antibiotics. Derm
Surg 2006;32(6):819–827.
Edwards PS, Lipp A, Holmes A. Preoperative skin
antiseptics for preventing surgical wound infec-
tions after clean surgery. Cochrane Database Syst
Rev 2004;3: CD003949.
Futoryan T, Grande D. Postoperative wound infec-
tion rates in dermatologic surgery. Dermatol Surg
1995;21:509–514.
ERRNVPHGLFRVRUJ
Mangram AJ, Horan TC, Pearson ML, et al. Guide-
line for prevention of surgical site infection, 1999.
Hospital Infection Control Practices Advisory
Committee. Infect Control Hosp Epidemiol
1999;20:250–278.
Patton LL, Shugars DA, Bonito AJ. A systematic
review of complication risks for HIV-positive
­patients undergoing invasive dental procedures.
J Am Dent Assoc 2002;133:195–203.
Seal LA, Paul-Cheadle D. A systems approach to
preoperative surgical patient skin preparation. Am
J Infect Control 2004;32(2):57–62.

Local anesthetics
Key Points
• Local anesthetics are commonly used in skin
surgery, avoiding the risks associated with
general anesthesia.
• Anesthetics may be delivered through topical
application, local infiltration, or regional nerve
blocks.
• The choice of anesthetic agent and method of
delivery depends on the type of surgery planned,
anatomic location of surgery, and patient
characteristics.
History
Modern local anesthesia was revolutionized in
1905 with the synthesis of procaine by Einhorn.
Procaine use was limited, however, owing to the
potential for severe allergic reaction to one of
its metabolites, para-aminobenzoic acid (PABA).
Tetracaine, a more potent ester anesthetic, was
introduced in 1930, but its use was also limited
because of similar allergic reactions.
In 1943, lidocaine was developed by Lofgren.
It is an amino amide that does not metabolize to
PABA. Lidocaine replaced procaine as the local
anesthetic of choice because of its low allergic
potential.
Mechanism of action
Local anesthetics produce their effect by prevent-
ing depolarization of the nerve cell membrane.
Stimulation of a nerve causes an influx of sodium
ions into the cell from the extracellular space.
The rapid influx of sodium ions starts the proc-
ess of depolarization and produces an action po-
tential. Local anesthetics prevent the rapid influx
of sodium ions through the voltage-gated sodium
channels (as well as interfering with potassium
channels), thereby preventing depolarization and
the production of an action potential.
It is believed that local anesthetics reversibly
block the internal portion of the sodium chan-
nels. To reach this intracellular portion of the
ERRNVPHGLFRVRUJ
3
Chapter
Jon G. Meine
s­ odium channel, the local anesthetic must first pass
through the lipophilic (phospholipid bilayer) nerve
cell membrane. Local anesthetics are ­supplied in an
acidic solution, in which most of the drug is present
in its ionized state (H+), which is hydrophilic and
lipophobic. The drug must convert to its un-­ionized
(base) state to pass through the nerve cell mem-
brane (Fig. 3-1). The proportion of drug available
in its base form is determined by the pKa of the
drug (Table 3-1) and the pH of the ­ tissue/inter-
stitial fluid. Once the drug enters the intracellular
space, the lower pH converts the drug back to its
ionized/cationic (active) form, which can block the
internal portion of the sodium ­channel.
For an anesthetic to function, it must:
• Reach the target nerve in sufficient
concentration
• Diffuse through the cell membrane’s lipid
bilayer
• Convert to an active (cationic, NH+) form.
Pain and temperature sensation are carried by
small unmyelinated type C fibers and myelinated
type A delta fibers (Table 3-�2). Local anesthetics
have the greatest effect on these smaller fibers, so
that pain is the primary sensation blocked, while
touch, pressure, and motor function are minimally
affected.
Structure
Local anesthetics have a similar basic chemical
structure (backbone) (Fig. 3-2). They consist of
three portions: an aromatic portion, and inter-
mediate chain, and a terminal amine group. The
aromatic component is typically a benzene ring,
which is lipophilic.
The terminal amine portion is hydrophilic, or
water soluble. The amine portion is a weak base
that accepts hydrogen ions (H+) and converts
the anesthetic into an active (cationic) form. The
­intermediate chain is composed of either an ­ester
50 Dermatologic Surgery

RNH+ RN + H+ (C-O-O-) or an amide (NH-), which links the

aromatic and amide ends.
Outside membrane
Diffusable form
Nerve cell membrane Classification
Active form Inside membrane Local anesthetics (Table 3-�
3) are classified into
two groups based on their intermediate chain
RNH+ RN + H+ (Fig. 3-�
3). The intermediate chain determines
the pathway by which the local anesthetic is
Figure 3-1  Acid–base equilibrium of local anesthetics ­metabolized.

Table 3-1  pKa and onset of action of local anesthetics

pKa % RN at pH 7.4 Onset (min)
Mepivacaine 7.6 40 2–4
Etidocaine 7.7 33 2–4
Articaine 7.8 29 2–4
Lidocaine 7.9 25 2–4
Prilocaine 7.9 25 2–4
Bupivacaine 8.1 18 5–8
Procaine 9.1 2 14–18
RN is the uncharged base molecule (the molecular form of the anesthetic that is able to diffuse through the lipid membrane of the nerve cell); it relates
to the potency (onset) of the anesthetic.

Table 3-2  Size and conduction velocity of nerve fibers

Namea Function External diameter (μm) Conduction velocity (m/s)
Myelinated fibers
A-α or IA Motor to skeletal muscle; 12–20 70–120
sensory from muscle spindle
proprioceptive endings (phasic,
annulospiral type)
A-β or IB Sensory from tendons (tension); 10–15 60–80
also Ruffini endings in skin
II Sensory from Meissner’s and 5–15 30–80
Pacinian corpuscles, and similar
endings in skin and connective
tissue; from large hair follicles
and tonic proprioceptive endings
(flower-spray type) of muscle
spindles
A-γ Motor to intrafusal fibers of 3–8 15–40
muscle spindles
A-δ or III Sensory from small hair follicles 3–8 10–30
and from free nerve endings for
temperature and pain sensation
B Preganglionic autonomic (white 1–3 5–15
rami and cranial nerves 3, 7,
9, 10)
Unmyelinated fibers
C or IV Pain and temperature; olfaction; 0.2–1.5 0.5–2.5
postganglionic autonomic
aLetters are used for any nerve; Roman numerals are for sensory fibers in dorsal spinal roots.

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 3

Chapter
Local anesthetics 51

Ester anesthetics are metabolized via ­hydrolysis
by pseudocholinesterase, a widely available ­plasma
enzyme, and excreted in urine. One of the me-
tabolites of ester anesthetics is PABA, which is a
well documented allergen. Patients with defects in
pseudocholinesterase have a decreased ability to
metabolize ester anesthetics; this could ­potentially
lead to high serum drug levels. Ester ­ anesthetics
should be avoided in patients with such conditions
and in those with a documented allergy to PABA.
Amide anesthetics are metabolized in the liver
via microsomal enzymes, specifically cytochrome
P-4503A4. Patients with liver disease and ­patients
taking medications that interfere with the metab-
olism of the anesthetic may be at increased risk
for adverse effects due to high serum drug levels
(Box 3-1). Antihypertensive medications, such
as beta-blockers, and congestive heart failure can
R1
r­ educe blood flow to the liver and therefore slow
the metabolism of amide local anesthetics.
Adverse effects
Local anesthetics are very safe when administered
properly and within the recommended dosage
(Table 3-�4). Allergic reactions, local toxicity, and
systemic toxicity are rare but potential complica-
tions of local anesthetics.
Local effects
Pain is a common local effect with injection of
­local anesthetics, but can be minimized with
good technique (Box 3-2). Less common adverse
­effects at the site of injection include ecchymosis,
hematoma, infection, nerve laceration, and tissue
necrosis. Nerve laceration can result in temporary
or longer-lasting pain or paresthesias.

Amide or
Ester linkage
N Systemic effects
R2 Systemic adverse effects occur due to raised plas-
ma concentrations of local anesthetics. Inadvertent
Lipophilic aromatic ring Hydrophilic amine
intravascular injection or excessive doses of local
Figure 3-2  Generic structure of local anesthetic agents anesthetic are usually responsible for systemic

Table 3-3  Local anesthetics

Maximum doseb
Brand Primary Relative Durationa Maximum doseb with epinephrine
Generic name name use potency Onset plain plain (mg) (mg)
Amides
Bupivacaine Marcaine Infiltration 8 2–10 min 3–10 h 175 250
Dibucaine Nupercaine Topical Rapid Short
Etidocaine Duranest Infiltration 6 3–5 min 3–10 h 300 400
Lidocaine Xylocaine Infiltration/ 2 Rapid 1–2 h 300 500 (3850 dilute)
topical
Mepivacaine Carbocaine Infiltration 2 3–20 min 2–3 h 300 400
Prilocaine Citanest Infiltration 2 Rapid 2–4 h 400 600
Prilocaine/ EMLA Topical 30–120 Short
lidocaine min
Esters
Benzocaine Anbesol, Topical Rapid Short
etc.
Chloroprocaine Nesacaine Infiltration 1 Rapid 0.5–2 h 600
Cocaine 45 min 200
Procaine Novocaine Infiltration 1 Slow 1–1.5 h 500 600
Proparacaine Ophthaine Topical Rapid Short
Tetracaine Pontocaine Infiltration 8 Slow 2–3 h 20
Tetracaine Cetacaine Topical Rapid Short
aIn clinical practice the duration of anesthesia appears to be less than stated above, especially for head and neck areas, and addition of epinephrine

prolongs anesthesia by a factor of 2.

bMaximum doses are given for a 70-kg person.

ERRNVPHGLFRVRUJ
52 Dermatologic Surgery

Aminoesters
Table 3-4  Maximum recommended dose of lidocaine
O CH2 CH3 Maximum dose (mg/kg)
H2N C C CH3 CH2 N Adults Children
CH2 CH3 With epinephrine 7.0 3.0–4.5
Without 5.0 1.5–2.0
Aminoamides epinephrine

CH3
O CH2 CH3 B ox 3 - 2
NH C CH3 N
Tips for reducing the pain of injection
CH2 CH3
CH3 Do not leave fluid on the needle when entering the skin.

Figure 3-3  Amino esters and amino amides Pinch the area before injecting.
Use the smallest (diameter) and longest needle possible.

B ox 3 - 1 Enter through a pore if possible.

Infiltrate slowly.
Commonly used medications known to inhibit
cytochrome P450 (adapted from Klein 2000) Use longer-acting anesthetic for long procedures.
Warm the anesthetic solution.
Antiarrhythmic agents • Itraconazole
• Amiodarone Preanesthetize
• Ketoconazole
• Quinidine • Ice
Antituberculous agents
Antibiotic agents • Topical lidocaine or lidocaine/prilocaine cream
• isoniazid
• Chloramphenicol • Benzocaine (mucosal surfaces)
Antiulcer agents
• Clarithromycin • Inject first with saline or plain lidocaine.
• cimetidine
• Erythromycin Methods for increasing pH – buffering local anesthetic
Benzodiazepines
solutions
• Tetracycline • Midazolam
• Mix plain lidocaine with fresh epinephrine (0.3 mL 1:1000
• Metronidazole • Triazolam epinephrine in 30-mL vial of lidocaine = 1:100 000)
Antidepressant agents Beta-blockers • Add sodium bicarbonate 8.4% – one part to nine parts
• Citalopram Calcium channel blockers lidocaine with epinephrine

• Fluoxetine • Diltiazem • Dilute lidocaine–epinephrine solution with plain

lidocaine.
• Paroxetine • Nicardipine
• Sertraline • Nifedipine
the central nervous system (CNS) and cardiovas-
Antiepileptic agents • Verapamil
cular system. The effects on the CNS are predict-
• Carbamazepine Immunosuppressants able and dose dependent (Table 3-�6).
• Valproic acid • Ciclosporin
Antifungal agents • Dexamethasone Cardiovascular
• Fluconazole • Methylprednisolone High serum levels of local anesthetics have a neg-
ative inotropic effect on the heart, resulting in de-
creased contractility, reduced cardiac output, and
e­ ffects (Table 3-� 5). Factors influencing plasma hypotension. Local anesthetics prolong conduc-
concentrations of these drugs include quantity of tion time in several pathways in the heart result-
the drug, concentration of the drug, vascularity of ing in an increased PR interval, prolonged QRS
the injection site, rates of absorption and metabo- complex, bradycardia, and atrioventricular block.
lism of the drug, and the weight, age, and health Arrhythmias are more common in patients with
of the patient. As mentioned above, local anes- underlying conduction irregularities. Bupivacaine
thetic use in patients with certain medical condi- has a higher risk for ventricular arrhythmias such
tions or taking drugs that affect the metabolism as ventricular fibrillation.
of local anesthetics should be limited because of Treatment of adverse cardiovascular effects
an increased risk of systemic toxicity. is primarily supportive. Advanced Cardiac Life
The systemic adverse effects of high levels of Support (ACLS) protocols should be initi-
local anesthetics in the serum primarily involve ated if the patient is symptomatic or unstable.

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 3

Chapter
Local anesthetics 53

Box 3-3 ­summarizes the differences in signs and Allergy

­symptoms between a vasovagal reaction, epine-
phrine reaction, anaphylactic reaction, and lido-
caine overdose.
Methemoglobinemia (hematologic)
Methemoglobinemia has been seen prima-
rily with prilocaine toxicity, but lidocaine and
­benzocaine have also been reported causative
agents. Infants under 6 months of age are par-
ticularly ­ susceptible. A metabolite of prilocaine,
O-toluidine, is a potent oxidizer of hemoglobin
to ­methemoglobin. Normal methemoglobin lev-
els are less than 1%. Slightly increased methemo-
globin levels may be asymptomatic, but patients
with higher ­ levels (10–40%) may present with
the following ­symptoms/complaints:
• cyanosis
• cutaneous discoloration (pale, gray, blue)
• dizziness and syncope
• dyspnea
• fatigue
• headache
• exercise intolerance
• mental status changes
• weakness
• tachypnea
True allergy to local anesthetics is uncommon.
The majority of reported adverse effects are side-
­effects of epinephrine added to the local anesthetic.
Type I (immediate hypersensitivity/anaphylaxis)
reactions account for the minority of true allergic
­reactions. The majority of type I reactions are seen
with the ester anesthetics in ­patients with a PABA
allergy. Patients allergic to an ester ­ anesthetic
and/or PABA should avoid all ester ­ anesthetics
because of cross-reactivity within the class ­
(Box 3-4). Most true allergic reactions to local
anesthetic are type IV (delayed hypersensitiv-
ity) reactions. Type IV reactions are seen with
both amide and ester anesthetics. ­ Preservatives
in multi-use vials of local anesthetics such as
­methyl­paraben and sodium metabisulfate can
cause ­adverse reactions in patients with an allergy
to esters and/or PABA.
Epinephrine
Most local anesthetics, with the exception of
­cocaine, act as vasodilators because they result
in relaxation of vascular smooth muscle. The net
result is increased bleeding at the operative site
and reduction of the duration of anesthesia due to

Table 3-5  Differential diagnosis of local anesthetic systemic reactions

Diagnosis Pulse rate Blood pressure Signs and symptoms Emergency management
Vasovagal reaction Low Low Excess parasympathetic tone; Trendelenburg, cold
diaphoresis, hyperventilation, compress, reassurance
nausea

Epinephrine reaction High High Excess α- and β-adrenergic Reassurance (usually

receptor stimulation; resolves within minutes),
palpitations phentolamine, propranolol
Anaphylactic reaction High Low Peripheral vasodilatation with Epinephrine 1:1000 0.3  mL
reactive tachycardia; stridor, SC, antihistamines, fluids,
bronchospasm, urticaria, oxygen, airway maintenance
angioedema
Lidocaine overdose
(μg/mL)
1–6 Normal Normal Circumoral and digital Observation
paresthesias, restlessness,
drowsiness, euphoria,
lightheadedness
6–9 Normal Normal Nausea, vomiting, muscle Diazepam, airway
twitching, tremors, blurred maintenance
vision, tinnitus, confusion,
excitement, psychosis
9–12 Low Low Seizures, cardiopulmonary Respiratory support
depression
>12 None None Coma, cardiopulmonary arrest CPR/ACLS
CPR, cardiopulmonary resuscitation.

ERRNVPHGLFRVRUJ
54 Dermatologic Surgery
Table 3-6  CNS effects of lidocaine
Serum level
(μg/mL) Effects
1–5 Drowsiness, tinnitus, circumoral tingling,
nausea, lightheadedness, vomiting,
talkativeness, double vision, metallic taste
5–8 Nystagmus, slurred speech, hallucinations,
localized muscle twitching, fine tremors of
face and hands
12–15 Focal or grand mal seizures,
cardiopulmonary depression
20–25 Apnea, coma, cardiopulmonary arrest
B ox 3 - 3
Treatment of CNS toxicity
Need to reduce hypoxia and acidosis
Oxygen
Leg elevation
Increase respiratory rate to produce a respiratory alkalosis
Convulsions:
• Valium 5–10 mg IV
• Thiopental 50 mg IV
• Succinylcholine 1mg/kg
B ox 3 - 4
Alternatives to local anesthetics
• Benzyl alcohol
• Diphenhydramine
• Saline
• Ice
• Dichlorotetrafluoroethane or ethyl chloride
i­ncreased absorption of the drug. ­Vasoconstrictors,
namely epinephrine, are commonly added to
­local anesthetics to counteract this effect (Box
3-5). Epinephrine is typically found in a 1:100 000
­concentration, but is an effective vasoconstrictor
at dilutions of up to 1:1 000 000 (Klein’s tumes-
cent formula). The maximal vasoconstrictive
­effect of epinephrine takes up to 10–15 min and
is evident by blanching of the affected skin.
Adverse effects of epinephrine can occur
with low doses. The most common side effect
is tachycardia. Higher doses (as with inadvert-
ent intravenous injection) can cause palpitations,
diaphoresis, pallor, angina, tremors, nervousness,
headache, and hypertension. The maximum dose
ERRNVPHGLFRVRUJ
B ox 3 - 5
Advantages of vasoconstrictors
• Decreased rate of absorption of anesthetic
• Reduced risk of systemic toxicity
• Prolonged duration of anesthesia
• Decreased bleeding at operative site
B ox 3 - 6
Contraindications to epinephrine
• Severe hypertension
• Severe cardiovascular disease
• Severe peripheral vascular disease
• Hyperthyroidism
• Pheochromocytoma
B ox 3 - 7
Relative contraindications to epinephrine
• Pregnancy
• Psychological instability
of epinephrine in a healthy patient is 1 mg, or
100 mL of a 1:100 000 concentration. Special
caution should be taken in patients with cardio-
vascular disease. See Boxes 3-6 through 3-8 for
contraindications and relative contraindications
to epinephrine.
Pregnancy and lactation
Local anesthetics can cross the placental membrane
by (passive) diffusion. Used conservatively, they
are considered to be safe in pregnancy. Although
elective or large procedures are best delayed until
after delivery, simple procedures such as biopsy
of a changing and/or atypical pigmented lesion
has little risk to the fetus with the use of a small
amount of local anesthetic. Some ­ obstetricians
recommend avoiding local ­anesthetics in the first
trimester when organogenesis occurs. Lidocaine,
etidocaine, levobupivacaine, prilocaine, and pro-
caine are considered pregnancy category B, while
bupivacaine, mepivacaine, articaine, tetracaine,
and chloroprocaine are category C. Epinephrine
is considered pregnancy category C and should
be used conservatively, as large doses can cause
decreased placental perfusion.
 3

Chapter
Local anesthetics 55

B ox 3 - 8 B ox 3 - 9
Drug reactions with epinephrine Anesthesia techniques
Methods of administration
Severe, prolonged hypotension or hypertension may be
produced if given to patients taking: • Local infiltration
• Monoamine oxidase inhibitors • Field block
• Tricyclic antidepressants • Nerve block
• Butyrophenones • Ring (digital) block
• Phenothiazines
• Vasopressors
• Oxytocin may be considered. Another option is to have
the patient pump her breast milk several hours
Non-selective beta-blockers can lead to unopposed after the procedure and discard the expressed
α-adrenergic stimulation:
milk.
• propranolol (Inderal)
• carvedilol (Coreg) Topical anesthesia
• labetalol (Normodyne, Trandate)
A number of agents are available for anesthe-
• nadolol (Corgard) tizing the skin and mucosal membranes (Table
• penbutolol (Levatol) 3-�7). The stratum corneum is a major barrier to
absorption of topical anesthetics through intact
• pindolol (Visken)
skin; ­ therefore application times are generally
• sotalol (Betapace) longer than for mucosal sites, and occlusion is
• timolol (Blocarden) frequently used to enhance absorption. Products
containing ­ benzocaine and prilocaine should be
Treatment for epinephrine toxicity:
avoided in infants due to the risk of methemo-
• Hydralazine 20 mg in 250 mL normal saline globinemia.
• Pentolamine 5 mg over 1 min
Anesthesia techniques
There are several methods of anesthesia ad-
Local anesthetics and epinephrine are ­excreted ministration in dermatologic surgery (Box 3-9).
in breast milk and should be used with caution The most common method is local infiltration,
in women who are nursing. Ester anesthetics where the anesthetic is injected directly into or
are preferred during lactation because they are below the lesion into the subcutaneous tissue.
­significantly metabolized in plasma before reach- This is most useful for small or limited surgical
ing breast tissue. Alternatives to “caine” ­anesthetics areas.

Table 3-7  Topical anesthetics for mucous membrane and intact skin anesthesia
Generic name Brand name Concentration (%) Type Primary use
Benzocaine Americaine otic 20 Ester Tympanic membrane
Benzocaine Hurricane 20 Ester Mucous membranes
Benzocaine/tetracaine Cetacaine 14/2 Ester Mucous membranes
Cocaine 2–10 Ester Nasal mucosa
Dibucaine (cinchocaine) Nupercainal 1 Amide Mucous membranes
Lidocaine LMX 4–5 Amide Intact skin
Lidocaine Topicaine 4 Amide Intact skin
Lidocaine Xylocaine 2–5 Amide Mucous membranes
Lidocaine in acid mantle cream 30–40 Amide Intact skin
Prilocaine/lidocaine EMLA 2.5/2.5 Amide Intact skin
Proparacaine (proxymetacaine) Alcaine 0.5 Ester Conjunctiva
Tetracaine Pontocaine 0.5 Ester Conjunctiva
Prilocaine–lidocaine mix Betacaine LA Proprietary Amide Intact skin

ERRNVPHGLFRVRUJ
56 Dermatologic Surgery
B ox 3 - 1 0
Nerve blocks
Advantages
• Anesthetizes the nerve before it reaches the operative site
• Affects a large area with small amount of anesthetic
• No distortion of operative site
Disadvantages:
• No vasoconstriction
• Longer onset
• Shorter duration
• Risk of nerve laceration
Technique – general principles
• Lidocaine and/or longer-acting anesthetic
• 5-mL syringe
• 27- or 30-gauge 1⁄2-inch needle
• Inject slowly into subcutaneous plane in vicinity of nerve
• Avoid directly hitting the nerve (back off if sharp pain when
inserting needle)
• Don’t inject directly into the foramen
• Pull back on the plunger before infiltrating
• Wait 10–15 min for the full effect
B ox 3 - 1 1
Supraorbital/supratrochlear nerve block (V1)
Provides sensation to forehead
Indications
• Hair transplantation
• Laser resurfacing
• Large surgical defects
Location
• Supraorbital nerve – mid-pupillary line along superior
bony orbit
• Supratrochlear nerve – superior/medial corner of
bony orbit
Inject about 1 mL lidocaine (± epinephrine) in subcutaneous
fat overlying supraorbital foramen
Inject about 1 mL at root of nose/medial border of orbit
A field block is the most common method
for achieving anesthesia for basic excisional sur-
gery. In this method, the anesthesia is infiltrated
around the periphery of the surgical site, provid-
ing anesthesia to the infiltrated area along with
the central portion within its boundaries. A bene­
fit of this technique is the potential to anesthetize
the entire site with only one painful needle stick.
ERRNVPHGLFRVRUJ
B ox 3 - 1 2
Infraorbital block (V2)
Provides sensation to lower eyelid, medial cheek, nose, and
upper lip
Indications
• Fillers
• Laser resurfacing
• Large surgical defects
Location
• Foramen is 1 cm inferior to the infraorbital ridge along the
mid-pupillary line
Approach through the oral cavity
The nerve is 0.5–1 cm above superior labial sulcus
Anesthetize oral mucosa with topical benzocaine first
Enter at apex of first bicuspid and direct needle towards
estimated location of foramen
Inject 1–2 mL with a 1⁄2-inch needle (27 or 30 g)
B ox 3 - 1 3
Mental nerve block (V3)
Sensation to lower lip, chin and mucous membranes
Indications
• Fillers
• Laser resurfacing
• Large surgical defects
Location
• Midway between upper and lower edge of mandible below
second bicuspid (mid-pupillary line)
Approach through the oral cavity
Anesthetize oral mucosa with topical benzocaine first
27- or 30-G 1⁄2-inch needle
Enter inferior labial sulcus between first and second bicuspids
Inject 1–2 mL around mental foramen
To achieve this, the surgeon anesthetizes the first
area and then reinserts the needle distal to the
first injection but still within the first area of an-
esthesia. In this way, the anesthesia is advanced
systematically around the periphery, each time
starting in an area of previous anesthesia [one
stick method]. One disadvantage of this meth-
od is that the volume of anesthetic may distort
­anatomic landmarks and time must be allowed
for the anesthesia to infiltrate. See Chapter 10,
Figure 10-4 for illustration.
Nerve blocks may be used in dermatologic
surgery to anesthetize a large area of skin and

B ox 3 - 1 4
Digital block
Paired dorsal and medial digital nerves
Indications
• Nail plate avulsion
• Nail unit biopsy
• Distal digit surgery
• Periungual warts
Plain lidocaine 1% or 2%
5-mL syringe
27- or 30-G needle
Topical anesthesia or ice prior to injecting
No more than 5 mL total volume
avoid distortion of the surgical site. Advantages,
­disadvantages and general principles of nerve
blocks are listed in Box 3-10. The indications for
and anatomy of supraorbital, supratrochlear, in-
fraorbital, and mental nerve blocks are listed in
Boxes 3-11 through 3-13.
A ring or digital block is when anesthesia is
infiltrated circumferentially around the proximal
base of an extremity, such as the penis or a digit
and provides anesthesia distally. This is much less
painful than injecting anesthesia directly into the
glans penis or tip of the finger. Historically there
has been concern regarding the use of epinephrine
in a circumferential ring block and its potential
to induce ischemia secondary to vasoconstric-
tion. There have been some recent studies docu-
menting the safe use of epinephrine-containing
­anesthesia in digital ring blocks; however, this has
not been universally accepted. Regardless of the
anesthetic choice, care must be taken to limit the
volume of anesthesia introduced in that it may
tamponade the blood supply, simply via a volume
effect. See Box 3-14 for indications and Chapter
15 for technique details.
Tumescent anesthesia
Jeffrey Klein revolutionized liposuction in 1987
when he published the tumescent technique for
liposuction. Tumescent anesthesia involves the
infiltration of a large volume of dilute ­ lidocaine
ERRNVPHGLFRVRUJ
3
Chapter
Local anesthetics 57
(0.05–0.1%) into the subcutaneous space. The
standard formula for tumescent anesthesia is
1000 mL of normal saline, 50–100 mL of 1%
­lidocaine, 1 mL of 1:1000 epinephrine, and
12.5 ml of sodium bicarbonate. This technique
causes significant vasoconstriction and profound
anesthesia, resulting in minimal blood loss, no
need for general anesthesia, or deeper sedation.
The absorption kinetics for lidocaine change
when administered using this method. Klein and
others have shown that doses of lidocaine between
35 and 55 mg/kg are safe with the ­ tumescent
technique for liposuction. Tumescent anesthesia
in dermatologic surgery has expanded to many
other applications, such as laser ­ resurfacing and
dermabrasion.
Summary
Local anesthetics are a staple in dermatologic
practice. Knowledge of the indications, limita-
tions, techniques of administration, and adverse
effects of local anesthetics is crucial for the safety
and effectiveness of cutaneous surgery.
Further reading
Gmyrek R, Dahdah M. Local anesthesia and regional
nerve block anesthesia. emedicine. Online. Avail-
able: http://www.emedicine.com/derm/topic824.
htm
Grekin RC, Auletta M. Local anesthesia in der-
matologic surgery. J Am Acad Dermatol
1988;19(4):599–614.
Huang W, Vidimos A. Topical anesthetics in derma-
tology. J Am Acad Dermatol 2000;43:286–298.
Jackson T, McLure HA. Pharmacology of local anes-
thetics. Ophthalmol Clin N Am 2006;19:155–161.
Klein JA, ed. Tumescent Technique: Tumescent
Anesthesia and Microcannular Liposuction.
St Louis: Mosby, 2000.
Klein JA, Kassarjdian N. Lidocaine toxicity with
tumescent liposuction. A case report of probable
drug interactions. Dermatol Surg 1997;23:
1169–1174.
Lynch C 3rd. Depression of myocardial contractility
in vitro by bupivacaine, etidocaine and lidocaine.
Anesth Analg 1986;65:551–559.
Upadya M, Upadya GM. Anesthesia for dermato-
logic surgery. Indian J Dermatol Venereol Leprol
2005;71:145–154.

Surgical instruments
Ashish C. Bhatia and Aashish Taneja
Surgical instruments are the most basic and
fundamental tools of the dermatologic surgeon.
Fortunately, the variety and quality of surgical
instruments available to the dermatological sur-
geon have improved tremendously over the past
few decades. The saying “Select the right tool
for the right job” truly has relevance in this field.
Each instrument has its own niche and pur-
pose, depending on the type of procedure that
will be performed. All surgical instruments are
available in different quality grades. In general,
­selecting higher quality grade instruments will
translate to longer lasting, better performing
instruments. It is important that the surgeon’s
instruments be of the highest quality possible.
Using inadequate instruments or equipment of
poor quality can lead to frequent replacement,
poor performance, and, in many cases, unneces-
sary tissue damage.
Knowledge of the core instruments used in
dermatologic surgery and understanding the
­capabilities and limitations of each will not only
enhance the life of the instrument and improve
performance of the instrument, but also expedite
the procedure and maximize the outcome for the
patient. In general, instruments utilized for der-
matologic surgery are small, fine, and lightweight,
thus allowing for proper atraumatic handling
of delicate tissue and minimal operator fatigue.
Modern instruments may be made from various
metals or a combination of metals, such as sur-
gical stainless steel with carbon alloy, chromium
nickel, and tungsten carbide. Tungsten carbide
is a very hard alloy that enhances function and
­durability of blades of scissors and jaws of needle
holders, and is usually incorporated as inserts on
otherwise steel-based instruments.
The following instruments are reviewed in
this chapter: biopsy instruments, scalpels, cu-
rettes, scissors, forceps, needle holders, chalazion
clamps, skin hooks, hemostats, periosteal eleva-
tors, and bone chisels. These form the set of core
instruments most often used in dermatologic
surgery.
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4
Chapter
Biopsy instruments
Key Points
• Biopsy instruments are those used to obtain
samples of cutaneous and/or subcutaneous
tissue.
• Both disposable and reusable biopsy
instruments are available, each having their own
distinct advantages and disadvantages.
Samples of integument can be obtained via punch,
shave, or excisional biopsy. While excisional biop-
sies are usually obtained using a scalpel, punch
­biopsies and shave biopsies can be performed
with specialized tools.
Punch biopsy instruments are available in vari-
ous sizes including 1, 1.5, 2, 3, 4, 5, 6, and 8 mm.
The instruments usually consist of a ­ cylindrical
handle and a blade, which is generally circular
with a hollow core. There are also elliptically
shaped punch biopsy instruments designed to
­excise lesions in an “easy to close” manner. As the
defect left by such a punch biopsy is elliptical
in shape, some minor undermining and layered
­sutures can provide a quick linear closure.
A shave biopsy can be executed with a No. 15
blade, Gillette® blade, or Dermablade®. The dif-
ference between a Gillette® and Dermablade® is
that the Dermablade® is sterile, more convenient,
and more expensive than the Gillette® blade.
However, Gillette® blades can be sterilized prior
to use. The Dermablade® also comes with a pro-
tective plastic support that offers better grip and
more safety to the surgeon.
Biopsy instruments can be disposable or re­
usable. Disposable instruments (Fig. 4-1) offer the
convenience of one time use, avoiding the hassle
of instrument cleaning, packaging, and steriliza-
tion. Another advantage of disposable instruments
is that each instrument is always sharp. Reusable
instruments (Fig. 4-2) need to be monitored for
dulling and wear, and sharpened or disposed of
when they become dull or damaged. The primary
60 Dermatologic Surgery
Figure 4-1  Disposable punch biopsies in various sizes
Figure 4-2  Reusable punch biopsy instruments
advantage of reusable instruments lies in their
economy. These instruments can be cleaned and
reused many times before dulling. They can also
be packaged conveniently into bundles of instru-
ments containing all of the necessary instruments
for a certain procedure. These bundles can be
marked as to their content and sterilized in one
package.
Scalpel
Key Points
• Scalpels consist of a handle and a blade, and
both are available in a variety of sizes and shapes
to accommodate both surgeon preference and
application.
• There are various methods for holding and using
a scalpel based upon the type of scalpel, handle,
and application.
A scalpel can be used for incising, puncturing, and
sectioning tissue as well as for scraping tissue in
certain circumstances. A scalpel generally con-
sists of a blade and a handle. The type of handle
and blade selected depends on the surgeon’s pre­
ference as well as the surgical application.
Blades are made of either carbon steel or stain-
less steel (Fig. 4-3). Proponents of carbon steel
prefer their sharper nature, although these blades
do dull rapidly with use. Stainless steel blades
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Figure 4-3  Blades can be stainless steel or carbon steel
Figure 4-4  Blades coated with Teflon™ to reduce
dragging
are not as sharp but maintain their sharpness for
longer. Blades are also available with Teflon™
coatings to minimize any dragging of the blade
against the tissue (Fig. 4-4). This allows them to
slide smoothly through the tissues being cut. In
dermatology, the most utilized blades are Nos 15,
10, and 11. The No. 15 blade is the most common
and popular blade used for excisional surgery
(Fig. 4-5). Its gentle curve makes it appropriate
for most procedures. The sharpest portion is the
tip. The greatest contact point lies where the flat
side meets the curved point of the blade; there-
fore the handle should be approximately 30° off
of the skin when cutting. A variant of the No. 15
is the No. 15c blade, which essentially is a smaller
version utilized in areas of thin, delicate skin. The
No. 10 is a larger version of the No. 15 (Fig. 4-6).
Its wide blade with a sharp convex belly is utilized
primarily for larger excisional procedures such as
on the back. The No. 11 blade has a straight, sharp
edge that tapers to a sharp point, and is used
primarily for incision and drainage of abscesses,
milia removal, “through and through” excisions,
and cutting sharp angles (Fig. 4-7). It is generally
wielded and utilized in a stabbing fashion.
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Chapter
Surgical instruments 61

Figure 4-5  No. 15 blade Figure 4-6  No. 10 blade Figure 4-7  No. 11 blade

Figure 4-8  The Beaver blades and handle

Figure 4-10  Various handles–from top to bottom: Siegel,
No. 7 and No. 3

Figure 4-9  The Beaver handle

Beaver blades, or the miniblade system, are

much smaller than standard blades (Fig. 4-8).
They are utilized for fine cutting, especially in
tight areas such as the medial canthus, in cavities,
and near the ear and the ear canal. Many shapes
are available. The two most commonly used in
dermatology are Nos 64 and 67. The No. 64 has
a rounded tip with a sharp cutting edge. The No.
67 is similar to the No. 15c in that it is curved
convexly with a sharp tip. These blades fit into
a beaver handle – a small pencil-like instrument
useful for working in concavities (Fig. 4-9). There
are also varieties of beaver blades that are bent
laterally at the midsection of the blade to allow
for easy maneuverability and use on the walls of a
cavity such as the ear canal. Figure 4-11  Disposable curettes in different sizes
The handle of a scalpel can be flat or round
and long or thin in shape (Fig. 4-10). The stand-
• Both disposable and reusable curettes are
ard system scalpel handles consist of the No. 3 available, and each has its advantages and
and the No. 7. The No. 3 is the most frequently disadvantages.
used handle in dermatologic surgery. It is available • The curette is held like a pencil and drawn
with an optional imprinted ruler. It can accom- towards the operator with the sharp side of the
modate a variety of scalpel blades including Nos. instrument touching the patient’s skin.
10, 11, and 15. The No. 7 is most commonly used
in plastic surgery. The Beaver handle is round or One of the first instruments used by a derma-
hexagonal. It holds much smaller, sharper blades tologist, the curette is utilized to treat benign or
such as Nos 64 and 67. These blades insert into low-grade malignant tumors and also to debulk
a collet, which tightens by rotating the collet tumors prior to Mohs micrographic surgery. It can
around the handle. also allow the surgeon to define tumor margins
better prior to excision. Curettes are available as
Curettes disposable or reusable instruments (Figs 4-11 &
4-12). The curette consists of a handle and a
Key Points head. The handle can be large or small, light or
• Curettes are a versatile therapeutic and heavy. The heads can be round or oval (Fig. 4-13),
diagnostic tool for the dermatologist. and are available in a variety of sizes, where the

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62 Dermatologic Surgery
Figure 4-12  Reusable curettes shown in different sizes
Figure 4-13  Reusable oval curettes
size refers to the width of the opening. The width
ranges from 1 to 10 mm. In general, smaller sizes
are utilized for finer procedures.
Some dermatologists prefer the reusable
curettes because of their physical weight and
“dullness.” This combination allows the physician
to get a better feel of the difference in consistency
between various tissue types, such as tumor, der-
mis, and subcutaneous tissues. These practitioners
find disposable curettes too sharp and light, essen-
tially cutting through any tissue almost equally
well, and providing minimal sensory feedback
­regarding the tissue being curettaged.
To obtain optimal sensory feedback from a
curette, it should be held like a pencil with the
sharp side of the tip angled downward. The scrap-
ing motion is towards the operator, and can be
performed in a linear or curvilinear method.
Scissors
Key Points
• A variety of scissors are available for the many
tasks involving cutting in a dermatology practice.
• There are a host of specialty scissors available
for very specific tasks in a dermatology office.
• Common uses for scissors in dermatology
include cutting or trimming tissue or grafts and
flaps, trimming bandages, cutting sutures, and
undermining tissues prior to closure.
ERRNVPHGLFRVRUJ
Figure 4-14  Tissue scissors–from top to bottom: iris, baby
Metzenbaum and strabismus
Figure 4-15  Scissors consist of tips, blades and handles
Scissors are a common instrument in the derma-
tologist’s office. They come in a variety of shapes
and sizes suited to different tasks (Fig. 4-14).
Common types of scissors include Gradle ­scissors,
tissue scissors, undermining scissors, suture-
­cutting scissors, and bandage-cutting scissors.
Dozens of specialty varieties of scissors are also
available for special purposes.
The basic anatomy of scissors consists of three
parts: the handle, the blade and the tip (Fig. 4-15).
The handle may be short or long. Generally, short
handles provide better control but less leverage,
and are utilized for fine work such as delicate sur-
geries on thinner tissues of the face. Long han-
dles not only provide greater leverage, but are
also optimal for surgeries requiring a long reach.
A longer reach may be necessary when operating
in cavities or undermining deeply under tissues.
Scissor handles are available in straight, curved,
or bent contours for increased visibility and
hand/wrist comfort for the surgeon. The blades
of scissors can also be straight or curved, for the
same reasons (Fig. 4-16). Straight blades allow for
straight cuts such as for gross trimming of flaps
and grafts, and are commonly used for cutting
sutures. Curved blades are often utilized for dis-
section, allowing easy movement around tumors
or cysts. They increase the surgeon’s visibility and
 4

Chapter
Surgical instruments 63

Figure 4-16  Scissors with a straight blade (top) Figure 4-18  Scissors reinforced with tungsten carbide
and a curved blade (bottom) (note the gold handle)

Figure 4-17  Scissors with serrated blade

allow a contoured cutting or dissecting path to be

followed easily.
The blades of scissors may be smooth or ser-
rated (Fig. 4-17). The serration on the blades of Figure 4-19  Scissors with blunt tips (left) and pointed tips
with ribbon handle (right)
surgical scissors are often very fine and difficult to
visualize; however, the “teeth” can easily be felt
when touching the blade. The advantage of the
serrated blade is that it helps to prevent slippage
of tissue out of the blades during cutting. The
serrated blade is particularly useful in areas with
thin skin and little subcutaneous fat, or when
trimming delicate flaps or grafts.
There are many different choices for the metal
used for the blades of scissors. Generally, they are
made with stainless steel. This can be reinforced
with tungsten carbide (TC) inserts to ­strengthen
the blade and prevent dulling. Scissors with
TC inserts are identified by their gold handles
(Fig. 4-18).
There are several options for scissor tips as well.
A scissor tip can be pointed, blunt, or occasion- Figure 4-20  Gradle scissors
ally hooked on one of the two blades (Fig. 4-19).
Pointed tips are optimal for more aggressive
­dissection, whereas blunt tips are used for more
atraumatic dissection such as when undermining delicate features and their sharpness and preci-
and freeing up of flaps. The single hooked tip can sion make them ideal for harvesting thin stages
be used to assist with suture removal. during Mohs micrographic surgery, or for cutting
and undermining delicate tissues.
Specialty scissors Iris scissors are the most commonly used in-
strument for dissecting and undermining on the
Gradle scissors have a high handle to blade ratio head and neck (Fig. 4-21). They generally have
and a small, delicate, sharp tip that is tapered to heavier handles and blades than Gradle scissors.
a fine point with a gentle curve (Fig. 4-20). Their The handle can be straight or curved, the blade

ERRNVPHGLFRVRUJ
64 Dermatologic Surgery
Figure 4-21  Iris scissors Figure 4-22  Westcott and Castroviejo
scissors
Figure 4-24  Mayo scissors Figure 4-25  Metzenbaum scissors
can be smooth or serrated, and the tip can be
sharp or blunt.
Westcott and Castroviejo scissors are one of the
most delicate and complicated scissors used in
dermatologic surgery (Fig. 4-22). Unlike ­ other
scissors, they are held like forceps and gently
squeezed to cut (Fig. 4-23). They are also unique
because of their spring action, which is used to
open the blades as pressure is released on the
­handles. They generally have very fine, pointed
tips and are good for delicate dissections such as
in periorbital surgery.
Mayo scissors are generally heavier scissors with
nearly a one to one handle to blade ratio (Fig. 4-24).
They are useful as general-use scissors. They are
not usually used for fine or delicate work, but
rather for coarse dissection.
Metzenbaum scissors are heavier, with a high
handle to blade ratio for maximal leverage and
length (Fig. 4-25). These long-handled scissors
are available in varying lengths. The blade can
be straight or curved, and the tip can be sharp
or blunt. These qualities make this instrument
ideal in areas that require long reach and for
ERRNVPHGLFRVRUJ
Figure 4-23  O’ Brien suture-cutting
scissors
Figure 4-26  Standard operating
scissors
tissues that are more difficult to cut or dissect.
They are commonly used for larger excisions
and undermining in areas such as the trunk and
scalp.
Like the Metzenbaum scissors, the Lagrange
scissors also have a high handle to blade ratio. Its
strongly curved tip with a reverse curve on the
handle shank makes this instrument useful to
harvest hair transplant donor grafts. It can also be
useful for freeing punch biopsy specimens with a
deep base.
Tissue scissors, such as most of the scissors
mentioned above, should generally be reserved
for cutting tissue. Surgical kits should contain
dedicated suture scissors for trimming and cut-
ting sutures. Using the same scissors to cut tissue
and sutures may result in premature dulling of
the tissue scissors. These scissors generally have
large, heavy-duty blades. Examples of good suture
scissors include standard operating scissors (Fig.
4-26) and Northbent scissors, which are specifi-
cally designed with a half-moon hook on the low-
er blade to remove sutures (Fig. 4-27). O’Brien
­scissors have a short-angled blade that ­allows the

Figure 4-27  Northbent scissors
Figure 4-28  Bandage scissors
surgeon to cut the suture with the tip of the blade
see (Fig. 4-23).
Bandage-cutting scissors tend to be large and
have blunt tips (Fig. 4-28). The blunt tips help
protect the patient’s skin during removal of band-
ages. One blade generally slides under a dressing
without injuring the underlying ­ integument.
These scissors are also used to trim bandages to
size prior to application.
Forceps
Key Points
• Forceps are versatile instruments in the
dermatology practice.
• They are used to hold or grasp items such as
tissue, sutures, or any other item handled in the
surgical field.
• Like scissors, several types of forceps are usually
ordered for various procedures to be performed
in the office.
Forceps are commonly used instruments in der-
matology. They are used to hold or grasp items
such as tissue, sutures, or any other item han-
dled in the surgical field. They are generally held
ERRNVPHGLFRVRUJ
4
Chapter
Surgical instruments 65
Figure 4-29  Variety of forceps
­ et­ween the thumb and index finger, and pressed
b
to bring the tips together.
Their anatomy consists of the handles, the tips,
and occasionally a platform which precedes the
tips. The handles can be long or short, heavy or
delicate, and occasionally textured or drilled for
added grip (Fig. 4-29).
The tips of these instruments can be delicate
(0.6 mm or less), regular (0.7–1.5 mm) or heavy
(greater than 1.6 mm) based upon the intended
use. Tips can be straight or curved (Fig. 4-30)
and can vary from smooth, serrated to toothed.
Smooth tips (Fig. 4-31) are good for removing su-
tures and splinters, and for grasping small bleeding
vessels. Serrated tips (Fig. 4-32) are generally used
for grasping tissues more firmly. Misuse of serrated
tips in delicate areas can lead to crush injury of
the tissue. Tips with teeth (Fig. 4-33) are used
to obtain a firm grasp of compliant tissue. These
also should not be used too aggressively because
they can leave marks on external tissues. Teeth
on a forceps vary in size and number. They can
be small, medium, or large. The most commonly
used toothed forceps has 1 × 2 teeth, meaning
one tooth on one tip and two teeth on the other
tip. Forceps with more teeth, such as 2 × 3 teeth
and multiple-tooth patterns, are also available
(Fig. 4-34). Furthermore, multiple-tooth patterns
may be arranged vertically or horizontally. Some
forceps come with a raised platform proximal to
the tooth to allow the surgeon to grasp the suture
needle firmly and to help remove it from tissues
(Fig. 4-35).
Adson forceps are the most common and versa-
tile tissue forceps used in dermatology (Fig. 4-36).
They are generally large forceps (4–5 inches in
length) used for grasping ­tissue during ­excisional
surgery on the trunk and ­extremities. They have a
relatively broad handle that tapers to a narrow tip.
The tip can be smooth, serrated, or toothed, and
is available with a suture-tying platform if desired
(see Fig. 4-35). The tying platform may be made
of stainless steel or of a TC insert. One variation
of the Adson forceps is the Brown–Adson forceps,
which has a row of eight or nine minute teeth
66 Dermatologic Surgery

Figure 4-30  Straight- and curved-tip Figure 4-31  Pointed smooth forceps Figure 4-32  Forceps with serrated tip
Semken forceps

Figure 4-33  Forcep with 1 × 2 teeth Figure 4-34  Brown–Adson forceps Figure 4-35  Forceps with needle
with multiple 8 × 9 teeth platform

Figure 4-37  Bishop–Harmon forceps without (left)

and with (right) teeth

Figure 4-38  Jeweler’s forceps

are much smaller than the Adson forceps, with

Figure 4-36  Adson single-toothed and dressing forceps
along the length of the tips for firmly grasping
­tissue (see Fig. 4-34). Both Adson and Brown–
Adson forceps can be ordered with fenestrated
handles for increased grip.
Bishop–Harmon forceps are generally the in­
strument of choice for grasping more delicate
­tissues, such as those of the face (Fig. 4-37). They
a total length of approximately 3½ inches with
the handles tapering to a fine tip that extends
for about 20% of the total length. They are de-
signed with three holes drilled into each side of
the ­handle. These holes contribute to their light
weight and sure grip. The tips on these forceps are
available with or without teeth.
Jeweler’s (splinter) and epilating forceps
are small and delicate forceps that taper to a
sharp pointed tip (Fig. 4-38). The tips of these

ERRNVPHGLFRVRUJ

i­nstruments are available in fine, extra fine, or
super fine varieties. These instruments are ideal
for grasping very small vessels, retrieving su-
ture fragments, or removing splinters. Jeweler’s
­forceps with angled or curved tips are often
­utilized in hair transplantation when placing the
delicate micrografts in the small recipient sites
on the scalp.
Iris forceps come in several varieties for various
uses. They have a narrower handle like that of the
Bishop–Harmon forceps, but of varying lengths
(Fig. 4-39). They have a high tip to handle ratio,
allowing less gripping force, which ­ minimizes
trauma to the tissues being handled. They of-
ten have a guiding pin, which extends from one
handle and is received by a hole in the opposing
handle. This helps prevent misalignment of the
tips when applying grasping force. The tips can be
smooth, serrated, or toothed. Iris forceps tend to
be utilized for more delicate tissues, with longer
Iris forceps used for working in deeper cavities.
Other varieties of forceps are the DeJardin
forceps (Fig. 4-40) and the Graefe and Harmon
Fixation forceps. These all have wide, horizontally
oriented, tips with eight or more horizontal teeth.
They are used in dermatologic surgery to prima-
rily handle cartilage.
Another style of forceps with a horizontally
oriented tip is the Allis forceps or clamp (Fig.
4-41). Unlike many other forceps, these have
ringed finger loops in the handle as well as a
mechanism to click the jaws closed with various
jaw pressure, much like towel clamps and needle
drivers. These are generally used to grasp tissues
Figure 4-39  Iris forceps Figure 4-40  DeJardin forceps
ERRNVPHGLFRVRUJ
4
Chapter
Surgical instruments 67
being removed, such as the wall of a cyst, or the
nail plate during an avulsion. They can also be
utilized as towel clamps for securing towels or to
secure the ­electrosurgical handle within the sur-
gical field or on the surgical tray.
The tremendous variety and subtypes of ­forceps
available make it a difficult choice when purchas-
ing forceps. It is best to purchase a few sets with
the type of forceps that one knows to be best
suited for the appropriate task. Once the basic kits
have been assembled, different varieties and sizes
of forceps can be tried to see whether they are well
suited for the task and for the surgeon’s hands. Not
all forceps work best for every surgeon, so finding
the right fit for the surgeon and task is essential to
help perform procedures efficiently and safely.
Needle holders (needle
drivers)
Key Points
• Needle holders come in a variety of shapes,
sizes, and compositions.
• Choosing needle holders for a practice is based
upon the type of procedures being done in the
practice.
• Generally, two or more sizes of needle holders
are required in most dermatology practices to
accommodate various suture needle types.
Although needle holders or drivers (Fig. 4-42) are
available in a variety of sizes and configurations,
one basic premise holds true: small needle holders
Figure 4-41  Allis forceps or clamp
68 Dermatologic Surgery
Figure 4-42  Large (top) and small Figure 4-43  Smooth surfaced needle
(bottom) needle holder holder
Figure 4-45  Crile–Wood needle holder Figure 4-46  Baumgartner needle
holder
should be used for small needles and large needle
holders for large needles.The options available with
needle holders include their size, the texture of
the jaws, the metal of the jaws, and the shape
of the jaws. The jaws of needle holders can be
smooth or fine toothed. A smooth surface
­minimizes damage to finer needles (Fig. 4-43).
One drawback, however, is that on a smooth sur-
face the small needles may tend to slip. As a re-
sult, small needle holders are available with fine
serrations that will not damage the needle. Nee-
dle holders that have fine serrations prevent the
twisting of needles during suturing (Fig. 4-44).
TC ­inserts are also available for increased durabil-
ity of the jaws. These inserts increase the strength
and ­ hardness of the instruments, and also allow
for secure gripping of needles.
Crile–Wood needle holders are large instru-
ments with blunt tips that are best utilized when
working on the trunk or extremities where larger
­suture materials and needles are needed (Fig.
4-45). Similarly, Baumgartner and Mayo ­ Hegar
needle holders are strong, durable drivers with ser-
rated jaws, making them suitable for procedures
on the trunk or extremities (Fig. 4-46).
ERRNVPHGLFRVRUJ
Figure 4-44  Serrated-surface needle
holder
Figure 4-47  Webster (Halsey) needle
holders
Webster (Halsey) needle holders are shorter dri­
vers with narrow jaws and tapered tips (Fig. 4-47).
The surface of the jaws can be smooth or serrated.
These drivers are suitable for finer needles.
Castroviejo needle holders are delicate instru-
ments that have a spring lock handle (Fig. 4-48).
They do not have finger loops in the handles. In-
stead, they are held like forceps. As the handles
are partially brought together, with a click, the
mechanism locks the jaws firmly to clamp the
needle in the needle holder. To release the ­need­le,
the handles are compressed further until they
click. At that point, the spring action separates
the jaws as the surgeon releases the handles. The
jaws of these instruments are very fine, making
them suitable for extremely delicate procedures
around the eyes and ears.
Another type of needle driver used by derma-
tologists is the Olsen–Hegar needle holder (Fig.
4-49). These, too, are available in several different
sizes. They differ from other needle holders be-
cause they serve a dual purpose. Just proximal to
the jaws, there is a suture-cutting scissor surface,
allowing the surgeon to suture and cut suture
with the same instrument. Care must be taken

Figure 4-48  Castroviejo needle holder with (left) and
without (right) lock
Figure 4-49  Olsen–Hegar needle holder
Figure 4-50  Chalazion clamp
not to cut the suture material accidentally during
the suturing process.
Chalazion clamps
Key Points
• Chalazion clamps are useful when operating on
mobile surfaces.
• Chalazion clamps are available in a variety of ring
diameters.
Chalazion clamps are a specialty instrument and are
quite useful when operating on mobile sur­faces (Fig.
4-50). These clamps consist of a flat arm that is op-
posed by a ring-shaped arm. As these are clamped
down on a mobile, vascular surface such as a lip, eye-
lid, or earlobe, the ringed arm provides stabilization
and hemostasis, while the flat arm provides a firm
ERRNVPHGLFRVRUJ
4
Chapter
Surgical instruments 69
Figure 4-51  Variety of skin hooks Courtesy of Acuderm
flat surface upon which the surface may cut, cu-
rette, or otherwise operate on the tissue. The clamp-
ing tension is adjusted by a thumbscrew, which can
be gradually tightened or released. It is important
to release these clamps quickly once the procedure
is completed, to avoid a tourniquet effect. They are
available in a variety of ring diameters.
Skin hooks
Key Points
• Skin hooks are available in single, double, or
multiple-pronged patterns.
• Skin hooks aid in manipulating tissue.
Skin hooks assist the surgeon in manipula­ting
tissue that needs to be sutured, assessing flap
movements, visualizing the surgical field for
electrocautery, reflecting skin edges during un-
dermining, placing dermal tissue, and correcting
dog ear defects. Skin hooks are available in single,
double, or multiple-pronged patterns (Fig. 4-51).
The prongs can be blunt or sharp tipped. Single
pronged hooks are commonly used for flap eleva-
tion and undermining of delicate skin. Skin rakes,
on the other hand, are utilized mainly for rhytid-
ectomies and large truncal procedures.
Hemostats
Key Points
• Hemostats assist the surgeon in hemostasis.
• Hemostats are available in a variety of sizes; the
tips can be curved or straight, and delicate or
regular tipped.
Hemostats assist the surgeon in hemostasis by
clamping the vessel, which later can be cauterized
or ligated with sutures. Hemostats vary in tip size,
curvature, and degree of serration (Fig. 4-52).
70 Dermatologic Surgery
Figure 4-52  Curved, serrated Figure 4-53  Jacobsen hemostat
hemostat
Figure 4-55  Periosteal elevator
Jacobsen hemostats are fine-tipped hemostats,
ideal for grabbing small vessels (Fig. 4-53). The tip
can be curved or straight.
Halstead mosquito hemostats are available in
3.5 or 5.0 inches, straight or curved, and delicate
or regular tipped (Fig. 4-54).
Periosteal elevators and bone
chisels
Key Point
• Periosteal elevators and bone chisels are used
to elevate periosteum or perichondrium, scrape
hard surfaces, and assist in nail surgery.
Both periosteal elevators and bone chisels are flat,
long, solid instruments. Generally, periosteal el-
evators have flattened, rounded tips on both ends
(Fig. 4-55). They are used to elevate periosteum
or perichondrium, or scrape hard surfaces. They
are versatile tools that can also be used to help
elevate and avulse fingernails and toenails.
Chisels have a sharpened, flattened end on one
side and a solid, wide end on the other (Fig. 4-56).
The wider end is used to strike the chisel with
a hammer, usually to biopsy bone or perios-
teum where it is suspected to be invaded by a
­neoplasm.
ERRNVPHGLFRVRUJ
Figure 4-54  Halstead mosquito
hemostats
Figure 4-56  Bone chisel and hammer
Conclusion
The selection of proper surgical instruments can
be a daunting task when setting up a dermatologic
surgery practice. Many surgical instrument com-
panies offer “excision packs” and various ­ other
instrument packages. Most dermatologists will
develop preferences for certain instruments dur-
ing their residency training, and gravitate towards
purchasing similar instruments. If one chooses
that route for the initial set of instruments, much
of the information can be gathered by recording
the make and model numbers of the instruments
used in training.
Choosing the right instruments for one’s hand
size and types of procedure to be performed is
crucial for efficient excisions, repairs and other
procedures.
Many varieties of instruments are available,
providing an overwhelming number of choices
in both cost and quality of surgical instruments.
A dermatologic surgeon’s instruments are a very
important investment, thus one should avoid low

cost or poor quality instruments. Higher ­ quality
surgical instruments are usually covered by longer
warranties as well. Although much can be learned
about the quality of various instruments from
speaking with colleagues and mentors, many
of the decisions will be personal ones, based upon
the surgeon’s hand size and practice type. Once
the proper instruments have been acquired, it is
important to keep them in good condition with
proper care, including periodic sharpening and
replacement when necessary. It is good to try out
new varieties of instruments if it may benefit one’s
practice. If useful, complete sets can be ordered.
Good care will optimize the instruments’ lifespan
and allow the surgeon to operate comfortably and
efficiently for many years.
ERRNVPHGLFRVRUJ
4
Chapter
Surgical instruments 71
Further reading
Bernstein G. Choosing the correct surgical instru-
ments. Adv Dermatol 1995;10:245–283.
Melissa BA, Joseph AK. Instruments and materials.
In: Robinson JK, Hanke WC, Sengelmann R, Siegle D,
eds. Surgery of the Skin. London: Elsevier-Mosby,
2005:59–66.
Neuberg M. Instrumentation in dermatologic surgery.
Semin Dermatol 1994;13:10–19.
Olhoffer IH, Goldman G, Leffell DJ. Wound closure
materials and instruments. In: Bolognia JL, Jorizzo
JL, Rapini RP, eds. Dermatology. London: Mosby,
2003:2248–2252.
Weber LA. The surgical tray. Dermatol Clin
1998;16:17–24.

Preoperative evaluation
of the dermatologic
surgery patient
Lisa M. Grandinetti and Susan Teri McGillis
The preoperative consultation and examination is
an integral component of the physician–patient
relationship. This interaction allows the surgeon
carefully to assess the problem, evaluate the
patient’s health status, identify risk factors,
educate the patient and discuss the surgery
in detail. The patient should gain a realistic
understanding of the proposed surgery, be
informed of treatment options and know what to
expect in the postoperative period. The additional
time to perform a preoperative evaluation is
well compensated for by a reduction in surgical
complications and an improved interaction
between patient and physician.
The consultation area
Key Points
• Should be clean and private with natural lighting
• Should include a place for patient to disrobe and
leave garments and a sink, with clean towels, for
patient to wash face and remove makeup
• Should have several mirrors on hand to help
patient point out their concerns or follow along
with the surgeon’s explanations.
The importance of a well planned consultation
area cannot be overemphasized. Patients are of-
ten anxious in anticipation of future surgery.
A clean, private area with natural lighting should
be arranged for conducting patient evaluations.
If needed, this area should include a place for
the patient to disrobe and store their garments.
Patients seeking consultation for facial cosmetic
reasons should be asked to remove all their make-
up so that a thorough assessment can be per-
formed. Additionally, it is helpful to have mirrors,
both hand-held and wall mounted, for patients
who may wish to point out their concerns or to
follow along with the surgeon’s explanations.
Allow ample time to address the patient’s
questions. A professional, yet personal demea­
nor, in both dress and actions will be ­appreciated
by your patients. During the course of the
ERRNVPHGLFRVRUJ
5
Chapter
c­ onsultation, there should be minimal distraction
from incoming phone calls, pagers or office staff.
Preoperative assessment
(Box 5-1)
General medical history
A preoperative questionnaire completed by the
patient or with the aid of the medical staff (nur­
ses, medical assistants, and physician assistants)
facilitates the consult and provides useful infor-
mation. Preprinted forms may be used or, as is the
case in the authors’ practice, an electronic medi-
cal record template assures that key components
of the preoperative assessment are addressed. The
patient’s response to these key questions helps to
identify potential problems and avert subsequent
complications. Additionally, forms can be tailored
to the anticipated procedure.
B ox 5 - 1
Basic components of preoperative
assessment
General medical history
• Existing and past medical history
• Allergies
• Medications
• Past surgical history
—response to previous procedures
• Review of social and family history
Physical exam
• Vital signs
• Problem-focused physical examination
—documenting the location of lesion (photographs)
Explanation of the procedure
Informed consent
74 Dermatologic Surgery

Existing and past medical problems B ox 5 - 2

In evaluating a patient’s past and current medi-
cal issues, the surgeon should be acutely aware
of possible complications and interactions that
may negatively impact the safety of the patient
or the outcome of the procedure. The more com-
monly encountered conditions are individually
addressed below.
Diabetes mellitus
Key Points
• Diabetes should be relatively well controlled prior
to procedure.
• Diabetics have compromised microvasculature.
• Diabetics have an increased risk of delayed
wound healing.
• Delaying procedure until diabetes control is
optimized may be necessary.
• Be aware of signs and symptoms of
hypoglycemia.
• Sweetened juices or glucose tablets should be
readily available.
Three main areas for evaluation
Angina and ischemic heart disease
• Sublingual nitroglycerin readily available
• Caution when using α-adrenergic agonists such as
­epinephrine
• Be prepared for possible cardiac related emergencies
—“crash cart” on site.
Valvular heart disease and prosthetic valves
• Higher risk of bacterial endocarditis and prosthesis infection
• Risks and benefits of prophylactic antibiotics must be
weighed
—prudent use of antibiotics is indicated in high-risk
­patients, certain anatomic locations, and the presence of
overt infection.
—updated guidelines (Tables 5-1 & 5-2)
—antibiotic regimens (Table 5-3)
Implantable electronic devices (pacemakers/defibrillators)

Patients with diabetes can have delayed wound

healing and an increased propensity toward
­infections. Ideally, the diabetic patient should be
fairly well controlled to achieve optimal surgical
Table 5-1  Antibiotic prophylaxis in cutaneous surgery
results. If this is not the case, consideration should
be made to postponing the procedure until con- High-risk patients Low-risk patients
ditions are optimized. This may require that the Prosthetic valves History of rheumatic fever
patient visit their primary care physician so that without valve dysfunction
History of bacterial
insulin dosing or oral diabetic medication may be
endocarditis H/O Kawasaki disease without
adjusted. valve dysfunction
Hypoglycemia is an additional concern that Mitral valve prolapse
must remain on the surgeon’s radar. It is prudent with regurgitation H/O coronary artery bypass
grafting
to have readily available sweetened juices or glu- Mitral valve prolapse
cose tablets on hand that may be administered without regurgitation Pacemaker/defibrillator
when potential signs of hypoglycemia are noted. (men >45 years of age)
Physiologic, functional,
Any cardiac valve or innocent murmur
Hypertension dysfunction
Mitral valve prolapse without
Patients with a history of hypertension can have Hypertrophic regurgitation
increased risk of intraoperative and postopera- cardiomyopathy
tive bleeding, particularly when the hypertension Ostium secundum atrial
Orthopedic prosthesis septal defect
is uncontrolled. If the patient is on antihyper-
tensive medications, they are instructed to con- Central nervous system Arterial grafts
tinue taking their medication on the day of the shunts
Penile prosthesis
procedure. The patient’s blood pressure should Shunts or fistulae with
be checked during the preoperative assessment nearby inflamed or infected Breast implants
and on the day of surgery. If a patient’s blood tissue
pressure is deemed elevated (a systolic pressure Adapted from Maragh SL, Otley CC, Roenigk RK, Phillips PK. Antibiotic
greater than 180 mmHg or a diastolic greater than prophylaxis in dermatologic surgery: updated guidelines. Dermatol Surg
100 mmHg), surgery may be postponed until the 2005;31(1):83–91.
pressure is under better control.
Cardiovascular disease (Box 5-2)
Patients with underlying cardiac disease may identified during the preoperative ­consultation.
have an increased complication risk during Sublingual nitroglycerin should be readily avail-
surgical procedures and therefore should be able for patients with a history of ischemic heart

ERRNVPHGLFRVRUJ
 5

Chapter
Preoperative evaluation of the dermatologic surgery patient 75

Table 5-2  Guidelines for prevention of endocarditis and prosthesis infection

Procedure Risk stratification Skin condition Prophylaxis
Mohs surgery High-risk patient All Yes
Excision High-risk patient Intact No (except with breach of nasal or oral mucosa)
Biopsy
Cryotherapy
Electrodessication and
curettage
Ablative laser
All High-risk patient Clinically infected Yes
All High-risk patient Eroded No (except with excision of eroded skin in
patient with prosthetic valve)
All Low-risk patient All No cardiac prophylaxis, but clinically infected
skin may require standard antibiotic treatment
Adapted from Maragh SL, Otley CC, Roenigk RK, Phillips PK. Antibiotic prophylaxis in dermatologic surgery: updated guidelines. Dermatol Surg
2005;31(1):83–91.

Table 5-3  Antibiotic regimens (1-h preoperative dose) Patients with pacemakers and implanted
Non-oral sites Oral and nasal mucosa defibrillators
Cephalexin 2 g PO Amoxicillin 2 g PO Key Points
Dicloxacillin 2 g PO Cephalexin 2 g PO • Consider an alternative procedure that allows
Clindamycin 600 mg PO Clindamycin 600 mg PO chemical cautery.
(PCN allergy) (PCN allergy) • Tie vessels when possible.
• Consider biterminal forceps, thermal cautery, or
Azithromycin or Azithromycin or carbon dioxide laser for hemostasis.
clarithromycin 500 mg PO clarithromycin 500 mg PO • Simple electrodessication of small lesions
(PCN allergy) (PCN allergy) located distant to the pacemaker poses
PCN, penicillin. Adapted from Maragh SL, Otley CC, Roenigk RK, Phillips negligible risk.
PK. Antibiotic prophylaxis in dermatologic surgery: updated guidelines.
Dermatol Surg 2005;31(1):83–91.
Patients with implantable electronic devices, such
as cardiac pacemakers, internal cardiac defibril-
disease or angina. The use of epinephrine, an lators (ICDs), or deep brain stimulators (DBSs),
α-adrenergic agonist, in local anesthetics in such should also be identified. Potential pacemaker,
patients may be cause for concern due to its ICD or DBS interference is a risk if using electro-
­vasoconstrictive and cardiostimulatory effects. surgery during the procedure.
Although the rate of bacteremia during skin Although most modern pacemakers and ICDs
surgery is very low, patients with valvular disease have technology that helps to shield external
or prosthetic valves are at higher risk of develop- electromagnetic currents, caution must be taken
ing bacterial endocarditis and thus may require to prevent adverse events, such as accidental fir-
antibiotic prophylaxis. ing of the ICD or the triggering of skipped beats.
Consideration may be given to changing pace-
Antibiotic prophylaxis (Table 5-3) makers to fixed-rate mode or to magnetically de-
Key Points activating the ICD during electrosurgery.
Devices that limit the area of the electromag-
• Endocarditis prophylaxis involves a single large netic current, such as biterminal forceps, or elimi-
preoperative dose of antibiotic.
nate the flow of current at all, such as in the case
• Wound infection prophylaxis can be
accomplished with a single dose of antibiotic or of electrocautery, are safer alternatives. Carbon
with antibiotic added to the local anesthetic. dioxide lasers provide an additional alternative
• Few skin surgery patients need prophylaxis. for hemostasis. Simple electrodessication of small
lesions located distant to the pacemaker poses
negligible risk.
Additionally, procedures that involve oronasal If appropriate safety precautions are taken
mucosa, genital, genitourinary and axillary tissues during the procedure, the vast majority of
may warrant prophylactic antibiotic ­coverage. ­patients will not need to undergo preoperative

ERRNVPHGLFRVRUJ
76 Dermatologic Surgery
cardiology consultation or intraoperative cardiac
monitoring. Should concerns arise preopera-
tively with regard to the viability of a patient’s
pacemaker or defibrillator, it is prudent to notify
the patient’s cardiologist for further evaluation.
Deep brain stimulators may be deactivated dur-
ing surgery, although this may cause a problem
with patient movement during surgery. Alterna-
tively, electrocautery or biterminal forceps may
be used to avoid interference and injury with
the DSB.
Pregnancy
Dermatologic surgery procedures can be per-
formed during pregnancy; however, nonemergent
and elective procedures should be postponed into
the postpartum period. This will avoid any po-
tential adverse effects during organogenesis. Anti­
biotics such as penicillin and erythromycin are
considered acceptable for use during pregnancy
(Food and Drug Administration [FDA] pregnancy
class B), whereas others such as tetracycline can
cause bone growth retardation and staining of the
dental enamel in the fetus, and should be avoided.
Lidocaine (FDA pregnancy class B) also ap-
pears safe in low dose; however, until more data
become available, caution should be used when
considering the use of lidocaine in pregnant
wo­men. Of note, epinephrine is classified as an FDA
pregnancy class C medication. Acetaminophen
(FDA pregnancy class B) is routinely used during
pregnancy despite its ability to cross the placenta.
Doubt about any administered medication should
trigger a call to the patient’s obstetrician.
Herpes simplex virus (HSV)
Key Points
• Resurfacing procedures carry a higher risk of
HSV reactivation.
• Consider viral prophylaxis in these patients.
A prior history of HSV is particularly important
when resurfacing procedures (carbon dioxide
laser, dermabrasion, chemoexfoliation, etc.) or
surgery in the genital or perioral areas is contem-
plated. Serious consideration must be given to
the fact that patients with a negative history of
HSV infection may have positive HSV serology
and, thus, are also at increased risk of develop-
ing herpetic infections postprocedure. Trauma or
stress, such as the surgery itself, can precipitate
a reactivation and warrants antiviral prophylaxis
(Table 5-4). It is the authors’ practice to begin an-
tiviral prophylaxis in all patients, unless otherwise
indicated (allergy to antiviral, patient refusal),
prior to resurfacing procedures. Antiviral prophy-
laxis should begin 1–2 days preoperatively and
­continue until reepithelialization has occurred
(approx. 10–14 days).
ERRNVPHGLFRVRUJ
Table 5-4  Antiviral prophylaxis
Drug Dosage
Acyclovir 200 mg 5 times a day or 400 mg 2 times a
day
Valacyclovir 500 mg 2 times a day
Famciclovir 250 mg 2 times a day
Begin 2 days before surgery and continue until reepithelialization occurs.
Liver disease
Knowledge of a history of liver disease helps the
surgeon to calculate the minor dose reductions
necessary for medications, such as acetaminophen
or postoperative narcotics. Additionally, the sur-
geon should be aware that patients with severe
liver disease may have an underlying coagulopa-
thy and an increased risk of intraoperative and
postoperative bleeding.
Renal disease
Additional consideration must be given to pa-
tients with chronic renal insufficiency or renal
failure. Antibiotics must be given at renal dosages.
It is often necessary to calculate the creatinine
clearance (mL/min) of these patients to calculate
the appropriate renal dose. This can be calculated
by the Cockcroft–Gault equation:
(140 − Age ) × Ideal bodyweight
Serum creatinine ( mg /dL ) × 72
For female patients, multiply by a factor of 0.85.
Psychiatric/psychological impairment
Psychological problems are often the cause of
“doctor shopping.” The astute physician must be
aware of these warning signs:
1. Unrealistic expectations regarding the
outcome of the procedure
2. Obsession about cosmetic appearance,
i.e. the problem is exaggerated beyond reality
3. Wrong perception of the surgery
4. Reluctance to accept the physician’s
explanation.
If a mutually satisfactory understanding has not
been established prior to the procedure, the
­patient may not be a surgical candidate. Patients
suspected of having body dysmorphic disorder
should be referred for psychiatric evaluation.
Allergies
Key Points
• Take a careful history.
• Distinguish true allergy from other events.
• True allergic reactions to local anesthetics are
rare.

Preoperative evaluation of the dermatologic surgery patient
The presence or absence of allergies to medica-
tions must be clearly indicated and easily vis-
ible on the patient’s medical record. This helps
to minimize the patient’s risk of accidental
exposure. Allergies of particular concern to the
dermatologic surgeon are addressed below.
Local anesthetics
True allergic reactions to local anesthetics are
rare. In many cases, substituting a different class
of anesthetic such as an amide (lidocaine) for an
ester (benzocaine) may be enough to prevent an
adverse reaction. The amide class of anesthet-
ics and the ester class display different antigenic
­determinants, therefore cross reactivity is low. Sen-
sitivity to the paraben preservatives in these agents
(methyl or propyl paraben) may be the true cause
of the reaction. Occasionally, patients may have
sensitivity to the adrenergic effects of epinephrine
(palpitations, flushing, and perspiration). This
should not be interpreted a true allergic reaction
to the anesthetic. Topical sensitization can also re-
sult from prolonged use of topical anesthetics.
Antibiotics
Both systemic and topical antibiotics are used
frequently by surgeons, necessitating inquiry into
possible adverse reactions. Topical antibiotics can
cause sensitization. White petrolatum is a safe
and less costly alternative to bacitracin for heal-
ing uncontaminated cutaneous wounds, with less
risk of allergy and secondary colonization.
Adhesives/tapes
Many of these products can induce acute allergic
contact dermatitis in previously sensitized per-
sons. Alternatives should be available for patients
with a history of adhesive allergy.
Latex
Latex allergy is a common problem, particularly
among healthcare workers. Symptoms can vary
from localized urticaria to anaphylaxis. Items
other than the surgeon’s gloves may be the issue
in the operating room, although most hospitals
are now required to have latex-free supplies avail-
able. Vinyl or other synthetic gloves should be
readily available for patients or medical staff with
such sensitivities.
Analgesics
Allergies or toxicities to analgesics should be
noted and avoided.
Medications
Key Points
• Take a careful history.
• Anticoagulants can usually be continued
(see below).
ERRNVPHGLFRVRUJ
5
Chapter
77
A vital part of any medical history is a list of
current medications, both prescription and
nonprescription. Such information can alert
the ­ physician to undisclosed medical problems, ­
potential drug interactions, and possible peri­
operative concerns.
Anticoagulant agents
Some degree of bleeding is anticipated during
any surgical procedure; however, excessive and/or
prolonged bleeding can be an unwelcome com-
plication. By inquiring into a patient’s anticoagu-
lant therapy prior to surgery, the surgeon has time
for advanced planning and can be better prepared
to deal with issues that arise during the course of
the procedure.
Aspirin, nonsteroidal anti-inflammatory agents
(NSAIDs), clopidogrel, warfarin, and low mole­
cular weight heparins are frequently encountered
anticoagulants in the outpatient setting .Vitamin E,
garlic, ginseng, ginkgo biloba, and fish oil have all
been implicated in decreasing platelet aggrega-
tion and increasing bleeding.
It is critical that the surgeon clarify whether
the patient is on medically necessary anticoagu-
lation. Recent literature from the Mayo Clinic
has shown that the risk of thrombotic events is
increased in patients in whom anticoagulation
therapy was discontinued preoperatively and that
this risk generally outweighs the risk of surgical
complications. Accordingly, Table 5-5 summarizes
suggestions for the management of anticoagulant
therapy. Patients on aspirin who have a normal
bleeding time appear to have no increased risk of
complications.
Immunosuppressive agents
Patients on glucocorticoids, cyclosporine, and other
steroid-sparing immunosuppressants may likely
have delayed wound healing and be predisposed
to infections. Close and regular follow-up of these
patients, and the addition of antibiotics if needed,
is prudent.
β-Adrenergic blockers
Although uncommon, epinephrine can cause
­malignant hypertension and reflex bradycardia
by creating unopposed α-receptor stimulation in
patients on beta-blockers. In the face of a crisis,
­intravenous hydralazine or chlorpromazine may be
effective. Modifications of a patient’s drug doses
should be done with guidance from their primary
care physician.
Isotretinoin
Patients on oral isotretinoin, currently or within
the past year, may have an increased risk of ad-
verse healing and scar formation. Elective proce-
dures should be deferred for 6 months to 1 year in
these instances.
78 Dermatologic Surgery

Table 5-5  Guidelines for anticoagulation therapy Transportation is another issue that is often
overlooked. If a patient is to receive conscious
Aspirin and sedation or will have vision-obstructing dressings,
NSAIDs Warfarin
they may need to have someone accompany them
On anticoagulation by Continue Continue on the day of the procedure. Likewise, if the pa-
physician order medication medication tient has a disability and requires special accom-
(INR should modations, the physician’s office can made aware
be within
of these needs in advance of the procedure.
therapeutic
range 2–3.5)
Alcohol
On anticoagulation Continue Continue Patients who drink socially should discontinue
due to history of medication medication consumption at least 48 h prior to surgery. If the
heart attack, angina, (INR should
patient is known to have an alcohol addiction, it is
transient ischemic be within
attack, or stroke therapeutic not advisable to stop alcohol consumption “cold
range 2–3.5) turkey,” as this may precipitate serious and life-
threatening alcohol withdrawal symptoms.
Prophylaxis for Discontinue ASA NA
stroke or heart attack 7 days prior
Smoking
prevention (no history Discontinue
of prior stroke or heart NSAIDs 3 days Cigarette smoking also affects the viability of
attack) prior (may be cutaneous tissue following surgical procedures.
resumed 3 days There is a risk of delayed wound healing, wound
postoperatively) dehiscence, and wound necrosis, particularly if
Used only for pain Discontinue ASA NA flaps or grafts were performed. Ideally, patients
control 7 days prior should cease smoking entirely. If the patient is
Discontinue ­unwilling to stop smoking completely, they should
NSAIDs 3 days be strongly encouraged to decrease consumption
prior(may be to less than one pack per day for 1week before
resumed 3 days surgery and for 3–4 weeks afterwards.
postoperatively)
The physical examination
INR, international normalized ratio; ASA, aminosalicylic acid (aspirin).
Modified from Otley CC. Continuation of medically necessary aspirin and A thorough examination of the lesion(s) in question
warfarin during cutaneous surgery. Mayo Clin Proc 2003;78:1392–1396. and any associated areas is essential. An assessment
of overall health status should also be performed.
Findings may mandate further evaluation. Appro-
priate laboratory tests and diagnostic studies can be
Response to prior procedures ordered in advance of the procedure and will allevi-
The purpose of eliciting the patient’s response ate any surprises on the day of the operation.
to prior procedures is to gain better understand- The lesion should be evaluated for size loca-
ing into the patient’s perception of their scars, tion, proximity to old scars, and relationship to
their pain tolerance and the need for postop- potential danger areas or natural skin lines. Any
erative analgesia, and difficulties they may have unusual feature or preexisting abnormalities such
had with postoperative care. If the patient has as eyelid ptosis or nasal alae asymmetry should
a history of hypertrophic scarring or keloid for- be photographed and recorded. This is especially
mation, steps can be taking postoperatively (in- important if it occurs in close proximity to the
tralesional steroid injection, silicone sheets/gel) proposed surgery site. Lesion location should be
to reduce the probability of a recurrence. Dis- carefully assessed for proper planning prior to the
cussing these issues with the patient enables the procedure. It is best documented by using several
physician better to address these issues prior to different methods concurrently. One option is to
the procedure. measure from two distinct anatomic landmarks.
Another possibility is to use standardized num-
Social and family history bering systems such as the New York University
Social and family issues often provide valu- numbers consistently to identify different ana-
able information about a patient and should not tomic sites. Perhaps the most important method
be overlooked. For example, it is wise to have the of documenting location is with photographs.
patient provide a “contact person,” should the Digital photography has become commonplace
physician need to provide information to some- among dermatologic surgeons. It provides an ex-
one other than the patient. If the patient is unable cellent means of documentation and allows for
to provide wound care to the operative site, an the easy storage and retrieval of patient photos.
assessment of the support available to help the Awareness of anatomic structures residing
patient is critical. close to the intended surgical field is essential.

ERRNVPHGLFRVRUJ

Preoperative evaluation of the dermatologic surgery patient
A thorough understanding of the vascular networks,
neural innervations, and structural anatomy is
needed. A detailed description of surgical anatomy
is discussed in Chapter 1 on Cutaneous anatomy.
Laboratory evaluations
At a minimum, each patient should have blood
pressure and pulse recorded during the examina-
tion. Further workup and laboratory testing (such
as magnetic resonance imaging, Doppler evalua-
tions, or blood work) will be at the discretion of the
surgeon, and directed by the history and physical
examination. Simple excisions and cosmetic pro-
cedures will require less evaluation than a ­patient
undergoing extensive skin cancer removal.
Explanation of procedure for patient education and, most importantly, it
and informed consent
Key Points
• Outline the risks, benefits, options, and
alternatives.
• Have a documented policy of how you obtain
consent (verbal or written).
At the completion of the history and physical ex-
amination, the physician should take the time to
discuss the nature of the problem with the patient.
Outline the risks, benefits, options, and alternatives
of a procedure. Make it clear to the patient that
the ultimate decision to undergo the procedure is
theirs, and that not going ahead with the planned
procedure is an option. In obtaining informed
consent, tell the patient or their legal guardians as
much as possible, including alternative forms of
therapy. Leave time for the patient to ask ques-
tions and try to answer all questions as fully as pos-
sible. It is important to stress to the patient that
unexpected complications may occur despite best
efforts, but as their physician you will help to sup-
port them and assist in any way possible.
Unfortunately, physicians practice in a litigious
era in which malpractice lawsuits are common.
Most are filed for reasons of unexpected compli-
cations or poor results, both of which reflect back
to the issue of informed consent. Accordingly,
it is integral to document completely what has
transpired during the discussion. Many physicians
have patients sign that they have received and un-
derstand the information that was discussed dur-
ing the informed consent.
Go over all preoperative details such as which
medications should be discontinued, and what
will be expected with regard to wound care and
follow-up. Prescriptions for prophylactic medica-
tions should be given to the patient or called into
the pharmacy.
Provide your patient with reading materi-
als. Numerous patient education pamphlets are
ERRNVPHGLFRVRUJ
5
Chapter
79
a­ vailable through the American Academy of
Dermatology and the American Society of Der-
matologic Surgery. Additionally, private printing
companies can individualize patient information
brochures that are tailored to your practice. These
pamphlets provide accurate information and will
often direct the patient to trustworthy websites
for additional information.
Although basic guidelines exist for the pre­
operative assessment of the dermatologic sur-
gery patient, they are just that – guidelines. Each
­patient must be evaluated on a case by case basis.
The previously discussed guidelines are designed
to eliminate avoidable risk and provide a posi-
tive outcome. The preoperative assessment helps
identify potential problems so that they can be
addressed prior to surgery. It provides an avenue
builds trust and strengthens the physician–­patient
relationship.
Further reading
Beeson WH, Rachel JD. Valacyclovir prophylaxis for
herpes simplex virus infection or infection recur-
rence following laser skin resurfacing. Dermatol
Surg 2002;28(4):331–336.
Fein H, Vidimos AT. Patient evaluation, informed
consent, preoperative evaluation and care. In:
Robinson JK, Hanke CW, Sengelmann RD,
Siegel DM, eds. Surgery of the Skin: Procedural
­Dermatology. Philadelphia: Elsevier Mosby, 2005:
67–76.
Kanzler MH, Gorsulowsky DC. Patients’ attitudes
regarding physical characteristics of medical care
providers in dermatologic practices. Arch Derma-
tol 2002;138:463–466.
McGillis ST, Stanton-Hicks U. The preoperative
evaluation: preparing for surgery. Dermatol Clin
1998;16(1):1–15.
Maragh SL, Otley CC, Roenigk RK, Phillips PK. Anti­
biotic prophylaxis in dermatologic surgery: updated
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Messingham MJ, Arpey CJ. Update on the use of
antibiotics in cutaneous surgery. Dermatol Surg
2005;31(8 Pt 2):1068–1078.
Otley CC. Continuation of medically necessary
aspirin and warfarin during cutaneous surgery.
Mayo Clin Proc 2003;78:1392–1396.
Otley CC. Perioperative evaluation and management
in dermatologic surgery. J Am Acad Dermatol
2006;54(1):119–127.
Smack DP, Harrington AC, Dunn C, et al. ­Infection
and allergy incidence in ambulatory surgery
patients using white petrolatum vs. bacitracin
­ointment. JAMA 1996;276:972–977.
Stasko T, Clayton AS. Surgical complications and
optimizing outcomes, In: Bolognia JL, Jorizzo JL,
Rapini RP, eds. Dermatology, 1st edn. New York:
Mosby, 2003:2341–2353.

Cutaneous wound healing
John A. Ebner and Edward V. Maytin
Introduction
Attempts to hasten the wound healing pro­cess
have likely occurred since the dawn of human-
kind. Recorded accounts dating back to the
Egyptians (3000–2500 bc) describe the use of
resin-covered linen strips to approximate wound
edges, and occlusive dressings made from grease,
honey, and lint to place on “diseased or sick
wounds.” Hair was used as suture material, and
insect mandibles were used as staples to close dis-
rupted tissues. Hippocrates (460–370 bc) wrote
about wound healing; he believed that pus was
beneficial, produced by the body as a means to
cleanse the wound. Infection was an unknown
entity back then, yet ancient Greek surgeons
empirically used wine, vinegar, honey, and metal-
lic salts because these compounds were seen to
­hasten wound closure and healing. Recently, it
has been shown that the bactericidal effects of
wine and vinegar-soaked bandages is attributable
to a polyphenol chemical, malvosid.
In the late 19th century, as the work of Pasteur
and Koch revealed a bacterial etiology for wound
infections, the search for specific therapies (an-
tibiotics) to augment wound healing began to
emerge. Further advances in wound healing have
come since then, but not until very recently has
this field truly exploded. Advances in molecular
and cellular biology have brought to light many
of the detailed biological processes involved in
wound repair and tissue regeneration. Bioengi-
neered skin substitutes have begun to revolution-
ize this field, as we improve our ability to hasten
the closure of wounds in the acute setting. Unfor-
tunately, advances in the area of chronic wounds
have been less robust, leaving many unanswered
questions and few solutions for patients suffering
from debilitating, nonhealing wounds.
Molecular and cellular biology
of wound healing
The material for this section derives from a clas-
sic research book by Clark et al (1996), supple-
mented by more recent reviews of Falabella et al
(2005) and Broughton et al (2006).
ERRNVPHGLFRVRUJ
6
Chapter
Normal wound healing
Acute wounds normally follow an efficient
­sequential pathway, progressing through dis-
tinct but overlapping phases of wound healing
(Fig. 6-1), which include:
1 Hemostasis
2 Inflammation
3 Proliferation
4 Tissue remodeling.
Chronic wounds share many physiologic charac-
teristics with acute wounds, but exhibit crucial
differences. Generally, chronic wounds experi-
ence a prolongation of one or more of the three
phases following hemostasis, often resulting in
prolonged ulceration and eventual fibrosis. The
major players in wound healing include platelets,
inflammatory cells (neutrophils, monocyte/mac-
rophages, mast cells), resident parenchymal cells
(fibroblasts, endothelial cells, epithelial keratino-
cytes, and nerve cells), soluble mediators, and the
extracellular matrix (Table 6-1).
Advances in the molecular and biological sci-
ences have led to an explosion of detailed knowl-
edge about wound healing and tissue regeneration.
A basic understanding of the biological steps
in wound healing, and what can go wrong with
them, is a prerequisite for any physician involved
in the creation and repair of wounds in the skin.
Phase 1: Hemostasis
Key Points
• Platelets serve as the original source for
cytokines and growth factors.
• Together with clotting factors from the blood,
they establish a provisional fibrin matrix.
Immediately after the induction of a cutaneous
wound, vasoconstriction of the damaged blood ves-
sels occurs. Closely following this, platelets become
activated, adhere, and aggregate at the site of injury.
Platelet activation is mediated by integrin receptors
on their surface that bind to exposed collagen in
the extracellular matrix (ECM). Activated platelets
then secrete glycoproteins ­ (fibrinogen, fibronec-
tin, thrombospondin, and von Willebrand factor)
82 Dermatologic Surgery
Inflammation
Proliferation
Hemostasis:
Platelets
Neutrophils Monocytes &
macrophages
Epithelial migration
Epithelial proliferation
Fibroblast proliferation
Fibroblast migration
01 2 3 12 1 2 3 4 5 6
Hours Days
– sticky molecules that ­assist platelet aggregation in
the wound. Clotting factors released from the vas-
culature produce a fibrin clot, forming a provisional
matrix. Proteases bind to the surface of platelets
trapped within this fibrin web, further activating
and accelerating the clotting cascade (Fig. 6-2).
This fibrin clot serves as a scaffolding for in-
vading cells. Certain growth factors released from
platelets (platelet-derived growth factor [PDGF]
and transforming growth factor β [TGFβ]), C5a
complement, and bacterial proteins help to initi-
ate the later states of wound healing by recruiting
cells to the wound (neutrophils and monocytes
first, then fibroblasts and endothelial cells later).
Vascular endothelial growth factor (VEGF),
TGFα and fibroblast growth factor (FGF) (all
platelet-derived growth factors) help to initiate
angiogenesis, whereas fibroblasts initiate the syn-
thesis of collagen and glycosaminoglycans (e.g.
hyaluronan) that will form the more permanent
ECM. All of these actions are initiated in the wan-
ing moments of the hemostasis phase.
Phase 2: Inflammation
Key Points
• Neutrophils and macrophages cleanse the
wound of bacteria, debris, and damaged tissue,
and are a secondary source of cytokines and
growth factors.
• Prolonged inflammation can interfere with healing
and increase scar tissue formation, as increased
protease activity destroys essential factors.
ERRNVPHGLFRVRUJ
Tissue remodeling
Maximal wound
strength 75–80%
Collagen synthesis
GAG synthesis (e.g. hyaluronan)
Angiogenesis
Myofibroblasts,
wound contraction
1 2 3 4 1 2 3 4 5
Weeks Months Years
The inflammatory phase begins within hours of
wounding and lasts for up to 2 weeks in normal
wounds (but much longer in chronic wounds).
The first cells to arrive are the neutrophils, repre-
senting 50% of all cells in the wound at 24 h post-
wounding. Neutrophils clear the wound of debris
and bacteria by releasing proteolytic enzymes
(metalloproteinases and elastases) that digest
bacteria, and degrade old ECM and nonviable tis-
sue. Neutrophils also release free radicals via the
myeloperoxidase system. These highly reactive
molecules help to sterilize the wound.
The process by which the neutrophil arrives
at the wound site is governed by the interaction
of leukocyte adhesion molecules (integrins) and
vascular endothelial receptors (selectins, cad-
herins, and the intercellular and vascular cell
adhesion molecules, ICAM and VCAM). These
interactions control the processes of adhesion,
rolling, and diapedesis, allowing the neutrophils
to squeeze through the vascular endothelium
and home toward the wound site along a gra-
dient of cytokines, growth factors, and soluble
ECM fragments. After 2–3 days, the neutrophils
undergo apoptosis and are cleared by the in-
coming monocyte/macrophages. As circulating
monocytes invade the wound, they are converted
into activated tissue macrophages, and after 48 h
represent the majority of inflammatory cells in
the area. Macrophages produce numerous inflam­
matory cytokines and growth factors, making
them the central players in the inflammatory
phase of wound healing. Macrophages continue
 6

Chapter
Cutaneous wound healing 83

Table 6-1  Different cell types in the skin and their roles in wound healing
Cell type Functions/comments
Platelets Wound hemostasis: neutrophil, monocyte, and lymphocyte chemotaxis
Release of hemostatic effectors: fibrin, factor XIII, complement, fibronectin, PAF, thromboxane A2
Cytokines/growth factors: PDGF, TGFβ, FGF, EGF, histamine, serotonin, prostaglandins, prostacyclin
Neutrophils First cell to arrive at wound; peak number at 24 h postwounding
Attracted by platelet-derived chemotactic signals: C5a complement, IL -1, TNFα, TGFβ, and bacteria
Adhere to endothelial cells via selectins, followed by rolling, margination, and diapedesis between endothelial
cells
Migrate through the ECM via integrin–receptor interactions
Provide wound debridement via phagocytosis and release of proteases and oxygen free radicals
Macrophages Migrate into wound at 48–96 h
Arrive as circulating monocytes, then transform into activated tissue macrophages
Orchestrator of wound healing. Release of cytokines and growth factors (paracrine signaling)
Help in wound debridement via phagocytosis and matrix metalloproteinases (MMPs)
Provide antimicrobial action (oxygen free radical: H2O2, O2, OH)
Recruit other cells (via growth factors: PDGF, TGFβ, TGFα, FGF; cytokines: TNFα, IL -1, IL -6, IL -8, fibronectin)
ECM synthesis (via growth factors: TGFβ, EGF, PDGF; cytokines: TNFα, IL -1, IFNγ; collagenases)
Angiogenesis (via growth factors: VEGF, TGFβ, FGF; cytokines: TNFα)
Keratinocytes Migration over wound surface in the first 24 h (over type I collagen and fibronectin)
Proliferation and differentiation into stratified layers occur later
Stimulated by fibroblasts secreting KGF-1, KGF-2, and IL -6 (paracrine signaling)
Wound edge keratinocytes secrete VEGF and promote neovascularization
Fibroblasts Primary cell type that rebuilds dermis in the proliferative phase
Induced by cytokines and growth factors from platelets and activated macrophages (primarily PDGF)
Synthesize collagen. Some are transformed into myofibroblasts (via TGFβ), which facilitate wound contraction
Endothelial Vasoconstriction after injury. Activation of coagulation cascade to achieve hemostasis
cells
Produce a host of mediators to stimulate chemotaxis and initiate the inflammatory stage
Selectins on cell surface bind circulating inflammatory cells, which then roll, adhere, and diapedese out of
vasculature
Release IL -1, TNFα, PDGF, VEGF, FGF
Activated by VEGF to sustain angiogenesis
Release nitric oxide, which assists in vasodilatation and perfusion of healing tissues
PAF, platelet activating factor; PDGF, platelet-derived growth factor; TGFβ, transforming growth factor β; EGF, epidermal growth factor; IL -1, interleukin 1;
TNFα, tumour necrosis factor α; ECM, extracellular matrix; IFNγ, interferon γ; MMPs, matrix metalloproteinases; KGF, keratinocyte growth factor;
VEGF, vascular endothelial growth factor.

the local cleansing process by generating large
amounts of nitric oxide (NO) and other oxygen
free radicals. Mast cells are another important
source of mediators, including histamine, and are
predominantly responsible for the classic signs
of rubor (redness), calor (warmth), dolor (pain),
and tumor (edema) seen during the inflamma-
tory phase.
While neutrophils and monocytes /macrophages
serve to cleanse the wound of infection and debris,
an equally important function is to initiate recruit-
ment of fibroblasts and epithelial cells via the release
of cytokines (interleukin (IL)-6, IL-8, and TNFα)
and growth factors (PDGF, FGF, and TFGα and
TFGβ). These growth factors stimulate the fibro­
blasts to synthesize ECM molecules and endothelial
cells to begin sprouting new vessels. Recently, “stop
signals” of inflammation have been elucidated. The
responsible molecules are called lipoxins (LXA4,
LXB4). Lipoxins are synthesized by lipoxygenase
enzymes, a pathway that produces the inflamma-
tory mediators in the prostaglandin family (e.g.
prostacyclins, thromboxanes, and leukotrienes).
Lipoxins have been shown to inhibit neutrophil
chemotaxis, degranulation and adhesion, and the
generation of superoxide free radicals.

ERRNVPHGLFRVRUJ
84 Dermatologic Surgery
Intrinsic pathway
Damaged endothelial
surface
XII XIIa
(Hageman
factor)
XI XIa
IX IXa
VIIIa
X Xa
Prothrombin
(II)
Fibrinogen
Final common pathway
Figure 6-2  Normal pathways of hemostasis
Phase 3: Proliferative
Key Points
• Keratinocytes rapidly migrate to cover the
granulation tissue and close the wound surface.
• Fibroblasts and endothelial cells move in, and
synthesize a relatively disorganized extracellular
matrix.
The term “proliferative” refers to the proliferation
of skin cells that will re-establish the structure of
the skin. Re-epithelialization occurs first. Epithe-
lial cells, from the wound margin or residual skin
appendages, lose their contact inhibition and mi-
grate into the wound area within the first 24 h after
wounding. This process is governed by key growth
factors (epidermal growth factor [EGF], keratino-
cyte growth factor [KGF], and TGFα) which help
to drive the migration of keratinocytes into the
wound bed and the proliferation of keratinocytes
at the wound edges. Migrating keratinocytes form
a confluent sheet of epithelial cells and re-establish
desmosomal and hemidesmosomal attachments
along a new basement membrane. Stratification of
epithelial cells completes the new intact epidermis.
The second aspect of the proliferative phase is
creation of granulation tissue. Granulation tissue is
composed of a dense network of blood vessels, cap-
illaries, fibroblasts, macrophages, and haphazardly
arranged collagen. This tissue is what ­ eventually
will become scar during the remodeling phase.
ERRNVPHGLFRVRUJ
Extrinsic pathway
Trauma
VIIa VII
Tissue factor (III)
X
Va
Thrombin
(IIa)
Fibrin
(I) (Ia)
XIIIa Fibrin clot
(cross-linked)
The process begins at 24–48 h after wounding,
as ­ fibroblasts migrate into the provisional matrix,
guided by interactions of their integrin receptors
with key ECM proteins (fibronectin, fibrin, and vit-
ronectin). Secretion of matrix metalloproteinases
(MMPs), collagenase (MMP-1), gelatinases (MMP-2
and MMP-9), and stromelysin (MMP-3) helps to
clear a path for the fibroblasts to migrate into the
wound site. TGFβ, secreted by platelets and mac-
rophages, is a key cytokine responsible for inducing
fibroblasts to synthesize matrix proteins, predomi-
nantly type III collagen along with proteoglycans,
including hyaluronic acid (HA). Endothelial cells
are the other key component of the proliferative
phase. Angiogenesis is stimulated by a host of local
conditions (low pH, low oxygen tension, high lactic
acid levels) as well as by the soluble growth factors,
FGF, TGFβ, and VEGF in the wound bed. Toward
the end of this phase, wound contraction begins
and continues through the remodeling phase.
Phase 4: Maturation and remodeling
Key Points
• As the number of fibroblasts gradually decreases,
early scar tissue is replaced by a more organized
matrix.
• Even in the best of circumstances, the final
tensile strength of a healed wound reaches only
70–80% that of the original tissue.

The defining feature of this phase is the deposi-
tion and reorganization of collagen. Early on, the
matrix is loose, pliable, and thin, allowing inflam-
matory cells as well as fibroblasts and endothe-
lial cell precursors to move freely. However, as
the matrix is remodeled and becomes denser
with thick, mature, collagen fibrils, it becomes
less compliant. As the matrix (scar) matures,
some fibroblasts in the wound differentiate into
myo­fibroblasts with contractile properties, initi-
ating a process of wound contraction. In rodents,
myo­fibroblast-mediated contraction is a power-
ful component of wound closure, but this is less
true in human skin. During the maturation and
remodeling phase, granulation tissue matures
into scar as capillaries are replaced by larger ves-
sels, cellularity decreases, and type III collagen
is replaced by type I collagen (the dominant
­collagen found in normal skin). Collagen synthe-
sis occurs for at least 4–5 weeks; by the end, the
relative content of type III collagen has ­decreased
from 30% to 10%. Remodeling is ­ assisted by
MMPs, which remove the early unorganized ma-
trix components (granulation tissue and collagen
type III).
Remodeling occurs over several months and is
regulated by a constantly changing mileu of cy-
tokines and growth factors. The dermis of healed
skin is usually thinner than that of unwounded
skin, and the collagen fibrils are oriented in par-
allel bundles rather than the basket-woven struc-
ture seen in normal skin. The tensile strength of
the tissue continues to increase during the re-
modeling phase, but will never exceed 75–80%
of normal. The wound strength is generally
7–10% of baseline by 1 week, 40% by 1 month,
and 75–80% by 3 months. Unfortunately, ap-
proximately 80% is the maximum ever attained:
a scar will never be as strong as the original
uninjured skin.
Biology of fetal wound healing
Key Points
• Fetal wounds heal without a scar until roughly
24 weeks’ gestation; after that, wounds heal with
scarring.
• Unlocking the secret of fetal scarless healing is
the “holy grail” for wound healing biology.
In adults, scarring and fibrosis are the usual end-
result of full-thickness wounding. This is not the
case for fetal wound healing. Up to 24 weeks’
gestation, fetal skin wounds heal with complete
restoration of epidermal and dermal architec-
ture, and the absence of scarring. This finding
has triggered intense investigation and significant
advances, yet the mechanisms remain largely
unknown.
Fetal and postnatal (adult) wounds differ
in their inflammatory responses, cellular and
ERRNVPHGLFRVRUJ
6
Chapter
Cutaneous wound healing 85
chemical mediators, growth factors, and ECM
(Table 6-2). The ECM, no longer viewed as just
inert scaffolding, is a dynamic structure com-
posed of collagen and proteoglycans that plays
important roles in cell adhesion, migration, dif-
ferentiation, and proliferation. The ECM of the
fetal wound is less compact than that in the
adult, partly due to higher levels of HA and
other glycosaminoglycans. Although type I col-
lagen is the most abundant collagen in both fetal
and adult skin, the ratio of type III to type I col-
lagen is higher in fetal skin. During fetal develop-
ment, this ratio slowly approaches that of adults
in the postnatal period. The high levels of HA
in fetal skin contribute to scarless healing. HA in-
creases water content of the ECM, perhaps allow-
ing easier cellular movement, but probably more
importantly it facilitates the adhesion, migration,
and differentiation of cells. In addition, high
HA levels in fetal skin are related to a lower
influx of inflammatory cells and to the produc-
tion of fewer proinflammatory cytokines, seen in
­fetal wounds.
Therefore, scarless fetal wounds exhibit a
relative lack of inflammation – a distinct differ-
ence from the robust inflammatory response in
the postnatal wound phenotype. This is further
­clarified by studies showing that the introduction
of inflammation into normally scarless wounds
induces increased wound neutrophils, macro-
phages, collagen deposition, and scarring. There-
fore, it appears that inflammation plays a critical
role in scar formation.
MMPs and tissue-derived inhibitors of metal-
loproteinases (TIMPs) function in opposition of
one another, regulating ECM turnover. A higher
ratio of MMPs to TIMPs is observed in scarless
fetal wounds than in adult wounds, indicating
a shift toward remodeling rather than toward
the accumulation of dense collagen fibrils (fi-
brosis). Another important aspect that favors
scarless wound healing in the fetus is the rela-
tive proportion of different isoforms of TGFβ.
TGFβ1 and β2 are profibrotic, whereas TGFβ3
is antifibrotic. The ratio of β1 to β3 appears to
be an important factor in determining wound
phenotype.
Other growth factors and cytokines are also
involved in determining scarless versus scarring
repair, but ultimately the differences between
these two phenotypes are controlled at the level
of gene expression. Certain transcription factors
(proteins that regulate gene expression) that
are implicated in many aspects of fetal develop­
ment, including skin embryogenesis, are also
differentially expressed during wound healing.
For ­ example, decreased expression of HOXB13
is seen in scarless healing, and adult HOXB13
knockout mice exhibit a nearly complete scarless
healing phenotype.
86 Dermatologic Surgery

Table 6-2  Comparison of fetal (scarless) and adult (scarring) wound healing
Mediator Function Fetal Postnatal
Type III collagen ECM component ↑ ↓
HA ECM component ↑ ↓
IL-1 Proinflammatory cytokine ↓ ↑
TNFα Proinflammatory cytokine ↓ ↑
IL-6 Monocyte chemotaxis, macrophage activation ↓ ↑
IL-8 Neutrophil chemoattractant, neovascularization ↓ ↑
IL-10 Anti-inflammatory, inhibits IL -6 and IL -8 production ↑ ↓
MMPs Wound remodeling ↑ ↓
TIMPs MMP inhibitors ↓ ↑
Platelets Hemostasis, secretion of growth factors, cytokines ↓ ↑
Neutrophils Phagocytosis of bacteria, damaged ECM ↓ ↑
Macrophages Debris removal, wound cleansing, cellular trafficking ↓ ↑
Fibroblasts Synthesis of ECM ↓ ↑
TGFβ1 Profibrotic cytokine ↓ ↑
TGFβ2 Profibrotic cytokine ↓ ↑
TGFβ3 Antifibrotic cytokine ↑ ↓
PDGF Profibrotic cytokine ↓ ↑
FGF Profibrotic cytokine ↓ ↑
VEGF Angiogenesis ↑ ↑
HoxB13 Homeobox gene (transcription factor) ↓ ↑
HA, hyaluronic acid; IL -1, interleukin-1, TNFα, tumor necrosis factor α; IL, interleukin; MMPs, matrix metalloproteinases; TIMPs, tissue inhibitors of
metalloproteinases; TGF, transforming growth factor; PDGF, platelet-derived growth factor; FGF, fibroblast growth factor; VEGF, vascular endothelial growth
factor; HoxB13, homeobox transcription factor B13.

Biology of chronic wounds • Increased protease activity within chronic

Key Points
• Chronic wounds are “stuck” at one stage of the
wound healing process, often at the inflammatory
stage. Such a wound must be debrided to
remove necrotic tissue and bacteria, essentially
converting it to an acute wound that can then
move freely through the remaining phases of
wound healing.
• For chronic wounds, topical or oral antibiotics
are helpful only in treating established infection.
Likewise for acute wounds, prophylactic antibiotics
are required only in select circumstances.
• Patients with chronic wounds require a thorough
medical evaluation and often benefit from a
multidisciplinary approach to diagnosis and
treatment.
The healing events in chronic wounds are gen-
erally haphazard, prolonged, and incomplete,
resulting in anatomic defects and poor func-
tional outcomes. Imbalances in wound cytokines,
growth factors, and proteases also contribute to
the persistence of nonhealing wounds. Several
key features appear to define the molecular envi-
ronment of chronic wounds:
wounds
• Raised levels of proinflammatory cytokines
(TNFα, IL-1, and IL-6)
• Reduced mitogenic activity.
Proteases (MMPs and neutrophil elastases) are in-
volved in the destruction of endogenous growth
factors, matrix proteins, and protease inhibitors,
all of which are necessary for wound healing.
Fibroblasts from some chronic wounds become
senescent, responding poorly to cytokines and
growth factors. Endocrine abnormalities includ-
ing insulin resistance, diabetes, low estrogen
states, and chronic glucocorticoid administration
all adversely affect wound healing, and reveal an
important endocrine function necessary to the
wound healing process. In addition to general
principles that identify the chronic wound phe-
notype, specific aberrant processes appear to be
more typical of certain types of chronic wound.
Venous stasis ulcers have problems with wound
epithelialization, whereas chronic pressure ulcers
show evidence of impaired ECM production.
Overall, given this background, a rational “ideal”
therapy for chronic wounds would eliminate

ERRNVPHGLFRVRUJ

hypoxia, supply the correct mixture of MMP in-
hibitors (TIMPs), add appropriate growth ­factors,
eliminate inflammation, and reduce protease
activity in order to shift the microenvironment
toward a more acute wound setting.
Clinical approaches
to wounds: evaluation and
preparation of the wound bed
Classification of cutaneous wounds
Erosions are wounds that involve only the epi-
dermis and can result from mild abrasive trauma,
microdermabrasion, and superficial chemical peels.
Erosions heal quickly, with minimal risk of scarring
or postinflammatory pigmentary alteration.
Partial-thickness wounds extend through the
epidermis and into some portion of the dermis.
These wounds do not affect dermal adnexal struc-
tures (hair follicles, sebaceous, eccrine or apocrine
glands), but some scarring is likely, depending on
the depth of dermal injury. Common dermatologic
procedures including shave biopsies/excisions,
electrodessication and curettage, dermabrasion,
medium-depth chemical peels, and some abla-
tive laser therapies (carbon dioxide laser, erbium
YAG) create partial-thickness wounds. Healing
of these wounds occurs relatively quickly, with
keratinocytes migrating out from nearby wound
edges and adnexal structures.
Full-thickness wounds extend through the full
depth of the dermis, exposing the underlying
subcutaneous adipose tissue. Damage to ad­nexal
structures and clinically obvious scarring are com-
mon. Examples are wedge excisions and deep
punch biopsies. Full-thickness wounds, whether
made by surgical instrumentation, trauma, or
other means, may be closed by approximating the
wound edges or instead left to heal by secondary
intention. Either way, full-thickness wounds will
heal but those with well approximated wounds
will experience fewer adverse effects from scar-
ring and wound contraction.
With proper wound care, most wounds heal
over a period of several weeks. Some wounds,
however, lapse into a state of chronicity that can
become exceedingly difficult to correct the longer
the wound remains unhealed. Chronic wounds
(ulcers) have a multitude of possible etiologies.
Identification of the underlying cause is essential
to provide patient-specific treatments. Therefore,
it is imperative that dermatologists understand
how to evaluate chronic wounds and what ad-
ditional diagnostic testing and consultations may
be required. A multidisciplinary approach involv-
ing dermatology, vascular medicine, and plastic
surgery is frequently required to arrive at the
­correct diagnosis and an adequate treatment plan.
ERRNVPHGLFRVRUJ
6
Chapter
Cutaneous wound healing 87
Table 6-3 lists some of the many possible ­etiologies
for chronic wounds that can be seen in practice.
Many are not obvious upon initial evaluation, and
require detailed investigation.
Cutaneous microbiology
Normal resident skin flora varies by anatomic
site. These organisms are generally nonpatho-
genic, and include Staphylococcus epidermidis,
Micrococcus species, Corynebacterium, Propioni-
bacterium, Acinetobacter species, and Pityrospo-
rum species. Staphylococcus aureus, normally not
part of the resident flora, can be isolated from
the intertriginous (20%) and nasal (20–40%)
passages of normal adults and is the most
common pathogen isolated from infected surgical
wounds. Group A β-hemolytic Streptococcus pyo-
genes is also a common wound pathogen, while
Streptococcus viridans, resident flora of the upper
respiratory tract, is the principal agent causing
infective endocarditis. Enterococci (Streptococcus
faecalis, S. faecium) represent an increasing cause
of infective endocarditis and are becoming
more antibiotic-resistant (vancomycin-resistant
­enterococci [VRE]), but are still uncommon in
cutaneous wound infections. Escherichia coli, res-
ident skin flora in the gastrointestinal and genito­
urinary regions, can cause wound infections in
those areas.
Surgical wounds: planning
the approach to optimize healing
As a whole, the field of dermatology creates more
cutaneous wounds, via a greater variety of meth-
ods, than does any other specialty in medicine.
Whether performing skin biopsies, excisions,
chemical peels, laser ablation, photochemother-
apy, Mohs surgery, or hair transplants, the derma-
tologist must be knowledgeable about maximizing
healing and cosmetic outcome while minimizing
complications. Necessary steps must be taken
prior to, during, and after surgery to optimize the
results. These steps may include prophylactic an-
tibiotics, proper selection of preoperative antisep-
tics, appropriate intraoperative sterile technique,
and postoperative wound care with or without
systemic antibiotics.
Antiseptics
Most antiseptics are applied to the intact skin
­prior to surgery in order to decrease bacterial
counts and reduce the risk of postoperative in-
fection. The ideal topical antiseptic should have a
wide antimicrobial spectrum, a persistent antibac-
terial effect, and minimal adverse or toxic effects.
Examples include:
• Povidone–iodine (Betadine) 10%
• Chlorhexidine gluconate (Hibiclens) 0.4%
88 Dermatologic Surgery

Table 6-3  Etiology of chronic wounds

Vascular disease Venous
Arterial: atherosclerosis, AV malformations, cholesterol emboli
Peripheral vascular disease (PVD)
Vasculitis:
• Small vessel disease – hypersensitivity vasculitis, rheumatoid arthritis, lupus erythematosus,
scleroderma, Sjögren’s syndrome, Behçet’s disease, atrophie blanche
• Medium and large vessel disease – polyarteritis nodosa (PAN), nodular vasculitis, Wegener’s
granulomatosis
Lymphedema
Metabolic Diabetes (ulcerating necrobiosis lipoidica diabeticorum)
Gout
Neoplasias Carcinomas: squamous cell carcinoma (SCC), basal cell carcinoma (BCC)
Sarcoma (Kaposi’s sarcoma)
Lymphoproliferative (CTCL and others)
Metastatic tumors: breast, colon, renal, prostate, etc.
Infectious Bacterial: furuncle, carbuncle, ecthyma, septic emboli, Gram-negative infections, anaerobic infections,
mycobacterial (including atypicals)
Fungal: Majocchi’s granuloma, deep fungal infections
Leishmaniasis
Infestations/bites (brown recluse spider)
Panniculitides Pancreatic panniculitis
α1-Antitrypsin deficiency
Traumatic panniculitis
Lipodermatosclerosis
Traumatic Pressure ulcers
Cold injury (pernio, frostbite)
Radiation dermatitis
Burns (thermal, chemical, electrical)
Factitial
Genodermatoses Epidermolysis bullosa (simplex, junctional, dystrophic, aquisita)
Pyoderma
gangrenosum
CTCL, cutaneous T-cell lymphoma.

• Dakin’s solution – sodium hypochlorite 0.5%
and boric acid 4%
• Sodium hypochlorite (bleach) in various
concentrations – 0.025%, 0.25%, 0.5%.
Povidone–iodine and chlorhexidine have become
the agents of choice in recent years. Of the two,
chlorhexidine exhibits superior antiseptic activ-
ity. Benzoyl peroxide 10% is also an effective anti-
septic with sustained broad-spectrum germicidal
activity and high liposolubility, making it a good
choice for the sebum-rich areas of the central
face. However, all of these agents are deleterious
to open wounds, causing neutrophil and fibroblast
cytotoxicity, increased inflammation, endothelial
cell damage, retardation of wound contraction,
and overall delayed wound healing.
Antibiotic ointments
Topical antibiotic ointments are designed to be
applied directly to wounds. They serve functions
over and above their antibacterial nature, includ-
ing keeping the wound bed moist and prevent-
ing tissue adherence to dressings. The three most
common topical antibiotics used in topical prepa-
rations are bacitracin zinc, polymyxin B sulfate,
and neomycin sulfate (either alone, or in any
combination of the three).
Bacitracin is effective against S. aureus, strep-
tococci, and Gram-positive bacilli. Bacitracin

ERRNVPHGLFRVRUJ

is also popular because of its activity against
more resistant staphylococcal species, notably
methicillin-resistant S. aureus (MRSA). S. ­aureus
is the most commonly isolated pathogen in
­surgical wounds, but Gram-negative bacteria
also represent a major share of pathogens found
in postsurgical wounds. Therefore, bacitracin is
often combined with neomycin for additional
coverage against most Gram-negative bacilli,
­except Pseudomonas aeruginosa.
Polymyxin B provides additional coverage for
P. aeruginosa as well as for other Gram-negatives.
Today, the most favored topical combination
is bacitracin and polymyxin B. Neomycin is ex-
cluded because roughly 10% of the US popula-
tion experiences an allergic contact dermatitis to
neomycin. Other agents include mupirocin (Bac-
troban) and silver sulfadiazine (Silvadene).
Despite their popularity, the use of antibacte-
rial ointments for postsurgical wounds has been
debated in recent years. A study by Smack and
colleagues in 1996 compared the effects of white
petrolatum versus bacitracin ointment in post-
operative wound infections, and found no differ-
ences in the rates of wound infection nor time to
healing. This suggests that the addition of anti-
bacterial ointments to uncontaminated postsurgi-
cal wounds may be unnecessary.
Hemostatic agents
Twenty per cent ferric subsulfate (Monsel’s solu-
tion) and 20–60% aluminum chloride solution are
two hemostatic agents used frequently in derma-
tologic surgery. Both agents act by causing protein
denaturation and vascular thrombosis, which has
been shown to delay wound healing by 2–6 days
and may result in larger scars by 0.5–2 mm. There-
fore, it is now recommended to use pinpoint
electrocoagulation, pressure, and/or sutures rather
than the chemical agents wherever possible, to re-
duce toxicity to the local wound environment.
Antibiotic prophylaxis
When considering antibiotic prophylaxis, surgical
wounds are generally classified in four categories:
1 Clean wounds – noncontaminated skin with
sterile surgical technique; infection rate <5%.
2 Clean-contaminated wounds – incisions
created in areas considered contaminated (oral
cavity, respiratory tract, axillae, perineum)
or with minor breaks in sterile technique.
These represent the majority of dermatologic
surgery procedures; infection rate <10%.
3 Contaminated wounds – created by trauma
or with major breaks in sterile technique;
infection rate 20–30%.
4 Infected wounds – grossly contaminated with
foreign bodies and necrotic tissue; infection
rate 30–40%.
ERRNVPHGLFRVRUJ
6
Chapter
Cutaneous wound healing 89
Clean wounds generally do not require prophy-
lactic antibiotics, but contaminated and infected
wounds will required the use of antibiotics (con-
sidered therapeutic rather than prophylactic).
The clean-contaminated wound may require
prophylactic antibiotics in select cases. Deci-
sion criteria include the surgical site, nature and
length of the procedure, level of contamination,
and the overall health status of the patient (e.g.
immune status). In general, incisions through
contaminated areas (oronasal mucosa, axilla,
and genitourinary) or in patients with implanted
prosthetic devices should be given prophylactic
antibiotics. A single preoperative dose is given
1 h prior to incision, and a postoperative dose is
sometimes given 6 h afterwards, depending on
the length of the procedure. For contaminated
or infected wounds, therapeutic antibiotic ad-
ministration requires a full 7–10-day course at
bactericidal doses.
Medical and surgical approach
to the pre-existing wound
The correct diagnosis of a wound’s etiology is
essential to reaching resolution and closure. It
is often necessary to incorporate a multidis-
ciplinary approach in difficult cases (chronic
wounds), which may include vascular medicine
and plastic surgery input along with dermatology.
Determination of wound etiology, local blood
flow (arterial and venous), medical problems,
and nutritional status are all critical elements.
An underlying principle is that a chronic wound
must be “converted” to an acute wound in order
to allow appropriate progression through the
normal phases of wound healing and achieve
closure.
Approach to the acute wound
Wounds of recent origin can be either surgical
or traumatic in origin. Patients with traumatic
acute wounds should be assessed for their
tetanus status; if unknown, or not up to date
(>5 years) the patient should receive a booster
immunization. Wound irrigation with normal
saline and debridement of dead tissues should
be carried out. Deep wound cultures should
be taken and empiric broad-spectrum antibiot-
ics initiated in suspected contaminated wounds,
including human or animal bites. Antibiotics
can be fine-tuned later, following the results
of the initial cultures. Traumatic acute wounds
should be reassessed daily and additional deb-
ridements performed as needed, every 24–48 h.
Normal wounds should show closure rates of
roughly 15% per day as a marker of normalized
wound healing. Wounds healing slower than this
should be continually reassessed to optimize
wound care.
90 Dermatologic Surgery

B ox 6 - 1
Approach to the infected wound
If infection is suspected, the edge of erythema Assessment of chronic wounds
surrounding the wound should be identified,
Wound history
traced with a pen, and the date and time recorded
to help identify progression/regression of the Timing of occurrence of ulcer/wound
infective process. In some cases, obtaining radio- Location
graphic evidence to rule out bony involvement
Prior ulcer/wound history
or gas within the tissues is critical. Gas within a
wound (a byproduct of the anaerobic bacterium Current and past treatment
Clostridium perfringens) is a surgical emergency. Complications of ulcer/wound
When quantitative bacterial counts reach greater Prior procedures
than 105 bacteria per gram of tissue, the wound’s
inflammatory response can overwhelm the local Drainage (quantified)
healing process, lead to failure of granulation and Pain
neovascularization, and thereby perpetuate the
infection. Deep tissue wound cultures should Complete medical history
be collected, to aid in guiding appropriate anti- Past medical history
biotic therapy after empiric coverage has been
Family history
implemented. Aggressive removal of all necrotic,
infected, and nonviable tissue prevents the devel- Surgical history
opment of an environment that fosters bacterial Social history
overgrowth. Wound debridement, along with ap-
propriate antibiotics, represents a critical element Physical exam
of proper wound care. Blood pressure (calculate ABI)
Approach to the chronic wound Wound exam
One difficulty in treating chronic wounds lies in ac- Location
curately determining the correct etiology. In these Wound measurements (length × width × depth)
cases, debridement may not be the proper first step, Drainage (quality/quantity)
as with vasculitic ulcers or pyoderma gangreno-
sum. These ulcers require medical treatment of the Surrounding skin appearance (cellulitis)
underlying illness before any debridement should Wound bed evaluation (granulation tissue, fibrinous debris,
take place. For example, an underlying coagulopa- eschar)
thy may be contributing to the patient’s wound Pain
persistence. A biopsy of the wound edge, including
Odor
normal skin, may be necessary to establish a diag-
nosis and guide further treatment. Additionally, Wound edge (undermining, active)
vascular studies (Doppler ultrasonography) can Wound details
help to assess arterial patency and venous valvular Tissue perfusion/oxygenation
competence. Chronic ulcers of long duration must
also be followed for signs of malignant degenera- • Palpation of peripheral pulses (macrocirculation)
tion, also known as a Marjolin’s ulcer. • Capillary refills (microcirculation)
Additional factors that can contribute to Wound contamination (bioburden ± infection)
chronic wound states include diabetes, smoking,
Wound bed (excess protease activity, inflammatory cytokines,
malnutrition, and hematologic abnormalities in-
altered growth factors)
cluding clotting abnormalities, cryoglobulinemias,
and antiphospholipid antibody syndrome. Only Nutrition and immune status
after the cause of the wound has been established Psychosocial details (depression, pain)
and medically treated should the wound be de­ Neuropathy
brided. Box 6-� 1 outlines the important questions
to ask in the evaluation of chronic wounds to help Weekly follow-up
in establishing a diagnosis.
Consider re-evaluation after 4 weeks
Debridement of wounds Consider biopsy if wound present for more than 3–4 months

Surgical debridement
In order to achieve complete removal of all non-
viable, necrotic, and infected material from the
wound bed, nontraumatic surgical methods are

ERRNVPHGLFRVRUJ

a b
Figure 6-3  (a) Adult and larval forms of the green bottle fly. The larvae can be obtained in a standardized and sterilized
form (b) and may be helpful for chronic wound debridement. (Photo from R. A. Sherman, © Monarch Labs, LLC, used
with permission)
recommended. Sharp dissection is most com-
monly employed to selectively remove nonviable
tissues, leaving only healthy, well vascularized tis-
sues in the new wound bed. Any damage to the
underlying healthy tissue (burning, crushing) cre-
ates a nidus for infection and prolongs the heal-
ing process. One should debride until there is
pinpoint bleeding, which identifies healthy viable
tissues. For most chronic wounds and for selected
acute wounds, debrided tissues may be sent for
pathologic analysis to assess for infection, vascu-
litis, and malignancy. After surgical debridement,
the wound must be irrigated well with normal sa-
line (without added antibiotics, as these have been
proven to add no additional benefit), to remove
any remaining loose debris, tissue, or bacteria.
Medical debridement
For patients unable to receive standard surgical
debridement, medical alternatives can be quite
effective under the right circumstances. Biologic
agents include the use of medical maggots, Phae-
nicia sericata (the green bottle fly). These maggots
are sterilized with radiation and do not progress
past the larval stage. Bottle fly maggots secrete
tissue-degrading enzymes that affect only devi-
talized tissues, dissolving them along with any
biofilms produced by invading bacteria into a
nutrient-rich fluid that the maggots ingest. Thirty
larvae can consume 1 g of tissue per day. Another
major advantage is that the maggots consume all
bacteria within the wound regardless of antibiotic
resistance, including MRSA and VRE. ­Obtaining
these maggots requires a prescription and they
ERRNVPHGLFRVRUJ
6
Chapter
Cutaneous wound healing 91
can be purchased only from Monarch Labs,
Irvine, California (www.monarchlabs.com). The
technique is completely painless, and useful for
a wide variety of wounds in patients not suitable
for surgical debridement.
Additional nonsurgical methods of wound de-
bridement include chemical debridement. These
chemicals are enzymes that function to degrade
the necrotic nonviable tissues, yet they have no
action against bacterial wound contamination or
infection (Fig. 6-3).
Wound dressings
Key Points
• Numerous wound dressings are available, each
with certain characteristics designed to treat
specific wound types: exudative, dry/necrotic,
wet/necrotic, macerated, infected.
• The ideal dressing should provide adequate
moisture levels in the wound bed, through a
combination of good absorption of excess wound
fluids and an adequate permeability barrier.
• Supportive dressings (compression stockings)
can reduce wound edema.
While the previous sections dealt with optimiz-
ing the wound bed for healing, this section de-
scribes the use of wound coverings (dressings)
to maintain a moist, clean wound environment
that allows the wound to progress through the
natural phases of healing. A revolution in wound
healing that began a few decades ago can be at-
tributed to the discovery that wound ­ dressings
92 Dermatologic Surgery
Table 6-4  Functions of wound dressings
Actions Benefits
Maintains Enhances epithelial migration. Reduces
moisture at pain in chronic wounds. Increases
wound/dressing autodebridement via retention of
interface enzymes and growth factors
Absorbs Avoids maceration while keeping wound
exudates moist
Provides Guards against contamination (microbes/
permeability foreign material) and trauma. Minimizes
barrier fluid loss. Increases angiogenesis
(hypoxic stimulation)
Compression Assists in hemostasis. Minimizes
edema. Prevents wound dehiscence
can dramatically hasten closure and healing. Prior
to 1958, it was believed that wounds healed best
when left dry and open to the air, but Odland’s
observation that blisters heal faster when left un-
broken challenged that assumption. In addition,
in 1962 it was shown that superficial wounds
covered with a moist film dressing healed twice
as fast as wounds exposed to the air. Later stud-
ies in humans found similar superior healing
with moist dressings.
While the benefits of occlusion is well estab-
lished for acute wounds, the same cannot be said
for chronic wounds in which exudative fluids can
be very abundant. Despite this concern, most evi-
dence still advocates the use of occlusive dressings,
but choosing the correct dressing type/function
becomes of paramount importance. No single
dressing is suitable for all wound types, and many
wounds require adjustment of the dressing type
as the wound progresses to healing and closure. In
general, though, all wound dressings should em-
ploy the strategies outlined in Table 6-4.
Table 6-5 lists some of the most common
wound dressings available today, and their char-
acteristics. Dressings are classified by their com-
position and appearance, but the most important
consideration is their function. Proper choice of
the appropriate dressing depends upon first defin-
ing the wound bed characteristics:
• Dry/dessicated wounds need moisture.
• Draining wounds need absorptive dressings.
• Necrotic wounds need debridement.
• Infected wounds need antimicrobial
treatment.
A newer advance involves dressings that contain
nanoparticles of silver, a broad-spectrum anti­
biotic agent. Silver-containing dressings should
be used only in infected wounds; although not
highly toxic to human cells, the silver particles do
affect keratinocytes in culture and therefore may
inhibit epithelialization of wounds.
ERRNVPHGLFRVRUJ
Cadexomer iodine, an iodophore with mul-
tiple properties, is a three-dimensional starch
lattice structure with iodine-containing micro-
spheres embedded within a gel dressing. This
allows the slow release of antimicrobial iodine
into the wound as the starch lattice structure
exercises a tremendous absorptive capacity. One
gram of cadexomer iodine can absorb up to 7 g
of fluid, making this dressing an ideal choice for
highly exudative wounds with concurrently high
microbial bioburden. Of note, cadexomer iodine
is active against S. aureus, specifically MRSA.
In addition to these antimicrobial dressings, there
is a multitude of other dressings available to fit vir-
tually all wound characteristics. Table 6-5 includes
many of the available dressings with their general
use and the manufacturer listed for reference.
Skin substitutes (“biologic” or “living”
dressings)
Key Points
• In recent years, several different skin substitutes
have emerged that contain epidermal, dermal, or
combined epidermal and dermal components.
• These substitutes are gaining acceptance as
a valuable resource to aid in healing chronic
recalcitrant wounds.
• Improvements in wound healing therapy must
come from research. Stem cells derived from a
multipotent population found in the hair follicle
bulge are known to be involved in epidermal
repair postwounding. These cells, or patient-
derived (autologous) bone marrow stem cells,
may eventually prove to be important as wound
healing adjuvants for the healing of chronic
intractable wounds.
Prompt wound coverage is the foundation of wound
management. Most wounds can be covered imme-
diately after cleansing, debridement, and appropri-
ate wound bed preparation. However, sometimes
wound closure must be delayed and the wound
allowed to heal by secondary ­ intention. For rela-
tively simple or small wounds, coverage can often
be provided by the synthetic and natural dressings
described in Table 6-5. However, for more exten-
sive or recalcitrant wounds, autologous skin grafts
used to be one of the few options. Now, however,
a number of artificial skin substitutes have evolved
that can be used instead of autologous skin grafts,
thereby avoiding the additional pain and scarring
at donor sites. Three general categories of skin sub-
stitutes are listed in Table 6-6, as follows:
1 Cultured epidermal cells, devoid of dermal
components
2 Dermal components without the epidermal
overlay
3 A bilayer containing both the dermal and
epidermal components.

Cutaneous wound healing
Table 6-5  Wound dressings and topical agents
Characteristics
Dressings
Impregnated Maintains moisture at wound bed; non-absorbent
gauze
Non-adherent primary dressing
Substances impregnated into gauze materials (iodinated
agents, petrolatum, zinc)
Hydrogels Gels or sheets of cross-linked polymers
Waterproof, protects against contamination
Poor absorptive capacity for exudates
Change daily to every 7 days
Hydrocolloids Occlusive or semiocculusive
Various shapes, sizes, adhesive properties
Forms include wafers, pastes, powders
Autolytically debride necrotic tissues
Impermeable to bacteria/contaminants
Transparent films Polyurethane, semipermeable, adhesive
Variable thickness, sizes
Waterproof, impermeable to contaminants
Allow visible observation of wound
No absorptive capacity
Not useful for exudative wounds
Foam dressings Hydrophilic polyurethane/polymer or gel-coated
Pads, sheets, cavity dressings
Supports autolytic debridement
Minimal to moderate absorptive capacity
Maintains moist wound environment
Not useful over dry eschars
Change daily to every 7 days
Alginate dressings Brown seaweed derivative
Absorbs 20 times its weight in fluid
Wicks fluid away from wound bed
Moderate to heavily exudative wounds
Effectively fills dead spaces in wound
Silver ion Prevents colonization of wound bed
dressings
Broad spectrum
Activity against MRSA, VRE, Pseudomonas
Resistance to silver not yet shown
Instant delivery and sustained release available
Use only in infected wounds as may adversely affect
keratinocytes
ERRNVPHGLFRVRUJ
6
Chapter
93
Brands/ingredients
Adaptic Dressings (J&J Wound,
Summerville, NJ)
Scarlet Red (Tyco Healthcare, Mansfield, MA)
Xeroform (Tyco Healthcare, Mansfield, MA)
AquaGauze (DeRoyal, Powell, TN)
Aquasite (Dumex Medical, Toronto, Canada)
Curasol (Healthpoint, Fort Worth, TX)
Intrasite (Smith & Nephew, Largo, FL)
Skintegrity (Medline, Mundelein, IL)
DuoDERM (Convatec, Skillman, NJ)
Exuderm (Medline, Mundelein, IL)
3M Tegasorb (3M Healthcare, St Paul, MN)
Comfeel (Coloplast, Marietta, GA)
Restore (Hollister, Libertyville, IL)
Tegaderm (3M Healthcare, St Paul, MN)
OpSite (Smith & Nephew, Largo, FL)
Bioclusive Transparent (J&J, Somerville, NJ)
Mefilm (Molnlycke, Newtown, PA)
Mepilex Border (Molnlycke, Newtown PA)
Tielle (J&J Wound, Somerville, NJ)
Lyofoam (Convatec, Skillman, NJ)
Allevyn (Smith & Nephew, Largo, FL)
Curafoam (Tyco Healthcare, Mansfield, MA)
Optifoam (Medline, Mundelein, IL)
Aquacel (Convatec, Skillman, NJ)
SeaSorb (Coloplast, Marietta, GA)
Silvercel (J&J Wound, Somerville, NJ)
Maxorb (Medline, Mundelein, IL)
Kalginate (DeRoyal, Powell, TN)
Acticoat Absorbent (Smith & Nephew,
Largo, FL)
Actisorb (J&J Wound, Somerville, NJ)
Aquacel Ag (Convatec, Skillman, NJ)
Silvasorb (Medline, Mundelein, IL)
Silverlon Pad (Argentum Medical,
Willowbrook, IL)
Continued
94 Dermatologic Surgery

Table 6-5  Wound dressings and topical agents­—cont’d

Characteristics Brands/ingredients
Topical agents
Antiseptics Destructive to bacteria and tissues Acetic acid 0.025%
Nonselective in activity Chlorhexidine (Hibiclens; Regent, Norcross,
GA)
Dakin’s solution 0.5%
Povidone–iodine
Gentian violet
Antimicrobial For critically colonized or infected wounds Mupirocin 2% (Bactroban; Glaxo Smith Kline,
agents UK)
Choice determined by wound culture Silver sulfadiazine 1% (King Pharmaceuticals,
Bristol, TN)
Most provide broad-spectrum coverage Metronidazole 1% (Flagyl/Metrogel;
Galderma, Fort Worth, TX)
Many contain silver-containing agents Gentamicin (Garamycin 1%)
Cadexomer iodine (Iodosorb; Smith &
Nephew, Largo, FL)
Bacitracin, polymyxin B, neomycin
Enzymatic Remove devitalized tissues Accuzyme (Healthpoint, Fort Worth, TX)
debriders
Can epithelialize areas of skin grafts that fail to take Collagenase Santyl (Ross Labs, Columbus, OH)
Activate proteolysis, collagenase, fibrinolysis Gladase-C (Smith & Nephew, Largo, FL)
Panafil (Healthpoint, Fort Worth, TX)
Maggot therapy Debridement of necrotic and devitalized tissues Monarch Labs, Irvine, CA
(www.monarchlabs.com)
Effective for venous ulcers, pressure ulcers, neuropathic foot
ulcers, and nonhealing traumatic or postsurgical wounds
Fly larvae sterilized and cannot progress past the larval stage
Must be used within 24 h of delivery
Miscellaneous Topical PDGF Becaplermin (Regranex 0.01% gel; J&J Wound,
Somerville, NJ)
Silicone nonadherent mesh Mepitel (Molnlycke, Newton, PA)
MMP binder ORC/collagen (Promogran Prisma, J&J)
MMP binder with silver ORC/collagen with silver (Promoran Prisma,
J&J)
Capillary bed stimulant, promotes epithelialization and Xenaderm (Healthpoint, Fort Worth, TX)
promotes healing
ORC, oxidized regenerated cellulose.

In general, these skin substitutes are gradually re-
placed by the host epidermal and dermal compo-
nents, but while present are a primary stimulus for
the host to produce the variety of cytokines and
growth factors needed for timely wound healing.
In turn, these soluble mediators promote the se-
quential steps of wound healing while at the same
time promoting appropriate inflammation and
wound granulation, and preventing dessication.
Epidermal skin substitutes
The science of epidermal tissue culture emerged
in 1975 when scientists discovered how to grow
sheets of human keratinocytes. This was a major
advance: a patient’s own skin keratinocytes could
now be expanded in culture and used to cover
large burns and other kinds of wounds, ­providing
permanent coverage of large areas. Although
scarring and wound contraction still occurred,
the technique was life saving. Unfortunately,
­keratinocyte autografts are still quite expensive
and considerable time (2–4 weeks) is required to
culture the epidermal sheets.
To avoid the long wait times needed for au-
tologous grafting, cultured allografts have been
­developed. Keratinocytes for allografts come from
cadavers or unrelated adult donors. ­Entire sheets
of decellularized human dermis (Alloderm) are

ERRNVPHGLFRVRUJ
 6

Chapter
Cutaneous wound healing 95

Table 6-6  Skin substitutes

Brand name
Epidermal constructs
Epicel (Genzyme Biosurgery,
Cambridge, MA)
Celaderm (Celaderm
Science, LLC, Brookline, MA)
Dermal constructs
Dermagraf (Smith &
Nephew, Largo, FL)
Alloderm (LifeCell Inc,
Woodlands, TX)
Integra (Integra Life
Sciences, Plainsboro, NJ)
Combined epidermal and
dermal constructs
Apligraf (Organogenesis,
Canton, MA)
OrCel (Ortec International,
New York, NY)
Components
Autologous (self)
Allogeneic (nonself)
Allogeneic skin – fibroblasts
grown on neonatal foreskin,
generates a 3-D matrix, serves
as a dermal replacement
Decellularized allogeneic
human dermis
Bovine collagen with
chondroitin 6-sulfate
Bovine collagen, allogeneic
fibroblasts and epidermal
cells
Allogeneic fibroblasts and
epidermal cells grown on a
porous cross-linked bovine
collagen sponge matrix
Advantages
No rejection, permanent
coverage, high take rate; large
coverage area
Readily available, inexpensive
(relative); no biopsy needed
Readily available; mimics
functional dermis; used
as matrix for cultured
autologous epidermal cells;
cryopreserved, sterility tested
Readily available, not rejected;
used as matrix for epidermal
grafts; 2-year shelf-life
Readily available; reduced
scarring; good barrier
function; moderate shelf-life
Readily available, no need
for subsequent autografting;
mimics functional skin;
cryopreserved
Cells secrete growth factors
and cytokines, closely
mimicking normal acute
wound fluid; porous nature
allows easy flow of wound
fluid and exudates to and from
wound bed
Disadvantages
2–4-week delay; fragile,
custom preparation; 1-day
shelf-life.; poor cosmesis
Temporary, superficial
coverage; poor cosmesis
Need to harvest from host;
some risk for infection
transmission; requires thaw/
rinsing before use; fragile
Need for harvesting from host;
lacks cellular components;
increased risk of infection
transmission (low)
High cost, risk of infection;
operative removal of silicone
layer required; autograft
required; need to excise
wounds
Limited viability; infection
risk (low); 5-day shelf-life;
expensive
Limited quantity; infection risk
(low); expensive

also available. These products are quite effective
in treating burns, skin-graft donor sites, chronic
pressure sores, and venous stasis ulcers. As they
are temporary, they are unsuitable for permanent
closure of full-thickness wounds.
Dermal skin substitutes
The primary advantage of using a dermal com-
ponent is to minimize wound contraction and
provide more stability. Dermal allografts from
human cadavers must be chemically modified to
remove their antigenic components to avoid graft
rejection. These dermal grafts are often overlaid
with autologous epidermal grafts to enhance the
overall wound healing effect. Currently available
products are listed in Table 6-6.
Composite skin substitutes
These grafts have a collagen-based dermal com-
ponent with incorporated living fibroblasts and
keratinocytes on top, to provide as natural a sub-
stitute as possible. Although effective, the main
drawback of these composite grafts is their high
cost, limiting their use to relatively small recalci-
trant wounds.
Optimizing outcomes: wound
care guidelines
Guidelines for patients
After a wound has been dressed appropriately in
the office or postoperative setting, the patient or
their caregiver will be responsible for the con-
tinued care of the wound at home. Therefore, he
or she must be provided detailed information on
how to care for their specific wound. Written in-
structions are most effective. Instructions should
be formatted in a stepwise manner to avoid con-
fusion about the proper order of cleansing and
dressing applications. Patients should keep the
wound dressing dry and untouched for 24 h,
unless the bandage becomes soiled and soaked

ERRNVPHGLFRVRUJ
96 Dermatologic Surgery
through. After this, the dressing may be removed
and the wound cleansed with tap water and a
mild soap or normal saline solution. Hydrogen
peroxide should be used only to remove dried
­serous crusts that may have accumulated between
dressing changes. Indiscriminate use of hydrogen
peroxide may inhibit wound healing. If antibiotic
ointments and nonadherent gauze are used, dress-
ings can be changed once to twice daily. With the
newer occlusive dressings, the timing of dress-
ing changes will be governed by the quantity of
­exudate and the anatomic location.
After most dermatologic surgical procedures,
patients should be told to expect some post­
operative swelling, bruising, and discomfort. Dis-
comfort in the first 48 h after surgery should be
manageable with acetaminophen. Alcohol, aspi-
rin, aspirin-containing products, and nonsteroidal
anti-inflammatory drugs (including ibuprofen)
should be avoided because these compounds can
increase the likelihood of inadvertent postopera-
tive bleeding. If discomfort worsens or persists,
the situation should be re-evaluated.
Patients should be told how to modify their
bathing routine. After a preliminary 24-h period,
most patients can bathe if the wound area is kept
relatively dry. Some newer occlusive dressings
even allow patients to shower within the first 24 h.
That said, any activity in which the wound may
be submerged (bathing, swimming) should be
avoided because immersion does increase the risk
of infection and wound dehiscence. In addition, pa-
tients must be specifically instructed to limit their
physical activity for 24–48 h postsurgery, because
the stress placed on the wound can cause dehis-
cence. Patients are often surprised to learn that the
strength of their healing wound will be only 7–10%
of normal at 1 week, and only 40–50% at 1 month.
Smoking is a critical inhibitor of wound heal-
ing and a major cause of graft failure, and this
should be stressed to patients in a direct manner.
Smoking causes vasoconstriction, inhibits wound
epithelialization, decreases oxygen tension at
the wound bed, and inhibits collagen deposition.
Patients should be strongly encouraged to mini-
mize or hold their smoking for several weeks
prior to their surgery, and for up to 4 weeks
afterwards, to achieve the best outcome. This
may even motivate them to quit.
Patients should also be advised about long-term
symptoms: the tingling, twitching, pain and itch-
ing that commonly occur at the wound site for
­several months after surgery. Patients should also
be counseled about the possibility of postopera-
tive erythema and pigmentary alteration. These
are real issues that may present themselves sev-
eral months down the line. Patients are far more
understanding if they are warned of these pos-
sible complications up front, rather than having
them appear without warning.
ERRNVPHGLFRVRUJ
Guidelines for physicians
In 2003, the Wound Healing Foundation com-
missioned the Wound Healing Society to develop
minimal standards for the diagnosis and treat-
ment of the four most common types of chronic
wound: venous ulcers, pressure ulcers, diabetic
ulcers, and arterial insufficiency. The consensus
guidelines were published in the November 2006
issue of Wound Repair and Regeneration, and are
summarized below.
Venous ulcers
Diagnosis
• Accurate diagnosis is made by color duplex
ultrasonography using proximal compression.
• Rule out gross arterial disease by palpating
pedal pulses and calculating the ankle:brachial
index (ABI). If significant arterial disease is
present, treatment of raised venous pressure
alone will not succeed.
• Biopsy all lower-extremity ulcers that show
no signs of healing over 3 months.
• Ulcers that are persistently painful and
enlarge after debridement should be
evaluated for pyoderma gangrenosum,
Wegener’s granulomatosis, or mycobacterial/
fungal infection.
Compression
• External compression, constant or
intermittent, is a mainstay of therapy in
venous ulcers, but is contraindicated in more
severe arterial disease.
• Compression therapy should be permanent
and lifelong as venous hypertension is ongoing
in these patients.
Infection control
• Debride all necrotic or devitalized tissue
using sharp, enzymatic, mechanical, biologic,
or autolytic techniques.
• Bacterial colonization (bioburden) impairs
wound healing and is best treated with topical
antimicrobials. Save systemic antibiotics for
overt infection.
• Edema inactivates the normal bactericidal
properties of the skin and inhibits wound
healing.
Wound bed preparation
• Evaluate for coexisting medical illness
(autoimmune illness), medication use
(immunosuppressive medications), nutritional
status, and tissue perfusion/oxygenation.
• Monitor wound characteristics frequently
for location, size, base, exudate, surrounding
skin condition, and pain, to assess for wound
healing rates and complications.

• Maintain a moist (not macerated) wound bed,
along with use of compression.
Dressings
• Combine dressing applications with
debridement and/or antimicrobial activity;
optimize moisture control and compression.
• Select a dressing that will manage wound
exudate and protect the periulcer skin.
Maceration impedes healing.
• Select dressings that minimize shear and
friction, yet stay in place to avoid additional
tissue damage – more easily accomplished
when covered with appropriate compression
bandages.
Surgery
• For venous ulcers, skin grafting without
attending to underlying venous disease is
prone to recurrent ulceration.
• Surgical treatment should be combined with
compression therapy.
• Surgical treatment of the deep perforator
veins is sometimes necessary when less
extensive measures/surgery have failed.
Adjuvants (topical, device, systemic)
• Cytokine growth factors have not been shown
to demonstrate statistically significant results
in the treatment of venous ulcers.
• Biologically active dressings (bilayered
artificial skin) used in conjunction with
compression can increase healing.
• Cultured epidermal autografts or allografts do
not show increased healing of venous ulcers.
• Electrical stimulation may be useful.
• Sclerotherapy may be useful as an adjunct to
compression therapy.
• Pentoxifylline in conjunction with compression
improves healing of venous ulcers.
• Stanozolol, an anabolic steroid, enhances
fibrinolytic activity when used in conjunction
with compression and may be useful in treating
lipodermatosclerosis in venous ulcer disease.
Long-term maintenance
• Recurrence rates are as high as 70%.
• Patients with healed or surgically repaired
venous ulcers should use compression
stockings constantly and forever.
Pressure ulcers
Positioning and support
• Establish a repositioning schedule and avoid
pressure on the ulcer itself.
• Head of the bed should be at the lowest
degree of elevation; limit the amount of time
that head of bed is elevated.
• Assess pressure ulcer risk in patients and use
pressure-reducing devices to lower this risk.
ERRNVPHGLFRVRUJ
6
Chapter
Cutaneous wound healing 97
Nutrition
• Nutritional assessment should be performed
upon entry to a new healthcare setting and
after all changes in health status.
• Nutritional supplementation can help to
prevent pressure ulcers.
Infection
• Treat distant infections (e.g. urinary tract,
endocarditis) in pressure ulcer-prone patients.
• Remove all necrotic or devitalized tissues
by sharp, enzymatic, biologic, mechanical, or
autolytic debridement.
• If any suspected infection remains after
appropriate debridement, then swab and
obtain tissue biopsy for culture.
• When the wound bioburden passes 1 × 106
colony forming units (CFU)/g tissue, or there
is any level of β-hemolytic streptococci,
topical antimicrobials are indicated.
• Prior to attempting any surgical closure,
achieve a bacterial balance of <105 CFU/g
tissue without any β-hemolytic streptococci.
• Bone biopsy to rule out osteomyelitis is
warranted in suspected cases of pressure
ulcer. If found, bone debridement is
needed and coverage with muscle or fascia
recommended.
Wound bed preparation
• Evaluate patient for concurrent systemic
disease, medications, nutritional status, tissue
perfusion and oxygenation.
• Debride to remove necrotic tissue, excessive
bioburden, devitalized cells and tissue.
• Cleanse wounds with a neutral, nonirritating,
nontoxic solution, and with minimal
mechanical trauma.
• Manage wound moisture balance by
controlling exudate and guarding against
dessication.
• Regularly document wound characteristics to
following the progression of healing.
Dressings
• Maintain moist wound healing environment
by managing exudate and protecting periulcer
skin from maceration.
• Wound dressings should adhere without
excessive shearing, friction or additional
pressure.
Surgery
• Sinus tracts and cavities in pressure ulcers
must be explored and unroofed, and then
treated.
• Necrotic tissue must be managed with topical/
systemic antibiotics and/or debridement.
• Fecal and urinary diversion are rarely needed
to heal a pressure wound.
98 Dermatologic Surgery
• Pressure sores/ulcers should be closed surgically
if they do not respond to wound care.
• A composite bilayered skin substitute
represents the best chance for sustained
wound closure.
Adjuvants (topical, device, systemic)
• Growth factor therapy may be of benefit in
treating recalcitrant pressure ulcers.
• Consider negative-pressure wound therapy
(NPWT) in stage III or IV pressure ulcers that
fail to progress with conventional
therapies.
• Electrical stimulation may be beneficial with
pressure ulcers.
• Hyperbaric oxygen therapy does not have any
statistically significant effect on the healing of
pressure ulcers.
Diabetic ulcers
Diagnosis
• Diabetic ulcers can result from arterial
insufficiency and/or neuropathy.
• Rule out significant arterial disease (pedal
pulses and ABI) using color duplex
ultrasonography.
• Significant neuropathy is tested with a
10-g Semmes–Weinstein monofilament.
• Neuropathy causes a lack of protective
sensation, allowing ulceration in areas of high
pressure.
Offloading
• Protective footwear is a critical requirement
in at-risk diabetic patients with neuropathy.
• Offload with crutches, walkers, wheelchairs,
custom shoes, total contact casts.
Infection control
• Debride all necrotic or devitalized tissue by
sharp, enzymatic, mechanical, biologic, or
autolytic means.
• If epithelialization from wound margin is not
progressing after debridement and 2 weeks
of offloading, evaluate and quantify whether
infection may be present (tissue culture and
swab).
• When wound bioburden passes 1 × 106
CFU/g tissue, or there is any tissue level of
β-hemolytic streptococci after debridement,
topical antimicrobials are indicated.
• Acute diabetic foot infections, including
cellulitis, respond well to systemic
antibiotics.
• Vigorous surveillance for osteomyelitis is
recommended and appropriate diagnostic
measures (X-ray, magnetic resonance
imaging, computed tomography, and
radionuclide scan) are indicated when
it is suspected.
ERRNVPHGLFRVRUJ
• Osteomyelitis is best treated by removal of
infected bone and systemic antibiotics for
2–4 weeks.
• Before attempting any surgical closure, obtain
a bacterial balance of <105 CFU/g tissue and
absence of β-hemolytic streptococci.
Wound bed preparation
• Evaluate patient for concurrent systemic
disease, medications, nutritional status, tissue
perfusion and oxygenation.
• Debride to remove necrotic tissue, excessive
bioburden, devitalized cells and tissue.
• Cleanse wounds with a neutral, nonirritating,
nontoxic solution, and with minimal
mechanical trauma.
• Manage wound moisture balance by controlling
exudate and guarding against dessication.
• Regularly document wound characteristics to
follow the progression of healing.
• Optimizing glucose control improves wound
healing.
Dressings
• Maintain moist wound healing environment
by managing exudate and protecting periulcer
skin from maceration.
• Wound dressings should adhere without
excessive shearing, friction, or additional
pressure.
Surgery
• Achilles tendon lengthening may improve
healing of diabetic forefoot wounds.
• Patients with ischemia should be evaluated
for revascularization surgery.
Adjuvants (topical, device, systemic)
• PDGF is effective in treating diabetic
neurotrophic foot ulcers.
• Other cytokine growth factors do not have
sufficient data to recommend their use in
diabetic foot ulcers.
• Negative-pressure wound therapy (NPWT)
may be beneficial.
• Living skin equivalents (composite bilayered
skin substitutes) may be of benefit in treating
diabetic ulcers.
• Electrical stimulation may provide some
benefit.
• Hyperbaric oxygen therapy may provide
some benefit in reducing amputation rates
in patients with ischemic diabetic foot
ulcers.
Long-term maintenance and prevention
• Patients with healed ulcers should wear
protective footwear.
• Good foot care and daily inspection of feet
will reduce recurrences.

Arterial insufficiency ulcers
Diagnosis
• Decreased or absent pedal pulses and/or a
resting ABI <0.9 is an indication of peripheral
artery occlusive disease (PAOD).
• Referral to a vascular medicine specialist is
necessary.
• Patients with significant risk factors
for atherosclerosis (smoking, diabetes,
hypertension, hyperlipidemia, advanced age,
obesity, hypothyroidism) who have ulcers are
more likely to have arterial ulcers and should
be closely evaluated.
• Patients with rest pain or gangrene need
an urgent referral to a vascular medicine
specialist as these conditions can progress
rapidly and involve an increased risk of limb
loss.
Surgery
• An anatomic “roadmap” is recommended
prior to any revascularization procedure
(angiography, duplex angiography, magnetic
resonance angiography).
• Surgical revascularization (endovascular
or open) is likely to be more successful if
combined with adjuvant therapies.
Infection control
• Debride all necrotic or devitalized tissue by
sharp, enzymatic, mechanical, biologic, or
autolytic means
• Arterial ulcers with dry gangrene or an
eschar require the re-establishment of
arterial inflow prior to attempting
debridement.
• Patients with neuroischemic ulcers (e.g.
diabetics) should consider a course of
systemic antibiotics even if clinical signs
of infection are absent. These chronic
wounds can have a significant bacterial
load before any clinical evidence of infection
arises.
• Adequate oxygenation is paramount in
healing arterial ulcers.
• Topical antimicrobial dressings may be
beneficial in achieving bacterial balance and
aiding wound healing.
Wound bed preparation
• Evaluate patient for concurrent systemic
disease, medications, nutritional status, tissue
perfusion and oxygenation.
• Maximize oxygen delivery to the area by
avoid smoking and dehydration.
• Debridement of nonviable tissues should be
delayed until after revascularization.
• Compression therapy may be of benefit in
mixed etiologies (venous and arterial).
ERRNVPHGLFRVRUJ
6
Chapter
Cutaneous wound healing 99
Dressings
• Autograft and allograft dressings can
accelerate wound closure in these patients,
yet revascularization is still required.
• Maintain moist wound environment by
managing exudate and protecting against
maceration.
• Wound dressings should adhere without exces­
sive shearing, friction, or additional pressure.
Adjuvants (device, systemic agents)
• Electrostimulation seems to offer a promising
adjuvant therapy in arterial ulcers.
• Spinal cord stimulation is a promising
adjuvant to managing lower limb ischemia,
ulcers, and pain.
• NPWT appears promising for mixed arterial
and venous ulcers.
• Intermittent pneumatic leg compression
increases impaired distal perfusion both
before and after revascularization.
• Hyperbaric oxygen therapy should
be considered in patients with
nonreconstructable anatomy or in those not
healing even after revascularization.
• There is no evidence to support the use of
pentoxifylline or prostaglandins (PGE1) in
the treatment of arterial ulcers.
• Stem cell therapy is a promising field, but
there are insufficient data to recommend its
use at present.
• VEGF gene therapy may be of some benefit.
Long-term maintenance
• Risk factor reduction (smoking, diabetes,
raised homocysteine levels, hyperlipidemia,
hypertension) is vitally important to combat
PAOD and arterial ulcers.
• Antiplatelet therapy is advocated, as these
medications offer vasodilatory and antiplatelet
effects, and improve fibrinolytic activity.
• Exercise, which increases arterial blood flow,
provides a significant long-term benefit for
ulcer prevention.
Further reading
Attinger CE, Janis JE, Steinberg J et al. Clinical
approach to wounds: debridement and wound
bed preparation including the use of dressings
and wound-healing adjuvants. Plast Reconstr Surg
2006;117(7 Suppl):72S–109S.
Broughton G 2nd, Janis JE, Attinger CE. The basic
science of wound healing. Plast Reconstr Surg
2006;117(7 Suppl):12S–34S.
Clark R. Wound repair: overview and general
­considerations. In: Clark R, ed. The Molecular
and Cellular Biology of Wound Repair. New York:
Plenum Press; 1996:3–50.
100 Dermatologic Surgery
Falabella A, Kirsner R. Wound Healing (Basic and
Clinical Dermatology). Boca Raton, Florida: Taylor
and Francis, 2005.
Leveriza-Oh M, Phillips TJ. Dressings and postopera-
tive care. In: Robinson JK, Hanke CW, Sengel-
mann RD, Siegel DM, eds. Surgery of the Skin:
Procedural Dermatology. Philadelphia, Elsevier
Mosby, 2005:117–135.
Robson MC, Barbul A. Guidelines for the best
care of chronic wounds. Wound Repair Regen
2006;14(6):647–648.
Robson MC, Cooper DM, Aslam R. Guidelines for
the treatment of venous ulcers. Wound Repair
Regen 2006;14(6):649–662.
ERRNVPHGLFRVRUJ
Singer AJ, Clark RA. Cutaneous wound healing.
N Engl J Med 1999;341(10):738–746.
Steed DL, Attinger C, Colaizzi T. Guidelines for the
treatment of diabetic ulcers. Wound Repair Regen
2006;14(6):680–692.
Whitby DJ, Ferguson MW. The extracellular matrix
of lip wounds in fetal, neonatal and adult mice.
Development 1991;112(2):651–668.
Whitney J, Phillips L, Aslam R. Guidelines for the
treatment of pressure ulcers. Wound Repair Regen
2006;14(6):663–679.

Electrosurgery
Oliver J. Wisco and Paula S. Vogel
Clinical overview
The utilization of electricity to cause thermal tis-
sue destruction has revolutionized the approach
to surgery. This chapter discusses the basic sci-
ence and the various types of electrosurgery, and
how they can be utilized effectively in dermato-
logic surgery.
Basic science and terminology
Key Points
• The interaction of the electricity principles of
current, resistance, voltage, work, and power
determine the functionality of an electrosurgical
unit.
• Whether an electrosurgical unit is monoterminal
or biterminal will determine the spread of the
electrical current through the patient.
Electricity principles (Table 7-1)
Pearl
• Tissue must be patted dry before using an elec-
trosurgery unit as blood decreases the resist-
ance and prevents heat from being generated.
Waveform (Table 7-2 & Fig. 7-1)
• Shape of the electromagnetic fields generated
from a high-frequency alternating current.
• Determines the effect of the current on the
tissue.
Pearls
• Spark-gap electrosurgery units are typically used
for electrodessication, electrofulguration, and
electrocoagulation.
• Vacuum-tube electrosurgery units are typically
used for electrosection.
Monoterminal versus biterminal
The terms monopolar and bipolar are misnomers.
Instead, “monoterminal” and “biterminal” should
be used, as electrosurgery does not use electrodes
that are true positive or negative poles.
ERRNVPHGLFRVRUJ
7
Chapter
Monoterminal
• Only one electrode delivers current to the
patient and electrons are randomly dispersed
to the environment.
• Used in electrodessication and
electrofulguration.
Biterminal
• Two electrodes are applied, with the current
flowing from one electrode to the other to
complete an electrical circuit.
• Used in electrocoagulation and electrosection.
Medical treatment options
Key Points
• Preoperative assessment is crucial when
performing electrosurgical procedures.
• Electrodessication, electrofulguration,
electrocoagulation, and electrosection are the
four types of electrosurgery.
Preoperative assessment
• Determine risk for excessive blood loss.
• Determine risk for poor wound healing.
• Identify patients with cardiac pacemakers
and implanted cardiodefibrillators as
electrosurgery may cause these devices to
malfunction.
• Have the patient remove all metal objects,
including jewelry, prior to surgery.
Electrosurgical procedures
Outlines of the procedures of electrodessication,
electrofulguration, electrocoagulation, and elec-
trosection are shown in Tables 7-3 & 7-�4.
Electrosurgery adverse reactions
See Box 7-1
Pearl
• Superficial electrosurgical wounds heal by
secondary intention and require only standard
postoperative wound care.
102 Dermatologic Surgery

Table 7-1  Electricity principles

Principle Definition Units Pearls/Application
Current Flow of electrons through a conductor per second Amperes The thinner the electrosurgical tip,
the greater the current density,
• Density = current/conductor cross-sectional area
resulting in greater tissue
destruction
Direct Electron flow is in one direction Used in iontophoresis and
electrolysis
Alternating Electron flow is constantly alternating direction; Frequencies of 500–2000 Hz generate
with high frequencies there is no cellular heat with no/minimal neuromuscular
depolarization resulting in the generation depolarization
of heat
Resistance A conductor’s ability to impede the passage of an Ohms Muscle: low resistance
electric current
Fat: high resistance
• Directly proportional to the length of the substance Skin: high when dry, low when wet
• Inversely proportional to the cross-sectional area
Voltage Electrical force that induces electron flow Volts Little heat is created with low
resistance
• Current flows from high to low electron
concentration
• Volts = current × resistance
Work Current flow over a distance due to voltage Joules Tissue resistance to current results
difference in heat generation
• Work = force × distance
Power Rate of heat generated due to tissue resistance Watts (joules/s) Power increases are greater with
to the passage of current created by a voltage increased current rather than voltage
potential
• Power = current × voltage

Tissue effect
Table 7-2  Waveform factors Continuous, undamped

Factor Description Pearls/Application

Undamped Pure sine wave Pure cutting Pure cutting
with minimal
hemostasis
Damped Amplitude Greater dampening Continuous, damped
decreases causes increased
progressively tissue destruction
and hemostasis Cutting and
coagulation
Continuous Uninterrupted Increased tissue
waveform heating, due to
longer current flow
Discontinuous, undamped
Discontinuous Interrupted Decreased tissue
waveform heating, due to
shorter current
Pure cutting
flow

Discontinuous, damped
Surgical approach (Box 7-2)
Key Points Desiccation and
coagulation
• Multiple conditions can be treated with
electrosurgery. The most common are those with
a superficial process.
• Electrodessication and curettage is an effective Figure 7-1  Types of waveform. Adapted from Robinson
option for superficial cutaneous malignancies. et al (2005) with permission from Mosby Publishing

ERRNVPHGLFRVRUJ
 7

Chapter
Electrosurgery 103

Table 7-3  Electrodessication and electrofulguration

Electrodessication
Use: superficial destruction, capillary hemostasis
Properties: monoterminal, high voltage, low amperage
Description: Touch the electrode to the skin to cause direct
superficial tissue dehydration with resultant damage localized
to the epidermis with lower settings. Higher power settings can
cause scarring due to dermal involvement
Electrofulguration
Use: superficial destruction
Properties: monoterminal, high voltage, low amperage
Description: Hold the electrode 1–2 mm from the skin to cause
superficial skin dehydration through sparks with resultant damage
localized to the superficial epidermis

Superficial tissue Sparks cause superficial

No electrode
Electrode dehydration epidermal carbonization
contact
contact

Epidermis Epidermis

Dermis Dermis

Adapted from Robinson et al (2005) with permission from Mosby Publishing Company.

Electrodessication and curettage • The element is very hot in electrocautery,

• Used for the treatment of superficial benign
and malignant neoplasms.
• Sequence of curettage followed by
electrodessication repeated two or three times.
• Not effective for deeper lesions or lesions that
extend down the hair follicles.
• Limited use in areas of high cosmetic
importance due to the risk of scarring.
Comparative outcomes
Key Points
• Electrocautery is not a true form of electrosurgery
as no current flows through the patient.
• Electrosection primarily has the benefit of a
faster incision time and less incisional blood loss
compared with scalpel surgery.
Electrocautery
• Low voltage, high amperage and direct or
high-frequency current that heats an element
causing superficial tissue destruction or
hemostasis through the direct transfer of heat.
• Useful in the setting of an implanted cardiac dev­
ice as no current is transferred into the patient.
whereas the electrode in electrosurgery
remains cool.
Electrosection versus conventional
scalpel surgery
• Incisional time and incisional blood loss are
less for electrosurgery.
• There is no significant statistical difference in
infection rate or healing time.
• Electrosection may have a superior cos­metic
outcome and decreased postoperative
pain.
Controversies
Key Points
• One of the most important issues when
employing electrosurgery is its use in the
setting of implanted cardiac devices such as
pacemakers and automatic defibrillators.
• Bipolar forceps are useful in the setting of
implanted cardiac devices as the forceps’ electrode
tips allow pinpoint electrocoagulation without
the spread of electrical current to the rest of the
body.

ERRNVPHGLFRVRUJ
104 Dermatologic Surgery

Table 7-4  Electrocoagulation and electrosection

Electrocoagulation
Use: deep tissue destruction, arteriole hemostasis
Properties: biterminal, low voltage, high amperage
Description: Place indifferent electrode on opposite side of the
body from the surgical site. Touch the electrode to the skin to
cause direct deep tissue destruction and coagulation
Electrosection
Use: tissue cutting
Properties: biterminal, low voltage, high amperage
Description: Place indifferent electrode on opposite side of the
body from the surgical site. Apply the electrode to the tissue
in the same fashion as incising with a scalpel, but with less
pressure, to cut through the tissue. Undamped current allows
cutting without coagulation, whereas damped current causes
cutting with coagulation

Electrode contact and

Deeper tissue tissue cutting with
Electrode coagulation or without coagulation
contact

Epidermis Epidermis

Dermis Dermis

Indifferent electrode Indifferent electrode

Adapted from Robinson et al (2005) with permission from Mosby Publishing Company.

B ox 7 - 1

Electrosurgery pitfalls and their management

Burns • The surgeon should not make or break contact with the
patient during current delivery.
• Use a nonflammable cleanser such as chlorhexidine or
povidone–iodine.
Transmission of infection
• Avoid alcohol cleanser, ethyl chloride anesthesia, and flowing
oxygen. • Use a smoke evacuator with the intake nozzle 2 cm from the
operative site.
• Ensure that the indifferent electrode has broad contact with
skin and is not placed over a bony prominence, scar tissue, or • Wear a surgical mask and eye protection when working with
implanted metal. human papillomavirus-related lesions.

• Ensure the patient is not touching grounded metal objects. Eye injuries
• Place the indifferent electrode away from vital structures to • Avoid using treatment electrode close to the eye, if
decrease the risk of current channeling into a substance that is possible.
more conductive than skin (e.g. nerve or vessel), especially if
it leads to an isolated region such as the penis or finger. • Use plastic corneal shields if working close to the eye.

Electric shock Interference with implanted cardiac devices

• Use a three-pronged receptacle that is not overloaded. • See discussion in the Controversies section.

• Do not use treatment table outlets.

Adapted from Robinson et al (2005) with permission from Mosby Publishing Company.

ERRNVPHGLFRVRUJ
 7

Chapter
Electrosurgery 105

B ox 7 - 2 B ox 7 - 3

Common dermatologic indications Guidelines to minimize interference with

for electrosurgery cardiac pacemakers and implantable
cardiodefibrillators
Electrofulguration/ • Sebaceous hyperplasia
electrodessication Use the following:
• Squamous cell
(superficial skin • Bipolar forceps
carcinoma
ablation)
• Syringoma • Battery-operated heat generating electrocautery device
• Acrochordon
• Telangiectasia • Short bursts (<5 s)
• Actinic keratosis
• Trichoepithelioma • Minimal power
• Angioma (small)
• Verruca vulgaris • Ground away from device
• Basal cell carcinoma
(all locations) • Avoid electrosurgery near device (preferably more than
(superficial and nodular)
10 inches away)
• Bowen’s disease Electrosection (skin
• Epidermal nevus incision/excision)

• Hemostasis • Acne keloidalis nuchae

(capillary bleeding) • Blepharoplasty incision
• Lentigo • Debulking procedures Further reading
• Verruca plana • Hair transplant strip Bolognia JL, Jorizzo JL, Rapini RP, eds. Dermatology.
• Seborrheic keratosis harvesting Edinburgh: Mosby, 2003.
• Rhinophyma repair Hainer BL. Electrosurgery for the skin. Am Fam
Electrocoagulation Physician 2002;66(7):1259–1266.
• Rhytidectomy incisions
(deep skin ablation) Massarweh NN, Cosgriff N, Slakey DP. Electrosur-
and undermining
• Angiofibroma gery: history, principles, and current and future
• Scar revision uses. J Am Coll Surg 2006;202(3):520–530.
• Angioma (large) Pollack SV. Electrosurgery. In: Bolognia JL, Jorizzo JL,
• Shave removal of benign
• Basal cell carcinoma skin lesions (fibromas, Rapini RP, eds. Dermatology. Edinburgh: Mosby,
(superficial and nodular) nevi, etc.) 2003:2197–2203.
• Bowen’s disease • Skin flap incisions and Robinson JK, Hanke CW, Sengelmann RD,
undermining Siegel DM, eds. Surgery of the Skin: Procedural
• Hemostasis Dermatology. Philadelphia: Mosby, 2005.
(arterial bleeding) • Skin resurfacing (under Soon SL, Washington CV. Electrosurgery, electro­
investigation) coagulation, electrofulguration, electrodessication,
• Hirsutism
• Surgical excision of electrosection, electrocautery. In: Robinson JK,
• Ingrown
malignant or benign skin Hanke CW, Sengelmann RD, Siegel DM, eds.
toenail matrixectomy
lesions Surgery of the Skin: Procedural Dermatology.
• Banal melanocytic nevi Philadelphia: Mosby, 2005:177–190.
Yu SS, Tope WD, Grekin RC. Cardiac devices and
Adapted from Bolognia et al (2003) with permission from Mosby Publishing electromagnetic interference revisited: new radio­
Company. frequency technologies and implications for der-
matologic surgery. Derm Surg 2005;31:932–940.

Dermatologic electrosurgery
interference with pacemakers
and defibrillators
The use of electrosurgery in dermatologic sur-
gery may cause interference with pacemakers
or defibrillators (Box 7-3). It is recommended to
­discuss with the patient’s cardiologist the need
for preop­erative/postoperative evaluation and/or
intra­operative monitoring.

ERRNVPHGLFRVRUJ

Cryosurgery
Leonid Benjamin Trost and Philip L. Bailin
Key Points
• Cryosurgery is a versatile and cost-effective
method of treating many benign, premalignant,
and malignant lesions.
• The most commonly used cryogen is liquid
nitrogen.
• The most common cryosurgical technique is the
open spray technique.
• To kill all malignant cells, a final temperature used salt solutions containing crushed ice (−8
of −20 to −30°C must be achieved.
• For malignant lesions, the depth of freeze should
be roughly equal to the radius of the surface
frozen area. A thermocouple can be inserted at
the base of the lesion for greater accuracy.
• If an intermittent spray technique is used, the
resultant ice ball will have a greater depth and
more limited lateral spread. If a continuous spray
technique is used, the resultant ice ball will be
more shallow and will have a greater lateral
spread.
• The greatest possible depth of the ice ball is
about 10 mm.
• Benign lesions usually require only one freeze–
thaw cycle.
• Premalignant lesions usually require one
freeze–thaw cycle, although two may be used.
• For cryosurgery of malignant lesions, the goal of
therapy is to destroy the same mass of malignant
tissue by freezing as would be removed by
excision. Therefore, an adequate margin around
the tumor must be frozen. Malignant lesions
usually require two freeze–thaw cycles, although
three may be used in some cases.
• For malignant lesions, the halo thaw time, or the
duration of surface thawing of marginal tissue
beyond the target site, should be greater than
60 s. The total thaw time of the entire lesion
should be more than 90 s.
• A large lesion may first be debulked surgically to
create a thinner lesion that freezes more rapidly.
• The combination of rapid freezing and slow thaw
produces maximal tissue damage.
Introduction
Cryosurgery is a versatile and cost-effective
­method of treating many benign, premalignant,
and malignant lesions. A cryogenic agent is applied
ERRNVPHGLFRVRUJ
8
Chapter
directly or indirectly to the skin. This causes local
tissue destruction, and healing occurs by second
intention. Today, cryosurgery is commonly used
by most dermatologists.
History
In 1845, James Arnott, an English physician,
to −12°C) to treat advanced cancers in sites that
were easily accessible, such as breast and cervi-
cal cancer. The goal was reduction in tumor
size and pain control. Olszenski was the first to
­liquefy air in 1885. In 1899, A. Campbell White
used liquefied air to treat nevi, warts, boils, and
herpes zoster. Over the next several decades, car-
bon dioxide snow (−78.5°C) and liquid ­ oxygen
(−182.9°C) were used. In 1950, Allington was
the first to use liquid nitrogen (−195.6°C) to
treat skin diseases such as warts, keratoses,
hemangiomas, and keloids.
Initially, cotton-tipped applicators and solid
copper cylinder disks chilled in the cryogen
were used. For the next several years, cryosur-
gery was limited by the depth of tissue dam-
age that could be achieved (maximum 7 mm).
In 1961, Cooper and Lee developed a closed
system with a vacuum-insulated probe that was
used in neurosurgery to treat conditions such
as Parkinsonism. In 1965, two American der-
matologists, Douglas Torre and Setrag Zacarian,
helped to develop a nitrogen spray device that
could be used with different cryoprobe tips.
These developments allowed deeper tissue in-
jury. In 1968, a handheld spray device was first
developed at Brooke Army Medical Center, us-
ing a rubber bulb to create pressure and force
the liquid nitrogen through the aperture. Later
versions were high-pressure systems that har-
nessed the pressure created by the evaporating
nitrogen.
The most common method of cryosurgery uses
a handheld device that contains liquid nitrogen.
A direct spray is used most commonly, but a cryo-
probe is sometimes used as well.
108 Dermatologic Surgery

Table 8-1  Cryogens and their boiling points Table 8-2  Factors that affect the freezing of tissue
Cryogen Boiling point (°C) Factor Key principles
Chlorodifluoromethane −40.8 Rate of tissue freezing Rapid freezing (<60 s)
Solidified carbon dioxide −78.5 causes more cell death

Nitrous oxide −88.5 Rate of intermittent Faster rate of intermittent

spraying spray gives deeper but
Oxygen −182.9 narrower depth of freeze
Liquid nitrogen −195.6 Slower rate of intermittent
Helium −268.9 spray gives more superficial
but wider depth of freeze
Rate of thawing Slow thawing (>90 s)
causes more cell death
Tissue temperature Final tissue temperature of
< −20 to −30°C will kill all
malignant cells
Duration of freezing Having the tissue remain
adequately frozen for a longer
period of time causes more
tissue injury
Maximum cell death rate
occurs at 100 s
Repetition of freeze–thaw More freeze–thaw cycles
cycles cause more cell death
Malignant tumors require
multiple freeze–thaw cycles
All cellular structures
show damage by electron
microscopy after two cycles

Figure 8-1  Temperature gradients formed within the ice

ball during cryosurgery. Note that the gradient ranges
from 0°C at its most lateral edge to-195.6°C at its center,
corresponding to the temperature of the liquid nitrogen
Cryogenic agents
Many cryogens have been used, but liquid nitro-
gen (boiling point −195.6°C) is employed most
widely (Table 8-1).
Cryobiology
During cryosurgery, an ice ball is formed in the
skin. Within the ice ball are temperature gra-
dients ranging from 0°C at its most lateral edge
to -195.6°C at its center, corresponding to the
temperature of the liquid nitrogen (Fig. 8-1).
­Cryosurgery causes injury via two mechanisms.
First, ice crystals form within the cells. Second,
vascular thrombosis occurs during freezing, and
vascular stasis occurs after thawing. These ­changes
in the vasculature lead to ischemic necrosis.
Table 8-2 describes factors that affect the
freezing of tissue. This includes the rate of tis-
sue freezing, rate of intermittent spraying, rate of
thawing, tissue temperature, duration of freezing,
and repetition of freeze–thaw cycles. Figures 8-02
and 8-03 depict how some of these factors relate
to the surface radius and depth of freeze.
Rapid freezing (100–260°C per min) leads
to increased cellular death. When cells are fro-
zen rapidly, intracellular ice formation damages
organelles and leads to irreversible cell destruc-
tion. Larger ice crystals cause more damage and
may even rupture the cell membrane. If cells are
frozen slowly, the cytoplasm becomes hyper­tonic
and resistant to freezing. Extracellular rather
than intracellular ice is formed. This is less lethal
to cells. Slow thawing (10°C per min) is associ-
ated with recrystallization and increased cellular
death. Intracellular water is increased, and rapid
electrolyte transfer further damages cellular
proteins. A second freeze–thaw cycle greatly
increases tissue injury. After two freeze–thaw
cycles, all cellular structures show damage on
electron microscopy. Malignant tumors require
multiple freeze–thaw cycles. This is discussed in
greater detail below.
Tissue temperature is crucial to achieving cel-
lular death. Table 8-� 3 shows the key events during
freezing. For malignant lesions, a final tempera-
ture of −20 to −30°C is necessary to kill all ma-
lignant cells. A final temperature of −50 to −60°C
kills all cells in the field. Having the tissue remain

ERRNVPHGLFRVRUJ

Figure 8-2  Relationship between depth of freeze to
spraying factors. (a) The depth of the ice ball is equal to
the surface radius of the ice ball. This tends to occur when
the spray is intermittent and when the spray tip is close
to the skin. (b) The depth of the ice ball is less than the
surface radius of the ice ball (R΄ < R). This tends to occur
when the spray is continuous and when the spray tip is
further from the skin. It can also occur when the liquid
nitrogen is “painted on’’ and/or the rate of intermittent
spray is too slow. Note that if the depth of the ice ball is
too shallow, then entire tumor may not be destroyed even
though the frozen surface margins appear to be adequate
Table 8-3  Key events during freezing
Temperature
(°C) Event
+11 to +3 65% of capillaries and 35–40% of
arterioles and venules develop thrombosis
−0.6 Freezing begins to occur in tissue
−4 to −7 Melanocytes die
−15 to −20 100% of blood vessels develop thrombosis
−20 Cells in sebaceous glands and hair
follicles die
−21.8 Ice crystals theoretically form in the tissue
(the eutectic temperature of sodium
chloride solution)
−20 to −30 Keratinocytes and malignant cells die
−30 to −35 Fibroblasts die
−50 to −60 All cells die
ERRNVPHGLFRVRUJ
8
Chapter
Cryosurgery 109
Figure 8-3  Relationship between the Therapeutically
Lethal Isotherm (TLI) (–30°C) and the edge of the ice ball
(0°C isotherm). In both A and B, the sizes and shapes of
the ice balls (0°C isotherm) are the same. In A, the TLI is
close to the edge of the ice ball. This tends to occur when
the spray is intermittent and when the spray tip is close to
the skin. In B, TLI is farther from the edge of the ice ball
(Y > X). Note that if the location of the TLI is too far from
the edge of the ice ball, the entire tumor may not be
destroyed even though the frozen surface margins appear
to be adequate
adequately frozen for longer periods of time leads
to higher rates of cell death, but at 100 s the rate
of cell death rates reaches a plateau.
Indications and
contraindications
Cryosurgery is effective at treating benign, prema-
lignant, and malignant lesions (Boxes 8-1–8-3).
For malignant lesions, cryosurgery is especially
appropriate for primary lesions less than 2 cm in
diameter with clearly demarcated borders in the
elderly, high-risk surgical patients, patients with
pacemakers or coagulopathy, patients who do not
wish to have excisional surgery, and when exci-
sional surgery is not practical. Cryosurgery also
can be used as a palliative therapy in metastatic
cancers to reduce tumor size.
Cryosurgery is contraindicated in patients with
cold sensitivity or diseases that are aggravated
by cold (cryoglobulinemia, cryofibrinogenemia,
pernio, etc.). It is also inappropriate for lesions that
overlie nerves, tumors with poorly demarcated
110 Dermatologic Surgery

B ox 8 - 1 B ox 8 - 2
Benign lesions that can be treated Premalignant lesions and in situ cancers
with cryosurgery that can be treated with cryosurgery

• Acne vulgaris, cystic • Actinic cheilitis

• Angiolymphoid hyperplasia • Actinic keratosis
• Angiokeratoma – Fordyce and solitary type • Squamous cell carcinoma in situ
• Angioma, cherry and spider • Leukoplakia
• Chondrodermatitis nodularis chronicus helicis
• Dermatofibroma
B ox 8 - 3
• Disseminated superficial actinic porokeratosis
• Epidermal nevi Malignant lesions that can be treated
with cryosurgery
• Granuloma faciale
• Granuloma fissuratum • Basal cell carcinoma

• Hemangioma, strawberry and cavernous • Squamous cell carcinoma (invasive) – includes

­keratoacanthoma
• Hidradenitis suppurativa
• Kaposi’s sarcoma
• Keloid
• Other malignancies (palliative only)
• Leishmaniasis
• Lentigines, lentigo simplex, solar lentigo
• Lichen planus, hypertrophic form
• Lichen sclerosus et atrophicus
• Lymphocytoma cutis
• Molluscum contagiosum
• Mucocele
• Myxoid cyst
• Nevus flammeus
• Porokeratosis of Mibelli
• Porokeratosis plantaris discreta
• Prurigo nodularis
• Psoriatic plaques
• Pyogenic granuloma
• Rosacea
• Sebaceous hyperplasia
• Seborrheic keratosis
Figure 8-4  Storsge Tank
• Steatocystoma multiplex
• Syringoma
• Trichiasis Cryosurgery is relatively contraindicated for
• Venous lake lesions on the scalp, lower legs, and digits, as well
• Verrucae (bowenoid papulosis, condyloma acuminatum,
as for lesions for lesions near the vermilion border,
periungual verruca, verruca plana, verruca palmaris et free margins of the ala nasi, and near the auditory
plantaris, verruca vulgaris) canal. Caution should be used in dark-skinned
patients because of the risk of postinflammatory
hypopigmentation.

borders, and tumors with deep invasion. Some Techniques

sites, such as the inner canthi, are more prone
to deep invasion. Finally, cryosurgery is contra­ Liquid nitrogen is stored long term in storage
indicated for recurrent tumors, as well as tumors tanks (Fig. 8-4). For temporary storage, portable
larger than 2 cm in diameter. storage units are available (Fig. 8-5).

ERRNVPHGLFRVRUJ
 8

Chapter
Cryosurgery 111

Figure 8-5  Portable storage unit

b
Table 8-4  Cryosurgery techniques and the lesions
that can be treated with each technique Figure 8-6  Instruments used in the dipstick technique:
(a) a cotton-tipped applicator and (b) a metal cryoprobe
Lesion type applicator
Technique Benign Premalignant Malignant
Dipstick Yes No No
Open spray Yes Yes Yes
Closed Yes Yes Yes

The three main cryosurgery techniques are the

dipstick, open spray, and closed techniques. The
open spray technique is used most commonly.
Table 8-� 4 describes the techniques that may be
used for benign, premalignant, and malignant
­lesions.
Dipstick technique
The dipstick technique involves dipping a cotton-
tipped applicator (Fig. 8-6a) to absorb the liquid
nitrogen or a metal applicator (Fig. 8-6b) chilled
to the temperature of the liquid nitrogen and then
applying it to the lesion. The latter method may
be safer clinically as there is no risk of dripping Figure 8-7  Handheld liquid nitrogen unit
liquid nitrogen onto the patient. This may have
to be repeated multiple times in one session un-
til the clinical endpoint is reached. The freezing patient. This small temporary supply can then be
spread is slow compared with other techniques. reused for the patient.
This method is generally reserved for small be-
nign epidermal lesions, especially warts, lentigo
Open spray technique
simplex, and solar lentigo. It is inappropriate for The open spray technique is probably the most
malignant lesions. common technique used by dermatologists. Liq-
Once the applicator has been used on a ­patient, uid nitrogen is stored in a handheld unit (Fig. 8-7)
it should never be placed back into the original and emitted as a spray through a specialized tip
liquid nitrogen supply. Rather, a small amount of (Fig. 8-8). The tip is held 1–2 cm from the target
liquid nitrogen should be poured into a dispos- site at a 90° angle. The handheld unit should be
able container (such as a styrofoam cup) for each vertical – otherwise liquid nitrogen may leak from

ERRNVPHGLFRVRUJ
112 Dermatologic Surgery
Figure 8-8  Spray tips. (A) has the largest diameter, (D) the
smallest
Figure 8-9  Neoprene cones used in the closed cone
technique
the unit. In addition to the factors listed in Table
8-�2, the distance between the tip and the target
tissue plays an important role in tissue freezing.
A greater distance between the tip and the target
tissue results in a slower rate of tissue freezing. In
addition, the width of freeze will increase and the
depth of freeze will decrease.
The most common lesions treated with the
open spray technique are seborrheic keratoses,
cystic acne, actinic keratoses, warts, actinic cheili-
tis, squamous cell carcinoma in situ (Bowen’s
disease), squamous cell carcinoma, and basal cell
carcinoma.
Cone spray technique
The cone spray technique is similar to the open
spray technique. However, the spray is directed
into a neoprene cone (Fig. 8-9) placed over the
target lesion. The cone serves to contain the liq-
uid nitrogen within a specified area. The cone has
two important characteristics: the diameter of
the opening that covers the target lesion, and the
­diameter of the wall of the cone. An ­appropriate
ERRNVPHGLFRVRUJ
Figure 8-10  Cryoprobe attached to a handheld liquid
nitrogen unit
cone is chosen corresponding to the measure-
ment of the target lesion and the desired margins,
respectively. The appropriate amount of freezing
is achieved when the lateral spread of the freeze
is seen beyond the walls of the cone. This is most
appropriate for round lesions and lesions close to
sensitive areas, such as the eye.
Closed technique
The closed technique is also called the cryoprobe
technique or contact therapy. A cryoprobe is used
(Fig. 8-10). The handheld liquid nitrogen unit is
connected to the cryoprobe by a tube, forming
a closed system. The probe is made of a metal
­conductor and can come in different shapes,
which can match the shape of the lesion. This
technique is used primarily for malignant ­lesions.
It also may also be used with venous lakes,
­hemangiomas, dermatofibromas, myxoid cysts,
sebaceous ­hyperplasia, and granuloma annulare.
Cold instrument technique
In this technique, a pair of flat forceps or a hemo-
stat is placed in a cup of liquid nitrogen until it is
chilled. The lesion is then grasped. The process is
repeated until the ice ball extends proximally to
the base of the lesion. This technique is sometimes
used for pedunculated lesions as little discomfort
is felt until the very end of the procedure.
Monitoring
The depth of freeze can be monitored in several
ways. It is roughly equal to the radius of the surface
area. If an intermittent spray technique is used,
the resultant ice ball will have a greater depth
and more limited lateral spread. If a ­ continuous
spray technique is used, the resultant ice ball will
be more shallow and will have a greater lateral
 8

Chapter
Cryosurgery 113

Figure 8-11  Pyrometer–thermocouple needle device
spread. Using liquid nitrogen, the greatest ­possible
depth of the ice ball is roughly 10 mm. Larger
lesions should be debulked surgically (e.g. curet-
ted) before cryosurgery is performed.
For malignant lesions, tissue temperature and
depth of freezing may be monitored by a py-
rometer–thermocouple device (Fig. 8-11) using
implanted 25–30-guage needles. The tip of the
needle should lie beneath or lateral to the lesion.
For malignant lesions, the final tissue ­temperature
should be −20 to −30°C. This pyrometer–
­thermocouple technique is rarely used today, and
then only in specialized circumstances.
Applications
Cryosurgery technique depends on the type of le-
sion being treated. Table 8-�
5 shows the general
treatment guidelines for benign, premalignant,
and malignant lesions.
Benign lesions
Benign lesions usually require only one freeze–
thaw cycle. See Table 8-� 5 for treatment param-
eters. Some of the most common benign lesions
treated are warts, molluscum contagiosum, sebor-
rheic keratoses, and lentigines. Each lesion on a
patient may require a slightly different technique.
The open spray technique is used most frequent-
ly. If the cryoprobe is used, the time for which
the tissue remains adequately frozen may be two
to three times longer. The lateral spread of freeze
is usually to the edge of the lesion or 2–3 mm
­beyond its border.
Benign neoplasms such as seborrheic kera-
toses and senile lentigos should be frozen
superficially, as they are epidermal. Vascular le-
sions such as venous lakes and spider nevi can
be frozen with one freeze–thaw cycle with or
without a 2–3-mm margin. For other benign
neoplasms such as warts, dermatofibromas, and
myxoid cysts, the lateral spread of freeze may
be 2–3 mm.
Premalignant lesions
Premalignant lesions usually require one freeze–
thaw cycle, although two may be used. See Table
5 for treatment parameters. For actinic kera-
8-�
toses, the lateral spread of the freeze may go just
to the edge of the lesion or slightly beyond. For
squamous cell carcinoma in situ, the optimal lat-
eral spread depends on the lesion and location.
The lateral spread of the freeze is usually 3–5 mm,
but may be less.

Table 8-5  Treatment guidelines for cryosurgery

No. of
freeze– Tissue Lateral spread
thaw Freeze Total thaw Halo thaw temperature Cure of freeze beyond
Lesion cycles time (s) time (s) time (s) (°C) rate (%) lesion (mm)
Benign 1 3–60 Variable NA <0 0

Premalignant
Actinic 1 <60 Variable Variable −10 98.8 1
keratosis
Leukoplakia 1–2 <60 >90 >60 −20 to −30 96.2 2–3
Squamous 2 <60 >90 >60 −20 to −30 2–3
cell carcinoma
in situ
Malignant
Basal cell 2–3 <60 >90 >60 −20 to −30 >98.6 5
carcinoma
Squamous cell 2–3 <60 >90 >60 −20 to −30 >98.6 5
carcinoma,
invasive
Times are for open spray technique. NA, not applicable.

ERRNVPHGLFRVRUJ
114 Dermatologic Surgery
Malignant lesions
Malignant lesions usually require two freeze–
thaw cycles, although three may be used in some
cases. See Table 8-� 5 for treatment para­meters.
The most common technique is the open spray
technique because of its speed and ease of use.
Other ­options are the cone spray and closed (cry-
oprobe) techniques. A thermocouple-mounted
needle may be used to monitor tissue depth of
freeze to detect a temperature of −20 to −30°C.
Large lesions may first be debulked surgically to
create a thinner ­lesion that requires less spraying.
The halo thaw time, or the duration of mar-
ginal surface thawing of tissue beyond the lesion
border, should be greater than 60 s. The total thaw
time of the entire lesion should be more than 90 s.
Large tumors may be treated in sections, in either
one or several sessions, if appropriate freeze–thaw
parameters cannot be achieved by freezing the
entire lesion at one time.
Keratoacanthomas should be treated as
­squamous cell malignancies with two freeze–
thaw cycles. Cryosurgery is not recommended for
lentigo maligna because of the documented high
rate of recurrence.
Postoperative course and care
During cryosurgery, pain is minimal and is worse
during thawing than during freezing. More pain-
ful areas include the forehead (where migraine
headaches may be triggered), plantar surfaces of
the feet, paronychial areas, ears, eyelids, lips, and
mucous membranes. Local anesthesia is used if
thermocouple needles are to be placed, but it will
not effectively block the discomfort of the actual
cryogenic effect.
Common postoperative responses include
pain, tenderness, swelling, and erythema. Blisters
and crusting also may occur, as well as eschar for-
mation following treatment of deeper malignant
tumors.
The resulting scar is usually hypopigmented
and atrophic. Although acceptable to light-
skinned patients, the scar may not be acceptable
to darker-skinned patients. Hyperpigmentation
may also occur, usually in intermediate skin types.
These pigmentation changes are usually transient,
but may be permanent.
The postoperative course is relatively simple.
Healing time can be from 2 to 5 weeks. As with
other modalities of surgery, factors such as in-
creased age, comorbidities such as diabetes, and
­location (e.g. lower legs) can prolong healing time.
Postoperative care includes washing daily
with soap and water, and keeping the wound
­protected. Hydrogen peroxide may be added if
a crust develops. If a tense blister forms, it can be
drained with a sterile needle, leaving the roof of
ERRNVPHGLFRVRUJ
the ­ blister ­ intact. Acetaminophen is usually suf-
ficient for pain control.
Complications
Hypopigmentation, large bullae, nerve damage,
and secondary infection are the most important
complications. Rarely, hypertrophic scars and
­keloids may form. Hemorrhage, either early or
delayed, has been reported.
Surrounding structures may be damaged per-
manently. Common examples include alopecia
(hair follicles), nail dystrophy (nail matrix),
­dysesthesia (superficial cutaneous nerves), and
notching of the ear or nose (cartilage).
PEARLS
• Make sure the handheld liquid nitrogen unit is
vertical at all times. If it is held at an acute angle
or horizontally during treatment, liquid nitrogen
may leak from the unit or the pressure valve may
discharge.
• Pare down hypertrophic lesions before freez-
ing them so that the base may be treated
­sufficiently.
• Darker-skinned individuals have a higher risk of
hypopigmentation.
• Prolonged spraying may cause the valve in the
handheld liquid nitrogen unit to freeze in an open
position, making it spray continuously without
closing. Running the valve under warm water will
unfreeze the valve and allow the unit to shut off.
• Be certain that the spray tip (or any attachment)
is tightly screwed onto the handheld unit. If the
tip is loose, the force of the liquid nitrogen may
propel it against the patient.
• Steady continuous spraying leads to a relatively
wide, but shallow, zone of frozen tissue. This is
ideal for benign or premalignant lesions.
• Intermittent spraying results in a relatively
­narrow, but deeper, zone of freeze. This is ideal
for malignant or deeper lesions.
• Likewise, “painting” the target by moving the
spray back and forth yields a wide but shallow
freeze. For deeper malignant lesions, the spray
should be held on a central target zone, allowing
the zone of freeze to be deep enough.
• Pain from cryogens is not blocked effectively
by local anesthesia. Therefore, unless thermo­
couple needles are being inserted, infiltration
with a local anesthetic is of little value and may
actually interfere with effective tissue freezing.
• Many units come with a choice of apertures.
Become familiar with how quickly and broadly
each delivers the cryogen. Be sure the correct
aperture is in place.

• Some storage tanks have a metal hose. This
should never be grasped by hand, as the hand
may freeze to the hose while the unit fills.
Further reading
Alam M, Ratner D. Cutaneous squamous-cell carci-
noma. N Engl J Med 2001;344:975–983.
Arlette JP, Trotter MJ, Trotter T, Temple CLF. Man-
agement of lentigo maligna and lentigo maligna
melanoma: seminars in surgical oncology. J Surg
Oncol 2004;86:179–186.
Castro-Ron G, Pasquali P. Cryosurgery. In: Robinson JK,
Hanke CW, Sengelmann RD, Siegel DM, eds. Surgery
of the Skin. Philadelphia: Elsevier Mosby, 2005:
191–202.
Dachow-Siwiec E. Treatment of cryosurgery in
premalignant and benign lesions of the skin. Clin
Dermatol 1990;8:69–79.
Drake LA, Ceilley RI, Cornelison RL, et al. Guide-
lines of care for cryosurgery. J Am Acad Dermatol
1994;31:648–653.
Elton RF. Complications of cutaneous cryosurgery.
J Am Acad Dermatol 1983;8:518–519.
Gage AA. History of cryosurgery. Surg Oncol
1998;14:99–109.
Gage AA, Caruana JA, Garamy G. A comparison
of instrument methods of monitoring freezing
in cryosurgery. J Dermatol Surg Oncol
1983;9:209–214.
ERRNVPHGLFRVRUJ
8
Chapter
Cryosurgery 115
Graham GF. Cryosurgery. Clin Plast Surg
1993;20:131–147.
James WD, Berger TG, Elston DM. Dermatologic
surgery. In: Andrews’ Diseases of the Skin: Clinical
Dermatology, 10th edn. Canada: Saunders Elsevier,
2006: 869–887.
Kokoszka A, Scheinfeld N. Evidence-based review
of the use of cryosurgery in treatment of basal cell
carcinoma. Dermatol Surg 2003;29:566–571.
Kuflik EG. Cryosurgery updated. J Am Acad Derma-
tol 1994;31:925–944.
Kuflik EG. Cryosurgery for cutaneous malignancy.
Dermatol Surg 1997;23:1081–1087.
Kuflik EG, Gage AA, Lubritz RR, Graham GF. His-
tory of dermatologic cryosurgery. Dermatol Surg
2000;26:715–722.
Lubritz RR, Smolewski SA. Cryosurgery cure
rate of actinic keratoses. J Am Acad Dermatol
1982;7:631–632.
Mallon E, Dawber R. Cryosurgery in the treatment
of basal cell carcinoma: assessment of one and
two freeze–thaw cycle schedules. Dermatol Surg
1996;22:854–858.
Sterling JC, Handfield-Jones S, Hudson PM. Guide-
lines for the management of cutaneous warts. Br J
Dermatol 2000;144:4–11.
Zouboulis CC. Principles of cutaneous cryosurgery:
an update. Dermatology 1999;198:111–117.

Biopsy techniques
Lisa B. Campbell and Victor J. Marks
Biopsies are vital in dermatology and dermatologic
surgery, allowing for dermatopathologic assess-
ment with resulting diagnostic information. Cli-
nicians choose from several biopsy techniques,
although the ultimate goal is to provide adequate
tissue for microscopic examination. In doing a
biopsy, the clinician may wish to sample part of
or a whole lesion or inflammatory process. Also
taken into consideration are the size and location,
cosmetic concerns, and depth of the pathologic
process.
Overview
• Preoperative planning
• Choosing the appropriate biopsy technique
based on diagnosis
• Incisional vs excisional biopsy
• Shave biopsy technique
• Punch biopsy technique
• Full-thickness/elliptical biopsy technique
• Biopsy specimen handling
Preoperative planning
Key Points
• Obtain informed consent, verbal or written.
• Be aware of underlying medical conditions and
adjust procedure accordingly.
• Take photographs where appropriate.
• Consider biopsy location for healing
characteristics.
Choosing the appropriate
Planning any surgical procedure, including a
­simple biopsy, requires consideration of the
biopsy technique
­following:
• Informed consent. Notify your patient of the
most common adverse outcomes: bleeding,
infection and scarring. Discuss the possibility
of requiring more surgery or other therapy
based on the biopsy results.
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9
Chapter
• Underlying medical conditions. Atrial
fibrillation, hypertension, pregnancy,
prosthetic heart valve or joint surgery,
prior vasovagal response, and other medical
conditions may alter your preoperative
management of a patient.
• Photography. Digital photography is now
easily accessed in many dermatology clinics.
Consider utilizing this technology as it can be
useful in clinicopathologic correlation, assist
in confirming location of biopsy at a later
time, and serve as visual history in a medical
chart.
• Location. Legs heal poorly in many individuals
and upper trunk procedures may result in
hypertrophic scarring.
• Antibiotics. Preoperative antibiotics are not
necessary for biopsy (considered a clean
surgical procedure) according to American
Heart Association guidelines, when the
biopsy is performed through clinically
uninfected skin. (See Chapter 5: Preoperative
evaluation.)
• Antisepsis. Generally, an alcohol swab for
10 s is adequate antisepsis for small biopsies.
Other surgical scrubs can be employed for
larger procedures or for patients at higher risk
for infection. (See Chapter 2: Antisepsis.)
• Anesthesia. Most dermatologists use lidocaine
(0.5–1%) with or without 1:100,000 or
1:200,00 epinephrine. (See Chapter 3: Local
anesthetics.)
Key Points
• Consider type of lesion, depth, and location.
• In general, melanoma requires full-thickness
biopsy.
• Broad, thin shaves may show lentigo maligna
best.
118 Dermatologic Surgery

The appropriate technique is ultimately the deci- • Inflammatory lesions:

sion of the clinician based on diagnostic concerns a. Consider biopsy of both established and
and suspicion. The two major techniques are new areas, and possibly multiple areas of
­incisional and excisional biopsy (Table 9-�
1). similar duration, to maximize diagnostic
information.
Special diagnostic considerations b. If a dermal process is suspected, a deep
shave or punch is preferable. If epidermal,
(Figs 9-1 & 9-2) a thinner shave may be adequate.
• Most melanomas: • Scalp biopsy for hair pathology:
a. Depth is critical for prognosis and a. A minimum of one 4-mm punch biopsy
therapeutic decision-making. parallel to the direction of hair growth
b. Full-thickness excisional biopsy preferred, b. A second punch biopsy can provide
with 2-mm margin. the pathologist with tissue for
• Lentigo maligna: transverse sections, vertical sections, and
a. Broad, superficial shaves are preferred over immunofluorescence. One specimen is
smaller biopsies. bisected transversely, 1 mm above the fat.
b. Broad, thin biopsies usually establish the The other is bisected vertically, with half
diagnosis, whereas the false-negative rate sent for immunofluorescence and the
for a 4-mm punch is as high as 80%. other half placed in the same bottle as the
transversely bisected specimen. Let the
lab know what you are doing. Pathologic
Table 9-1  Major biopsy techniques
examination utilizing both horizontal and
Incisional Excisional vertical sectioning enhances diagnostic
biopsy biopsy yield.
Goal To remove a part To remove c. A biopsy from a burnt-out scar can
of the lesion for entire lesion to demonstrate characteristic elastic tissue
diagnosis subcutaneous fat patterns of scarring when other biopsies
Considerations Too large for Depth needed have not been diagnostic. They can also
excisional biopsy for diagnosis demonstrate the potential for regrowth.
(i.e. suspected d. Suturing a scalp biopsy site can be
melanoma) cumbersome. Gel foam produces rapid
Cosmesis of Cosmesis hemostasis and is generally preferred.
complete removal improved if Location
not acceptable if lesion removed
benign process completely • Nail biopsy is discussed in Chapter 15: Nail
Diffuse Malignant process surgery.
inflammatory suspected • Eyelid (or other thin skin) biopsy may be
process not accomplished with the use of Gradle or
amenable to curved Iris scissors as a modified excisional or
excisional biopsy shave biopsy (Fig. 9-�3).
Method Shave Deep “scoop” a. Lift lesion gently with forceps.
shave b. Snip at base with Gradle scissors.
c. Hemostasis is achieved with gentle
Punch Punch
pressure or cautious use of aluminum
Ellipse Ellipse chloride.

Pigmented lesions

Large,diffuse or Suspected lentigo Suspected melanoms Nevus

sensitive cosmetic area maligna

Incisional biopsy Broad, thin shave Shave or punch

Excision 2-mm margin
2-mm margin if dysplastic

Figure 9-1  Algorithm for pigmented lesion biopsy

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Inflammatory lesions
Dermal process Epidermal process
Deep Shave Shave
Punch
Figure 9-2  Algorithm for an inflammatory lesion
Figure 9-3  Eyelid or pedunculated lesion biopsy.
A forceps is used to grasp and elevate the lesion while
a Gradle scissors evenly cuts the lesion at its base
• Pedunculated lesions are also easily biopsied
with scissors technique.
• Mucosal lesions are quickly anesthetized with
topical anesthetic gel followed by injection of
anesthetic. Also consider a chalazion clamp to
control bleeding, and silk or other soft suture
material to avoid irritation.
• Scalp lesions along suture lines or midline
spine lesions may involve intracranial or spinal
structures. Consider preoperative imaging or
consultation with neurosurgery.
Surgical instruments
• Shave biopsies may be performed with a
scalpel blade, razor blade (available with
plastic handle), or curette (disposable or
multiple use with sterilization) (Fig. 9-�4).
• Punch biopsy devices may be either
disposable or reusable (Fig. 9-�5).
• Elliptical incisional or excisional biopsies are
accomplished utilizing a scalpel and standard
excisional technique (see Chapter 10: Basic
excisional surgery). Blade choice depends
on the location and thickness of the skin.
For fine surgery on thinner skin, consider a
small blade (15, 15c). Trunk and extremity
lesions may require a larger blade (10). (For
further discussion see Chapter 4: Surgical
instruments.)
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9
Chapter
Biopsy techniques 119
Figure 9-4  Biopsy tools. From left to right: scalpel blade,
double-edged razor blade, DermaBlade™, curette,
disposable curette
Figure 9-5  Punch biopsy tools. Disposable (left); multiple
use (right)
Shave technique
Key Points
• Become comfortable with several biopsy
techniques.
• Practice with a skin substitute – tomatoes and
oranges work well.
Scalpel blade (Fig. 9-�
6)
• Enter skin with curve of blade (15 or 10
blade most common) while holding skin taut.
• Use a short sawing motion with blade parallel
to skin surface.
• Depth is controlled by downward pressure of
the blade.
• Exit the skin by decreasing downward
pressure and angling slightly upward, allowing
the blade to resurface smoothly to complete
biopsy.
• A cup-shaped defect is produced in the skin.
• Hemostasis can be achieved with 35%
aluminum chloride on a cotton-tipped
applicator. Alternatives include Monsel’s
solution and electrocautery.
120 Dermatologic Surgery

b
a

c d

Figure 9-6  Scalpel shave technique. After anesthetizing the skin, hold the blade parallel to the skin surface, entering with
the curve of the blade (a). Using a short sawing motion, draw the blade across the base, elevating slightly to exit the skin (b).
A thin defect results (c) and aluminum chloride can be used for hemostasis (d)

a b c

Figure 9-7  Razor shave technique. After anesthesia, hold curved edge of blade parallel to skin surface (a). Using a short
sawing motion, push the blade across the base, elevating to exit the skin (b). The resulting specimen and defect can be
seen in (c)

the blade to resurface smoothly to complete

Razor blade (Fig. 9-�
7)
• Curve the blade by applying inward pressure
on the blade from the sides.
• Stretch the skin taught for a superficial shave.
• Enter the skin in the center of the curved
blade.
• Use a short sawing motion with the center of
the blade.
• Depth is controlled by the amount of curve on
the blade (more curve, more depth; less curve,
more shallow) as well as downward pressure.
• Exit the skin by decreasing downward
pressure and angling slightly upward, allowing
the biopsy.
• May produce a cup-shaped defect in the skin
(minimized by flattening the blade).
• Useful for deep saucerizations.
• Can also produce broad, thin specimens with
little to no cup-shaped defect when the blade
curvature is minimized.
• Blade curvature can be inverted for convex
surfaces.
• Surgeons with small hands generally prefer to
break the blade in half. This is done by folding
the blade in half lengthwise with the wrapper
still in place.

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Curette (Fig. 9-�
8)
• The desired biopsy area must fit within the
circumference of the curette.
• Stretch skin to provide a firm surface.
• Entry, central depth, and exit are controlled
by downward pressure.
• A single fluid motion is preferred, as a
fragmented specimen can compromise
diagnosis and margin analysis.
PEARLS
• Techniques may be practiced on tomatoes or
oranges to simulate required force and motions
to achieve even, controlled biopsies of appropri-
ate depth (Fig. 9-�
9).
• To avoid a cup-like defect and maintain an even
skin surface after biopsy of a raised lesion, anes-
thetic should be placed in the deep dermis and
allowed to diffuse for 10–15 min (Fig. 9-10). The
skin should be stretched taught during the shave.
Punch technique
Using a disposable or reusable punch (Fig. 9-11):
• Punch should be placed perpendicular to skin
surface.
• Stretch the surface of the skin to provide a
firm surface.
• Apply even downward pressure while rotating
the punch until desired thickness is achieved.
• Withdraw punch.
• Grasp gently with toothed forceps without
crushing the specimen.
Figure 9-8  Curette technique. Begin with curette nearly
perpendicular to the skin
a b
Figure 9-9  Shave technique practice
ERRNVPHGLFRVRUJ
9
Chapter
Biopsy techniques 121
• Tissue scissors may be required to free base
of biopsy.
• Hemostasis may be achieved with surgical gel
foam, suturing, or pressure.
• Apply pressure dressing.
PEARLS
• To avoid inadvertent pinching with forceps, a
bent needle may be used to elevate the biopsy
out of the skin.
• To make an oval defect with a circular punch,
apply lateral pressure on the skin in the direction
in which the short radius of the oval is desired
(Fig. 9-12).
Elliptical incisional/excisional
biopsy technique
When performed as a standard excision (see also
Chapter 10: Basic excisional surgery):
• Place scalpel perpendicular to skin surface
and incise through to subcutaneous fat along
predetermined outline.
• Outline may be elliptical to allow linear
closure, or circular for healing by secondary
intention.
• Once appropriate depth is obtained, elevate
the tissue to reveal its base.
• Using scalpel or tissue scissors, free the base
of the biopsy parallel to the surface.
• Undermine edges for linear closure.
• Achieve hemostasis.
• Place buried absorbable sutures to relieve
tension, and top sutures to align skin edges.
Biopsy specimens
Each laboratory will have specific handling instru­c­
tions for biopsy. As a minimum, specimens must
be labeled with the patient’s name and, if there
are multiple specimens, an appropriate number
or letter. They should be placed in an ­appropriate
medium: formalin is used for routine light micro-
scopy. Alternatively, specimens sent for direct im-
munofluorescence should be placed in Michel’s
solution or taken directly to the laboratory in
normal saline. Any special requests should first be
discussed with the pathologist to ensure optimal
specimen processing. Clinical history and lesion
c d
122 Dermatologic Surgery

a b

Cut
Cut

Figure 9-10  Deeper placement of anesthesia minimizes the depth of the defect. (a) Shallow placement which displaces
skin upward, obscuring the edge of a raised lesion. (b) Deeper placement, preserving the elevation of the lesion and
allowing a more shallow biopsy defect

a b c

Figure 9-11  Punch biopsy technique. After anesthesia, place the punch perpendicular to the skin. While applying
downward pressure, rotate the punch until desired depth is achieved (a). Elevate the specimen and snip the base (b).
Hemostasis can be achieved with a suture or gel foam (c)

a b c

Figure 9-12  Oval defect from a punch. To make an oval shape, apply tension outward on the skin perpendicular
to relaxed skin tension lines (a–c)

description are also imperative so that clinico-

pathologic correlation can be made.
Further reading
Chen TM, Mellette JR. Surgical pearl: Tomato – an
alternative model for shave biopsy training. J Am
Acad Dermatol 2006;54(3):517–518.
Dalton SR, Gardner TL, Libow LF, Elston DM.
Contiguous lesions in lentigo maligna. J Am Acad
Dermatol 2005;52(5):859–862.
Dzubow LM, Halpern AC, Leyden JJ, et al.
Comparison of preoperative skin preparations for
the face. J Am Acad Dermatol 1988;19:437–441.
Elston DM, Ferringer T, Dalton S, Fillman E, Tyler W.
A comparison of vertical versus transverse sections
in the evaluation of alopecia biopsy specimens.
J Am Acad Dermatol 2005;53(2):267–272.
Garcia C. Skin biopsy techniques. In: Robinson JK,
Hanke CW, Sengelmann RD, Siegel DM, eds.
Surgery of the Skin: Procedural Dermatology.
Philadelphia: Elsevier Mosby, 2005:203–212.

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Basic excisional surgery
Christine Poblete-Lopez
Key Points
• The simple excision is the bread and butter of
any dermatologist’s surgical practice.
• Performed for diagnostic or therapeutic
purposes, it is a relatively simple procedure that
one should master.
• Knowledge of surgical anatomy is of utmost
importance!
• There are variations in the ellipse that are
particularly useful in certain anatomic regions noma on the extremity can usually be excised
of the skin, such as the crescent, S-plasty and
M-plasty excisions.
• If proper surgical technique and meticulous
hemostasis are maintained, surgical
complications can be minimized and a
cosmetically elegant scar can result.
Introduction
The simple excision is the foundation of cuta-
neous surgery. Though seemingly complex to a
novice, it should be mastered by any dermatolo-
gist seeking to perform this relatively simple pro-
cedure in an office-based setting. Knowledge of
surgical anatomy, tumor biology, local anesthetics,
instrumentation, and suturing techniques is cru-
cial prior to performing any cutaneous surgery.
In addition, a thorough preoperative evaluation
is essential to help minimize postoperative com-
plications. When performed properly and meticu-
lously, a fine cosmetically acceptable scar results.
Application
The simple excision is designed to remove entire
lesions for histopathologic examination, as well as
surgical cure. Whether it is a benign lesion that
is troublesome (e.g. cyst, lipoma, or dermato­
fibroma) or cosmetically bothersome (e.g. nevus
on the chin or cheek), or a lesion of uncertain
biologic behavior (e.g. clinically atypical nevus on
the back), these lesions can be excised in an ellip-
tical fashion to achieve definitive histopathologic
ERRNVPHGLFRVRUJ
10
Chapter
diagnosis, as well as complete removal. On
the other hand, a surgical excision can be the
­definitive treatment of choice for selected malig-
nant lesions that have been diagnosed on a prior
biopsy. However, in this case, margins for cure, as
well as cosmetic and functional challenges regard-
ing the final scar, must be taken into considera-
tion, making the excision a bit more challenging.
For example, a well demarcated basal cell carci-
with a 4–5-mm margin of normal appearing skin
around the circumference of the lesion. A super-
ficial spreading melanoma on the forearm with
a Breslow level of 0.43 mm, for example, can be
excised with a 10-mm margin down to the fascia.
See Table 10-� 1 for general recommendations on
margins of excision.
Techniques
Orienting the ellipse
Whether one is working on the head and neck
region, or the trunk and extremities, a work-
ing knowledge of anatomic danger zones (see
­Chapter 1) and surface anatomy, with regard to
relaxed skin tension lines, contour lines, and cos-
metic units is essential (Figs 10-� 1 & 10-2). Plan-
ning your incision lines along relaxed skin tension
lines, natural skin lines, cosmetic units, and bound-
aries can increase the likelihood of a cosmetically
acceptable scar, by providing optimal camouflage
and allowing the wound to be closed under the
least amount of tension.
Relaxed skin tension lines are formed by the
pull of the underlying muscles at the site of their
insertion on the overlying skin. In general, the
skin creases form in a pattern that is perpendic-
ular to the direction of the underlying muscle
contraction. Wounds oriented parallel to the skin
creases or skin tension lines close under less ten-
sion, and result in well camouflaged, thin scars.
Although Figures 10-1 and 10-2 show these lines
124 Dermatologic Surgery
Table 10-1  General rules for margins of excision
Type of lesion Margin (mm)
Benign lesions 0–2
Atypical nevi 3–4
Nonmelanoma skin cancer 4–6
(not an indication for Mohs
surgery)
Melanoma (Breslow level 10
≤ 1 mm)
Melanoma (Breslow level 20–30
>1 mm)
in general, many variations exist. Therefore, one
should ­ consider each patient individually. In
elderly patients, the lines are quite evident. In
younger individuals, asking them to make an ex-
aggerated facial expression or pinching the skin
and identifying the natural skin lines will aid in
determining the axis of orientation. If there is
question as to optimal suture line orientation,
the lesion should first be removed in a circular
fashion, and undermined. This maneuver allows
the skin’s inherent elasticity to determine along
which axis it will form an oval. The surgeon can
then extend the incision along this axis to form
an ellipse.
Cosmetic subunit junction lines are formed at
the borders of fixed structures on the face, and
divide the face into cosmetic units that have simi-
lar skin color, texture, sebaceous gland quantity
and quality, and hair content (see Fig. 10-�
2). Exci-
sions should be designed and contained within a
single cosmetic unit and resultant scars planned
so that they lie within cosmetic subunit junction
lines. This best maintains the normal anatomy of
the face, in particular, as well as making the scar
less conspicuous than one that crosses multiple
cosmetic units. Some surgeons even enlarge their
excisions so that the resultant scar will lie along
a subunit junction line, emphasizing the impor-
tance of these boundary lines over relaxed skin
tension lines.
As a general rule, the length of the ellipse
should be three to four times the width, and the
tips drawn at an angle ranging from 30° to 75°
(Fig. 10-�3). This ensures that the wound edges
will come together without “dog ears” or redun-
dancies at the apices of the ellipse, and that the
scar will lay down flat against the skin. If pos-
sible, the length of the ellipse should be drawn
along the length of the lesion, to minimize the
length of the scar. However, there are times
when a longer, well placed scar, such as one that
is oriented within a contour line or along skin
tension lines, will result in a more cosmetically
acceptable scar than a shorter, more conspicu-
ous, one.
ERRNVPHGLFRVRUJ
Preparing for the excision
Planning the excision should be done with the
patient upright, to minimize apparent distortion
of the relaxed skin tension lines. Marking of the
planned excision should be done prior to infiltrat-
ing the anesthetic. This minimizes distortion of
the skin tension lines and avoids obscuring the
lesion margins.
Prior to marking, the area should be cleansed
with 70% isopropyl alcohol. Any hair in and
around the operative site that will interfere with
the surgical procedure should be secured away
from the operative field or clipped with scissors.
Preoperative shaving creates microabrasions in
the skin and should be avoided due to increased
risk of wound infection.
Lines of planned excision may now be drawn
using a skin marking pen, fine-tipped perma-
nent marker, or a wooden applicator dipped in
gentian violet. The surgical site is then anesthe-
tized, including a sufficient margin to allow for
wide undermining (Fig. 10-� 4). The area is then
prepped with an appropriate surgical scrub (e.g.
povidone–iodine, chlorhexidine) (see Chapter 2:
Antisepsis). Chlorhexidine should be used with
caution around the eye, as it can cause corneal
ulceration, and avoided completely around the
ear if there is chance of a tympanic membrane
perforation. Povidone–iodine should be avoided
in patients with known allergy to iodine. Univer-
sal precautions should be employed at this point,
including the use of sterile gloves, masks, and eye
protection for surgical personnel. The surgical
field is then draped with sterile towels, or dispos-
able sheets, and the excision carried out under
aseptic conditions.
Performing the excision
For the majority of basic excisional surgery, a
no. 15 scalpel blade attached to a Bard Parker han-
dle, is appropriate (see Chapter 4: Surgical instru-
ments). For small, delicate excisions, the scalpel
should be held vertically like a pen. For larger ex-
cisions, it may be preferable to hold it horizontally,
like a steak knife. Prior to starting the incision,
traction should be placed on the wound edges by
the surgeon’s nondominant hand or by a surgical
assistant. Next, the skin is incised at a 90° angle,
starting at the distal tip of the ellipse. The incision
should be carried out toward the surgeon, ideally
with enough pressure to incise the skin up to the
subcutaneous fat. The angle of the scalpel is de-
creased to about 45° when incising along the cur-
vature of the ellipse, with the belly of the blade in
contact with the skin. This is the sharpest part of
the blade (Fig. 10-�5). Again, the angle of the blade
is held at 90° when approaching the other apex
of the ellipse (Fig. 10-�6). The incision is ­repeated
 10

Chapter
Basic excisional surgery 125

Figure 10-1  Relaxed skin tension lines. (a) face; (b) trunk; (c) extremities

ERRNVPHGLFRVRUJ
126 Dermatologic Surgery

Lateral ridge
of nose
Infraorbital
crease
Nasofacial Nasoalar
sulcus crease
Nasal ala Melolabial
Nasal tip crease

Philtral Vermillion
crest border
Labiomental
crease
a

Figure 10-2  Contour lines and cosmetic units

1 cm 30º

3 cm

b
Figure 10-3  Dimensions of the ellipse
Figure 10-5  With the nondominant hand providing tension
opposite the side of incision, the tip of the blade is used
to incise the apex of the ellipse (a) and the belly of the
blade incises the curvature of the ellipse (b)

Figure 10-4  Anesthetizing a previously marked planned

excision

ERRNVPHGLFRVRUJ

Figure 10-6  The angle of the blade during incision
Figure 10-7  Avoid “fishtail” or “cross-hatching”
Correct
Figure 10-8  “Staircasing”
at the other side of the ellipse. Care should be
taken to avoid “cross-hatching” or “fishtails” at
the apices of the ellipse (Fig. 10-�
7). Try to avoid
multiple shallow incisions, in order to minimize
“stair-­casing” of the wound margins (Fig. 10-�
8).
ERRNVPHGLFRVRUJ
10
Chapter
Basic excisional surgery 127
Variations of the ellipse
Crescentic excision
Sometimes also referred to as the “pregnant
belly,” the crescentic excision takes advan-
tage of sides of unequal length, and results in a
­curvilinear scar. As the arc of the crescent de-
termines the resultant scar, the ellipse could be
oriented along curved skin tension lines or cos-
metic subunit junction lines. The wound should
be closed using the rule of halves, thereby mini-
mizing any resulting Burrow’s triangles from the
unequal sides. Areas of potential use include the
cheek (along the malar eminence) and the chin,
for example (Fig. 10-�9).
S-plasty excision
Also called “lazy S,” the S-plasty excision is use-
ful when performing an excision along a convex
surface, for example the forearm, shin, or jaw.
This minimizes the contraction and buckling
seen along the length of the scar. Similarly, clos-
ing the wound with the rule of halves is helpful
(Fig. 10-10).
M-plasty excision
The M-plasty excision is effective in reducing the
length of scar when it would otherwise encroach
on a neighboring functional or cosmetic structure.
This may be planned prior to the excision, or may
be used in repairing a redundant standing cone
(or “dog ear”) deformity. At the apex of the el-
lipse used to perform the M-plasty, a tip stitch
may be helpful to minimize necrosis of the tip
(Fig. 10-11).
128 Dermatologic Surgery

Figure 10-9  Crescentic excision

Figure 10-10  S-plasty excision

Specimen removal and undermining

Once you have incised through the full thickness of
the skin, the lesion is transected at its base, sharply,
with the blade, or bluntly with dissecting scissors,
at the level of the subcutaneous fat (Fig. 10-12 &
Table 10-� 2). To aid removal of the specimen, a skin
hook or toothed forceps is used to pick up the dis- b
tal apex of the ellipse, and the base is transected as
described. Try to remove the specimen with uni-
form thickness and avoid beveling the wound edges Figure 10-11  M plasty excision. (a) Design of the M plasty
when making your incision, to minimize “scoop- and end result; (b) M plasty excision illustrating tip stitch
ing” or “boating” of the specimen and wound edges,
as this will ultimately affect the proper apposition
of the wound edges (Fig. 10-13).
Undermining serves a number of purposes that
result in a more cosmetically pleasing scar:

• It reduces the tension on the wound edges.

• It creates a horizontal scar band that parallels
the skin surface.
• It restores the contour of the skin surrounding
the excision.

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 10

Chapter
Basic excisional surgery 129

a b

Figure 10-12  Sharp or blunt transection of the base of the specimen

Figure 10-13  Avoid “boating” or “scooping” the specimen

a b

Figure 10-14  Blunt undermining of the wound edges using the closed–open technique. Note the use of a skin hook to
minimize trauma to the skin edge

Undermining is performed by blunt dissection of scissors (see Chapter 4: Surgical ­ instruments),

the surrounding wound edge, around the entire
border of the excision, including the apices of the
ellipse. The level for undermining is dictated by the
anatomic location of the wound (see Table 10-� 2).
This may be done using a blunt-tipped dissecting
or sharply with caution using the blade. Using
the scissors, the closed to open technique is used
(Fig. 10-14). To minimize damage to the wound
edge, a skin hook is used to visualize the field and
expose the level of undermining. The scissors is

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130 Dermatologic Surgery

Table 10-2  Planes of undermining 1 cm would necessitate undermining 1–2 cm later-
ally. Ultimately, undermining is done to the extent
Location Plane of undermining that is necessary to facilitate placement of subcuta-
Face Superficial fat neous/intradermal sutures with minimal tension.
Scalp Subgaleal
Neck Superficial fat Obtaining hemostasis
Trunk and extremities Mid to deep subcutaneous fat Complete hemostasis should be achieved to min-
above muscular fascia imize the risk of hematoma formation after sur-
Hands and feet Immediately subdermal gery. One should be very meticulous, taking into
consideration the effects of epinephrine ­ during
the procedure and its expected vasodilatation
inserted with its tips closed, and then opened to postoperatively. This can be achieved using elec-
separate fibrous attachments aside, as well as cut- trodessication and electrocoagulation techniques.
ting the intervening fibers. For small bleeding vessels, a direct touch to the
The extent of undermining depends on the lax- vessels using the handheld electrode is sufficient.
ity of the surrounding skin. In general, the width of When larger vessels are transected, use of a tissue
undermining is the distance equal to, or up to dou- forceps to elevate and isolate the vessel is help-
ble the length of, the short axis of the ellipse. For ful. The electrode is then touched to the distal
example, excision of a lesion with a diameter of aspect of the forceps, which transmits the energy

a b

Figure 10-15  (a) Direct touch to smaller vessels; (b) isolation of larger vessels with tissue forceps; (c) transmission of
energy by touching the electrode tip to the tissue forceps.

ERRNVPHGLFRVRUJ

Figure 10-16  “Figure of 8” technique of suture ligation
to the isolated vessel (Fig. 10-15). This minimizes
­extensive tissue destruction in the surrounding
area, as well as optimizing the ability of the elec-
trode to coagulate in a drier wound bed.
Be meticulous but do not be overzealous in
coagulating the bleeding, especially that seen
along the epidermal/dermal wound edge (resulting
from visible telangiectasias), as this may increase
the risk infection and prolonged healing, and
adversely affect the resultant appearance of the
scar. Even larger bleeding vessels, especially vis-
ible arteries, are more reliably treated with ­suture
ligation, using the figure-of-eight technique
(Fig. 10-16). Using an absorbable suture, such as
chromic, the vessel is visualized and isolated with
a fine-tipped hemostat, and the suture is passed
in and across the vessel in a diagonal and out,
and again, from the opposite side, in and across
the vessel in a diagonal and out, and tied off as the
hemostat is removed. This effectively clamps the
actively bleeding vessel.
Closing the surgical wound
Once meticulous hemostasis is achieved, and wide
undermining is performed, the wound is ready
for closure. The goal of closure is to ­ produce a
a b
Figure 10-17  Layered closure of the excision
ERRNVPHGLFRVRUJ
10
Chapter
Basic excisional surgery 131
well approximated and everted wound edge with
minimal tension, thereby resulting in a cosmeti-
cally elegant scar. The nature of the surrounding
skin, and the size and depth of the wound, will
determine which suture material and closure
technique is appropriate (see Chapter 12: Suture
materials).
In general, excision of full-thickness lesions
necessitates a layered closure, which consists of a
buried inverted layer of absorbable ­ intradermal/
subcutaneous sutures and a percutaneous layer
of suture, tissue adhesive or adhesive tapes
(Fig. 10-17). The intradermal/subcutaneous su-
tures provide the support following removal of
the percutaneous sutures, when the wound has
only achieved 5% of its final tensile strength. A
layered closure (see Chapter 11: Suture tech-
niques) achieves the following:
• Allows elimination of any potential dead
space, thereby minimizing the risk of
hematoma or seroma formation, which can
serve as a nidus for infection
• Approximates the wound edges with proper
eversion
• Reduces the tension along the wound edges,
thereby resulting in a well healed scar.
Dog ear repair
Burrow’s triangles, standing cone deformity, and
“dog ears” – all refer to redundant skin that is
formed from wounds with apical angles greater
than 30°, or those with unequal lengths at the
time of closure. In general, this tissue redundancy
is located at the apices of the ellipse, but may
occur along the length of the longer wound edge.
The repair is performed by pulling the
redundant tissue perpendicular to the direction
of closure, incising one half of the tissue until
another apex is reached. This incised flap is
draped over the incision, and the other half of
132 Dermatologic Surgery

Figure 10-18  Management of dog ear deformity

ERRNVPHGLFRVRUJ

Figure 10-18, cont’d.
the redundant tissue excised. Undermining this
newly formed apex will minimize pseudo-dog
ear formation. The wound is then closed accord-
ingly (Fig. 10-18). Dog ear deformity may also be
repaired using the M-plasty technique described
above (see Fig. 10-11).
Postoperative course and care
Patients should receive written and verbal post-
operative instructions relating to the excisional
surgery just performed. When the patients are
properly educated about postoperative expec-
tations, instructions for care and potential com-
plications, their anxieties are tempered and
the risks for complications are minimized. Al-
though considered a relatively minor procedure,
­patients should be prepared to experience some
­limitations in their daily activities, at least for
the first 24–48 h. This is especially stressed with
regard to strenuous activities, including heavy
lifting and vigorous exercise. Further restric-
tions on physical activity are individually tailored
according to the patient’s age, preoperative level
of activity, and extent, location, and depth of the
wound.
Certain situations warrant special attention dur-
ing the postoperative period. Surgery performed
on dependent areas, such as the hand, wrist, or leg,
are more likely to result in edema. Surgery around
ERRNVPHGLFRVRUJ
10
Chapter
Basic excisional surgery 133
thin lax skin, for ­example the periorbit, is also more
prone to edema. As such, elevation of the limb or
head is often ­recommended. Excisions around and
over joints often require special immobilization
to give the wound the time to strengthen, and to
minimize the risk of wound dehiscence.
Patient education is the key to avoiding post-
operative complications (see Chapter 17: Surgical
complications). The patient should understand
that some edema, ecchymosis, ­erythema, and ten-
derness is normal and should be expected. These
expected sequelae of surgery may be alarming if
the patient has not been forewarned. Patients who
are anticoagulated should be cautioned regarding
the difference between exaggerated bruising ver-
sus an expanding hematoma. All patients should
be provided with a 24-h contact telephone
number and instructed to contact their surgeon
with any concerns. All information should be
explained verbally to the patient and any family
member who may be accompanying them. These
same instructions should be provided in written
form for ready reference at home.
Wound care
Most excisions require a simple pressure dressing
that should remain intact for 24 h. Basically, this
is prepared as follows: a thin layer of ointment
(­petrolatum ointment, Aquaphor®, or antibiotic
134 Dermatologic Surgery

a b

c d

Figure 10-19  Postoperative dressing

ointment), a nonadherent gauze (such as Telfa®, Table 10-3  Suture removal recommendations
cut to fit the dimensions of the suture line), an ab-
sorbent layer of gauze, and secured with an outer Location No. of days
layer of surgical tape (e.g. Mefix®, Micropore™). Eyelid 2–4
Oftentimes a liquid adhesive (tincture of benzoin
Face 4–7
or Mastisol®) is used to secure the surgical tape in
place (Fig. 10-19). Neck 5–7
Patients are instructed to remove the pres- Scalp 7–10
sure dressing in 24–48 h. The wound surface is
Trunk 7–12
cleansed with soap and water. Hydrogen perox-
ide may be used sparingly to remove any dried Extremities 10–14
blood or crust. Occlusive ointment is reapplied,
and, depending on location and level of activity,
a light dressing or strip bandage may be required. provide further support to the wound edges after
This wound care is repeated two to three times the percutaneous sutures have been removed.
daily until the sutures are removed. These typically stay on for about 5–7 days. Pa-
tients are instructed to leave these alone, and
allow them to fall out on their own. Table 10-�3
Suture removal outlines general recommendations on suture
The timing of removal of the percutane- ­removal.
ous sutures is of utmost importance. Sutures
should be left long enough to permit complete Complications
­epithelialization across the wound margins, but
early enough to avoid suture tracking. Obviously, Although relatively infrequent, patients need to
there is ­ individual variability in wound healing. be informed about the potential complications of
For example, sutures may be removed a little skin surgery at the time of informed consent, and
earlier for young, healthy, nonsmoking individu- be educated about how these may be manifested
als, compared to older, smoking, diabetic patients, immediately after surgery. When they do occur, the
because of problem with delayed wound healing. surgeon should be able to recognize and ­manage
Occasionally, wound closure tapes are used to them appropriately. The four most frequently

ERRNVPHGLFRVRUJ
 10

Chapter
Basic excisional surgery 135

encountered complications (see Chapter 17:
Surgical complications) are:
• Hematoma formation
• Infection
• Wound dehiscence
• Necrosis.
PEARLS
• Handle the skin with great care. This will be
evident in the final scar that results. To minimize
trauma to the wound edges, use of a skin
hook is quite helpful. If not, with the toothed
forceps, grasp the relatively acellular dermis or
fascia, rather than the epidermis, which may
leave permanent scars (Fig. 10-20). When the
middle finger is placed between the tongs of the
forceps about half way down, the forceps are
held open and one side can be used in place of
a skin hook.
• When placing sutures, both intradermally and
percutaneously, the square knot can be secured
by drawing one end of the suture toward you,
while keeping steady tension on the other end
of the suture. This will avoid slippage of the
knot and separation of the wound edges
(Fig. 10-21).
• As much as possible, try to use your
instruments to help you perform the procedure
in an efficient manner. When performing a
running percutaneous suture, try to minimize

Figure 10-20  Grasp the dermis, rather than the epidermis, to minimize trauma to the surface that might potentially leave
a permanent scar

Figure 10-21  Securing square knots

ERRNVPHGLFRVRUJ
136 Dermatologic Surgery

a
d

Figure 10-22  Use instruments to aid closure of the wound in an efficient manner. (a) Secure the exit point on the skin with
a skin hook. (b) Grasp the needle while maintaining tension on the needle’s exit point. (c) Grab the needle at the body,
ready to place the next bite. (d) Pick up the suture and provide sufficient tension to help placement of the next bites

ERRNVPHGLFRVRUJ

Figure 10-23  Closure using strip suture method for thin
atrophic skin
your movements by using your forceps to
stabilize your exit point, and push the needle
through with your needle-holder. This movement
will allow you to grasp and lock the needle at
the intended body of the needle, ready to take
the next bite. You or your assistant can also hold
onto the suture, providing just enough tension
along the already sutured wound edge; this
provides tension along the wound edge
that you are about to place the needle in
(Fig. 10-22).
• Management of cysts: For noninflamed cysts,
mark the margin of the cyst, but perform a
punch biopsy or elliptical excision within the
margins, carefully dissect around the well
demarcated cyst, and perform a layered closure.
This minimizes the resulting scar.
• Management of lipomas: Similarly, carefully
palpate the lesion to assess the depth and size
of the lipoma, and mark the presumed size.
Plan for an incision well within the margins of
the lesion, or a punch biopsy. A lipoma can be
delivered through a very small opening when
pressure is placed on both sides. Carefully
dissect the lesion out. When involving the
forehead, attempt to dissect the frontalis muscle
bundles in a vertical orientation, and repair the
muscle and fascial planes if necessary.
A layered closure will minimize the risk of
seroma or hematoma formation.
ERRNVPHGLFRVRUJ
10
Chapter
Basic excisional surgery 137
• Closure on atrophic skin: use of the strip
suture technique: The use of Steri-Strips™ along
the wound edges, or perpendicular to
the incision, will aid the application of
percutaneous sutures along the wound edges
that would have otherwise pulled through
(Fig. 10-23).
Further reading
Bennett RG. Fundamentals of Cutaneous Surgery.
St Louis: CV Mosby, 1988:353–444.
Dunlavey E, Leshin B. The simple excision. In:
McGillis ST, ed. Dermatologic Clinics, Excision
and Repair. Philadelphia: WB Saunders, 1998:
49–64.
Leshin B. Proper planning and execution of surgical
excisions. In: Wheeland R, ed. Cutaneous Surgery.
Philadelphia: WB Saunders, 1994:171–177.
Jackson IT. Local Flaps in Head and Neck
Reconstruction. St Louis: CV Mosby, 1985.
Olbricht S. Biopsy techniques and basic excisions. In:
Bolognia J, Jorizzo J, Rapini R, eds. Dermatology.
London: Mosby, 2003:2269–2286.
Paolo B, Stefania R, Massimiliano C, et al. Modified
S-plasty: an alternative to the elliptical excision
to reduce the length of suture. Dermatol Surg
2003;29:394–398.
Perry AW, McShane RH. Fine tuning of the skin
edges in the closure of surgical wounds. J Dermatol
Surg Oncol 1981;7:471–476.
Robinson JK, Hanke CW, Sengelmann RD, Siegel
DM, eds. Surgery of the Skin: Procedural
Dermatology. Philadelphia: Elsevier Mosby, 2005.
Sadick N, D’Amelio DL, Weinstein C. The modified
buried vertical mattress suture. J Dermatol Surg
Oncol 1994;20:735–739.
Salasche SJ, Bernstein G, Senkarik M. Surgical
Anatomy of the Skin. Norwalk: Appleton & Lange,
1988:13–35.
Zalla MJ, Padilla RS. Excision. In: Roenigk RK, Ratz
JL, Roenigk HH, eds. Roenigk’s Dermatologic
Surgery: Current Techniques in Procedural
Dermatology, 3rd edn. New York: Informa
Healthcare, 2007:131–139.
Zitelli JA. Tips for a better ellipse. J Am Acad
Dermatol 1990;22:101–103.
 11

Chapter
Suture techniques
Brittany Wilson, Andrea Willey,
and Ken K. Lee

Key Points
• Suturing is one of the mainstays of cutaneous General guidelines for suture
surgery. placement
• Closing a wound by first intention helps achieve
hemostasis, decreases the risk of infection, and Typically, the needle should penetrate the skin at
closes dead space. a 90° or greater angle. This helps facilitate wound
• The primary goals of suturing include eversion and minimizes trauma to tissue. Simi-
achieving wound eversion, decreasing tension larly, the needle should exit perpendicular to the
on the wound, and approximating wound
skin surface. It may be helpful to use forceps to
edges.
• Wound eversion helps to decrease the risk of a grasp the needle as it exits the tissue. This can help
spreading or depressed scar. stabilize the needle and minimize the chance of
• Various suture techniques can be selected loosing the needle in the soft tissue. Needle safety
based upon anatomical location, tension on the is paramount when suturing. The following steps
wound, tissue quality, and wound depth. are important in preventing needle sticks:

1. Always use the needle holder or

forceps initially to grasp and stabilize
Loading the needle the needle.
2. When handling the base of needle with
Correct placement of the needle is important in your thumb and index finger, always apply
gaining appropriate angle of entry into the tissue the forceps or needle holder between your
and avoiding a bent needle. Grasp the needle with fingers and the needle tip.
the needle holder in the mid to distal portion of
the needle, approximately one half to three quar-
ters of the distance from the tip of the needle
(Fig. 11-�
1).

Grasping the needle holder Swag

Point
There is more than one proper way to hold the
needle holder. Some surgeons prefer to hold it in
the palm of the hand without placing fingers in Body
the loops. This method offers maximum dexte­
rity. Alternatively, the needle holder is grasped by
placing the thumb and the fourth finger in the
loops and placing the index finger at the fulcrum.
This method offers maximum stability.

Tissue stabilization
Tissue stabilization aids in proper suture place-
ment. Depending on the setting, tissue may be
stabilized using the hands, forceps, or skin hooks.
Tissue should always be handled delicately to
avoid excessive trauma.

ERRNVPHGLFRVRUJ
140 Dermatologic Surgery

3. Use your third, fourth, and fifth fingers 3. Open the needle holder and grasp the short
to shorten any extra slack in the suture. (cut) end of the suture.
One technique is to “figure 8” the 4. Gently pull the loops off the needle holder
slack between the third and fifth fingers and reverse your hands. This knot should be
(Fig. 11-�
2). slightly looser than the final desired tension
of the wound (the second knot will tighten
Instrument tie the tie).
5. Bring the needle holder across the wound
The square knot is the basic surgical knot and is again and make a single loop (in the opposite
the primary knot used in cutaneous surgery. direction of the first knot) with the long
(needle) end of the suture.
Tying a square knot (Fig. 11-�
3) 6. Open the needle holder and grasp the short
1. Place the suture using the desired technique (cut) end of the suture.
and leave approximately 4–5 cm of suture 7. Gently pull the loops off the needle holder,
on the short (cut) end. Grasp the base of the reverse your hands and tighten.
needle between the index finger and thumb of 8. Repeat steps 5–7 again. The important point
your nondominant hand (as described above). is to reverse the direction of the loop and
2. Bring the needle holder across the wound the direction in which the needle holder is
and loop the suture twice around the tip of pulled across the wound.
the holder.
Simple interrupted suture
The simple interrupted suture (Box 11-1) is the
fundamental suture in cutaneous surgery:

• Place the suture by entering with the needle

at least perpendicular to the skin surface
(Fig. 11-�4).
• To obtain wound eversion, the suture should
be placed in a flask shape with the wide end
inferiorly (Fig. 11-�
5). Sutures that do not
follow the flask shape can lead to an inverted
suture line.
• Wounds of uneven height can be closed by
placing the suture deep on the low side and
shallow on the high side (Fig. 11-�6).
• Larger wounds or thicker skin may require
larger bites, perhaps necessitating reloading of
a
the needle from the center of the wound.

Box 11-2 lists the disadvantages of simple inter-

rupted sutures.

Vertical mattress suture

A properly placed vertical mattress suture can evert
skin edges better than any other suturing tech-
nique. Additionally, vertical mattress sutures pro-
vide eversion with less tension than other suturing
techniques. The vertical mattress is a strong suture
that can provide support to a wound under stress.

Placing the vertical mattress suture

(Fig. 11-�
7)
1. Place the deep suture first by entering the
epidermis approximately 5 mm from the
b wound edge and exiting from a similar
distance on the opposite skin edge with the
Figure 11-2  (a, b) Suture technique needle coursing deeper in the wound.

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 11

Chapter
Suture techniques 141

Pull gently

Pull gently

Figure 11-3  (a, b) Instrument tie

Continued

ERRNVPHGLFRVRUJ
142 Dermatologic Surgery

Pull gently

Pull gently

Figure 11-3  (a, b) Instrument tie

ERRNVPHGLFRVRUJ

B ox 1 1 - 1
Simple interrupted sutures
These are useful for:
• Closing small low-tension wounds, including punch biopsy
sites
• Top suture for layered repairs
• Correcting wound edges of unequal heights (“step off”)
Figure 11-4  Simple interrupted suture
Figure 11-5  Simple interrupted suture
2. Place the second, shallower, bite by entering
and exiting in the opposite direction from
the first pass, approximately 1–3 mm from
the wound edge.
3. The distance of the sutures from the wound
edge will vary depending on tension on the
wound and the amount of dead space to be
closed.
ERRNVPHGLFRVRUJ
11
Chapter
Suture techniques 143
Figure 11-6  Simple interrupted suture for wounds of
uneven height
B ox 1 1 - 2
Disadvantages of simple interrupted sutures
• Potential for “railroad track” scarring
• Inadvertent inversion of the wound edges
• Uneven tension on the wound
• More time consuming than other methods
Figure 11-7  Vertical mattress
Advantages and disadvantages of vertical mattress
sutures are shown in Boxes 11-�
3 & 11-4.
Half-buried vertical mattress suture
A vertical mattress suture in which one side of
the suture remains subcuticular is called a half-
buried vertical mattress suture (Fig. 11-�8). This
suture can be useful to close dead space ­without
144 Dermatologic Surgery
B ox 1 1 - 3
Advantages of vertical mattress sutures
• Excellent wound eversion
• Decreased wound tension
• Provide added support to defects under stress
• Useful for closing dead space
B ox 1 1 - 4
Disadvantages of vertical mattress sutures
• Potential for railroad tracking
• More time consuming than some other methods
• Tissue strangulation may occur if tied too tight
Figure 11-8  Half-buried vertical mattress
leaving track marks on the subcuticular side of
the wound. It is valuable when closing wounds
near hair-bearing skin where one side of the clo-
sure can be hidden. It does not provide as much
tension as the classic vertical mattress ­suture.
Near–far adaptation of the vertical
mattress suture
The near–far adaptation of the vertical mattress
suture is employed by beginning the suture near
the wound with a small epicuticular bite, then
re-entering deep and exiting far from the wound.
Next, the direction of the needle is reversed, and a
near epicuticular bite is taken, followed by a deep
ERRNVPHGLFRVRUJ
bite that exits far from the wound (Fig. 11-� 9).
This suture is useful in elevating the deep tissue
in which it is placed, for example when closing
the orbicularis oris muscle in a lip wedge.
Pulley suture
The pulley suture can be very helpful when ­closing
wounds under tension. The critical feature of the
pulley suture is multiple passes through the ­tissue,
creating significant resistance and making the ­suture
unlikely to slip. Although variations exist, the ­suture
is typically initiated by entering the epidermis dis-
tant to the defect, traveling across the defect and
exiting nearby. The needle is then redirected to en-
ter the epidermis near the wound, traveling across
the defect and finally exi­ting far from the wound
(Fig. 11-10). The suture may be left in place after
wound closure, or used to decrease tension while
placing additional sutures and then removed.
Horizontal mattress sutures
The horizontal mattress suture is an invalu-
able “stay” suture, and can be helpful to achieve
­hemostasis. Used by itself, it reduces wound
­tension, everts wound edges, and closes dead space.
It is also often used in conjunction with a second,
more superficial, interrupted suture placed closer
to the wound edges. Some surgeons remove this
suture once suturing is complete. Others wait
days to weeks to remove the suture. If the latter is
the case, consider placing a bolster to prevent the
­suture from cutting into the skin and lea­ving “rail-
road track” scarring. Owing to the risk of decreased
wound edge perfusion, this suture is generally not
used on poorly vascularized wounds or flaps.
Placing the horizontal mattress
suture (Fig. 11-11)
1. Place the initial suture in same fashion as the
simple interrupted suture.
2. Without tying, travel approximately 2 mm
parallel to the wound edge and place a
second suture entering on the same side and
traveling to the opposite side. Gently tie the
knot lateral to the wound edge, with care not
to strangulate the tissue.
Advantages and disadvantages of horizontal mat-
tress sutures are shown in Boxes 11-�
5 & 11-6.
Canal suture
The canal suture is a horizontal mattress suture
placed in the reverse direction (Fig. 11-12). It
can be used intentionally to invert the wound
edge into which it is placed, and everts the deep
edge of the wound. For example, this suture can
be placed on the outside (cutaneous side) of a

Figure 11-9  Near–far adaptation of vertical mattress suture
Figure 11-10  Pulley stitch
wound to evert the underlying mucosal surface of
full-thickness mucosal defects.
Three-point corner (tip) suture
This important variation on the horizontal mat-
tress suture can be employed when closing acute
tissue angles. This suture involves passing the
­needle subcuticularly through the “tip” to be
ERRNVPHGLFRVRUJ
11
Chapter
Suture techniques 145
closed (Fig. 11-13). An overly tight or improperly
placed corner suture can lead to tissue necrosis.
Four-point corner (tip) suture
Another variation on the horizontal mattress su-
ture can be employed when closing two acute tis-
sue angles. This suture involves passing the needle
subcuticularly through the two “tips” to be closed
146 Dermatologic Surgery
Figure 11-11  Horizontal mattress
B ox 1 1 - 5
Advantages of the horizontal
mattress suture
• Hemostasis
• Helpful as a “stay” or anchor suture
• Decreases and redistributes tension
• Eversion of wound edges
• Closes dead space
B ox 1 1 - 6
Disadvantages of the horizontal
mattress suture
• “Railroad track” scarring
• Overly tight horizontal mattress sutures can result in tissue
hypoxia and poor wound healing
• Time consuming when compared to other methods
(Fig. 11-14). Again, an overly tight or improperly
placed corner suture can lead to tissue necrosis.
Running sutures
Simple running cuticular sutures
The running superficial suture is a fast, efficient
way to close wound edges under little or no
­tension. Appropriate sites for this suture include
eyelids, neck, scrotum, and any tissue under little
tension where dead space has been closed pre-
viously. When beginning a running subcuticular
suture, it is important to place one end perpen-
dicular to the suture line. To anchor the loose
ends of the suture, tie them back on themselves
(Fig. 11-15).
Boxes 11-� 7 & 11-8 show the advantages and
disadvantages of running subcuticular sutures.
ERRNVPHGLFRVRUJ
Running locked suture
A running locked suture is useful for achieving
hemostasis in wounds with a high potential for
bleeding. However, if placed too tightly, tissue
necrosis may occur. To place a running locked
­suture, pass the needle through the loop created
by each previous stitch (Fig. 11-16).
Running horizontal mattress suture
The running horizontal mattress suture is a
time-efficient suture that provides good wound
eversion. The technique is similar to the stand-
ard horizontal mattress suture described above,
­except that it is run continuously until the end
of the incision (Fig. 11-17).
Combination running simple
and vertical mattress suture
The use of alternating vertical mattress sutures
with simple running sutures also produces good
wound eversion in a time efficient manner. Simple
cutaneous sutures are followed by vertical mat­t­
ress sutures in an alternating pattern (Fig. 11-18).
Buried sutures
Interrupted buried sutures
Buried sutures are typically used to reduce ten-
sion and evert the wound edges. They can be
placed to reapproximate deep structures (muscle
and fascia), the dermis, or both.
Placing the interrupted buried suture
(Fig. 11-19)
1. Enter deep and exit on the same side of the
wound superficially, typically at the level of
the mid dermis.
2. Continuing in the same direction, enter the
opposing side of the wound edge and travel
to the deep aspect, opposite the initial entry
point. This results in the knot being buried in
the deep aspect of the wound and minimizes
its extrusion.

Figure 11-12  Canal stitch
Figure 11-13  Three-point corner (tip) stitch
Advantages and pitfalls on buried sutures are
shown in Boxes 11-�
9 & 11-10.
Buried vertical mattress suture
This is a modification of the simple buried suture
that further optimizes wound eversion. To initi-
ate the suture, place a deep suture by entering
the undersurface of the dermis and traveling with
the needle in a superficial direction almost to the
level of the epidermis. Then travel back down to
exit at the level of the mid dermis. On the oppos-
ing side of the wound, again enter at mid dermis,
travel superficially, then dive down and exit deep.
The path of the suture creates a heart shape when
complete (Fig. 11-20).
Modified buried vertical it leaves no suture exit and entrance marks along
mattress suture
The buried vertical mattress suture can be modi-
fied to produce similar wound eversion in areas
too small to perform a standard buried mattress
suture, such as a small punch biopsy defect or
ERRNVPHGLFRVRUJ
11
Chapter
Suture techniques 147
flap repair. The modified version is performed
by entering the wound edge deep and exiting
through the epidermis lateral to the wound. The
needle is then redirected to enter back through
the same hole and to exit within the mid dermis.
The suture is repeated on the opposite side by
entering the contralateral mid dermis and exiting
through the epidermis. Again the needle re-enters
the same hole, but exits deep (Fig. 11-21). The
modified heart-shaped suture path yields superior
eversion. Care must be taken to ensure that the
suture is placed sufficiently in the mid dermis to
prevent “pull through.”
Running subcuticular suture
When used properly, the running subcuticular
­suture can yield superior cosmetic results because
the edge of the suture line (Fig. 11-22). This ­suture
should be used only when the wound is well
­approximated, the edges are everted, and wound
tension is minimal. If a deep space is present, it
should be closed with a separate ­ buried suture.
If using a nonabsorbable suture that will need
148 Dermatologic Surgery

Figure 11-14  Four-point corner (tip) stitch

ERRNVPHGLFRVRUJ
 11

Chapter
Suture techniques 149

Figure 11-15  Running cuticular stitch

B ox 1 1 - 8
B ox 1 1 - 7
Disadvantages of the running
Advantages of the running subcuticular suture
subcuticular suture
• Cannot be used on wound under tension due to tissue
• Efficient use of time ­strangulation
• Applies equal tension to wound edges • Does not close dead space
• Can allow for excellent wound eversion • Can leave “track lines”

ERRNVPHGLFRVRUJ
150 Dermatologic Surgery

to be removed, the suture should have an exit

point ­ every 2–3 cm for ease of removal. When
­using absorbable suture material, the technique
is ­modified.

1. The running subcuticular is initiated with a

simple dermal interrupted suture. Cut only
the short end after tying the knot.
2. After completing the running subcuticular,
the suture end is tied off with another
dermal interrupted suture. Cut only the
short end.
3. The needle end is then passed through the
end of the incision and exited distal to the
incision. The needle is pulled with tension.
This pulls the knot deeper into the wound.
The suture is then cut at the skin surface.

Purse-string suture
The purse-string suture is a variation on the
­buried dermal or simple continuous suture that
is useful for fully or partially reducing wound
­diameter or closing dead space. Circumferentially
placed intradermal or epidermal sutures can be
applied to redistribute tension equally around the
wound. In some cases the purse-string suture is
used to close a defect entirely. Alternatively, it can
be used to decrease the defect size and optimize
secondary intention. Multiple bites are oriented
horizontally around the wound edge and pulled
taught (Fig. 11-23).

Figure 11-16  Running locked stitch
Suture removal
Proper suture removal technique is often under-
appreciated. The suture should be cut and the
freed knot should be pulled across the suture line.
This allows the suture to be pulled out in the di-
rection in which it was placed and avoids placing­
tension opposite the axis of closure. Improper
­suture removal can place tension on the suture
line and put the wound at risk of dehiscence.

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Chapter
Suture techniques 151

Figure 11-17  Running horizontal mattress

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152 Dermatologic Surgery

Figure 11-18  Running combination simple and vertical mattress

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 11

Chapter
Suture techniques 153

Figure 11-19  Interrupted buried stitch

B ox 1 1 - 9
Advantages of the buried suture

• Closes dead space

• Provides wound stability and reduces tension
• Helps to evert wound edges

B ox 1 1 - 1 0
Pitfalls of the buried suture

• A suture that is pulled too tightly can result in tissue necrosis.

• A buried suture placed only in the fat can pull through. If
­possible, try to include a portion of the dermis or fascia
with the suture.
• If placed too superficially, a subcutaneous suture can pucker
the wound and may extrude or “spit” through the final wound.

Figure 11-20  Buried vertical mattress

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154 Dermatologic Surgery

Figure 11-21  Modified buried vertical mattress

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 11

Chapter
Suture techniques 155

Cut the short end of

the suture at the knot

Pull the needle through

the skin and cut at the
skin surface

Figure 11-22  Running subcuticular stitch

Figure 11-23  Purse-string suture

ERRNVPHGLFRVRUJ
156 Dermatologic Surgery
Further reading
Adams B, Anwar J, Wrone DA, Alam M. Techniques for
cutaneous sutured closures: ­variants and ­indications.
Semin Cutan Med Surg 2003;22(4):306–316.
Adams B, Levy R, Rademaker AE, Goldberg LH,
Alam M. Frequency of use of suturing and repair
techniques preferred by dermatologic surgeons.
Dermatol Surg 2006;32(5):682–689.
Alam M, Goldberg LH. Utility of fully buried
horizontal mattress sutures. J Am Acad Dermatol
2004;50(1):73–76.
Collins SC, Whalen JD. Surgical pearl: percutaneous
buried vertical mattress for the closure of narrow
wounds. J Am Acad Dermatol 1999;41(6):
1025–1026.
Harrington AC, Montemarano A, Welch M, Farley M.
Variations of the pursestring suture in skin cancer
reconstruction. Dermatol Surg 1999;25(4):
277–281.
Krunic Al, Weitzul S, Taylor RS. Running combined
simple and vertical mattress suture: a rapid skin-
everting stitch. Dermatol Surg 2005;31:
1325–1329.
ERRNVPHGLFRVRUJ
Moody BR, McCarthy JE, Linder J, Hruza GJ. En-
hanced cosmetic outcome with running horizontal
mattress sutures. Dermatol Surg 2005;31:1313–
1316.
Odland PB, Murakami CS. Simple suturing tech-
niques and knot tying. In: Wheeland RG, ed.
Cutaneous Surgery. Philadelphia: WB Saunders,
1994:178–188.
Olbricht S. Biopsy techniques and basic excisions. In:
Bolognia J, Jorizzo J, Rapini R, et al, eds. Derma-
tology. Philadelphia: Mosby, 2003:2269–2286.
Starr J. Surgical pearl: the vertical mattress tip stitch.
J Am Acad Dermatol 2001;44(3):523–524.
Stasko T. Advanced suturing techniques and layered
closures. In: Wheeland RG, ed. Cutaneous Surgery.
Philadelphia: WB Saunders, 1994:304–317.
Swanson NA. Atlas of Cutaneous Surgery. Boston:
Little, Brown, 1987.
Vistnes L. Basic principles of cutaneous surgery. In:
Epstein E, Epstein E Jr, eds. Skin Surgery, 6th edn.
Philadelphia: WB Saunders, 1987:44–55.
Zelac D, Swanson N, Simpson M, Greenway H. The
history of dermatologic surgical reconstruction.
Dermatol Surg 2000;26(11):983–990.

Suture materials
Oliver J. Wisco and Matthew R. Ricks
Clinical overview
The needle and suture are the foundation of
wound closure. This chapter discusses the prin-
ciples of the needle and suture and how to em-
ploy their strengths and weaknesses effectively in
dermatologic surgery.
Basic science and terminology
Key Points
• Curved needles with triangular tips are typically
used in dermatology as they give the highest
precision for fine detailed closures.
• The properties of a suture determines its utility in
the closure of certain body regions and the type
of closure to be used.
Needles
• Curved needles with triangular tips are
typically used in dermatology.
• The 3/8 circle is used most commonly.
• The 1/2 circle is commonly used for small flaps.
• Other sizes include 1/4 and 5/8 circles.
• The surgical needle is composed of three
parts (Fig. 12-1):
1 Shank – where the needle attaches, the
weakest part.
2 Body – middle part (strongest part), where
the needle should be held with the needle
driver.
3 Point – sharp end extending to the largest
cross-section of the body; do not handle
the needle in this area.
PEARL
For finer needles, use needle holders with smaller,
smoother jaws.
Types of needle (Fig. 12-2)
1 Triangular – conventional cutting:
• Cutting edge on the inside of the arc.
• Puncture faces the wound incision.
ERRNVPHGLFRVRUJ
12
Chapter
• Sutures may tear through tissue when
tied.
2  Triangular – reverse cutting:
• Cutting edge on the outside of the arc.
• Puncture faces away from the wound
incision.
• Less tearing of tissue than conventional
needle.
3 Rounded:
• Tapered rounded shape.
• Useful with fascia and delicate areas.
PEARL
Triangular needles are typically preferred over
round ­needles because they are easier to pass
through tissue.
Needle nomenclature
• There are several major suture brands,
each using different nomenclature
(Fig. 12-3).
• Ethicon produces 80% of the surgical needles
in North America (Table 12-1).
PEARLS
Use smaller needles for areas of high cosmetic
importance.
Use larger needles to close large wounds.
Suture properties
• The properties of a specific type of suture
determine how it is used (Table 12-2).
• Each property influences the other
properties.
PEARL
T
 here is an increased rate of suture
absorption on mucosal surfaces and areas
of infection.
158 Dermatologic Surgery

Table 12-1  Ethicon needle abbreviations

Abbreviation Meaning
P Plastic
PC Precision Cosmetics
PS Plastic Surgery
FS For Skin
Tip
Adapted from Robinson et al (2005) with permission from Mosby
Grasp needle Shank
Publishing Company.
in this region

Options
Body Key Points
Figure 12-1  Curved needle. Adapted from Robinson et al • All sutures are absorbed to some degree if left in
(2005) with permission from Mosby Publishing Company long enough (except stainless steel).
• Sutures are defined as absorbable or
Conventional Reverse Round nonabsorbable according to whether the suture
loses its tensile strength by 60 days (Tables 12-3
& 12-4).
• The rate of absorption is dependent on the
suture type, the location, and the presence of
infection.

Surgical approach
Key Points
• Choose the smallest suture that can provide
adequate strength for the closure but still
minimize tissue trauma.
• For subcutaneous suturing in areas of high
tension, use sutures with longer absorption rates.
• Use sutures with minimal tissue reactivity in areas
of high cosmetic importance.

For recommendations on which suture material and

needle to use in different locations see Table 12-5.

Comparative outcomes
Figure 12-2  Different needle types. Adapted from
Key Points
Robinson et al (2005) with permission from Mosby • While suturing is typically the preferred method
Publishing Company of wound closure, staples, tissue adhesives,
and skin closure tapes can be good alternatives
P-1 PS-1 (Table 12-6).

Controversies
P-3
PS-2 Key Points
• Data on the risk of infection with braided sutures
P-4 has historically been controversial.
• It has been theorized that the braids in braided
sutures harbor microorganisms, thus increasing
PS-4 the risk of infection.
PC-1 • However, a study published in 2001 by
Gabrielli et al showed that age, sex, wound
site and length, and surgeon experience were
more important in predicting complications
PC-3 PS-6 than the choice of suture materials and suturing
techniques.

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 12

Chapter
Suture materials 159

Table 12-2  Suture properties

Material Synthetic vs natural
Configuration Monofilament: single strand, low coefficient of friction allows it to slide easily, good for exterior suturing
Multifilament: braided/twisted, increased strength, easier handling but higher coefficient of friction, good for
subcutaneous suturing
Capillarity The ability to absorb and transfer fluid; it is controversial whether increased capillarity allows the suture to
harbor organisms
Tensile strength Determined by the force in pounds to snap the suture; synthetic sutures are generally stronger than natural
sutures; the greater the diameter the stronger the suture
Size Size ranks tensile strength - the thicker the suture, the greater the strength and the fewer the zeroes (3-0 is
wider and stronger than 4-0 for the same type of suture) dependent on the type of the suture
Elasticity The ability to return to the original size after being stretched; good elasticity allows for stretch with tissue
swelling, but also will recoil to maintain tissue approximation when the swelling resolves; use sutures with
good elasticity for exterior suturing
Plasticity The ability to maintain a new shape after it has been manipulated; allows for a more secure knot; good
plasticity accommodates tissue swelling without cutting tissue but does not hold tissue approximation well
when the swelling resolves
Memory A measure of a suture’s elasticity and plasticity; sutures with increased memory have a greater tendency
to return to their original configuration after being manipulated and are more difficult to handle; increased
memory causes suture knots to untie themselves, requiring extra knots
Coefficient of friction Determines how easily a suture will pull through tissue; the lower the coefficient, the easier it is for the
suture to slide through tissue, but it will also unravel more easily; sutures with a low coefficient are useful for
running subcuticular suturing
Pliability A measure of how well a suture bends; good pliability allows ease in knot tying and increased knot strength
Coating Sutures may be coated with various materials to lower the coefficient of friction or to increase the
antimicrobial properties
Tissue reactivity A measure of how much the suture will illicit a foreign body reaction; sutures with increased tissue reactivity
are natural, multifilament, absorbable, and large

Table 12-3  Commonly used absorbable sutures

Tensile Ease of Knot Tissue Time to
Suture Configuration strength handling security reactivity absorption Uses & pearls
Surgical gut Multifilament, Low, lost in Fair Poor Moderate 70 days Rarely used
(plain) twisted 7–10 days in skin;
unpredictable
absorption
rates
Surgical gut Multifilament, Low, lost in Fair Poor Low 21–42 days Skin grafts,
(fast-absorbing) twisted 3–7 days surface
sutures
Surgical gut Multifilament, Low, lost in Poor Fair Moderate 90 days Skin grafts;
(chromic) twisted 10–21 days unpredictable
absorption
rates
Polyglycolic Multifilament, Moderate, Good Good Low 60–90 days Dexon S:
acid (Dexon®) braided 20% at uncoated
21 days Dexon II: coated
Polyglactin Multifilament, High, 75% at Good Fair Low 56–70 days Subcutaneous
(Vicryl®, braided 14 days, 50% closure, vessel
Polysorb®) at 21 days ligature, high
memory
Continued

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160 Dermatologic Surgery

Table 12-3  Commonly used absorbable sutures—cont’d

Tensile Ease of Knot Tissue Time to
Suture Configuration strength handling security reactivity absorption Uses & pearls
Polydioxanone Monofilament High, 70% at Poor Poor Low 90–180 Subcutaneous
(PDS II®) 14 days, 50% days closure (high-
at 30 days, tension areas)
25% at
42 days
Polytrimethylene Monofilament Very high, Fair Good Low 60–180  Subcutaneous
carbonate 81% at days closure (high-
(Maxon®) 14 days, 59% tension areas)
at 28 days
Poliglecaprone Monofilament High, Good Good Minimal 90–120  Use when
25 (Monocryl®) 50–60% at days minimal tissue
7 days reactivity is
essential; good
for running
subcuticular
suture
Glycomer 631 Monofilament 75% at Good Poor Minimal 90–110  Subcutaneous
(Biosyn®) 14 days, 40% days closure (high-
at 21 days tension areas)
Rating scale: very low – low – poor – fair – good – moderate – intermediate – relatively high – very high – very good – highest. Adapted from Bolognia et al
(2003) and Robinson et al (2005) with permission from Mosby Publishing Company.

Table 12-4  Commonly used nonabsorbable sutures

Tensile Ease of Tissue
Suture Configuration strength handling Knot security reactivity Uses & pearls
Silk Multifilament, Low Gold standard Good High Mucosal
braided surfaces
Nylon
Ethilon® Monofilament High Good to fair Poor Low May tear
through
Dermalon® Good
delicate tissue
Surgilon® Multifilament, High Good Fair Moderate
braided
Nurolon®
Polypropylene Monofilament Moderate Good to fair Poor Low Running
(Prolene®, subcuticular
Surgilene®, suture
Surgipro®)
Polyester Multifilament, Very high Very good Very good Moderate Mucosal
(Dacron®, braided surfaces
Mersilene®)
Polyester Good Moderate Polybutylate-
(Ethibond coated
Excel®)
Polybutester Monofilament High Good to fair Good Low Exhibits
(Novafil®) elasticity
Rating scale: very low – low – poor – fair – good – moderate – intermediate – relatively high – very high – very good – highest. Adapted from Bolognia
et al (2003) and Robinson et al (2005) with permission from Mosby Publishing Company.

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 12

Chapter
Suture materials 161

Table 12-5  Suture recommendations

Location Needle Suture type and size Time to removal Clinical pearls
Scalp
Deep PS-2 Vicryl, 4-0 NA Use large needle
Superficial P-3 Prolene or Ethilon, 4-0 10–14 days Can use staples
Ears
Deep Not typically used
Superficial P-3 Prolene or Ethilon, 5-0 7 days Use small needle
Other face
Deep P-3 Vicryl, 5-0 NA
Superficial P-3 Prolene or Ethilon, 7 days
5/6-0
Nose
Deep P-3 Vicryl, 5-0 NA
Superficial P-3 Prolene or Ethilon, 7 days
5/6-0
Eyelids
Deep PS-6 Vicryl, 6-0 NA Not typically used
Superficial P-3 Prolene or Ethilon, 6-0 7 days Can also use fast-
absorbing gut or silk
Lips
Deep P-3 Vicryl, 5-0 NA
Superficial P-3 Prolene or Ethilon, 6-0 7 days Can also use fast-
absorbing gut or silk
Neck
Deep P-3 Vicryl, 5-0 NA
Superficial P-3 Prolene or Ethilon, 5-0 10–14 days
Trunk
Deep P-3 Vicryl, 4-0 NA Use PDS for large
high-tension wounds
on the back
Superficial P-3 Prolene or Ethilon, 4-0 10–14 days
Arms
Deep P-3 Vicryl, 4-0 NA
Superficial P-3 Prolene or Ethilon, 4-0 10–14 days
Hands
Deep P-3 Vicryl, 5-0 NA
Superficial P-3 Prolene or Ethilon, 5-0 10–14 days Use silk for delicate
skin
Legs
Deep P-3 Vicryl, 4-0 NA
Superficial P-3 Prolene or Ethilon, 4-0 10–14 days
Feet
Deep P-3 Vicryl, 4-0 NA
Superficial P-3 Prolene or Ethilon, 4-0 10–14 days
Continued

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162 Dermatologic Surgery

Table 12-5  Suture recommendations—cont’d

Location Needle Suture type and size Time to removal Clinical pearls
Penis
Deep P-3 Vicryl, 5-0 NA
Superficial P-3 Silk, 5-0 7 days
Vulva
Deep P-3 Vicryl, 5-0 NA
Superficial P-3 Silk, 5-0 7 days

Table 12-6  Closure material alternatives

Material
Staples
Tissue adhesives
(cyanoacrylate compound)
Skin closure tapes
Benefits
Fast application; good wound
eversion; decreased risk of
infection/reactivity
Fast application; no need
for removal by a medical
professional; may have
decreased risk of infection/
reactivity
Fast application; low cost; no
need for removal by a medical
professional; may have
decreased risk of infection/
reactivity
Disadvantages
Increased risk of necrosis
with flaps; painful on back,
intertriginous areas, and over
bony prominences
Little eversion of wound
edges; expensive; risk of
allergic reaction; can be
removed easily by repeated
washing
Little eversion of wound
edges; little wound support if
used alone; can be removed
easily
Pearls
Can be used on the scalp and
trunk; can be used to secure
grafts
Used for superficial/low-
tension incisions or wounds;
useful for children
Used to support sutured
wounds; can be used alone
for superficial/low-tension
incisions or wounds; not to
be used alone in cosmetically
sensitive areas

Further reading Oljoffer IH, Goldman G, Leffell DJ. Wound closure

Adams B, Levy R, Rademaker AE, Goldberg LH,
Alam M. Frequency of use of suturing and repair
techniques preferred by dermatologic surgeons.
Dermatol Surg 2006;32:682–689.
Bolognia JL, Jorizzo JL, Rapini RP, eds. ­Dermatology.
Edinburgh: Mosby, 2003.
Coulthard P, Worthington H, Esposito M, Elst M,
Waes OJ. Tissue adhesives for closure of surgical
incisions. Cochrane Database Syst Rev 2004;
(2)CD004287.
Eaglstein WH, Sullivan T. Cyanoacrylates for skin
closure. Dermatol Clin 2005;23:193–198.
Gabrielli F, Potenza C, Puddu P, Sera F, Masini C,
Abeni D. Suture materials and other factors associ-
ated with tissue reactivity, infection, and wound
dehiscence among plastic surgery outpatients. Plast
Reconstr Surg 2001;107(1):38–45.
Kanegaye JT, Vance CW, Chan L, Schonfeld N.
Comparison of skin stapling devices and standard
sutures for pediatric scalp lacerations: a rando­
mized study of cost and time benefits. J Pediatr
1997;5:808–813.
materials and instruments. In: Bolognia JL, Jorizzo
JL, Rapini RP, eds. Dermatology. Edinburgh:
Mosby, 2003:2243–2253.
Raza SL, Sengelmann RD. Instrumentation and
sutures. In: Snow SN, Mikhail GR, eds. Mohs
Micrographic Surgery. Madison: Wisconsin Press,
1999:33–42.
Robinson JK, Hanke W, Sengelmann RD, Siegel DM.
Surgery of the Skin: Procedural Dermatology.
St Louis: Mosby, 2005.
Weitzul S, Taylor RS. Suturing technique and other
closure materials. In: Robinson JK, Hanke CW,
Sengelmann RD, Siegel DM, eds. Surgery of
the Skin: Procedural Dermatology. Philadelphia:
Mosby, 2005:225–243.

ERRNVPHGLFRVRUJ

T. Minsue Chen,
Rungsima ­Wanitphakdeedecha, and Tri H. Nguyen
Key Points
• “Function before form, and form before
cosmesis” are inviolable principles of
reconstructive surgery.
• The most useful flap classification schemes are
based on location (with respect to the defect),
movement, and vascular supply.
• Most flaps in dermatologic surgery are local,
being harvested from adjacent skin.
• There are two essential local flap movements:
advancement (linear) and rotation (pivotal).
• Transposition flaps have both a linear and a
pivotal movement, but the flap is not directly
contiguous with the defect. These flaps transfer
tissue across an area of normal skin to reach the
defect.
• The flap pedicle, or vascular supply, is critical to
tissue viability and flap survival. Pedicles may be
random pattern or axial based.
• This is especially true of flaps with axial pedicles.
Elasticity, restraints to movement, tension
vectors, free margins, and effects of closing the
secondary defect are all factors to consider in
flap design.
Introduction
A key tenet in reconstructive surgery is: function
before form (contour, shape); form before cosmesis.
A beautiful scar is worthless if nasal inspiration
is obstructed. Form is primary, because contour
depressions and elevations are difficult to cam-
ouflage. Scar quality, although important, is sec-
ondary, as a wide or red scar may be hidden with
cosmetics as long as it is flush (contour) with its
surroundings.
Accurate wound assessment is critical to re-
constructive planning; Box 13-1 outlines issues to
consider.
When these details are factored, the best re-
pair usually becomes evident. The surgeon should
be able to discuss with the patient the ­ inherent
ERRNVPHGLFRVRUJ
13
Chapter
Flaps
a­ dvantages and limitations of each closure
­method. The simplest option (fewest incisions,
least tissue alteration, fewest stages, etc.) is usually
the best option provided that function and form
are optimized – in order of simplicity: second
­intention > primary closure > skin grafting > flap.
A wound closure algorithm is useful for a system-
atic approach (Fig. 13-1). Flaps are usually per-
formed when other closures are less optimal due
to issues with tension, function, or form. In gen-
eral, flaps are ideal for reducing, redirecting, and
redistributing tension from the primary defect,
and for providing bulk or thickness for deeper
wounds.
Flaps have a wide range of applications and
can provide excellent functional and cosmetic
outcomes when designed and executed precisely.
The goals of this chapter are to discuss: (1) how
flaps are classified, (2) the principles and biome-
chanics of flap movement, and (3) common flap
designs in dermatologic surgery.
Definition
A flap is a section of partially detached tissue.
The attached portion of a flap contains its vascu-
lar supply and is its pedicle (Fig. 13-2). All flaps
share the following features:
• The recruitment of nearby (but not
necessarily contiguous) donor skin that is
mobile and lax.
• The ability to reduce, redirect, and/or
redistribute tension from the primary defect
(original wound to be repaired).
• The creation of a secondary defect once the
flap moves into and closes the primary defect.
The secondary defect is the space that the
donor flap tissue occupied. The tension on
the primary defect is partially redirected and
redistributed to the secondary defect.
164 Dermatologic Surgery
B ox 1 3 - 1
Wound analysis
Wound characteristics
How large is the defect?
What tissue layers are missing – epidermis, dermis,
subcutaneous fat, fascia, muscle?
Is there a need for structural support – bone, cartilage?
Is the wound located in a convex or concave region of the
body?
Are any critical structures exposed – bone, tendon, nerve,
vessel)?
What caused the wound – malignancy, trauma, infection?
If cancer, are the margins clear? What is the risk of recurrence?
Will adjuvant therapy (radiation, topical chemotherapy) be
necessary?
Cosmetic unit, boundary
Is the defect in an area of visual significance?
Is there baseline asymmetry?
What cosmetic units and subunits are involved? What
proportion of the subunit is involved? If more than 50%, should
the remainder be removed and the entire subunit replaced?
What cosmetic boundaries are nearby?
Relevant anatomy
Where are the regional relaxed skin tension lines and
rhytids?
Is there baseline functional compromise – nerve injury/palsy,
ectropion, nasal valve collapse, etc.?
What free margins are affected – eyelids, nose, lips?
What neurovascular structures are at risk?
Is the location in an area of inherent high tension – extremity,
trunk?
Adjacent skin
Where is there lax and mobile skin – donor reservoir?
What is the quality of the adjacent skin – Thickness? Elasticity?
Sebaceousness? Compromised (actinic damage, prior scarring
or radiation)? Hair growth patterns?
How does positional change (upright versus supine, static
versus dynamic) affect the defect and closure plans?
Patient-specific considerations
What are the patient’s aesthetic expectations?
Is the patient willing to undergo a staged reconstruction?
Wound care compliance?
May patient comorbidities (venous stasis, diabetes, smoking)
affect wound healing?
Does the patient take any prescription and/or over-the-counter
products that may complicate reconstruction – anticoagulants,
antineoplastic, immunomodulating medications, herbal
supplements?
ERRNVPHGLFRVRUJ
• The alteration of tension vectors (directional
movement under tension) when both primary
and secondary defects are closed.
Classification
There are numerous ways to classify flaps
(Fig. 13-3):
• Location with respect to the surgical
defect – local, regional, or distant
• Movement – advancement, rotation
• Vascular supply – random pattern, axial, or
microvascular
• Stage – single or multistaged
• Configuration – note, rhomboid, bilobed,
banner, etc.
• Eponym – Abbe, Reiger, Mustarde, etc.
No single classification accounts for every design
or definition variation. Eponyms should generally
be avoided. Most flaps in cutaneous surgery are
local (adjacent and contiguous skin) and regional
(nearby but not directly adjacent). Within this
context, the most useful classification scheme is
based on movement and vascular supply.
Movement
There are two basic local flap movements: linear
­(advancement) and pivotal (rotational) (Table
13-1). Advancement flaps move adjacent/contigu-
ous skin in a linear fashion into the defect. Rota-
tion flaps move adjacent/contiguous tissue in an
arc or curvilinear fashion. Although these defini-
tions help in concept and classification, in practice
many flaps involve both types of ­movement.
A transposition flap may incorporate both
a pivotal and a linear movement. However,
­although a pure rotation or advancement flap
moves contiguous tissue into a wound, a transpo-
sition flap transfers noncontiguous tissue across an
inte­rvening area of normal skin to close the pri-
mary defect (Fig. 13-4). Local transposition flaps
are one-stage procedures (excluding revisions).
Regional transposition flaps, however, are staged
repairs (more than one stage for completion) and
are also known as interpolation (interpolate = to
insert between parts) flaps. Interpolation flaps or
staged flaps, therefore, are subtypes of transposi-
tion by moving tissue across areas of unaffected
skin to reach the wound.
Vascular supply
The vascular supply or pedicle to a flap is the
portion that remains attached. A pedicle may
be random or axial based. Random pattern flaps
include all local flaps and are nourished by der-
mal and subdermal vascular plexus. Axial flaps
are regional and are based on a named artery
­(either ­ septocutaneous or musculocutaneous,
 13

Chapter
Flaps 165

No: FTSGd
Vascular
base poor?
Yes: STSGe or
allograft/xenograft
Superficial

Second intentc

Low tension: Primary closure

or delayed FTSG
Defecta

Degree of Moderate tension: Plication

tension? + primary, local flap, or
delayed FTSG
Yes: Local flapf
Deepb
High tension: Is there
adjacent tissue laxity?
No: Composite graftg,
regional flapf
No
Structural
support?
Yes: Cartilage graft Local or regional flap

Figure 13-1  Algorithm for defect closure. The algorithm is not all inclusive. Repair depends greatly on the location of
the defect; for instance, a 1-cm defect on the nose demands greater consideration and complexity than a wound of the
same size on the cheek. aSmall (<1 cm), medium (1–3 cm), large (>3 cm). Location is critical. bDefects greater than
3 mm in depth will likely heal with a contour depression (unless in concave area), especially if overlying convex surfaces
or sebaceous skin. cSmall, superficial defects in concave areas are ideal for second intention healing. Avoid second
intention if bare bone, tendon, or neurovascular structures are exposed. Large defects will also heal well if superficial.
However, anticipate significant wound contraction and its impact, if any, on free margins or function. dA full-thickness skin
graft (FTSG) may be applied to any defect that is well vascularized. Superficial defects with FTSGs will maintain contour. If
deep defects are repaired with FTSGs, contour depressions may result unless delayed (partial granulation to fill the depth)
skin grafting is performed. eSplit-thickness skin grafts (STSGs) have less metabolic demand and survive better in poorly
vascularized defects. However, significant graft contraction (with potential effect on free margins) is assured compared
with FTSGs. fCombination closures (flap + flap, flap + graft, flap + second intention) should be considered for wounds
involving multiple subunits. gComposite grafts work best for small deep wounds at free margins. Owing to their bulk and
high metabolic demand, composite grafts survive poorly if sized above 1.5 cm

e.g. ­ supratrochlear artery in a paramedian fore-
head flap, labial artery in a lip-switch flap) (Table
13-2). All axial flaps are multistaged flaps. Not all
staged flaps, however, are axial in vascular supply.
The cheek to nose staged flap, for example, is a ran-
dom pattern flap (incorporates arterial perforators
from the angular artery but the angular itself is
not in the flap pedicle), despite being a two-stage
repair. Due to a more robust and reliable vascular
supply, axial designs permit flaps to reach farther
and close more complex defects. Axial flaps can
even become free flaps if the ­vessels are divided,
and the flap is moved and reanastomosed with
microsurgical techniques at the recipient site.
Flap biomechanics and design
The physics mantra “for every action, there is an
equal and opposite reaction” is applicable to flap
design. Poor flap design may have deleterious
outcomes, such as inadequate flap length, tissue
ischemia, edema, and/or inability to close the sec-
ondary defect. The best flap designs must account
for and overcome a variety of tissue restraints. All
flap movement is limited by inherent, vertical,
and lateral restraints.
Inherent restraint refers to the intrinsic laxity of
the flap tissue. For example, scalp tissue is more re-
strained than cheek skin due to the inherent rigidi­
ty of the galeal fascia. Similarly, the sebaceous nasal
tip is more restrained than the nasal sidewall. Flap
design must compensate for inherent tissue re-
straint. A rotation flap on the scalp must be greater
than the 3–4 : 1 ratio (flap diameter = 3–4 × defect
diameter) because of the scalp’s reduced mobility.
Vertical restraint refers to the fibrous fibers that
tether the flap to its base. Vertical restraints are
released by appropriate undermining. A form of
restraint that combines both inherent and vertical
restraint is pivotal restraint, which is a term that

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166 Dermatologic Surgery

a b

c d

Figure 13-2  Flap lexicon. (a) A = primary defect; B = pedicle, attached portion of flap; C = primary standing cone
(excises redundancy at primary defect). (b) Flap is rotated superiorly to close the defect. Note how the tension from the
primary defect is reduced, redirected, and redistributed to the secondary defect (D). (c) Length discrepancy at secondary
defect will be excised in the secondary standing cone (E), which is strategically placed at the submentum; (C) is the
primary standing cone that has been excised at the temple. (d) Outcome at 6 months

is specific to rotation flaps. It refers to the point
(usually between the pedicle and the primary
standing cone) on which the flap rotates into the
defect. If a door is the flap, then the door hinge is
the area of pivotal restraint. Pivotal restraint teth-
ers the flap during rotation so that the flap’s supe-
rior leading edge falls short of the superior border
of the defect. Wide undermining and elongating
the rotation flap height is required to overcome
pivotal restraint (Fig. 13-5).
Lateral restraints are the attachments of the
flap to its periphery (see Fig. 13-5). A cheek flap,
for instance, is laterally restrained by its attach-
ments to the temporal and preauricular fascia.
Lateral restraints can be overcome only by prop-
erly placed incisions. These “relaxing or releasing”
incisions separate peripheral anchors and allow
for flap movement. Once these restraint concepts
are understood, flap design may begin.
Next to flap restraints, the secondary defect
closure is the most important factor to consider.
When designed accurately, closure of the second-
ary defect can facilitate flap movement. Improp-
erly designed, however, untoward tension may
result with subsequent complications. Closing the
secondary defect usually involves lines of unequal
lengths, which may be resolved by a number of
techniques (see below in Operative technique).
An advancement flap is simply a method of dis-
placing a standing tissue cone from the primary
defect. The best example is the Burow’s wedge
advancement flap (BWAF), in which one stand-
ing cone is displaced laterally in a linear fashion
(Fig. 13-6). Rarely used advancement flaps are

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Chapter
Flaps 167

Flap classification
schemes

Location of Movement Vascular Staged Configuration Eponym

donor site supply
Flap is named Flap is
by its shape named after
(e.g. comet flap, its originator
hatchet flap) (e.g. Abbé flap,
Rieger flap)

Local Regional Distant Advancement Rotation Random Axial Single stage Multi-staged
pattern
Donor Donor tissue Distant Linear Pivotal Named artery Additional Additional
tissue is nearby donor site movement movement Dermal, nourishes flap (e.g. procedures procedures
is adjacent but not (e.g. tubed subdermal septocutaneous, not required required (e.g.
and directly pedicle plexus musculocutaneous) flap delay,
contiguous contiguous flap, radial nourishes flap inset,
with defect with defect forearm flap pedicle
(e.g. free flap, division, flap
paramedian rectus debulking,
forehead abdominis scar
flap) free flap, Transposition Microvascular revision)
latissimus
Flap tissue Division of flap and
dorsi flap)
transferred over an axial blood supply,
area of unaffected followed by
skin to reach defect reanastmosis by
microvascular
techniques

Regional Local transposition

transposition
(interpolation) Flap pedicle
contiguous with
Flap pedicle is not defect
contiguous with Random pattern
defect pedicle
Axial pedicle Single stage
Multi-staged

Figure 13-3  Flap classification

the U-plasty or H-plasty, as they result in long
narrow pedicles and unnatural box-like incisions
(Fig. 13-7). Other variations of advancement
flaps, such as A to T or crescenteric designs, are
more useful and aesthetic (Figs 13-8–13-10).
­Island pedicle flaps (IPFs) are especially ­ flexible
advancement designs. Also known as a Kite or
V to Y advancement flap, an IPF is separated
from its ­ peripheral skin (hence its label as an
­island). Its only attachment is a subcutaneous or
­myocutaneous pedicle that is either underneath
the flap or to its side. Rather than displacing a cone
laterally, an elongated standing cone is developed
as a flap and advanced directly into the defect. IPFs
are the most tissue sparing of all flaps as there is
no secondary or primary standing cone resection
(Fig. 13-11). IPFs are categorically a local, single-
stage advancement flap. However, they may also
rotate and or be transposed into the defect.
A rotation flap is more complex, in that the
surface area of the defect itself (and its tension)
is redirected and redistributed laterally in a cur-
vilinear fashion into the secondary defect. The
length, height, and arc of the curvilinear exten-
sion determine where the secondary defect is lo-
cated and how well it closes (Figs 13-12–13-15).
An O to Z flap is a bilateral rotation design that
is useful for larger defects, especially on the scalp
(see Fig. 13-15).
Transposition flaps are most demanding in geo-
metric accuracy. Several eponym versions exist,
such as DuFourmental, Limberg, and Webster.
The most commonly applied designs in derma-
tologic surgery are the 30° transposition flap
­(Webster), the bilobe, and the trilobe transposi-
tion flaps (Figs 13-16–13-19). Z-plasties are a
form of transposition flaps used in scar revision.
Transposition flaps recruit donor laxity that is

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Table 13-1  Flap movement: advancement versus rotation
Advancement flap
Examples Unilateral designs:
• Burow’s wedge advancement (Fig. 13-6)
• Crescentic advancement (can be unilateral
or bilateral (Figs 13-8 & 13-10)
• V to Y or island pedicle (kite) (Fig. 13-11)
Bilateral designs:
• H-plasty
• A to T (Fig. 13-9)
Interpolation subtype:
• Retroauricular staged flap – this is
a staged flap that has linear movement.
However, it may also be classified as a
transposition design because it crosses
over intervening island of normal skin to
reach the defect
Movement Linear
Vascular supply Random pattern
Flap : defect ratio 2–4 : 1
Tension Tension is reduced and redistributed but is
not redirected
Mobility Recruits some adjacent tissue laxity laterally
Restraint Lateral restraint
nearby but not directly contiguous with the de-
fect; this is why flap tissue is transferred over an
area of unaffected skin.
Staged flaps require two or more stages (sepa-
rated by 2–3 weeks) to complete, not including
any revisions (Fig. 13-20). Stage I involves flap
harvest, pedicle creation, and coverage of the
defect. Stage II usually divides the pedicle and
finalizes the repair. However, stage II may also
be an intermediate stage in which the flap is par-
tially elevated and debulked (see Fig. 13-20d). If
this intermediate step occurs, then pedicle divi-
sion occurs in stage III (see Fig. 13-20e,f). Staged
designs included both random pattern and axial
based pedicles. An example of a staged flap that
has a random pattern pedicle is the cheek-to-
nose (melolabial interpolation) staged flap (Fig.
13-21). Indications for staged repairs include:
ERRNVPHGLFRVRUJ
Rotation flap
Rotation (Figs 13-12–13-15):
• Cervicofacial rotation (Figs 13-12 & 13-13)
• Dorsal nasal flap (Rieger, hatchet) (Fig. 13-14)
• O to Z bilateral rotation (Fig. 13-15)
• Innervated myocutaneous lip and cheek (Karapandzic)
• O to T
• Comet flap
Transposition subtype:
• Rhombic or rhomboid (Limberg, Dufourmental)
• Webster 30° transposition
• Note or Banner flap (Fig. 13-16)
• Bilobe (Figs 13-17 & 13-18)
• Trilobe (Fig. 13-19)
Interpolation subtype:
• Paramedian forehead flap (Fig. 13-20)
• Lip-switch (Abbé) flap
• Cheek to nose (melolabial) interpolation (Fig. 13-21)
Pivotal (movement is in an arc)
Random pattern or axial (paramedian forehead flap,
lip-switch flap)
2–4 : 1 (flap : defect ratio may be greater with axial flap)
Tension is reduced, redistributed, and redirected
Optimizes recruitment of lax donor tissue laterally and
distant from the defect
Pivotal restraint (Fig. 13-5):
• Arises from inherent tissue stiffness at the flap’s pivot point
and prevents tip of flap from reaching distal margin of
operative defect. Secondary movement expected at primary
defect
• Large defects and/or more than 50% subunit
loss
• Deep defects that require tissue bulk and
contour
• Infrastructure loss (i.e. cartilage)
• Adjacent tissue reservoir inadequate for
reconstruction.
Supplementary operations in staged flaps may
include:
• Flap delay – when distal flap perfusion and
viability is questionable, flaps may be delayed
after incision.
• Flap inset – after flap delay, a subsequent
procedure is necessary to inset the flap to the
recipient site.
 13

Chapter
Flaps 169

a b c

Figure 13-4  Rhombic transposition flap. (a) A = primary defect; B = flap; C = intervening area of skin. (b) Transposition
flap (B) crosses over an intervening area of unaffected skin (C) to close the primary defect. (c) Closure

Table 13-2  Flap vascular supply: random versus axial pattern flap
Random pattern flap Axial flap
Illustration Rotation flap – random pattern Paramedian forehead flap – axial pedicle (in this
example the left supratrochlear artery at the left
medial eyebrow is contained within pedicle)

Vascular Dermal and subdermal plexus Septocutaneous artery or myocutaneous artery

supply
Stages Usually single stage; occasionally Multi-staged (at least two stages)
multi-staged – cheek to nose (melolabial)
interpolation flap, retroauricular staged flap
Length :  1.5–4 : 1 Greater than random pattern flap
width ratio
Example All single-staged flaps and some multi-staged flaps, Paramedian forehead flap (based on supratrochlear
such as the cheek to nose (melolabial) interpolation artery)
flap and the retroauricular staged flap
Lip-switch interpolation (Abbé) flap (based on labial
artery)

• Flap debulking – to improve contour and
aesthetic outcome, flaps may require incision
and removal of excess tissue.
• Pedicle division – once a flap has established
vascular connection with the recipient site,
the pedicle may be divided, most commonly
in 3 weeks’ time.
• Scar revision – procedures to optimize surgical
scars may include scar excision, Z-plasty, laser,
and dermabrasion.

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170 Dermatologic Surgery

a b

Figure 13-5  Pivotal and lateral restraints. (a) Arrows represent lateral restraints that prevent donor tissue mobility. Black
arrows are in areas where tissue movement should be avoided to prevent an eclabium. Blue arrows are preferred donor
flap tissue. Note how rotation incision (gentian violet) cuts through lateral restraints, thereby releasing their tethers on the
flap. Pivotal restraint (PR) is the area on which the flap will rotate into the defect. (b) Pivotal restraint (PR) prevents flap
from fully covering the defect and tethers the flap downward. Proper design and wide undermining in this area helps to
minimize the anchoring effect of pivotal restraint

a b c

Figure 13-6  Burow’s wedge advancement flap closure. (a) The BWAF displaces one standing cone laterally: (B) is
the displaced standing cone that extends laterally and linearly to the looser donor cheek and is the same size as (A) or
slightly wider; (C) is the linear vector of closure for this advancement flap. (b) Closure lines are camouflaged along natural
creases: (A) hides along the nasal dorsum; (B) hides at the melolabial fold, and linear extension hides at the superior alar
sulcus. (c) Long-term results demonstrating functional and cosmetic restoration

Preoperative planning 3 Is one flap sufficient or are combination

The patient should be examined in the upright
position in both static and dynamic situations.
Baseline and postoperative functional compromise
and asymmetry should be noted (i.e. nerve injury/
palsy, ectropion, nasal valve collapse, oral incompe-
tence, etc.). Aesthetic boundaries, relaxed tension
lines, rhytids, and, finally, the flap design should be
marked prior to infiltration with local anesthetic.
The final checklist before the first incision
should successfully answer these questions:
1 Has the defect been evaluated accurately?
(see Box 13-1)
2 Is the pedicle sufficient to supply this size of flap?
closures needed (more then one flap, flap
plus second intention/primary closure/
graft)?
4 Does this design overcome inherent and
lateral restraints?
5 How much undermining is needed to
overcome pivotal and vertical restraints?
6 Is “reaction for every action” accounted for?
In other words:
a. What will happen to the surrounding
structures at the primary and secondary
defect if the flap is moved as drawn?
b. Will closing the secondary defect be
possible without excessive tension or free
margin distortion?

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Chapter
Flaps 171

a b

Figure 13-7  U-plasty advancement flap design and anticipated final suture line conformation if this closure was chosen.
(a) U-plasty design displaces two standing cones (A) and (B) laterally compared with the BWAF. These are the same
cones that would be excised if the defect were closed primarily. Two parallel linear incisions extend laterally to form the
flap; (P) is the long narrow pedicle. (b) Rectangular box shape incision lines are less camouflaged than with a BWAF

a b c

Figure 13-8  Crescenteric advancement flap. (a) The crescenteric advancement flap is similar to the BWAF in that one
standing cone is displaced laterally (A); however, the displaced standing cone is crescentic in shape (A) rather than
triangular, thus conforming better to areas such as the lateral alar curve (shown here) or lateral eyebrow. (b) Suture lines
show how the crescenteric cone blends into the lateral alar sulcus. (c) Appearance 1 week after surgery

a b

Figure 13-9  A to T advancement flap. (a) A to T design: flap incisions camouflaged at mental crease, primary standing
cone placed inferiorly. (b) “T” closure as flaps advance bilaterally. Eversion is needed only at the center, where tension is
greatest

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172 Dermatologic Surgery

a b c

Figure 13-10  Bilateral advancement flap. (a) A bilateral crescenteric advancement flap is ideal for larger midline lower
lip defects. Two crescenteric standing cones are removed along mental crease. The bilateral movement maintains lip
symmetry and minimizes tension on any one side. (b) A wedge of lip (skin, muscle, mucosa) has been removed centrally
and crescenteric cones have been resected and advanced medially. Note how crescenteric cones are concealed along
mental crease. (c) Final closure. (d) Long-term results

a b c

Figure 13-11  Island pedicle flap (V to Y, or kite advancement flap). (a) Length : width ratio of island flap is 2–3 : 1
relative to defect. Smaller white outline is the final flap dimension. (b) Flap incised and pedicle (myocutaneous) created
underneath. Circular defect is angulated to enhance aesthetic closure. (c) Closure

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Chapter
Flaps 173

7 Where will the primary and Operative technique

secondary standing tissue cones (dog
ears) be?
8 Are the incisions placed where they can best
be hidden (along subunit boundaries, within
rhytids)?
9 Is any anesthesia needed beyond local infiltra-
tion (tumescent anesthesia, nerve blocks)?
10 Is the patient in proper position?
11 Are all instruments and supplies available?
The surgical field should include the contralateral
aspect of the surgical wound (i.e. the entire face
should be prepped in the usual sterile fashion).
This will allow the intraoperative assessment
of flap movement on tissue symmetry and free
­margins.
Undermining should be performed to release
vertical and pivotal tissue restraint and elasticity,

a b

c d

Figure 13-12  Cervicofacial rotation flap. (a) Lateral restraints are circumferential to defect. Dark blue arrows represent
best laxity and donor skin, and are released by flap curvilinear incision (white curve). There is also some movement from
the medial cheek (light blue arrows); movement from black arrows is undesirable. (b) Flap incised and undermined. Note
incision onto upper neck, which serves as a back-cut and releases additional restraint. (c) Flap rotated to close defect;
note displacement of defect and tension vectors onto secondary defect (zygoma, preauricular, upper neck). Primary
standing cone at medial cheek. (d) Closure – secondary standing cone revised behind ear at postauricular sulcus

a b

Figure 13-13  Cheek rotation flap. (a) Classic rotation design, which begins rotation curve level with superior edge
of defect. Pivotal restraint (P) tethers flap inferiorly and brings its leading edge A down to A′; this leaves a secondary
defect below the eyelid (may lead to ectropion once closed). (b) Modified rotation height, which is above the level of the
defect’s superior edge. The elevated rotation height compensates for pivotal restraint and minimizes the risk of ectropion.
Secondary standing cone excised posteriorly at sideburn.

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174 Dermatologic Surgery

c d

Figure 13-13, cont’d (c) Elevated height of flap allows suspension of flap to lateral orbital rim, thus minimizing the
gravitational pull on lower eyelid that inevitably occurs with time and wound contraction. (d) Six-month follow-up: there is
no ectropion and ipsilateral eyelid is properly supported

a b

c d

Figure 13-14  Dorsal nasal rotation flap (Rieger). (a) Rotation flap extended to superior glabella, with back-cut to optimize
movement. (b) Flap is broadly undermined – above perichondrium on the nose. (c) Flap rotates inferiorly. (d) Long-term
results. Note flap thickness relative to thinner nasal root area

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Chapter
Flaps 175

a b c

Figure 13-15  O to Z bilateral rotation on scalp. (a) Bilateral rotation design recruits donor laxity from parietal scalp
bilaterally. White arrow is tension vector of primary defect. (b) Flap elevated subgaleally and rotated to close defect. Note
that tension vectors are redirected and redistributed to smaller secondary defects. (c) Final closure. Length discrepancies
resolved by using rule of halves suturing

a b

c d

Figure 13-16  Melolabial transposition flap. (a) Flap width B and D must equal defect diameter at points A and C
respectively. Flap length is extended to lower melolabial fold to form a 30° angle (*), which prevents standing cone
formation. (b) Flap transposes across lateral ala to close the defect. The distal edge of the flap at D will be trimmed.
(c) Closure. (d) Long-term results. Note blunting of superior alar sulcus, which is typical of the melolabial transposition flap

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176 Dermatologic Surgery

a b c

Figure 13-17  Laterally based bilobe transposition flap. (a) The pedicle is laterally based (vascular supply from cheek
laterally). The length of the primary cone (P) is intentionally longer in order to optimize flap movement, and is placed at
the alar sulcus for camouflage. The entire arc of movement from C to A is less than 90°. The diameter of the first lobe (B)
equals that of the defect (A). The diameter of second lobe (C) may be equal to or no less than 75% that of the primary
lobe. The two arcs radiating from the defect (A) emanate from the mid and superior edges of the defect. These arcs
ensure that the first and second lobes are properly positioned and proportioned when rotating towards the defect. (b) The
flap is rotated inferiorly and the defect is closed. The primary lobe (B) closes the defect (A), the second lobe (C) moves
into where (B) was, and the donor site at (C) is closed linearly along the upper nasal dorsum. (c) Long-term results

a b

Figure 13-18  Medially based bilobe transposition flap. (a) Pedicle is medially based (vascular supply from medial nose).
Note intentional elongation of primary cone, now positioned at lateral nasal tip. (b) Closure. (c) Long-term results

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Chapter
Flaps 177

a b c

Figure 13-19  Trilobe transposition flap. (a) Three lobes may be used for larger defects under tension. The first lobe (A)
equals the defect diameter; the second and third lobes (B) and (C) may be equal to or less than (A), depending on the
laxity of donor skin. Angles of movement from (B) to (A) and from (C) to (B) are 90° of rotation. (b) Closure. (c) Short-term
results

a b

c d

Figure 13-20  Staged axial flaps. (a) Stage I: a paramedian forehead flap, based on the left supratrochlear artery is
being developed to repair complex defect on the left nasal tip (a cartilage batten graft has been inserted across the alar
rim defect for infrastructure support). (b) Stage I: the forehead flap has been rotated, transposed, and interpolated 180°
inferiorly to close the nasal defect. The supratrochlear artery is within the pedicle tube attached at the left medial eyebrow.
(c) Healthy appearance of paramedian forehead flap 3 weeks later, before stage II. (d) Stage II: the flap is partially elevated
and excess subcutaneous tissue is debulked for better sculpting of the nasal tip. The vascular pedicle is still attached at
the medial eyebrow.
Continued

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178 Dermatologic Surgery

e f g

Figure 13-20, cont’d (e) Stage III: the pedicle is divided and donor site closed primarily. (f) Stage III: pedicle tube is
discarded; flap is sculpted and inset into nose. (g) Outcome 6 months after surgery: note restoration of contour, alar rim
stability, and symmetry of eyebrows

a b

c d

Figure 13-21  Cheek to nose staged random pattern flap. (a) Flap based on melolabial fold; defect has cartilage batten
graft inserted for support of alar rim. (b) Pedicle is random pattern, based on arterial myocutaneous perforators of nasalis
muscles. (c) Cheek flap inset onto nasal alar defect. (d) Long-term results after pedicle division in stage II

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a b
Figure 13-22  Lengthening shorter line. (a) Burow’s wedge advancement flap: note curved upper line (A) that eliminates
need for standing cone revision inferiorly (line B) by equalizing line A with line B. (b) Closure without standing cone
inferiorly. (c) Final long-term results
and the plane of flap elevation and ­undermining
should match the wound depth closely. This
should be performed cautiously to minimize in-
jury to vital structures and to maximize the flap’s
vascular supply.
Flap insetting requires at least two layers of su-
tures. Subcutaneous–dermal sutures approximate
skin edges and minimize wound closure tension
on epidermal edges. Suspension or tacking sutures
may be necessary to anchor a portion of the flap,
in order to shift tension off the leading edge of
the flap, reorient tension, and/or reduce ­potential
wound dead space. Fascial plication sutures may
also be placed to reduce wound tension and
defect size.
Borders of unequal length will result from the
discrepancy between the primary and secondary
defects. To equalize this discrepancy, a standing
tissue cone (dog ear, Burow’s triangle) may need
to be removed from the longer side, or the shorter­
sides may need to be lengthened (Fig. 13-22).
­Alternatively, if the incision lines are long enough
(rotation flap with length : width ratio of 4 : 1), the
discrepancy may be sewn out either by closing
the wound by the “rule of halves.”
Postoperative care
Wound care after flap reconstruction is similar to
that for most other wounds. A pressure dressing,
including ointment and nonstick pad, should be
applied over the flap. This initial dressing should
be removed after 24–48 h, the area cleaned, and
a dressing of ointment, nonstick pad, and tape
reapplied. In selected patients, the first dressing
change should be performed in the office by the
ERRNVPHGLFRVRUJ
13
Chapter
Flaps 179
c
surgical team, especially in patients with complex
dressings and/or intricate reconstructions.
Patients and their caretakers should be encour-
aged to view the wound prior to bandage place-
ment to avoid any surprises with the first dressing
change at home. They also should be educated on
the anticipated postoperative wound appearance,
phases of healing, and potential complications.
Written instructions should include recommen-
dations to enhance flap survival, as well as when
to seek medical attention.
Summary
Aesthetic flap reconstruction requires careful as-
sessment of patient and wound characteristics,
an expansive knowledge of surgical anatomy,
meticulous flap design and execution, an artistic
sense of function and form, and an understand-
ing of flap biomechanics and tissue movement.
A systematic approach to design considerations
will optimize an outcome that is both functional
and beautiful.
Further reading
Baker SR. Reconstructive surgery for skin cancer.
In: Rigel DS, Friedman RJ, Dzubow LM, Re-
intgen DS, Bystryn JC, Marks R, eds. Cancer of
the Skin. Philadelphia: Elsevier Saunders, 2005:
573–592.
Cook JL, Goldman GD. Random pattern flaps. In:
Robinson JK, Hanke WC, Sengelmann R, Siegel D,
eds. Surgery of the Skin: Procedural Dermatology.
St Louis: Mosby, 2005: 311–343.
180 Dermatologic Surgery
Cook J, Zitelli JA. Axial pattern flaps. In: Robinson
JK, Hanke WC, Sengelmann R, Siegel D, eds.
Surgery of the Skin: Procedural Dermatology.
St Louis: Mosby, 2005: 345–365.
Dzubow LM. Facial flaps: biomechanics and
regional application. Norwalk: Appleton & Lange;
1990.
Fazio MJ, Zitelli JA. Flaps. In: Ratz JL, Geronemus
RG, Goldman MP, Maloney ME, Padilla RS, eds.
Textbook of Dermatologic Surgery. Philadelphia:
Lippincott-Raven, 1998: 223–245.
Nguyen TH. Staged cheek-to-nose and auricular
interpolation flaps. Dermatol Surg 2005;31(8 Pt
2):1034–1045.
ERRNVPHGLFRVRUJ
Nguyen TH. The nose. In: Roenigk RK, Ratz JL,
Roenigk HH, eds. Roenigk’s Dermatologic Surgery:
Current Techniques in Procedural ­Dermatology3rd
edn, New York: Informa Healthcare, 2007: 219–230.
Stotland MA, Kerrigan CL. Principles of skin flap
­surgery. In: Weinzweig J, ed. Plastic Surgery Secrets.
Philadelphia: Hanley & Belfus, 1999: 414–416.
Tromovitch TA, Stegman SJ, Glogau RG. Flaps and
Grafts in Dermatologic Surgery. St Louis: Mosby,
1989.
Verheyden CN, Losee J, Miller MJ, Rockwell WB,
Slezak S, eds. Essentials for Students: Plastic Sur-
gery, 6th edn. Arlington Heights, IL: Plastic Surgery
Educational Foundation, 1979.

Skin grafts
Daihung Vu Do and Christine M. Hayes
Key Points
• Skin grafts offer a one-step procedure for repair
of defects in anatomic areas in which there is little
skin laxity.
• Full-thickness skin grafts are the most commonly
performed skin graft and can offer excellent
cosmesis if the appropriate donor site is selected.
• Split-thickness grafts may be used to cover
very large defects but their cosmetic outcome is
poorer than that of full-thickness grafts.
• Composite grafts are useful for repairing small
but deep defects that may include loss of
cartilage.
Introduction
A skin graft is defined as a piece of tissue har-
vested from a donor site, separated from its vascu-
lar supply, and placed in a distant location. When
implanted at the recipient site, the graft must
re-establish its vascular supply if it is to survive
(Table 14-�1).
Classification
Grafts are classified by their thickness. Split-
­thickness grafts contain the epidermis and por-
tions of the dermis with little to no adnexal
structures. Full-thickness skin grafts include the
entire epidermis and dermis as well as adnexal
structures. Composite skin grafts contain the
complete epidermis, dermis, and deeper struc-
tures such as cartilage.
Indications
Skin grafts are useful when other options for
repair such as primary closure, granulation, and
local skin flaps are not ideal. For example, large
defects of the nasal tip have little surrounding
skin laxity to draw upon and heal poorly with
secondary intention. For patients unwilling to
undergo a two-stage interpolation flap such
as the paramedian forehead flap, grafts can be
ideal. They offer a one-step repair procedure
that can provide exceptional aesthetic results
ERRNVPHGLFRVRUJ
14
Chapter
if donor tissues with a good color and texture
match can be identified. For deeply invasive
­tumors with a high incidence of local recur-
rence, a split-thickness skin graft may be the best
repair choice so that postoperative surveillance
may be facilitated.
Contraindications
Before undertaking a graft, the recipient site
should be assessed for graft suitability. Of para-
mount importance is the vascularity of the graft
bed. Grafting should be avoided in sites with ex-
posed cartilage or bone because they are poorly
vascularized and unable to support a graft. These
sites should be allowed to granulate prior to the
placement of a skin graft. Alternatively, a hinge
flap in which a flap of fat adjacent to the defect
is raised and turned over onto the defect can be
used to cover exposed bone or cartilage and allow
immediate graft placement.
Full-thickness skin grafts
Technique
An overview of how skin grafts are performed is
shown in Figure 14-�
1.
Donor site selection
Donor sites should be selected to match the
­recipient site as closely as possible with regard to
color, texture, skin thickness, sebaceousness, and
absence or presence of hair. There should be rela-
tive skin laxity at the donor site in which harvest
scars can easily be hidden. The most common do-
nor areas are the preauricular area, postauricular
area, supraclavicular area, and the conchal bowl.
In some instances, closure of a defect will require
the excision of a redundant cone of tissue, which
may be used as a graft. This is known as a Burow’s
graft because it arises from a Burow’s triangle.
Burow’s grafts provide a better texture and color
match than more distant donor sites, and closure
of the donor site is usually simpler.
182 Dermatologic Surgery
Table 14-1  The three stages of postoperative graft
physiology after placement
Stage Events
Imbibition Ischemic period in which
fibrin forms underneath the
graft and keeps it attached.
The graft relies on passive
diffusion of nutrients from the
graft bed
Inosculation Dermal vessels in the graft
become connected to
vessels in the wound bed.
During this phase, the graft
becomes reperfused
Neovascularization Capillaries grow into
the graft from the graft
bed. This phase may
occur concurrently with
inosculation. Lymphatic flow
is re-established
Complications
Hematoma
Prior to placing a graft, meticulous hemostasis
should be carried out to prevent the development
of a hematoma underneath the graft. Although the
development of a thin layer of fibrin beneath the
graft is normal, the presence of a large ­hematoma
inhibits diffusion of nutrients into the graft and
limits the development of capillary ingrowth nec-
essary for graft survival.
Basting sutures and bolsters are employed to
prevent hematoma formation. Basting sutures
(Fig. 14-�2) are sutures that attach the graft to the
base of the recipient site. They may be placed
percutaneously (going through the full thickness
of the graft) or subcutaneously (intradermal bite
on the graft side). They mechanically prevent a
hematoma from forming underneath the graft.
Bolsters (Fig. 14-� 3) are large cotton or gauze
dressings that are sutured on top of the graft.
They apply pressure to the graft and hold it flat
against the recipient bed to maximize contact
between the graft and the wound bed to prevent
hematoma formation. More recently, thermo­
plastic bolster dressings have been described.
The thermoplastic dressing is heated in a water-
bath to 160°F so that it can be molded to fit the
contours of the recipient site. Once it cools, it
hardens and immobilizes the graft. It can be su-
tured or stapled to the recipient site for 5–7 days.
Thermoplastic bolsters are most advantageous on
convex or concave areas such as the nose and ear.
However, they are more costly than traditional
cotton bolster dressings.
ERRNVPHGLFRVRUJ
Necrosis
If an adequate vascular supply cannot be estab-
lished, partial or full necrosis of the graft will
occur. This is heralded by a black, thick, tightly
adherent crust or eschar (Fig. 14-� 4a). It is best to
leave the necrotic graft intact to act as a biological
dressing and to provide a scaffold for regenerating
tissue. The site should be dressed with petroleum
jelly and covered to promote wound healing. In
time, the eschar will fall off revealing pink viable
tissue underneath (Fig. 14-� 4b).
Wound infection
The development of wound infection at the graft
site is rare but can occur if there has been a break
in sterility, or may be due to seeding of the site
in the postoperative period. It is characterized
by edema, erythema, and purulence. Incision and
drainage of abscesses, oral antibiotics directed at
the causative organism, and conservative wound
care should be carried out.
Postgraft cosmetic considerations
Contraction
Traditionally, it was thought that full-thickness skin
grafts contracted minimally. However, one study
showed that skin grafts contract by about 40% in
the postoperative period. Infection of the graft was
associated with a slightly greater degree of contrac-
tion (50%), presumably because part of the graft
healed via secondary intention. Grafts on the nose
and periorbital area contracted more than those on
the scalp and temple. There did not seem to be an
association between the degree of contraction and
donor site, graft area, or patient age.
Pincushioning/scarring
During the immediate postoperative period, grafts
become edematous due to limited lymphatic
drainage. This resolves with the re-establishment
of lymphatic flow. Persistent elevation of the graft
(Fig. 14-� 5) can be due to the development of a
hypertrophic scar or pincushioning. Distinguish-
ing between these possibilities can be difficult.
A hypertrophic scar is characterized by a firm,
smooth, elevated graft surface devoid of adnexal
structures. Pincushioning occurs due to the for-
mation of a plate-like scar beneath the graft that
then contracts as the scar matures, pushing the
center of the graft upwards. Wide undermining
has been advocated to avoid pincushioning be-
cause the plate-like scar occurs over a greater area
and is not confined solely to the area underlying
the graft. Persistent graft elevation can be treated
with dermabrasion, ablative resurfacing lasers,
­serial steroid injections, shave excision of fibrous
tissue, or may spontaneously improve with scar
maturation.
 14

Chapter
Skin grafts 183

a b c

d e f

g h i

j k l

Figure 14-1  Full-thickness skin graft. (a) Biopsy-proven basal cell carcinoma of the left ala prior to Mohs surgery.
(b) Defect on the left nasal ala following Mohs micrographic surgery for a basal cell carcinoma. (c) A Gentian violet marker
is used to mark the perimeter of the defect. (d) The reverse side of the suture cardboard label is pressed against the defect
to create an imprint of the defect to serve as a template. Scissors are used to cut the template out. (e) The cardboard
template is placed on the donor site and used to draw an appropriately sized ellipse. (f) A no. 15 Bard–Parker scalpel is
used to excise the donor tissue. The deep surgical margin is shown to illustrate the yellow color of the adipose tissue, which
must be removed. (g) Curved iris scissors are used to defat the graft. The graft is placed with the epidermis facing down.
Curved scissors are used to remove the fat. Fat is relatively soft and easily removed by the scissors. The dermis is relatively
tough and not easily cut by the scissors. (h) After the graft has been defatted, the white appearance of the dermis can be
appreciated. (i) The donor tissue is laid onto the recipient site and positioned correctly. ( j ) Two simple interrupted sutures are
placed at opposite ends of the graft to secure it in place. Curved scissors are then used to trim the graft to fit the recipient site
exactly. (k) Simple interrupted sutures are placed to secure the graft in place. (l) Donor site repair with simple running suture

Hyper/hypopigmentation
Color mismatch may occur if the donor and
­recipient tissue have different degrees of actinic
damage. Superficial dermabrasion, dermasanding,
Erbium or carbon dioxide resurfacing can result
in a better color match when performed as early
as 6–8 weeks postgraft. However, these proce-
dures require additional wound care.
Pearls
• For grafts on the nose, place basting sutures oriented
along the alar groove to help recreate it (see Fig. 14-������
2�����
).
• If pleats develop along the circumference of
the graft, the graft is oversized and needs to be
trimmed down to size.
• Some surgeons prefer to harvest the graft using a
45° bevel, to match the bevel of the recipient site
following Mohs micrographic surgery.

ERRNVPHGLFRVRUJ
184 Dermatologic Surgery

Split-thickness grafts allows it to cover an even larger area while ena-

Indications
Split-thickness skin grafts are useful to cover
large defects and are more likely to take than full-
thickness grafts. Fenestrating or meshing the graft
Figure 14-2  Basting sutures help to secure the graft to the
wound bed and prevent shearing forces from disrupting
the graft–host interface
bling blood and serum to drain from beneath the
graft. For aggressive tumors and tumors with a
high chance of local recurrence, split-thickness
grafts are particularly useful because tumor recur-
rence can be easily observed due to the thinness
of the graft.
Contraindications
Split-thickness grafts have a poorer cosmetic out-
come than full-thickness grafts in terms of tex-
ture, color, and skin thickness. Contraction of the
recipient site is greater for split-thickness grafts
and, therefore, should be used with caution near
free margins. Specialized equipment is necessary
and creates a donor site that heals by secondary
intention.
Donor site selection
Donor sites heal by secondary intention and usu-
ally appear hypopigmented. Sites that are non-
exposed and easily accessible to the patient for
wound care tend to be favored, such as the upper
thigh, lateral hips, medial arms, lower back, and
abdomen.

a b

c d

Figure 14-3  Bolsters. (a) Full-thickness skin graft after placement. (b) Simple interrupted sutures are placed around
the perimeter of the graft. One end of the suture is cut short and the other end is left long. (c) Gauze impregnated with
petroleum jelly is placed over the graft to keep it moist. (d) The long ends of the suture are tied to one another to secure
the bolster

ERRNVPHGLFRVRUJ

a b
Figure 14-4  Necrosis. (a) Necrosis is characterized by a black, thick, tightly adherent crust or eschar. (b) It is best
to leave the necrotic graft intact to act as a biological dressing. With conservative wound care, the eschar will fall off,
revealing pink viable tissue underneath
Figure 14-5  Persistent elevation of the graft may be due
to the development of a hypertrophic scar or pincushioning
Technique (Fig. 14-�
6)
Free-hand grafts
A no. 10 or 15 blade can be used to harvest small
split-thickness grafts by hand. Alternatively, a
Weck blade, which is a long straight blade, may be
used to obtain larger split-thickness grafts by hand.
Free-hand grafts can be performed quickly and do
not require the use of specialized ­equipment.
Dermatome grafts
Powered dermatomes (driven electrically or pneu-
matically) can be used to harvest larger split-
thickness grafts and allow the harvesting of grafts
with consistent thickness. Graft thickness can be
selected by means of a lever on the dermatome.
Most grafts of the head and neck are 0.012–
0.016 inches thick. For recipient sites on the trunk
and extremities, grafts of 0.020–0.024 inches
are used.
ERRNVPHGLFRVRUJ
14
Chapter
Skin grafts 185
Complications
Split-thickness grafts are subject to many of the
same complications that may occur with full-
thickness grafts. Hematoma and seroma forma­
tion can be avoided by meshing the graft in
addition to tacking sutures or bolster dressings.
Owing to the decreased nutritional requirements,
split-thickness grafts are less likely to undergo
necrosis than full-thickness grafts. Split-thickness
grafts are not as durable and tend to develop ul-
cers in areas of mechanical trauma. Pain at the
donor site is common and may be ameliorated
with occlusive dressings.
Composite grafts
Composite grafts are used to replace defects that
are missing both cartilage and skin, such as full-
thickness loss of the alar rim. These grafts require
revascularization from the graft’s edge and thus
are usually small in size (less than 1 cm).
Donor site selection
The cartilage and skin of the ear is most often
used to repair nasal defects. Donor sites are se-
lected so that the harvested graft matches the
missing nasal tissue as closely as possible. The
crus or the helical rim is most commonly used
to reconstruct the ala. The conchal cartilage is
most commonly used to repair the nasal sidewall
or columella.
Technique (Fig. 14-7)
First, the recipient site must be made smooth so
that the planned graft may fit in precisely. Be-
cause revascularization from the sides is manda-
tory for graft survival, it is critical that a template
of the wound be drawn and then transferred to
the selected donor site. The template should be
slightly oversized to account for postoperative
186 Dermatologic Surgery

a b c

d e

g h i

Figure 14-6  Split-thickness skin graft. (a) This patient presented with a large morpheaform basal cell carcinoma on
the right cheek. (b) There is a large defect on the cheek following Mohs surgery. (c) A template on the right thigh is
drawn for the split-thickness skin graft. The graft taken may be smaller than the recipient site if meshing will be
performed. Hair within the template is shaved and a drop of mineral oil is applied to the donor site to facilitate the
harvest. (d) An electrically powered dermatome is used to harvest the graft using firm, steady, downward pressure on
the device. (e) Donor site after harvesting of the graft. Note the pinpoint bleeding. The donor site is allowed to heal by
secondary intention. (f) The split-thickness graft is put in a Petri dish with normal saline to keep it moist. (g) The graft has
been put through a mesher to increase its size and placed over the wound bed. Absorbable sutures may be placed to
secure the graft to the recipient bed. (h) The graft 4 days after placement. (i) Some 2.5 months later, the graft has fully
healed

contra­ction. The graft may be designed with wings
or struts that extend beyond the cutaneous por-
tion and fit into grooves at the recipient site for
additional mechanical security. If cartilaginous
wings are used, then a scalpel should be used to
incise a groove or pocket in the tissue adjacent to
the recipient site into which the struts of the com-
posite graft may be placed.
Sutures are placed to secure the graft to the
mucosal surface of the nose first. This secures and
aligns the graft at the recipient site. The cartilaginous
struts are placed into the pockets created previ-
ously. Sutures are placed around the perimeter to
secure the graft. Intranasal packing is placed fol-
lowed by petroleum jelly and gauze externally.
Complications
Composite grafts are subject to necrosis due to
inadequate revascularization. This is a particular
problem in smokers.

ERRNVPHGLFRVRUJ
 14

Chapter
Skin grafts 187

a b

c d

Figure 14–7  Composite graft. (a) Nasal ala defect following Mohs surgery for basal cell carcinoma. (b) Donor site of
composite graft at crus of helix drawn approximately 10% larger than the defect. (c) Donor site following excision of
composite graft. (d) Underside of helical composite graft illustrating cartilage on left side of graft, which will provide support
to the alar rim. (e) Composite graft sutured into place with petrolatum-coated dental roll in nostril

Christensen DR, Arpey CJ, Whitaker DC. Skin graft-

Further reading
Adams DC, Ramsey ML. Grafts in dermatologic
surgery: review and update on full- and split-
­thickness skin grafts, free cartilage grafts, and
composite grafts. Dermatol Surg 2005;31(8 Pt 2):
1055–1067.
ing. In: Robinson JK, Hanke CW, Sengelmann RD,
Siegel DM, eds. Surgery of the Skin. New York:
Elsevier Mosby, 2005:365–379.
Fader DJ, Wang TS, Johnson TM. Nasal reconstruc-
tion utilizing a muscle hinge flap with overlying
full-thickness skin graft. J Am Acad Dermatol
2000;43(5 Pt 1):837–840.

ERRNVPHGLFRVRUJ
188 Dermatologic Surgery

Geyer AS, Pasternack F, Adams C, Ratner D. Use of
a skin–fat composite graft to prevent alar notch-
ing: an alternative to delayed postoperative repair.
Dermatol Surg 2005;31(5):602–607.
Gloster HM Jr. The use of full-thickness skin grafts
to repair nonperforating nasal defects. J Am Acad
Dermatol 2000;42(6):1041–1050.
Gurunluoglu R, Shafighi M, Gardetto A, Piza-Katzer H.
Composite skin grafts for basal cell carcinoma de-
fects of the nose. Aesthetic Plast Surg 2003;27(4):
286–292.
Meads SB, Greenway HT, Eaton JS. Surgical pearl:
thermoplastic bolster dressing for full-thickness
skin grafts. J Am Acad Dermatol 2006;54(1):
152–153.
Shook BA, Peterson J, Wells MJ, Butler DF. The
beveled edge technique for harvesting of full-
thickness skin grafts. Dermatol Surg 2005;31(9 Pt
1):1128–1130.
Silapunt S, Peterson SR, Alam M, Goldberg LH.
Clinical appearance of full-thickness skin grafts of
the nose. Dermatol Surg 2005;31(2):177–183.
Stephenson AJ, Griffiths RW, La Hausse-Brown TP.
Patterns of contraction in human full thickness
skin grafts. Br J Plast Surg 2000;53(5):397–402.

ERRNVPHGLFRVRUJ

Nail surgery
Elizabeth Magill Billingsley
Key Points
• Nail surgery can be relatively painless when
performed properly.
• Patient relaxation is important for nail surgery to
run smoothly.
• It is important to discuss the risk of permanent
nail dystrophy and obtain informed consent prior
to the procedure.
• Avoid unnecessary trauma to the proximal nail
matrix to minimize the chance of permanent nail
dystrophy.
• Perform biopsies no larger than 3 mm if possible.
• Orient excisions in the nail matrix transversely,
and excisions in the nail bed longitudinally for
optimal results.
• The distal matrix produces the undersurface
of the nail plate. Small wounds in this area are
unlikely to produce a visible nail defect.
• The proximal matrix produces the dorsal surface
of the nail plate. Large wounds in this area have
the greatest potential to produce a visible nail
defect.
• Explain postoperative instructions clearly.
Introduction
Surgical procedures involving the nail unit may
be necessary to diagnose inflammatory disorders
or neoplasms. They may also be therapeutic, as
when removing a growth or relieving the discom-
fort of an ingrown nail. Many nail procedures,
such as avulsions, matrixectomy, and biopsies, can
be simple to perform in an office setting. With
experience, they can be performed quickly, and
planned so as to minimize the risk of permanent
nail dystrophy (Box 15-� 1).
Anatomy
Before undertaking any nail procedure, it is
­important to have a thorough understanding of
nail unit anatomy (Fig. 15-�
1).
The most important structure in the nail unit
is the nail matrix. The matrix is the germinative
epithelium from which the nail plate is gener-
ated. The distal nail matrix, often visible through
ERRNVPHGLFRVRUJ
15
Chapter
the proximal nail plate, is called the lunula. The
proximal matrix forms the dorsal surface of the
nail plate, and the distal matrix is responsible for
the ventral portion, or underside, of the plate. This
anatomic concept is important when performing
nail unit surgery because damage to the proxi-
mal matrix is likely to produce a visible perma-
nent nail dystrophy. This is in contrast to surgery
of the distal matrix, which may produce a nail
deformity that is not visible because it is on the
undersurface of the nail plate. The nail bed, some-
times called the sterile matrix, extends from the
lunula to the hyponychium. The hyponychium is
the end of the nail bed and the beginning of the
normal volar epidermis. The proximal and lateral
nail folds surround and support the nail plate. The
cuticle is the distal extension of the proximal nail
fold, and serves to seal and protect the proximal
nail fold from external pathogens and irritants.
The vascular supply to the nail unit and distal
digit is derived from the paired proper palmar and
plantar arteries. These arteries travel along the lat-
eral aspects of the digit, and form a series of arcades
supplying blood to the proximal nail fold, matrix,
nail bed, and end of the digit. The paired palmar
and plantar nerves run in close apposition to the
blood vessels, along the lateral aspects of the digit.
The extensor tendon of the digit is an impor-
tant anatomic structure. This tendon attaches in
a broad distribution approximately 12 mm proxi-
mal to the proximal nail fold. Extensive damage
to this tendon attachment, either with a ­surgical
B ox 1 5 - 1
Keys to successful nail surgery
• Patient relaxation – calm atmosphere, positioning
• Communication – expectations of the procedure and post­
operative period
• Painless anesthesia (relatively!) and painless procedure
• Proper instruments
• Appropriate knowledge of nail anatomy and surgical technique
190 Dermatologic Surgery
Proximal nail fold
Bone Nail matrix
Figure 15-1  Nail unit anatomy
instrument or through excessive heat with ­cautery
or laser, could result in difficulty with full exten-
sion of the tip of the digit.
Preoperative considerations
As with any surgical procedure, a thorough
medical history should be obtained prior to
performing nail surgery. Although not absolute
­contraindications to surgery, a history of pe-
ripheral vascular disease, collagen vascular dis-
ease, diabetes, or a bleeding disorder should be
noted. Prophylactic antibiotics may be indicated
in ­ patients who have artificial heart valves or
other risk factors for endocarditis. The patient’s
medications should be reviewed, with specific
attention to anticoagulants. Patients on aspirin,
warfarin, clopidogrel, and certain supplements
may have increased operative and postoperative
bleeding, and will need extra attention paid to
hemostasis. Allergies to medications should be
recorded.
Photographs should be taken preoperatively,
especially for pigmented streaks, neoplasms, and
where there is significant risk of permanent nail
dystrophy. These photos could be helpful in a
medicolegal situation to document the location
of the lesion and the need for the procedure to
be performed. Photos are also very helpful for
teaching purposes. When there is suspicion that
there may be an underlying bony process, such
as a subungual exostosis, or invasive malignancy,
radiographs are helpful to delineate the extent of
the neoplasm.
Prior to the procedure, it is extremely impor-
tant to spend time in consultation with the patient
explaining the procedure, expectations of pain,
and postoperative limitations. Risk of permanent
nail dystrophy should also be explained fully and
informed consent should be obtained. Patients
generally have many questions, and time spent
ERRNVPHGLFRVRUJ
Cuticle
Lateral nail fold
Nail plate
Hyponychium
Nail bed
a­ ddressing these concerns prior to undergoing
the procedure is extremely beneficial (Box 15-�
2).
Anesthesia
Perhaps the most anxiety-provoking aspect of nail
surgery is the patient’s fear of pain from adminis-
tration of the local anesthetic. Nail surgery can be
performed with significantly less anxiety when at-
tention is focused on minimizing the discomfort
of this part of the procedure. Patient relaxation is
very important to lessen the real and perceived
discomfort of the injection. Placing the patient in
a supine position and creating a relaxed atmos-
phere in the surgical room, through a reassuring
and confident staff, can help to calm an anxious
patient. Music can also be helpful.
A digital nerve block is an excellent means
of decreasing the pain of achieving anesthesia in
the distal nail unit. This is far less painful than
­injecting directly into the nail unit. As small vol-
umes of anesthetic are needed for this procedure,
2% plain lidocaine is an excellent choice of an-
esthetic. If prolonged anesthesia is required, sup-
plemental 0.25% bupivacaine can be also be used.
Recent literature has suggested the use of epine-
phrine in digital blocks is generally safe, and may
be helpful for minimizing operative bleeding, but
should be avoided in patients with peripheral vas-
cular disease.
To perform the digital nerve block, a 30-
gauge needle is placed at the midline of the
medial and lateral aspects of the base of the
digit. An initial small bleb of anesthetic is in-
jected very ­ superficially (Fig. 15-� 2). Addi-
tional anesthetic is administered slowly, while
advancing the needle deep in the skin toward
the bone. The needle is then withdrawn slightly
and advanced toward the dorsal and then vol-
ar aspects of the digit. It is important that the
needle is advanced in a linear fashion and that

B ox 1 5 - 2
Preoperative considerations
• Medications: anticoagulants
• Allergies
• Medical history: peripheral vascular disease, diabetes, bleed­
ing diathesis, prosthetic valves, collagen vascular disease
• Photos or digital images
• X-rays: subungual exostosis, enchondroma, tumor with bony
invasion
• Counseling: expectations of discomfort, time for nail regrowth,
postoperative footwear, possible difficulty with work
• Consent: risk of permanent nail dystrophy
Figure 15-2  Digital block at base of thumb
great care is taken to avoid any lateral motion,
which may cause laceration of the digital neu-
rovascular bundle. ­ Approximately 1.0–1.5 mL
of anesthetic on each side of the digit should
be adequate, Another approach that may pro-
duce even less discomfort is to inject the lido-
caine into the adjacent web space to access a
more proximal aspect of the nerve (Fig. 15-� 3).
It is very important to allow enough time for
the anesthesia to take effect. Usually 10–15 min
is sufficient. Sensation of the distal digit should
then be assessed. If the patient still has sensa-
tion, the options include allowing more time for
the block to become fully effective, or adding
supplemental anesthetic in a wing block fash-
ion. A wing block is accomplished by injecting
a small amount of anesthetic at the junction
of the proximal and lateral nail folds (Fig. 15-
4). The needle is advanced slightly toward the
tip of the digit, and then across the proximal
nail fold. Many surgeons choose the wing block
as the preferred method for anesthesia of the
digit.
ERRNVPHGLFRVRUJ
15
Chapter
Nail surgery 191
Figure 15-3  Digital block in web space
Figure 15-4  Wing block of thumb
Surgical instruments
The instruments needed on a surgical tray for a
nail procedure will be determined by the pro-
cedure being performed (Fig. 15-� 5). The Freer
­septum elevator is very useful for nail avulsions,
and the English nail splitter is important for
­partial nail avulsions. Other instruments that are
often used are listed in Box 15-�3.
Hemostasis
Hemostasis during nail surgery may be obtained
by a variety of means. Electrocautery is effective
for spot hemostasis during biopsies and along
lateral nail fold incisions. Gel foam and pressure
may be useful for punch biopsies or on an oozing
wound. Aluminum chloride may also be useful,
especially on the nail bed. Lateral compression of
the digital artery by a surgical assistant is very ef-
fective in minimizing bleeding during the proce-
dure. For larger procedures, and ones where a very
dry field is necessary, a clamped Penrose drain can
192 Dermatologic Surgery
Figure 15-5  Surgical tray for nail procedures. From left to
right – bottom: English nail splitter, Freer septum elevator,
hook, hemostat, curette, nail-pulling forceps, penrose
drain; top: gauze, scalpel, marker, urethral swabs, phenol
B ox 1 5 - 3
Surgical instruments
• Freer septum elevator or nail spatula
• English nail splitter
• Hemostat
• Nail-pulling forceps
• Scalpel
• Marker
• Penrose drain
• Miscellaneous: curette, punch biopsy, forceps, scissors
serve effectively as a tourniquet. ­Another option
for hemostasis is placing a sterile glove on the pa-
tient’s hand with the glove fingertip cut off and
rolling it back on itself to the base of the digit
(Box 15-� 4).
Procedures
Nail avulsion
Nail avulsion is the most basic nail surgical proce-
dure and may involve partial or complete removal
of the nail plate. Avulsions are often performed to
allow visualization of the underlying nail unit for
biopsy or excision. Partial or complete avulsions
may also be performed to improve discomfort
of an ingrown nail, or allow drainage of a paro-
nychia. The basic surgical concept of an avulsion
is to ­remove the nail plate from its attachments
to the nail bed, nail matrix, and surrounding nail
folds.
Distal nail avulsion
After cleansing the hand or foot with surgical
antiseptic scrub, a digital block or wing block is
performed. Once adequate anesthesia is obtained,
ERRNVPHGLFRVRUJ
B ox 1 5 - 4
Hemostasis
• Cautery
• Penrose drain
• Gel foam
• Aluminum chloride
• Pressure, lateral compression
Figure 15-6  Freer septum elevator being used to separate
nail plate from nail bed
a Freer septum elevator or dental spatula is used
to separate the distal end of the nail plate from
the nail bed (Fig. 15-�
6). The instrument is pushed
firmly in a proximal direction, aiming it upwards
toward the nail plate to avoid injury to the under-
lying nail bed. The instrument is then removed
and reinserted multiple times, gradually advanc-
ing proximally until the matrix is reached, identi-
fied by a marked decrease in resistance. Care must
be taken to avoid damaging this area of the nail
unit with aggressive pushing. After the nail plate
has been separated from the nail bed and the sur-
rounding nail folds, a hemostat or nail-pulling
forceps may be used to gently remove the nail,
either in a rolling side-to-side motion or with a
direct pulling motion (Fig. 15-� 7). After the nail
is removed, hemostasis can usually be accom-
plished with direct pressure (Box 15-� 5). If that
is inadequate, spot electro­cautery or aluminum
chloride may be used.
Proximal nail avulsion
Nail avulsion via a proximal approach may be
necessary when there is significant distal sub-
ungual debris or damage, or if there is no distal
free nail edge. In these cases, the instrument is
inserted beneath the proximal nail fold, and
aimed proximally until it reaches the beginning
of the nail plate. It is then rotated under the nail
plate, and advanced distally, gently separating the
nail matrix and nail bed from the plate (Figs 15-8
& 15-9).
 15

Chapter
Nail surgery 193

a b

Figure 15-7  Nail avulsion performed by (a) direct pulling motion or (b) rolling the nail plate, assuring removal of lateral
aspects of nail

Figure 15-8  Proximal nail avulsion using Freer septum

elevator
Figure 15-9  Freer septum elevator gently separating nail
plate from nail bed in proximal approach

B ox 1 5 - 5
Nail avulsion Nail matrixectomy
Matrixectomy is performed when the goal is perma-
• Clean procedure
nently to remove all or part of the nail, and prohibit
• Digital block further nail growth. The most common indication
• Insert nail spatula or Freer septum elevator under distal free for this is recalcitrant ingrown nails (onychocrypto-
edge of nail sis), but this procedure may also be performed for
• Gently push instrument proximally, avoiding damage to the
other reasons, such as deformed nails or fungal dis-
nail bed and matrix ease. Matrixectomy may be achieved by excision or
ablation. Excisional techniques include cold steel,
• Remove and reinsert several times until plate is free from bed electrosurgery, or laser. More commonly, ablative
and nail folds
techniques that achieve chemical destruction of the
• Remove nail plate in rolling or pulling motion matrix are performed. The most common chemical
used for this purpose is phenol (88% carbolic acid),

ERRNVPHGLFRVRUJ
194 Dermatologic Surgery
which must be kept in a dark bottle, and must not
have exceeded its expiration date (Box 15-�
6).
Partial matrixectomy
Partial matrixectomy destroys the lateral aspect of
the nail matrix, and allows the central portion
of the nail to remain for cosmetic and functional
importance. Phenol matrixectomy is performed
as a clean, but not sterile, procedure. After a dig-
ital block is performed, an English nail splitter is
used to make an incision approximately 2–4 mm
from the lateral edge of the nail. The incision is
advanced proximally, by gently inserting the blunt
end of the splitter underneath the proximal nail
fold until the proximal aspect of the nail plate is
cut (Fig. 15-10). Next, the Freer septum elevator
is used gently to separate the nail plate from the
nail bed in this area, and this portion of the nail
plate is then removed. Care should be taken to
ensure that the most proximal and lateral aspects
of nail in the proximal groove are included.
The next step is the destruction of the matrix.
A bloodless field is necessary as blood minimizes
the effectiveness of phenol. Once this is achieved,
a cotton-tipped applicator is then saturated with
B ox 1 5 - 6
Nail matrixectomy using phenol
• Clean procedure
• Partial or complete nail avulsion
• Obtain a bloodless field
• Apply phenol with small cotton swab or urethral swab to
proximal matrix
• Apply to deep corners for partial matrixectomy, to entire
matrix for complete matrixectomy
• Rinse with alcohol or saline after 30–60 s
• Repeat phenol application and rinse again
Figure 15-10  English nail splitter being used to incise
lateral portion of nail plate
ERRNVPHGLFRVRUJ
phenol solution. It is inserted underneath the nail
fold and advanced onto the lateral corner of the
matrix. It is important that the swab reaches the
most proximal and lateral horns of the matrix to
prevent regrowth of nail spicules. Urethral swabs,
which are smaller than most cotton-tipped appli-
cators, can be more effective in reaching under-
neath the nail fold and limiting any inadvertent
contact with the nail fold (Fig. 15-11). Petrolatum
may be placed along the nail folds to prevent dam-
age to the surrounding skin. The phenol is left in
place for 30–60 s and rinsed with alcohol or saline.
This procedure is then repeated. A curette may
be helpful to remove any granulation tissue along
the nail folds or any residual necrotic tissue in
the treated area. Corticosteroid injected into the
proximal and lateral nail fold helps to minimize
postoperative discomfort. Triamcinolone, 5 mg/mL
is often used. Phenol is an effective coagulant, and
has antiseptic as well as local anesthetic properties.
Chemical matrixectomy can also be performed
using 10% sodium hydroxide, applied for 1 min,
and then neutralized with 10% acetic acid.
Complete matrixectomy
Complete matrixectomy is performed when the
goal is permanent removal of the entire nail plate.
A complete nail avulsion is performed, followed
by application of phenol to the entire nail matrix.
Electrodessication and curettage, electrosurgery,
laser, and surgical excision are other approaches
for complete matrixectomy.
Nail unit biopsy
Biopsy of the nail unit may be necessary to diag-
nose a dermatosis, such as psoriasis, a tumor such
as squamous cell carcinoma, or to determine the
cause of a pigmented streak. The biopsy may be
done via a punch through the nail plate, or after
nail avulsion. Nail matrix and nail bed lie in close
proximity to periosteum, and these procedures
should be performed using sterile technique to
Figure 15-11  Urethral swab saturated in phenol, prior to
placing underneath nail fold

prevent osteomyelitis. Also, great care should be
taken to handle the biopsy specimen carefully, as
crushing the tissue can produce artifact making
histologic interpretation much more difficult.
Biopsy of pigmented streak
Pigmented streaks should be biopsied at the
most proximal aspect of the streak. If the origin
of the streak is visible through the nail plate, a
punch ­biopsy may be adequate for diagnosis. This
is most easily done with a larger punch, such as
a 4 or 5 mm, to remove the overlying nail plate,
followed by a 3-mm punch to remove the desig-
nated nail bed or matrix. Ink placed on the super-
ficial surface of the biopsy can aid in specimen
orientation for proper embedding. If the origin of
the pigmented streak is proximal to the lunula,
the proximal nail fold may need to be reflected.
This is accomplished by making two 5-mm re-
leasing incisions at the junction of the proximal
and lateral nail folds. These should extend at an
angle towards the lateral aspects of the digit. The
proximal nail fold is then reflected back, and held
in place with retaining sutures that can be secured
with a hemostat, or by using a skin hook. The
proximal matrix should then be visible. A single
punch may be used for both the thin proximal
nail plate and the underlying tissue (Fig. 15-12).
Complete nail avulsion may be performed to
facilitate a biopsy and allows the entire nail unit
to be examined. Avulsion is also often necessary
for complete removal of tumors, or to obtain a
shave biopsy of the nail unit. It is very helpful to
ink the proximal nail fold in line with the area to
be biopsied prior to avulsing the nail, as biopsy
Figure 15-12  Punch biopsy of matrix after reflecting
proximal nail fold. Note ink on proximal nail fold indicating
location of streak
ERRNVPHGLFRVRUJ
15
Chapter
Nail surgery 195
location may become difficult to identify once
the nail plate is removed. To visualize the entire
matrix after nail avulsion, it may be necessary to
reflect back the proximal nail fold, as described
above (Fig. 15-13). A shave or saucerization can
be used to remove the lesion in question.
Nail matrix biopsy
When possible, biopsies of the nail matrix should
be performed in the distal matrix to minimize
visible permanent nail dystrophy. Ideally, punch
biopsies should be 3 mm or less, and these small
biopsies do not need to be sutured in the mid and
distal matrix. Biopsies 3 mm or larger in the proxi-
mal matrix should be sutured to minimize the po-
tential for nail dystrophy. Another technique for
sampling matrix tissue is the shave biopsy. Shave
biopsies can be performed for larger lesions and
for lesions in the proximal matrix. This method
has less risk for causing permanent nail dystrophy.
­Elliptical excisions of the nail matrix should be ori-
ented transversely, and with careful undermining
of the matrix, may be sutured with an absorbable
or nylon suture. This would result in a uniformly
thinner nail rather than a longitudinal split. It is
important not to interfere with the curvilinear dis-
tal border of the lunula in order to prevent distal
onycholysis and abnormal curvature of the distal
free nail edge (Box 15-� 7).
Nail bed biopsy
Punch biopsies of the nail bed that are 3 mm or
less do not need to be sutured. Elliptical excisions
of lesions, such as a glomus tumor, should be ori-
ented longitudinally, and with careful undermin-
ing above the periosteum they may be sutured to
minimize the risk of onycholysis.
Figure 15-13  Reflection of proximal nail fold using skin
hook, revealing matrix lesion
196 Dermatologic Surgery
En bloc excision
Longitudinal resection or wedge resection in-
volves the removal en bloc of nail folds, nail
plate, nail bed, matrix, and hyponychium. This
may be necessary to help with diagnosis of ­lateral
­longitudinal pigmented bands and for some in-
flammatory conditions that involve many parts of
the nail unit. It is performed by making an exci-
sion through the proximal nail fold, matrix, nail
plate and nail bed, and through the lateral nail
fold on the other side (Fig. 15-14). The specimen
is removed en bloc, and the wound is sutured or
allowed to granulate (Fig. 15-15).
Lesions arising in or underneath the proximal
nail fold, such as mucous cysts, can produce sig-
nificant nail dystrophy due to pressure on the un-
derlying matrix. These lesions can be excised by
reflecting back the proximal nail fold and remov-
ing the lesion, or by an en bloc excision of the
proximal nail fold. These en bloc excisions should
be symmetric across the width of the digit to al-
low for aesthetic healing, and are allowed to heal
by second intention. Significant care must be tak-
en not to damage the underlying matrix. A Freer
septum elevator placed underneath the proximal
nail fold can protect the matrix from inadvertent
damage (Fig. 15-16).
B ox 1 5 - 7
Nail matrix biopsy
• Sterile procedure
• May be performed through the nail plate or after nail avulsion
• 3 mm or smaller punch if possible
• Distal matrix rather than proximal matrix if possible
• Elliptical biopsies should be oriented transversely, under­
mined, and sutured
Figure 15-14  En bloc excision Figure 15-15  Sutured wound after
of lateral nail fold, including en bloc excision of lateral nail fold
hyponychium, nail plate, nail bed, lesion
matrix, and proximal nail fold
ERRNVPHGLFRVRUJ
Postoperative management
Immediately after the procedure, the area should
be cleansed and dried. It is helpful to hold direct
compression for a few minutes to ­ensure hemos-
tasis. The bandage should be absorbent, nonad-
herent, bulky, and nonconstrictive. An initial layer
of petroleum jelly should be used to protect the
wound bed. Vaseline-impregnated gauze is also
useful. The next layer consists of nonadherent
gauze, followed by an additional layer of gauze
for absorption and protection. The securing layer
must hold the bandage in place but not be con-
strictive, and can be a metal frame or tape. For
toe-nail surgery, an open-toed shoe may improve
comfort.
Patients need to be educated about their
­expectations of postoperative pain and possible
limitations in activities. Nail surgical patients may
or may not experience significant pain. Postop-
erative pain management should consist initially
of elevation of the affected area and adminis-
tration of acetaminophen or nonsteroidal anti-
­inflammatory agents (NSAIDs). If pain is not
adequately managed with these interventions,
a prescription pain medication may be needed.
A prescription sent home with the patient with
instructions to fill only if needed can be helpful.
Also, taking acetaminophen or NSAIDs before
the local anesthetic has worn off, and on a regular
schedule in the first 24–48 h, may minimize any
postoperative pain.
After 24 h, the initial bandage may be re-
moved. The wound should be cleansed once or
twice daily with soapy water, gently loosening
any debris. Soaking may be helpful to loosen an
adherent bandage or debris, or if there is much
swelling. The new bandage should be nonadher-
ent, absorbent, protective, and secure. Petroleum
Figure 15-16  En bloc removal of
proximal nail fold mucous cyst. Note
Freer septum elevator being used to
protect underlying matrix
 15

Chapter
Nail surgery 197

B ox 1 5 - 8 complications are rare. There are reports in the

Postoperative considerations
• Wound care – written and verbal instructions, bandaging
• Elevation
• Pain management – acetaminophen, ibuprofen, narcotics
• Soak wound – swelling, debris
literature of pyogenic granuloma formation and
reflex sympathetic dystrophy occurring following
nail surgery.
The most important complication of nail sur-
gery is permanent nail dystrophy. In most cases,
this can be anticipated, discussed with the patient
preoperatively, and, with surgical attentiveness,
minimized.

jelly and an adhesive bandage may be sufficient Pearls

for the fingers, but an additional layer of gauze
may be necessary on a toe, to help cushion as well Nail surgery pearls
as absorb drainage (Box 15-�8). Take preoperative photos
Good patient counseling
Complications Use a marker for biopsies prior to removing the nail
plate
As with all surgical procedures, complications
such as bleeding, infection, and pain may occur. DON’T CRUSH THE SPECIMEN
Antibiotics are not given routinely in nail surgery, Orient matrix biopsies transversely, nail bed
and an appropriate antibiotic should be prescribed biopsies longitudinally
only when there is a culture-proven infection. When possible, biopsy the distal matrix rather than
Osteomyelitis and septic arthritis can occur, but the proximal matrix
fortunately, with proper surgical technique, these

ERRNVPHGLFRVRUJ

Mohs micrographic
surgery
Justin G. Woodhouse and Allison T. Vidimos
Key Points
• Mohs micrographic surgery is a specialized
surgical technique for skin tumor extirpation.
• Mohs surgery incorporates horizontal frozen-
section processing and specialized mapping to
enable evaluation of the entire excised surgical
margin.
• For neoplasms of the skin that grow in continuity,
Mohs surgery offers the highest cure rate while
minimizing the amount of normal skin sacrificed
for tumor removal.
• Mohs surgery requires specialized training in
cutaneous tumor biology, surgical technique,
histopathologic interpretation, and subsequent
reconstruction.
• The success of Mohs surgery is predicated
on the concept of continuous tumor spread
from a single focus, and is also dependent on
the resources and skills of the surgeon and
histotechnician.
• When used for the proper indications, Mohs
surgery is cost effective, but generally more
expensive and labor intensive than conventional
methods of tumor removal.
• With proper technique and preoperative
preparation, Mohs surgery has an exceedingly
low complication rate.
History
Mohs micrographic surgery was initially concep-
tualized by Dr Frederic Mohs at the University of
Wisconsin in the 1930s when he began to use zinc
chloride paste for fixation of tissue in vivo. Zinc
chloride has been used as an escharotic treatment
of cancer since the 1800s but Mohs incorporated
microscopic examination of tissue at the time of
tumor removal. Subsequently, the need for addi-
tional marginal tissue could be determined while
the patient was still in the office. Using a special
method of tissue processing, he devised a way to
evaluate 100% of excised surgical margins. Sub-
sequently, Stegman and Tromovitch modified
the technique and used the currently preferred
method of fresh tissue processing, without the
ERRNVPHGLFRVRUJ
16
Chapter
use of zinc chloride paste . The ­American College
of Mohs Micrographic Surgery and ­ Cutaneous
­Oncology was established in 1967 and currently
has nearly 800 members, all of whom have re-
ceived advanced fellowship training in Mohs sur-
gery, pathology, and reconstructive surgery.
Skin cancer treatment
overview
Skin cancer is a general term for any tumor devel-
oping from the cutaneous structures within the
epidermis, dermis, or subcutaneous tissue imme-
diately deep to the dermis. There are more than
two dozen distinct tumors that arise from specific
cell types within any of these tissue planes. Basal
cell carcinoma (BCC) is the most common skin
cancer, and squamous cell carcinoma (SCC) is the
second most common.
Many treatment modalities have been devised
for the elimination of skin cancer. The most com-
monly used skin cancer treatments include simple
excision, electrodessication and curettage, cryo-
surgery, radiation therapy, topical chemotherapy,
and Mohs micrographic surgery. Many variables
should be taken into consideration when choosing
the most optimal therapy for any given patient
(Box 16-� 1). Certainly, the ultimate success of any
given modality is predicated on the skill and ex-
perience of the physician, but approximate cure
rates for each modality are listed in Table 16-1. In
general, all non-Mohs surgery modalities result in
lower cure rates when employed for tumors on
the head versus the trunk or extremities.
Mohs concepts
The two main advantages of Mohs surgery are
(1) histologic confirmation of tumor removal
with a very high cure rate, and (2) normal tissue
preservation. In all cases, the most important pri-
mary goal is eradication of the tumor. Regardless
of the final cosmetic outcome, tumor recurrence
200 Dermatologic Surgery

B ox 1 6 - 1 The outstanding cure rate offered by Mohs

surgery is due to the meticulous evaluation of
Important factors influencing treatment 100% of the excised surgical margins. This same
modalities for skin cancer aspect of Mohs surgery allows the surgeon to cut
in very close proximity to the perceived margin
Treatment factors of the tumor. This will inherently lead to maximal
Physician skill and competence tissue preservation, which is the secondary goal
of Mohs surgery. Oftentimes, the tumor is rela-
Cure rate inherent to treatment tively well demarcated and this approach permits
Morbidity a very small postoperative defect without sacrific-
Cost and access ing overall cure rates. On the other hand, aggres-
sive or recurrent tumors are better likened to an
Cosmetic outcome
iceberg with a substantial imperceptible tumor
Effect on/preservation of local anatomic structures vs other burden tracking under the surface of the skin. In
modalities this instance, the microscope helps to guide the
surgeon in determining where additional tumor-
Patient factors laden skin needs to be removed. In each case, the
General health and co-morbid conditions surgery is designed to remove only cancerous skin
(immunosuppression, diabetes, hypertension) and thus spares normal skin, inherently maximiz-
Patient support system and wound care needs ing cosmetic outcome and the function of local
anatomic structures.
Age and life expectancy
The relative importance of tissue preservation
Cosmetic concerns changes somewhat for any given patient and tu-
mor location. For example, tissue preservation on
Disease factors the cheek of an 87-year-old man with a multiply
Tumor type and subtype recurrent infiltrative BCC is less important than
Anatomic location in a 43-year-old woman with a primary BCC on
the cheek. In the case of the elderly man, the
Size value of Mohs over wide excision is margin con-
Presence or absence of perineural invasion trol and ultimate cure rate. Figure 16-� 1 depicts
Growth pattern a tumor with finger-like infiltrative extensions of
cancer under the surface of the skin. The initial
Primary vs. recurrent
saucerized portion of skin is removed and the skin
Prior irradiation of area edges and undersurface of the skin are evaluated.
The tumor is found in the deeper dermis in one of
the quadrants and a subsequent specimen is taken
in that area to clear the tumor.
Table 16-1  Cure rates for different skin cancer Mohs micrographic surgery has several indi­
treatment modalities cations, which are listed in Box 16-� 2. From a
5-year cure rate (%) practical standpoint, the indications are situa-
BCC SCC
tions where other modalities are much more
likely to lead to recurrence, increased morbid-
Surgical excision 89.9 91.9 ity and eventually increased cost. Several pub-
Cryotherapy 92.5 NA lications have validated the cost-effectiveness
Electrodessication and curettage 92.3 96.3
of Mohs surgery when used for appropriate
indic­ations.
Radiotherapy 91.3 90.0 Mohs is most commonly used for cutaneous
Mohs surgery 99.0 96.9 neoplasms on the face, and is particularly im-
NA, not applicable. Source: Rowe DE, Carroll RJ, Day CL J Dermatol Surg
portant in the H zone of the face (Fig. 16-� 2). In
Oncol 1989;15:315–328 & J Am Acad Dermatol 1992;26:976–990. these areas, tumors have higher recurrence rates
and are often more aggressive and invasive. This is
likely due in part to the relative ease of invasion
­ bviates success. Accordingly, tumor extirpation
o through natural embryonic fusion planes.
via Mohs surgery requires meticulous, precise Many different cutaneous tumors can be re-
surgical incisions and tissue markings to mini- moved via Mohs surgery and these are listed in
mize the possibility of error in the processing Box 16-� 3. By far the most common tumor is BCC,
stage of the operation. Likewise, timely and followed by SCC. Some of the tumors listed are
careful mounting, sectioning, and staining by the more commonly treated with other methods, or
Mohs laboratory histotechnician is paramount to the use of Mohs surgery is controversial. In the
cure and operational success. case of rare tumors, it is most beneficial for the

ERRNVPHGLFRVRUJ
 16

Chapter
Mohs micrographic surgery 201

Figure 16-1  The tumor is removed in a saucer-shaped section and divided into pieces for processing. Evaluation of all
excised margins reveals skin cancer present at one of the dermal edges of excision. This area is subsequently excised to
remove the rest of the tumor

B ox 1 6 - 2
Indications for Mohs surgery
• Facial tumors, particularly in H zone, lips, eyelids, ears
• Recurrent tumors
• Tumors 1 cm or greater on the neck or face
• Aggressive pathology on hands, feet, genitals
• Tumors 2 cm or greater in areas other than face
• Positive margins on recent excision Highest Intermediate Lowest
• Poorly defined borders obviating margin control
Figure 16-2  “H zone” of the face indicating areas of
• Radiation-induced tumors particular recurrence risk
• Tumors with perineural invasion on biopsy
• Deeply infiltrating tumors exhibiting difficulty in estimating
tumor depth patient to be treated at a center with more expe-
• Tumor occurring in an old scar or wound (Marjolin’s ulcer) rience of treating that particular type of cancer.
• Tumor in a patient with basal cell nevus syndrome
• Tumor in a patient with xeroderma pigmentosa Mohs preoperative evaluation
• Tumor in patients with proven difficulty with skin cancer – Prior to surgery, several factors are important to
immunocompromised or organ transplant patients address for optimal outcomes. Once Mohs surgery
has been deemed appropriate for the given tumor

ERRNVPHGLFRVRUJ
202 Dermatologic Surgery
B ox 1 6 - 3
Tumors potentially treated with Mohs
surgery
• Basal cell carcinoma (BCC)
• Squamous cell carcinoma (SCC)
• Lentigo maligna (LM)
• Dermatofibrosarcoma protuberans (DFSP)
• Atypical fibroxanthoma (AFX)
• Microcystic adnexal carcinoma (MAC)
• Desmoplastic trichoepithelioma (DTE)
• Verrucous carcinoma
• Keratoacanthoma (KA)
• Erythroplasia of Queyrat
• Extramammary Paget’s disease
• Sebaceous carcinoma
• Apocrine carcinoma
• Bowen’s disease
• Bowenoid papulosis
• Leiomyosarcomaa
• Malignant fibrohistiocytomaa
• Merkel cell carcinomaa
• Angiosarcomaa
• Melanomaa
aCase reports and controversial
and patient, various medical and psychologic issues
are taken into consideration during evaluation and
preparation of the patient for surgery. Important
questions to address are included in Box 16-�4.
The procedure
The area is cleansed with a surgical scrub, typi-
cally Betadine® or chlorhexidine. The perceived
tumor margins are carefully marked along with
important cosmetic lines and units using a surgi-
cal pen or gentian violet (Fig. 16-�3).
The area is infiltrated with local anesthetic, typ-
ically 1% lidocaine with epinephrine 1 : 100 000.
Lidocaine is the most commonly used anesthetic
but the surgeon may choose to use another an-
esthetic based on its duration of action, cost, or
allergenic potential. Some individuals have an
intolerance to epinephrine, and plain lidocaine
can be used in these circumstances. To minimize
the stinging sensation that occurs from injec-
tion of unbuffered acidic lidocaine, the lidocaine
can be buffered with sodium bicarbonate in a
ratio of one part bicarbonate to nine parts lido-
caine. Slow injection of the anesthetic will also
­decrease the uncomfortable burning sensation
ERRNVPHGLFRVRUJ
B ox 1 6 - 4
Preoperative evaluation
• Medications and allergies – anticoagulants, anesthetics, and
surgical scrubs may need to be adjusted
• Propensity for infection at surgical site or elsewhere –
indications for preoperative and postoperative antibiotics
• Alcohol and tobacco history
• Presence of implants such as defibrillators, pacemakers, or
deep brain stimulators that affect choice of hemostatic device
• Necessity of preoperative imaging based on tumor character-
istics and symptoms
• Preoperative consultations (plastics, oculoplastics, head and
neck surgeons)
• Psychological preparation of the patient, particularly when
defect is expected to be large, disfiguring, or potentially to
lead to long-term structural damage or nerve dysfunction
Figure 16-3  The estimated tumor margins are marked
with ink and the area is surgically scrubbed and
anesthetized
that can occur with infiltration. Furthermore,
pinching the adjacent skin while inserting the
needle through a pore can decrease the pain of
needle insertion. Ideally, the anesthetic is allowed
to penetrate the larger nerves in the area for
5–10 min, and this will also allow time for the
vasoconstrictive action of epinephrine to set in.
Typically, a debulking procedure is performed
prior to excision of the first Mohs layer (Fig. 16-�
4).
The tissue of most interest is the border of nor-
mal tissue surrounding the tumor. Accordingly,
gross pathologic tissue is usually removed and
discarded, although many exceptions to this oc-
cur. If the tumor is particularly large or exophytic,
tissue scissors or a scalpel may be used to remove
obvious tumor mass. More commonly, curettage
is employed to remove gross tumor and delineate
gross tumor margins. Skin cancer is usually very
friable and easily parts with normal tissue when
using a ­curette. A rough estimate of tumor width
 16

Chapter
Mohs micrographic surgery 203

Figure 16-4  Tumor is often debulked with a curette to aid Figure 16-6  Hash marks are placed in the skin and tumor
in determination of initial incisions for orientation purposes

Figure 16-5  Tumor is excised with a 1–2-mm margin of Figure 16-7  The tissue is excised, keeping the deep
normal appearing skin. The scalpel is kept at an angle to margin in the same plane parallel with the surface of the skin
bevel the skin edge and facilitate processing in the lab

and depth helps to guide the surgeon with regards

to the initial Mohs specimen (layer).
The initial layer is then excised with a scalpel
(Fig. 16-�5). Although some authors have argued
that incisions should be made perpendicular to
the skin, a traditional bevel of the scalpel is most
commonly employed. The bevel of approximately­
45° allows easier orientation of the skin edge in
the plane with deeper tissues, as discussed below.
A single smooth cut is made around the tumor
including a 1–2-mm margin of clinically normal
appearing skin. The skin is nicked with a scalpel
or marked with ink around the perimeter for ori-
entation purposes (Fig. 16-� 6). A scalpel or tissue
scissors may be used to transect the base of the
excision parallel to the surface of the skin under
the tumor. Care is taken to keep the deep margin
within the same plane (Fig. 16-� 7). This also op-
Figure 16-8  Information regarding tumor location and
timizes tissue processing and subsequent margin location of hash marks is transferred to the Mohs “map”
evaluation. The specimen can be processed in one while the piece of skin is marked with inks and prepared for
piece or it may be divided into two or more pieces­ processing
for processing. The tumor location, shape, size,
and orientation marks are transferred to paper on color of inks are transferred to a paper Mohs map.
the Mohs “map” (Fig. 16-� 8). Inks are used to mark The tissue pieces are laid on gauze for transfer to
the specimen and are placed carefully at the edges the Mohs histopathology laboratory (Fig. 16-10).
of the tissue; they will be used to map the location The wound is dressed temporarily with a pres-
of positive margins (Fig. 16-� 9). The location and sure bandage while the tissue is processed, and it

ERRNVPHGLFRVRUJ
204 Dermatologic Surgery

B C D E
A F

Figure 16-9  The tissue is marked for orientation with one

or more inks

Figure 16-10  The pieces are laid on gauze for transfer to

the lab. Here, by convention, the first piece is in the upper
left-hand corner closest to the ink dot and the skin edge
is away from the dot. The second piece is on the bottom
left and the third piece is on the upper right. Information
regarding the color and location of ink is transferred to the
Mohs “map”

is determined whether further layers need to be

taken or whether the tumor has been removed
completely and repair can begin. Figure 16-11  Standard elliptical excision of tumor followed
by vertical sectioning “bread-loafing.” Here, all margins
Tissue processing appear to be clear based on the sections evaluated at the
top of the figure. However, the positive margin between
and interpretation sections B and C was not evaluated

The success rate of Mohs surgery relates in part

to the fact that the surgeon doubles as the his-
topathologist and, as such, has a more complete
understanding of the many variables surround-
ing the case. Critical information is not lost in
the transfer between multiple doctors. The Mohs
surgeon is intimately familiar with the expected
tumor pathology, understands exactly how and
where the tissue was removed, and can readily
interpret various findings under the microscope
having just seen the patient clinically. Instant clin-
icopathologic correlation is obtained.
Prior to interpretation of the tissue by the
Mohs surgeon, the histotechnician has many key
steps and should be thoroughly trained to orient,
embed, freeze, section, mount, and stain sections
properly. Many sources of error can be introduced
at each step and the technician needs to be inti-
mately familiar with those sources of error so that
recognition and correction are an ongoing process
for quality control of the lab. If these steps do not
lead to complete and interpretable tissue margins,
the overall cure rate will suffer.
The key difference between standard histopa-
thologic processing and Mohs processing of the
tissue surrounds tissue orientation and plane of
sectioning. In standard histopathologic process-
ing, the excised specimen is “bread-loafed” with
multiple thin vertical sections cut from the
block and prepared for examination (Fig. 16-11).

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 16

Chapter
Mohs micrographic surgery 205

The sections give the pathologist a relative “sam-
pling” of the surgical margin. This method leads to
a handful of sections which are of the order of sev-
eral microns, although the actual specimen may
be several centimeters in multiple dimensions.
In fact, it is estimated that standard processing
presents less than 1% of the true surgical margin
for evaluation by the pathologist. Based on this
fact, it is not surprising that the cure rates for ex-
cision listed in Box16-1 are lower than with Mohs
surgery and are based on recommended standard
margins rather than histologic control.
In contrast, Mohs processing involves section-
ing the tissue in a horizontal rather than vertical
plane. The skin edge is bent into the same plane
as the deeper subcutaneous tissue margin, and
sections are taken in a horizontal plane parallel to
the surface of the skin (Fig. 16-12). In this ­manner,
sections contain both the skin edge margin and
the deeper subcuticular margins all within the
same section. The Mohs map is used to orient the
specimen, and the location of persistent tumor is
indicated on the map to guide further tissue re-
moval. A true section, as would be obtained based
on Figure 16-12, is seen in Figure 16-13.
Management of postoperative
defects and postoperative
course
Repair of postoperative defects is usually per-
formed by the Mohs surgeon, although consul-
tation with other surgical specialties is often

Slice

Slice section

Figure 16-12  Schematic portraying tissue removal and manipulation of the skin edge such that the entire skin edge is in
the same plane as the deeper tissue margin. Horizontal sections are taken in a bottom-up approach so that the first few
sections are a representation of the true surgical margin comprising both skin edge and deeper tissues

ERRNVPHGLFRVRUJ
206 Dermatologic Surgery
Figure 16-13  Hematoxylin and eosin stain of a frozen
section depicting half of the excised surgical margin. The
inks used (blue and red) are clearly visible at the deep
margin of the tissue, and the epidermis, dermis, and
subcutaneous fat are all seen and evaluated in the section.
In this case, the section is clear of tumor
appropriate. Some wounds are allowed to heal by
second intention. Repair options include primary
closure, flaps, grafts or delayed closure. Utiliza-
tion of various wound care principles and closure
techniques is addressed in other chapters.
Complications with Mohs surgery are rare. Ex-
pected postoperative events include at least some
degree of scarring, bruising, swelling, and post­
operative tenderness. Infection occurs in 1–2%
of cases, and excessive bleeding or hematoma
formation increases the likelihood of infection.
ERRNVPHGLFRVRUJ
Further reading
Cook J, Zitelli JA. Mohs micrographic surgery: a cost
analysis. J Am Acad Dermatol 1998;39:698–703.
Martinez JC, Otley CC. The management of
melanoma and nonmelanoma skin cancer: a review
for the primary care physician. Mayo Clinic Proc
2001;76:1253–1265.
Messingham MJ, Arpey CJ. Update on the use of
antibiotics in cutaneous surgery. Dermatol Surg
2005;31:1068–1078.
Rowe DE, Carroll RJ, Day CL. Long-term recurrence
rates in previously untreated (primary) basal cell
carcinoma: Implications for patient follow-up.
J Dermatol Surg Oncol 1989;15(3):315–328.
Rowe DE, Carroll RJ, Day CL. Prognostic factors for
local recurrence, metastasis, and survival rates in
squamous cell carcinoma of the skin, ear, and
lip: implications for treatment modality selection.
J Am Acad Dermatol 1992;26:976–990.
Thissen MR, Neumann MH, Schouten LJ. A
systematic review of treatment modalities for
primary basal cell carcinomas. Arch Dermatol
1999;135:1177–1183.
Tromovitch TA, Stegman SJ. Microscopically
controlled excision of skin tumors: chemosurgery
(Mohs): fresh tissue technique. Arch Dermatol
1974;110:231–232.

Surgical complications
Erin J. Allen and Summer R. Youker
Introduction
Even the most experienced surgeons will have
complications. With that in mind, preventing
complications is preferable to managing them.
Careful planning, meticulous technique, and
good patient communication help the surgeon
to avoid complications. It is important to give
patients ­ wri­t­ten postoperative instructions and
emergency ph­one numbers. Postoperative phone
calls to check on patients’ status is an easy way to
detect complications early and increases patient
satisfaction. Many surgical complications can be
avoided with careful preoperative planning (see
Chapter 5: Pre­operative evaluation). Fortunately,
overall complication rates are low for cutaneous
surgery, and overall rates as low as 1.6% have been
reported for Mohs micrographic surgery.
A surgical complication can set off a chain reac-
tion, causing further adverse events. Most compli-
cations are interrelated (Fig. 17-1). It is important
to detect problems in a timely manner as early
intervention can improve overall outcome.
Hematoma, ecchymosis,
and seroma
Key Points
• Preoperative evaluation of anticoagulants or
coagulopathies can help prevent excessive
intraoperative and postoperative bleeding.
• Practice meticulous intraoperative hemostasis to
prevent hematomas.
• Evacuation of large hematomas is necessary
to prevent further adverse outcomes (infection,
necrosis, dehiscence).
• Seromas are caused by collections of serous
fluid. Prevention of seromas is accomplished
by layered closure of all potential space during
surgery.
ERRNVPHGLFRVRUJ
17
Chapter
Contact dermatitis Seroma
Bleeding Infection Necrosis
Hematoma Dehiscence Tension
Widened scar
Figure 17-1  Surgical complications algorithm
Hematoma (Boxes 17-1 & 17-�
2,
Figs 17-2 & 17-�
3)
Preoperative evaluation of patients, their coagula-
tion history, and medications is important to help
prevent hematoma formation (see Chapter 5:
Preoperative evaluation). Warfarin and clopido­
grel are not routinely discontinued for derma-
tologic surgery. When possible, over-the-counter
herbal remedies, nonsteroidal anti-inflammatory
drugs (NSAIDs), and alcohol should be withheld.
Aspirin does not appear to increase the risk of sig-
nificant bleeding unless the bleeding time is pro-
longed, and bleeding time is prolonged beyond
the normal range in only about 25% of aspirin-
treated patients. For minor procedures, the risk
from aspirin is minimal. For larger procedures,
determination of the bleeding time can assess the
risk.
Bleeding can cause a number of problems for
both the patient and the surgeon. Intraoperative
bleeding obscures the surgical site. It is important
to maintain a dry field for visualization and to
prevent later hematoma formation. ­ Meticulous
hemostasis with precise ­ electrocautery during
208 Dermatologic Surgery

B ox 1 7 - 1 surgery is key to controlling bleeding. Pay ­careful

attention to the entire wound and explore the
Causes of excessive bleeding undermined edges for bleeding vessels. If the pa-
tient is in the Trendelenburg position, bleeding
Defects in coagulation cascade
can be exaggerated. Larger vessels may need to be
Platelet abnormality tied off at both ends with a figure-of-eight stitch
Medications with an absorbable suture. Vessels that have been
incompletely severed will often continue to ooze.
• Aspirin, NSAIDs, warfarin, clopidogrel, ethyl alcohol,
vitamin E, garlic, gingko biloba, ginseng Once completely transected, the vessel will often
contract and discontinue bleeding. Wound edge
Physical problems bleeding of the epidermal or papillary dermis can
• Hypertension also be problematic. Avoid direct cauterization
• Lack of vessel retraction (incomplete sever) of the wound edges as epidermal char impedes
healing. The placement of epidermal sutures
• Transient vasoconstriction will often stop superficial wound edge bleeding.
—epinephrine effect The mattress suture is a good choice when there
—traumatic vessel response is significant papillary dermal bleeding.
Other tools exist for patients in whom ade-
• Failure of adequate surgical hemostasis
quate attempts at hemostasis fail to stop bleeding.
Special dressings containing hemostatic materials
can be used in open wounds that continue to
bleed. Products that facilitate hemostasis include
gelatin sponges or powder (Gelfoam®), micro-
fibrillar collagen (Avitene®, Collastat®), topical
B ox 1 7 - 2
thrombin to speed coagulation, and oxidized
Treatment of hematoma cellulose (Oxycel®, Surgicel®). For particularly
large defects or in patients with excessive bleed-
Prevention ing, a small Penrose drain may be used. The drain
• Ensure international normalized ratio (INR) is not supra­ is placed in the wound bed in a direction that
therapeutic in warfarin patients allows it to exit the dependent portion of the
• Cessation of anticoagulants preoperatively when medically wound. The wound is then closed, with a small
appropriate opening left for the external portion of the drain.
The drain may be removed in 24–48 h or left in
• Meticulous intraoperative hemostasis
place for up to 1 week.
• Pressure bandage Postoperatively, a bandage composed of gen­
Long-term massage and warm compresses for smaller erous absorbable gauze and firm tape aids in
hematomas wound compression. Ice applied to the wound
site after surgery will also decrease bleeding due
Evacuation of larger hematomas
to vasoconstriction. Patients should limit their
• Syringe with large-bore needle postoperative activity. Surgeons should give
• Single suture removal their patients strict and explicit written instruc-
Placement of drains as appropriate
tions with activity restrictions including lifting
limitations and elevation of the site. This surgeon
Antibiotics ­instructs patients to avoid all exercise other than
walking, and to undertake desk duties at work for

a b c

Figure 17-2  (a) A stitch is removed from the bulging wound to reveal a hematoma. (b) Insertion of an instrument breaks
up the clot and aids evacuation. (c ) Firm pressure expels the clot from the wound bed. (Photos courtesy of John Skougee
MD)

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 17

Chapter
Surgical complications 209

a b c

d e

Figure 17-3  (a,b) The patient, on warfarin, underwent two stages of Mohs surgery to clear a basal cell carcinoma on
the lower back. Despite instructions to rest, the patient did yardwork and presented on postoperative day 1 with a rapidly
expanding hematoma. (c) The flaps were taken down. The bleeding vessels were identified and tied off. (d) Drains were
placed with the openings to the dependent portion and the flaps resutured into place. (e) There is necrosis of the left flap
tip as a result of a relatively long length : width ratio, hematoma, and tension

at least 7 days. There should be no lifting greater of hematoma as the nutrient-rich collection is a
than 10–15 pounds. breeding ground for infection. A first-­generation
When a hematoma occurs, there is often con- cephalosporin such as cefalexin is an appropriate
tinued oozing from the site and pronounced first-line treatment option.
swelling. Patients often complain of worsening
pain, ­ especially if the hematoma is ­ expanding.
Ecchymosis (Fig. 17-4)
Hematomas should be evacuated whenever Although often alarming to patients, ecchymosis
possible, as they delay wound healing, facili- alone rarely causes problems other than the tem-
tate epidermal necrosis, and serve as a nidus of porary cosmetic appearance. Make certain that
­infection. the ecchymosis is not masking a hematoma that
If a patient presents with a hematoma, evacu- should be addressed. Ecchymosis is more preva-
ation should be attempted if the hematoma is lent around the eyes, in the setting of blood thin-
large enough to palpate. The wound often does ners or coagulopathies, and in ­elderly skin. Surgery
not need to be anesthetized, as epidermal reinner- close to the eye, even when not on the eyelids, can
vation of the wound edges is not yet complete. If
anesthesia is needed, then avoid epinephrine as it
causes temporary vasoconstriction and can mask
the culprit vessel(s). The incision site should be
opened by removing the sutures; often, some of
the sutures can be left in place. A no. 11-blade
or large-bore needle on a syringe is then inserted
into the wound at the incision line. Direct pres-
sure or suction with the syringe is applied in
all directions to aid hematoma evacuation. Any
­actively bleeding vessels should be cauterized
or tied off.
Once the hematoma is evacuated, the wound
is flushed with copious amounts of sterile saline.
The wound can be packed with iodiform gauze
if a large space is present. Loose Steri-Strips can
also be applied to reapproximate the wound
­edges and facilitate further drainage. Most authors Figure 17-4  Ecchymosis. Note the extension well beyond
recommend empiric antibiotics in the setting the surgical site

ERRNVPHGLFRVRUJ
210 Dermatologic Surgery

cause significant eyelid ­ ecchymosis. All ­ patients B ox 1 7 - 4

should be warned of the risk of ­ ecchymosis,
­especially those at high risk. Preparing patients
for possible bruising can ­alleviate anxiety. Imme-
diate postoperative ice can ­decrease bruising.
Seroma
A seroma is a collection of serous fluid that
­accumulates in potential spaces after surgery.
A complete and layered closure during surgery
will eliminate potential space for fluid collection.
Seromas can be detected as a soft mass beneath
or adjacent to the suture line. They are often
clinically mistaken for a hematoma. Insertion
of a large-bore needle on a syringe with suction
applied will drain a seroma. The fluid should be
sterile. However, if the fluid is cloudy or other
signs of infection are present, it should be sent for
culture and antibiotics initiated. Seromas should
be drained when possible, because the collec-
tion impedes healing and places pressure on the
­healing epidermis.
Dehiscence and epidermolysis
(Boxes 17-3 & 17-4, Fig. 17-5)
Key Points
• Dehiscence is the separation of the layers of the
wound.
• Epidermolysis is the separation of only the edges
of the epidermis.
• Both occur as a result of other complications:
hematoma, seroma, infection, necrosis,
improper repair design, and/or premature suture
removal.
Epidermolysis and deeper dehiscence result from
increased wound tension that is often caused by
B ox 1 7 - 3
Avoiding dehiscence and epidermolysis
Treatment of dehiscence and epidermolysis
Resuture if <24 h
Allow granulation if patient presents >24 h
Steri-Strips for wound support
Minimal debridement as necessary
Antibiotics not necessary, but recommended for large or
high-risk areas
poor closure execution or by another complica-
tion. At the time of suture removal, the wound
is only approximately 10% of original strength,
and approaches 80% the tensile strength of ­uncut
skin only at 8–9 months. Once dehiscence has
­occurred, the wound is typically left open and
­allowed to heal by secondary intent.
If the wound is large, packing with an iodi-
form gauze dressing may be necessary to fill
the void. The packing should be placed loosely
in the wound and replaced with smaller pack-
ing every 3–5 days. The patient can also be in-
structed to remove a portion of the gauze each
day to make room for healing tissue. Conservative
debridement of fibrinous and devitalized tissue
to a bleeding base is important as it allows for
proper granulation. Closure can be attempted if
the wound is clear of all infected tissue, and is
best attempted within the first 24 h. If wound
closure is ­attempted, then a curette or scalpel is
used to freshen the wound edges to a bleeding
base and layered sutures are placed. Prophylactic
antibiotics can be started in cases of dehiscence if
infection is imminent or likely, but are usually not
necessary for epidermolysis.

Limit patient’s postoperative activity

Maintain a sterile field
Avoid crush injury of tissue
Avoid excess tension on wound
Appropriate design
• Adequate undermining
• Remove standing cones
Use proper suture material and placement
Limit patient smoking
Maintain hemostasis
Figure 17-5  Wound dehiscence

ERRNVPHGLFRVRUJ

Necrosis (Box 17-5, Fig. 17-6)
Key Points
• Necrosis is caused by compression of blood
vessels from sources such as tension on the
wound, crush injury, infection, hematoma, and
smoking.
• The best treatment is continued observance,
moist dressings, and antibiotics if there are signs
of infection.
• Extensive debridement is not recommended.
Necrosis occurs when vascular perfusion is com-
promised. Reiterating the relationship between
adverse surgical outcomes, necrosis is usually the
result of another complication. The superficial
dermal plexus provides the main supply to the
skin. Any of the previously mentioned compli-
cations can threaten this vascular plexus. Poor
closure design places tension on the wound that
is often evident after closure as pale and poorly
perfused tissue. Extensive undermining in an
excessively superficial plane will interrupt the
­feeding arterioles. Using the correct instrument
such as hooks instead of forceps to lift rather than
B ox 1 7 - 5
Causes of epidermal necrosis
Interference of blood supply
• Inadequate closure design
• Wound tension
• Crush injury from poor tissue handling
• Extensive superficial undermining
Infection
Hematoma
Smoking
a b
Figure 17-6  (A) Necrosis of a full-thickness skin graft. (B) Allowed to heal by secondary intent. (Photos courtesy of Mary
Maloney MD)
ERRNVPHGLFRVRUJ
17
Chapter
Surgical complications 211
crush tissue will prevent tissue crush injury. Su-
tures placed in a layered closure help ­eliminate
tension. Suture knots should be secure but not
so tight that they compromise blood supply to
the wound edges. Planning a flap or graft may
be necessary when a complex closure will not
suffice.
Flap and graft necrosis rates range from
1.9% to 10.4%. The tip of the flap is the most
­vulnerable region as it is the most distal from
the blood supply. Undersizing flaps is a rela-
tively ­common mistake that demands too much
of the flap, causes tension, and compromises
blood ­ supply. Back-cuts into the flap pedicle
or ­ improper length : pedicle ratio (3 : 1 is usu-
ally ­ appropriate) will also cause flap-tip necro-
sis. Lastly, the surgeon should not cut into the
pedicle when ­taking the standing cone, as it will
reduce the flap’s blood supply.
Grafts derive their blood and nutrient supply
from the wound bed. Cartilage and exposed bone
are not suitable for grafts owing to the relative
lack of blood supply. Areas of exposed cartilage
on the auricle greater than 1 cm2 can be fenes-
trated with a 2-mm punch to facilitate graft per-
fusion from the underlying dermis. Exposed bone
should be allowed to granulate, and a delayed graft
placed when the wound bed is ready to accept a
graft. Alternatively, the outer table of bone may
be burred to stimulate bleeding before a graft is
placed. A hematoma in the wound bed will inter-
fere with graft survival. A bolster dressing and/or
basting sutures aid adequate contact between the
graft and wound base.
Smoking contributes to numerous adverse
surgical outcomes by directly and indirectly de-
creasing blood flow. Smoking more than one pack
per day increases the risk of flap or graft necro-
sis threefold. All patients should be instructed to
decrease, or if possible stop, smoking for 1 week
before and 2 weeks after surgery.
Necrosis is typically partial thickness. When
wound necrosis is encountered, extensive
212 Dermatologic Surgery

­ ebridement is not recommended. Devitalized

d B ox 1 7 - 6
tissue is dusky and frequently has a densely ad-
herent eschar. Extensive debridement can in- Associations with increased surgical site
jure deeper viable tissue. The wound should be infection
cleansed frequently and kept moist with an oint- Location – ear, hair-bearing, distal extremities, mucous
ment-based product, such as petrolatum. membrane involvement, axillary or inguinal sites
Significant break in sterile technique
Infection and mimickers (Table
Surgery of a contaminated wound
17-1, Box 17-6, Figs 17-7–17-10)
Long duration of surgery – infection rate almost doubles with
Key Points each hour of surgery
• Infection usually begins at the time of surgery. Comorbidities – poorly controlled diabetes,
• Infection is evident after 4–8 days. immunosuppression, malnutrition
• Staphylococcus aureus is the most likely
organism – treat with a first-generation
cephalosporin or penicillinase-resistant penicillin.
• Abscesses should be drained and packed.
• Signs of infection include redness, drainage,
pain, crepitus, cellulitis, lymphangitis, fever, signs
of endocarditis, shock.
• Bacterial infection mimickers include viral
infection, candidiasis, allergic and irritant contact
dermatitis, and suture reaction.

Most dermatologic procedures are considered

“clean-contaminated” and, although infection rates
in these types of wound are accepted to be 5–10%,
most dermatologic studies report lower rates. Pain
or erythema that worsens with time should alert
the patient and physician to evaluate the wound
for infection. Most infections are introduced dur- Figure 17-7  Postoperative bacterial infection. (Photo
courtesy of Mary Maloney MD)
ing surgery, but poor postoperative wound care
can also contaminate the wound. Strict surgical

Table 17-1  Wound classification

Wound type Defined Infection rate
Clean Sterile technique, <5%
noninflamed skin
Clean- Small breaks in 10%
contaminated sterile technique;
gastrointestinal,
genitourinary, or
respiratory tracts
entered without gross
contamination
Contaminated Major breaks in 20%
sterile technique;
gross contamination
from gastrointestinal,
genitourinary, or
respiratory tracts
Dirty Acute bacterial 30–40% Figure 17-8  Postoperative candidal infection in the groin.
infection present (Photo courtesy of John Skougee MD)

ERRNVPHGLFRVRUJ

Figure 17-9  Allergic reaction from topical antibiotic
ointment. (Photo courtesy of Mary Maloney MD)
hygiene by both the surgical team and the patient
or persons doing dressing changes is imperative.
When infection is diagnosed clinically, ­antibiotics
should be started, and then tailored when
­culture and sensitivity results are available (see
Fig. 17-10).
Wound erythema can be caused by bacte-
rial infections, but the surgeon should watch for
­infection mimickers. Irritant contact dermatitis
caused by adhesives is often geometric in shape.
Pruritus, rather than pain, marks allergic con-
tact dermatitis that can be caused by antibacte-
rial ointments, tape, dressings, or ­ intraoperative
cleansers. Allergic and irritant dermatitis is treat-
ed with discontinuation of the offending agent
and a short course of midpotency topical steroids.
Individual pink granulomatous ­ papules found
along the incision line can be a sign of ­ suture
Routine skin
surface
Most likely causative agent S. aureus
Non-PCN allergic:
Treatment
First generation
cephalosporin
Figure 17-10  Infection treatment algorithm. PCN, penicillin
ERRNVPHGLFRVRUJ
17
Chapter
Surgical complications 213
reactions to ­absorbable sutures. Other ­infections,
such as herpes and candida, also cause wound
pain and erythema. Punched-out ­ erosions with
scalloped borders and vesicles are evidence of vi-
rus and can be confirmed by Tzanck smear, viral
culture, and cytopathic changes on skin biopsy.
Treatment is with oral aciclovir or derivatives.
Candidiasis can be confirmed with potassium
hydroxide preparations and culture, and treated
with topical azole or nystatin preparations. Treat-
ment may require oral ketoconazole or flucona-
zole if involvement is ­extensive or the patient is
immunocompromised.
Abnormal scarring and poor
wound appearance
(Figs 17-11–17-17)
Key Points
• Avoiding complications and early treatment will
improve wound outcome.
• Most wounds improve with time and may not
reach their final appearance until 1 year.
• Proper suture use, placement, and closure
technique decreases the risk of scarring.
• Dermabrasion is best performed 4–8 weeks after
surgery.
Even the most carefully planned and executed
operations can have poor scarring outcomes.
Proper understanding of common pitfalls and
­prevention through proper planning is key to
reducing that risk. See Table 17-2 for a list of fre-
quently encountered types of scarring complica-
tions. Chapters 13 & 14 also review complications
Signs of infection present
Send swab for culture and drain abscess if present
Site of infection
Skin folds
Gram
Pseudomonas
negatives
PCN allergic: Fluoroquinolone,
Fluoroquinolone
Clindamycin, sulfa, sulfa, or extended
tetracycline, spectrum
macrolide cephalosporin
214 Dermatologic Surgery

Figure 17-11  Alar notching. (Photo courtesy of Figure 17-14  Ectropion. (Photo courtesy of Scott W.
Scott W. Fosko MD) Fosko MD)

Figure 17-12  Hypertrophic scar. (Photo courtesy of Mary Figure 17-15  Hypertrophic scarring. (Photo courtesy
Maloney MD) of Scott W Fosko MD)

Figure 17-13  Scar spread or “fish mouth scar” Figure 17-16  Suture granuloma that resolved after
3 months. (Photo courtesy of Scott W. Fosko MD)

ERRNVPHGLFRVRUJ
 17

Chapter
Surgical complications 215

­ rovide tremendous improvement. Although a

p
difficult wait, it is best to delay scar revision for
6–8 months or more to assess the final scar.

Nerve deficits (Fig. 17-18)

Key Points
• There are three important danger zones for
cutaneous head and neck surgery:
a. Marginal mandibular nerve
b. Temporal nerve
c. Spinal accessory nerve (cranial nerve XI).
• Note pre-existing deficits and intraoperative
deficits caused by local anesthesia.
• Sensory deficits are expected and usually
temporary.
• In select cases, some motor nerves can be
reanastomosed. Early intervention is preferable.

Figure 17-17  Trap-dooring of a flap. (Photo courtesy
of Scott W. Fosko MD)
specific to flaps and grafts. When a wound is
­healing with an unacceptable scar, interven-
tion may be ­appropriate (see Table 17-2). How-
ever, patience and conservative therapy can also
Although sensory nerve deficits are more com-
mon, motor nerve deficits are of more concern.
Almost all patients can expect some sensory
nerve loss, which is more pronounced in flaps,
grafts, and areas of wide undermining. The loss
is usually temporary but may be permanent –
more so in grafts. Patients should be warned that,

Table 17-2  Complications of scarring

Likely causes
Ectropion Improperly sized closure with too
much tension on eyelid or too
much of eyelid margin removed
and not replaced
Trap-dooring or Oversized grafts and flaps, and lack
pin-cushioning of undermining around wound
“Train track” scarring Too much tension on epidermal
sutures and/or leaving them in
place too long
Ear bowing/cupping or Removal of cartilage/lack of
floppy ear structural support
Floppy or notched nasal Removal of supporting structure
ala
Terminal hair in flap or Follicles present in donor skin
graft
Widened or fish-mouth Too much wound tension
scars
Suture granulomas Tissue hyperresponsive to
absorbable sutures
Keloids Predisposed individuals. More
common in upper chest/back and
in black skin
Widened scars on the Dynamic movement
forehead and glabella
Hypertrophic scarring Any of the above causes
Treatment or prevention
Plan properly sized flaps and grafts. Place tension vectors
parallel to lid margin
Prevent with proper flap or graft size and undermining. Treat
with intralesional steroids, surgical debulking, scar massage,
and observation
Adequate use of buried sutures to close the majority of wound
tension and removal of epidermal sutures as early as possible
Replace cartilage with composite grafts or reduce size of ear
with wedge resection
Replace support structure with composite graft or generous flap
Harvest skin from site with similar wound characteristics, or
manually remove follicles from donor before placement
Prevent with adequately buried sutures, properly sized closures,
and limit patient’s postoperative activity
Prevent by placing buried sutures deeper. Treat by removing
protruding sutures, and reassurance
Early intralesional steroids, postoperative topical imiquimod
cream (Aldara) or radiation therapy
Consider preoperative botulinum toxin to limit movement
during healing phase
Silicone sheets, scar massage, dermabrasion, observance

ERRNVPHGLFRVRUJ
216 Dermatologic Surgery

a b

Figure 17-18  (a) The patient lost function of the temporal branch of the facial nerve after Mohs surgery on the right
temple. (b) Partial movement was recovered when local anesthesia resolved on postoperative day 1

as sensation recovers, some parasthesias or neu-
ropathic pain could occur along with the normal
healing process. Temporary motor nerve loss is
not uncommonly caused by the effect of local
anesthesia or nerve blocks. It is important to as-
sess the patient’s motor function prior to each
surgical procedure to ­ determine whether this
temporary phenomenon has occurred. Most mo-
tor nerves of the face are protected by the fascia.
There are three areas at particular risk during cu-
taneous surgery of the head and neck that place
the temporal, marginal mandibular, and accessory

Table 17-3  Life-threatening surgical complications

Type Possible causes Signs Treatment
Anaphylaxis Topical agents: Flushing, shortness • Maintain airway and administer oxygen
chlorhexidine, bacitracin of breath, lip or face • Obtain IV access
swelling, urticaria, • Epinephrine (IV, subcutaneous, or endotracheal) for
Local anesthetic: amide,
stridor, wheezing anaphylaxis
ester, preservative
Oral antibiotics: latex
allergy
Lidocaine toxicity Excessive administration Central nervous • Benzodiazepines for lidocaine toxicity or seizures
system: circumoral • Check blood glucose
Reduced metabolism
numbness, slurred • Initiate CPR or ACLS as appropriate
Delayed absorption speech, nystagmus, • Transfer to appropriate facility
tremor, seizure, coma
Cardiovascular:
vasodilatation,
hypotension,
arrhythmia
Seizure Vasovagal reaction, Sometimes preceded
pre-existing condition, by an aura, fainting,
hypoglycemia, lidocaine tonic–clonic
toxicity movements
Myocardial Pre-existing coronary Chest or arm pain,
infarction or disease, direct diaphoresis, cyanosis
arrhythmia epinephrine effect, or pallor, nausea
β-blocker and or vomiting, loss
epinephrine interaction, of consciousness,
anxiety, arrhythmia, sudden death
hypotension, tachycardia,
lidocaine toxicity

ERRNVPHGLFRVRUJ

(cranial nerve XI) nerves at risk. Chapter 1 pro-
vides ­detailed information of their anatomy and
deficits that occur when transected.
If transection of a major motor nerve is con-
firmed, early intervention offers the best results.
When no intervention occurs, recovery is possi-
ble but is ­unlikely and unpredictable. Colleagues
in Head and Neck Surgery or Neurosurgery can
sometimes reanastomose or patch the defect
if the transection is relatively proximal and the
nerve is not significantly arborized.
Life-threatening complications
(Table 17-3)
Key Points
• Relatively rare in cutaneous surgery.
• A vasovagal syncopal episode can initially mimic
an emergency.
• Complications include anaphylaxis or type 1
allergic reactions, lidocaine toxicity, seizures,
myocardial infarction, and arrhythmias.
Life-threatening complications are fortunately
rare in dermatologic surgery. All surgical staff
should have emergency training such as Basic Life
Support (BLS) or Advanced Cardiac Life Sup-
port (ACLS) certification. Surgeons should main-
tain up-to-date ACLS certification. Some offices
choose to keep an automated external ­ cardiac
defibrillator on site. Emergency plans should be
in place and all office staff knowledgeable as time
is limited in emergencies.
Further reading
Aasi SZ, Leffell DJ. Complications is dermatologic
surgery: how safe is safe? Arch Dermatol
2003;139:213–214.
Arpey CJ, Whitaker DC. Postsurgical wound man-
agement. Dermatol Clin 2001;19(4):787–797.
Billingsley EM, Maloney ME. Intraoperative and
postoperative bleeding problems in patients taking
warfarin, aspirin, and nonsteroidal antiinflamma-
tory agents. A prospective study. Dermatol Surg
1997;23(5):381–385.
Bolton L, Fattu AJ. Topical agents and wound heal-
ing. Clin Dermatol 1994;12:95–120.
Classen DC, Evans RS, Pestotnik SL, Horn SD,
Menlove RL, Burke JP. The timing of prophylactic
administration of antibiotics and the risk of surgi-
cal-wound infection. N Engl J Med 1992;326:
281–286.
Cook JL, Perone JB. A prospective evaluation of
the incidence of complications associated with
Mohs micrographic surgery. Arch Dermatol
2003;139(2):143–152.
ERRNVPHGLFRVRUJ
17
Chapter
Surgical complications 217
Futoryan T, Grande D. Postoperative wound infec-
tion rates in dermatologic surgery. Dermatol Surg
1995;21:509–514.
Gette MT, Marks JG Jr. Maloney ME. Frequency
of postoperative allergic contact dermatitis to
topical antibiotics. Arch Dermatol 1992;128:
365–367.
Goldminz G, Bennett RG. Cigarette smoking and
flap and full-thickness graft necrosis. Arch Derma-
tol 1991;127:1012–1015.
Haas AF, Grekin RC. Antibiotic prophylaxis in
dermatologic surgery. J Am Acad Dermatol
1995;32:155–176.
Helfman T, Ovington L, Falanga V. Occlusive
dressings and wound healing. Clin Dermatol
1994;12:121–127.
Kargi E, Babuccu O, Hosnuter M, Babuccu B,
Altinyazar C. Complications of minor cutaneous
surgery in patients under anticoagulant treatment.
Aesthetic Plast Surg 2002;26(6):483–485.
Khalifeh MR, Redett RJ. The management of
patients on anticoagulants prior to cutaneous
surgery: case report of a thromboembolic com-
plication, review of the literature, and evidence-
based recommendations. Plast Reconstr Surg
2006;118(5):110e–117e.
Kirsner RS, Eaglestein WH. The wound healing
­process. Dermatol Clin 1993;11:629–640.
Lawrence C, Sakuntabhai A, Tiling-Grosse S. Effect
of aspirin and nonsteroidal antiinflammatory drug
therapy on bleeding complications in derma-
tologic surgical patients. J Am Acad Dermatol
1994;31(6):988–992.
McGrath M, Simon R. Wound geometry and the
kinetics of wound contraction. Plast Reconstr Surg
1983;72:66–72.
Otley CC, Fewkes JL, Frank W, Olbricht SM. Com-
plications of cutaneous surgery in patients who are
taking warfarin, aspirin, or nonsteroidal anti-
inflammatory drugs. Arch Dermatol 1996;132:
161–166.
Salasche SJ. Acute surgical complications: cause,
prevention, and treatment. J Am Acad Dermatol
1986;15:1163–1185.
Singer AJ, Clark RAF. Cutaneous wound healing.
N Engl J Med 1999;341:738–746.
Smith AG. A prospective study of 134 consecutive
patients requiring diagnosis, excision and repair of
a facial cutaneous lesion. Br J Oral Maxillofac Surg
1992;30:157–160.
Whitaker DC, Grande DJ, Johnson SS. Wound infec-
tion rates in dermatologic surgery. J Dermatol Surg
Oncol 1988;14:525–528.
Witte M, Barbul A. General principles of wound
healing. Surg Clin North Am 1997;77:509–528.

Sclerotherapy of varicose
and telangiectatic leg veins
Allison Jo Moosally and Allison T. Vidimos
Key Points
• Varicose veins are a common problem affecting
one third of all Western adult populations; the
incidence increases with age.
• They can be a cosmetic problem due to their
appearance, or affect the quality of life of the
patient due to their symptoms.
• They typically involve the deep and superficial
venous systems of the legs.
• The prevalence is 25–33% in women and 10–20%
in men.
• Patients commonly complain of aching and
cramping in the affected areas.
Clinical overview
Varicose veins are a common problem in many
Western populations today, with a prevalence of
25–33% in women and 10–20% in men. They ap-
pear to be more common in Western or industrial-
ized societies, increase in frequency with age, and
vary among ethnic backgrounds. Varicose veins
are rare in childhood, but, when present, are more
commonly associated with a vascular malforma-
tion as in Klippel–Trenaunay syndrome. They not
only affect the patient by their cosmetic appear-
ance, but also cause symptoms that affect the pa-
tient’s quality of life. They are typically found on
the lower extremities but also can appear on the
spermatic cords (varicoceles), vulva, rectum (he-
morrhoids), esophagus (esophageal varices), and
even other less common sites such as the neck fol-
lowing administration of certain drugs or surgical
procedures that affect the vascular supply.
Pathophysiology
The venous system of the legs is divided into deep
and superficial vessels (Fig. 18-�
1). The superficial
venous system runs parallel to the deep venous
ERRNVPHGLFRVRUJ
18
Chapter
system. The deep veins lie within the muscular sys-
tem and the fascia, transporting the majority of the
deoxygenated blood returned from the legs to the
heart. The superficial veins, which transport only
about 10% of the blood, lie outside the muscles
and drain the venules from the skin. Perforator
veins connect the two systems and contain one-way
check valves (Fig. 18-�
2). These one-way valves pre-
vent backflow of blood. The blood is transported
from the superficial veins to the deep veins by the
perforator veins during muscle relaxation, when
pressure in the deep veins is less than the pressure
of the superficial veins. Conversely, contraction of
the leg muscles causes constriction of the veins,
moving blood upward through the vessels. This
mechanism of venous blood flow has been referred
to as the muscle pump or peripheral heart.
Varicose veins result from chronic venous insuf-
ficiency (valvular incompetence) with a number
of known causes (Box 18-� 1). They develop
most commonly at the communication point
(perforator veins) between the two systems, for
example at the saphenofemoral or saphenopop-
liteal junction. They are the result of structural
and functional defects in the venous system.
After a prolonged period of time, these defects
cause ambulatory venous hypertension, weak-
ening of the vein walls, abnormal distensibility
of surrounding connective tissue and seperation
of the valve cusps within the vein. The result is
valvular incompetence or reflux, and permanent
venous dilatation. Valvular incompetence can
occur anywhere within the deep or superficial
venous system. Incompetence of the perforat-
ing veins leads to reflux between the deep and
superficial veins. Prolonged dilatation of the
venules, the most distal branches, results in te-
langiectases clinically.
Varicose veins are classified as either a primary
or a secondary disorder. Primary varicosities are
more common in women and patients with a
220 Dermatologic Surgery

Superficial circumflex
Superficial
ilium v.
epigastric v.
Saphenofemoral
junction
Femoral v.
Anterolateral v. Superior external
pudendal v.

Posteromedial v.
Long saphenous v.

Saphenopopliteal
Femoral v. junction
Popliteal v. Hunterian perforator Intrasaphenous v.
Boyd’s perforator Long saphenous v.
Posterior tibial v.
Short saphenous v.
Anterior saphenous v. Paraperoneal perforator
Posterior arch v.

Crockett’s perforating v.
Anterior tibial v. Peroneal v.

Dorsal venous arch

Figure 18-1  Diagram of major veins in the lower extremities

a b c B ox 1 8 - 1
Etiologies of chronic venous dilatation
that can result in valvular incompetence
and resultant varicosities

• Pregnancy – the external pressure of the developing fetus on

Figure 18-2  Diagram of venous valves in the lower
extremities. (a) Normal venous valve opens when blood
flows from the lower extremities toward the heart.
(b) Competent venous valves close, preventing backflow
of blood into the lower extremities. (c) Diseased,
incompetent venous valves allow blood to flow backwards
into the lower extremities, resulting in varicose veins
the iliac veins causes distal vessel distention
• Obesity
• Prolonged standing (gravity) – often occupation dependent
• Pelvic obstruction that leads to venous obstruction
• Chronic increased intra-abdominal pressure – straining on
defecation or urination
• Habitual leg crossing
• Chronically wearing tightly fitted clothes
• Hormones
• Prolonged sitting
• Familial predisposition – inherited weakness in vein walls or
congenital deficiency in the number of valve cusps

ERRNVPHGLFRVRUJ

Sclerotherapy of varicose and telangiectatic leg veins
strong family history of varicose veins. Secondary
varicosities are a result of an acute or previous
venous thrombosis.
Clinical presentation
A majority of patients who present with vari-
cose or spider veins do so for cosmetic concerns.
However, frequent complaints including pain,
cramping, swelling, throbbing, burning, and the
sensation of heaviness in the legs prompt patients
to seek medical attention (Box 18-� 2). Symptoms
are exacerbated by prolonged standing, sitting,
and weight-bearing, whereas they improve with
leg elevation and walking. Varicose veins com-
monly present during pregnancy.
To date, studies have failed to show that the
size or number of varicosities directly correlates
with symptom severity. One patient with small
telangiectases or reticular veins may complain of
severe throbbing and burning, whereas another
patient with few but very large veins may be
asymptomatic and concerned only about the cos-
metic appearance.
Prolonged chronic venous insufficiency, if left
untreated, commonly leads to more severe signs
and symptoms including hemorrhage, dermatitis,
and ulceration. The ulcerations are commonly
present on the medial malleolus of the ankle.
The hyperpigmentation is due to hemorrhage
with extravasation of the red blood cells into the
skin and ulceration is from prolonged insufficient
blood supply to the affected area.
Severe complications of chronic venous insuf-
ficiency are superficial thrombophlebitis, stasis der-
matitis, lipodermatosclerosis, and atrophie blanche.
These complications are frequently seen in individ-
uals with varicosities. Atrophie blanche is a condi-
tion characterized by star-shaped ulcerations that
heal classically with white star-shaped scars around
the medial ankles. Lipodermatosclerosis is charac-
terized by edematous, hyperpigmented, firm, thick-
ened, painful legs with the classically described
“inverted champagne bottle” appearance. Stasis
dermatitis, a condition frequently seen by derma-
tologists, is characterized by edema, hyperpigmen-
tation due to hemorrhage, poor wound healing,
and pruritus with or without dermatitis. Superficial
thrombophlebitis is less common in patients with
varicose veins. It can be caused by trauma, a hyper-
coagulable state, or may occur spontaneously. The
greater saphenous vein is most commonly affected.
This condition manifests with warmth, tender-
ness, erythema, and swelling at the affected site. It
must be treated to prevent extension into the deep
venous system leading to a possible deep venous
thrombosis or pulmonary embolus.
ERRNVPHGLFRVRUJ
18
Chapter
221
B ox 1 8 - 2
Signs and symptoms
• Throbbing
• Aching
• Burning
• Cramps
• Fatigue
• Heaviness
• Pruritus
• Restless legs
• Tingling
• Swelling
• Hyperpigmentation
• Dermatitis
• Superficial thrombophlebitis
• Ulceration
Diagnosis
History
The diagnosis of varicose veins starts with a
thorough history and physical exam. Onset of
symptoms, aggravating factors, job description,
and a patient’s activity level are all valuable
pieces of information, not only for diagnosis
but for overall management. Determination of
events surrounding the onset of the varicosities
could lead to ­ relevant information regarding
a possible preceding deep venous thrombosis
(DVT) that may have been overlooked. A his-
tory of recent travel, ­pregnancy, chronic consti-
pation, change in medications, immobilization,
surgery, previous DVT, or clotting disorder pro-
vides valuable pieces of information that must
be elicited during the evaluation. A review of
the patient’s current medical problems, past
medical history, past surgical history, medica-
tions, and family history is all essential for di-
agnosis and management of varicose veins. It is
important to know how many hours per day the
patient is on their feet, if they wear high-heeled
shoes, and whether they cross their legs often.
Taking oral contraceptive pills or hormone re-
placement therapy, a recent pregnancy, or even
a change of occupation can all help to explain
the onset, worsening, or even improvement of
the varicosities (Box 18-� 3).
222 Dermatologic Surgery

s­ ystem. Careful palpation of the abdomen and

Physical exam pelvis could also reveal a mass that is compressing
A complete exam of the lower extremities, venous outflow, causing venous hypertension and
pelvic region, and abdomen should be done with varices in the lower extremities. Palpation of the
the patient in the supine and standing positions. main arterial vessels should also be preformed, in-
The location, size, configuration, and color of the cluding the femoral, popliteal, dorsalis pedis, and
varicosities should be noted, as well as the areas posterior tibial arteries.
that cause the most discomfort. Areas with sta- Varicose veins have several clinical appearances
sis dermatitis, edema, hyperpigmentation, and depending on extent and severity of involvement
ulceration should be noted; further work-up will (Figs 18-3 through 18-5). The Duffy–Goldman
likely be necessary as these signs typically signify a classification of abnormal veins can be used to
more complex disease process within the venous classify veins based on their size and appearance
(Table 18-� 1).
B ox 1 8 - 3 Testing
Risk factors Several specific diagnostic maneuvers have been
used in the past to assess varicose veins including
• Heredity
the Perthes test, the Brodie–Trendelenburg test,
• Age the percussion or Schwartz test, and the cough
• Sex test. For the purposes of our discussion we will
not consider these tests further, as they are not
• Occupation (prolonged standing)
accurate or consistent enough to allow for proper
• Sedentary lifestyle diagnosis and appropriate treatment. All have
• Immobility been largely replaced by noninvasive laboratory
ultrasound testing.
• Long flights or automobile trips
A Doppler ultrasound or a Doppler duplex
• Weight-lifting (increased intra-abdominal pressure) scan are the current tests of choice to assess the
• Obesity anatomy, flow, and patency of the valves in the
venous system, owing to their ease, noninvasive
• High heels
nature, and accurate diagnostic ability. With Dop-
• Pregnancy pler ultrasonography, a wand with a transmit-
• Hormones (oral contraceptives or hormone replacement ting and sensing crystal is passed over a vein, and
therapy) ­signals received provide diagnostic data. Doppler
• Diet (fiber deficient) duplex scanning, using a probe to pass over the
vessels, allows for direct visualization of the veins,
• Constipation luminal diameter, and any valvular incompe-
• Diverticular disease, inguinal hernias, hemorrhoids, pelvic tence or reflux. A DVT can be detected as well as
surgery ­narrowing of a vessel. With either test, a trained
professional is essential to achieve accurate and

a b

Figure 18-3  (a) Large tortuous, bulging blue varicosities. (b) Resolution of varicosites after sclerotherapy with sotradecol.

ERRNVPHGLFRVRUJ
 18

Chapter
Sclerotherapy of varicose and telangiectatic leg veins 223

Table 18-1  Duffy–Goldman classification of abnormal

veins
Type Features
1: Telangiectases/spider 0.1–1.0 mm in diameter
veins
Red to cyanotic
1A: Telangiectatic matting <0.2 mm in diameter
Red
1B: Communication Type 1 veins in direct
telangiectases communication with varicose
veins of the saphenous
system
2: Mixed telangiectatic/ 1.0–6.0 mm in diameter
varicose veins (no
Cyanotic to blue
direct communication
with varicose veins of
saphenous system)
Figure 18-4  Smaller reticular veins are typically 3: Nonsaphenous varicose 2–8 mm in diameter
blue–green, flat, and less tortuous veins (reticular veins)
Blue to blue–green
4: Saphenous varicose >8 mm in diameter
veins
Blue to blue–green
Source: Goldman MP, ed. Sclerotherapy: Treatment of Varicose and
Telangiectatic Leg Veins. St Louis: Mosby Year Book, 1991:56. Modified
by Goldman from Duffy DM. Small vessel sclerotherapy: an overview. Adv
Dermatol 1988;3:221–242.

venous pressure measurements, and light reflex

rheography. Most of these tests are not performed
routinely in clinical practice.

Figure 18-5  Telangiectases are the smallest vessels (less
than 1 mm in diameter) and may be blue, red, or purple in
color.
reliable results. Examination occurs in the stand-
ing or, more commonly, the reverse Trendelen-
burg position. The Valsalva maneuver or coughing
helps to elicit reflux.
Controversy still exists on whether the above
testing should be done universally on all patients
presenting with varicosities or telangiectases, or
whether only those with significant clinical dis-
ease and predisposing history should be tested.
Other diagnostic tests available to evaluate the
venous system include venography, air phlethys-
mography, photophlethysmography, ambulatory
Treatment
Treatment options for varicose veins vary from
conservative to invasive. Each patient is different,
presenting with a different type of varicosity, dif-
ferent contributing medical issues, and different
desired outcomes. Some patients present with
asymptomatic varicose veins and telangiectases
that are cosmetically displeasing and would like
treatment for cosmetic reasons only. Other pa-
tients are very symptomatic and seek treatment
for the relief of symptoms. After a careful his-
tory, physical, and laboratory testing, one should
be able to choose a treatment based on the
outcome of the work-up and the patient’s needs
(Box 18-�4).
Compression therapy
Compression therapy remains the standard of
care for most varicose veins and, if employed early
enough in life, may prevent or delay the onset of
symptoms. Compression hose can be used as mon-
otherapy or in conjunction with other therapies.
They can be ordered as socks, knee highs, thigh
highs or full pantyhose. Compression therapy is a
conservative and inexpensive approach, but many

ERRNVPHGLFRVRUJ
224 Dermatologic Surgery

B ox 1 8 - 4
Treatment options for varicose veins and
telangiectases

• Weight loss
• Leg elevation
• Compression stockings
• Sclerotherapy
• Laser or light therapy
• Endovenous obliteration
• Ambulatory phlebectomy, stab avulsion phlebectomy,
­transilluminated power phlebectomy Figure 18-6  A 3-mL syringe with a 30-gauge needle bent
to 145° in feeder vein of a telangiectatic cluster
• Vein stripping
• Vein ligation

B ox 1 8 - 5
Contraindications to compression therapy

• Allergy to any component of the compression hose or

­stockings used
• Active ulceration
• Arterial insufficiency – ankle/arm index <0.6 and/or ankle
pressure <65 mmHg

Figure 18-7  Injection of telangiectases and filling

of multiple tributaries
patients find them difficult to put on and wear
regularly due to discomfort. They are effective at
relieving swelling and pain symptoms, but have
minimal cosmetic benefit as monotherapy once
the varicosities have formed. It must be stressed
to the patients that without compression stock-
ings in their treatment plan more varicosities
and telangiectases will likely form despite more
aggressive treatment. Over-the-counter stocking
compression is 10–18 mmHg, which is typically
insufficient for patients with moderate to large
varicosities or chronic venous insufficiency. Most
patients require compression of between 20 and
40 mmHg. The stockings can be custom ordered
after appropriate measurements have been taken Figure 18-8  Erythema and edema following injection
and should be replaced at least yearly as they lose of telangiectases
their elasticity. Box 18-�
5 gives contraindications
to compression therapy.
hypertonic saline and dextrose ­ (SclerodexTM),
Sclerotherapy morrhuate sodium and sodium tetradecyl sul-
Sclerotherapy is the most common treatment fate (SotradecolTM). Osmotic agents work by
performed for patients with venous telangiectas- producing endothelial cell damage through
es, nonsaphenous varicosities, and reticular veins. ­dehydration. Detergents have a hydropho-
Surgical treatment is typically employed for larg- bic and hydrophilic pole. The hydrophobic
er saphenous vein varicosities. ­ Saphenous vein portion­ of the detergent molecule attaches to
insufficiency/reflux must first be ruled out and the cells in the vein walls, while the hydrophilic
treated prior to initiating sclerotherapy. Sclero- ­portion draws water into the cells causing ­rapid
sing agents include glycerin, hypertonic saline, overhydration and endothelial cell damage.

ERRNVPHGLFRVRUJ
 18

Chapter
Sclerotherapy of varicose and telangiectatic leg veins 225

Table 18-2  Important characteristics of sclerosing solutions

Sclerosing
solution Class Allergenicity Risks FDA approval Dose limitationa
Hypertonic saline Hyperosmotic None Necrosis of skin; Yes, as 6–10 mL (estimate
pain and cramping abortifacient based on authors’
experience)
Hypertonic saline Hyperosmotic Low (due only to Pain (much less No (sold in 10 mL of undiluted
and dextrose added phenethyl than hypertonic Canada) solution
(Sclerodex) alcohol) saline)
Sodium Emulsifier Rare, anaphylaxis Pigmentation; Yes 10 mL of 3%
tetradecyl sulfate necrosis of
(Sotradecol, skin (higher
Fibro-Vein, concentrations);
Thrombovar) pain with
perivascular
injection
Polidocanol Emulsifier Rare, anaphylaxis Lowest risk of No 10 mL of 3%
(Aethoxysklerol, necrosis; lowest
Aetoxisclerol, risk of pain;
Sclerovein) pigmentation
at higher
concentrations
Sodium Emulsifier Anaphylaxis Pigmentation; Yes (used 10 mL
morrhuate – highest risk necrosis or skin; primarily for
(Scleromate) pain; viscous, esophageal
difficult to inject varices)
Ethanolamine Emulsifier Urticaria, Pain on injection; No 10 mL
oleate anaphylaxis necrosis of
(Ethamolin) skin; dark brown
color makes
intravascular
placement more
difficult to confirm
Polyiodide iodine Corrosive Anaphylaxis, No 5 mL of 3%
(Varigloban, iodine
Variglobin) hypersensitivity
reactions
72% glycerin with Corrosive Extremely rare, Ineffective No 5 mL (estimated)
8% chromium anaphylaxis sclerosis (weak
potassium alum agent); very low
(Chromex, risk of necrosis;
Scleremo) lowest risk of
pigmentation
aIncreasedvolume per session is associated with an increased risk of allergenicity.
Source: Weiss RA, Weiss MA. Sclerotherapeutic agents used for treatment of spider and varicose veins: update 2002. J Drugs Dermatol 2002; 1 (1): 53-59

See Tables 18-2 & 18-3 for sclerosing agents and
­concentrations. Polidocanol (Aethoxysklerol)®
is not approved by the Food and Drug Admin-
istration. Box 18-�
6 lists the contraindications to
sclerotherapy.
At the time of consultation the preoperative
and postoperative instructions are discussed with
the patient. Some practical guidelines are included
in Box 18-� 7.
The appropriate technique for sclerotherapy
starts with appropriate positioning of the pa-
tient. The patient is placed in a supine position
and the areas to be treated are cleansed with
­alcohol. Shadow-free lighting of the affected ar-
eas allows for adequate visualization; additional
magnifying loupes/glasses may be necessary.
­Sclerotherapy should start proximally with the
feeder vessels and proceed distally down the legs.
A 3-mL ­ syringe with either a 30- or 33-gauge
needle bent to a 145° angle is inserted into the
feeder vein and the sclerosant is injected slowly
with a 5–15-s vein filling time (Fig. 18-� 6). This
allows for a slow low-pressure injection of the
sclerosant which optimizes results and allows for
maximum ­patient comfort during the procedure.
The injected telangiectases blanch as they fill

ERRNVPHGLFRVRUJ
226 Dermatologic Surgery

Table 18-3  Relative potency and use of sclerosing B ox 1 8 - 6

solutions
Contraindications to sclerotherapy
Sclerosing Concentration
Vein diameter solution (%) • History of or acute superficial thrombophlebitis
<0.4 mm Hypertonic saline 11.7 • Deep venous thrombosis or pulmonary embolism
Chromated glycerin 50 • Severe incompetence of the venous valves
Polidocanol 0.25 • Existing abdominal or pelvic tumors
Sodium tetradecyl 0.1 • Leg ulceration
sulfate
• Bedridden patients
Chromated glycerin 100
• Inflammatory bowel disease
Polidocanol 0.5
• Phlebitis migrans
Polyiodide iodine 0.1
• Cancer or those undergoing chemotherapy
Sodium morrhuate 1
• Unstable systemic disease
Ethanolamine 2
• History of venous stasis
oleate
• Obesity
0.4–3 mm Hypertonic dextrose
and saline • Pregnancy (also those breast-feeding)
Sodium tetradecyl 0.2–0.3 • Superficial varicose veins communicating to the deep venous
sulfate system
Polidocanol 0.5–0.75 • Allergy to the sclerosing agent
Polyiodide iodine 1 • Acute infection
Hypertonic saline 23.4 • Use caution in those taking oral contraceptives or hormone
replacement therapy (antiovulatory drugs)
Ethanolamine 5
oleate • Use caution in patients with arterial disease
Sodium morrhuate 2.5
3–5 mm Polidocanol 1–2
Sodium tetradecyl 0.5–1.0 be worn still varies. Studies reveal duration peri-
sulfate ods from 5 days to 3 weeks, but durations longer
Polyiodide iodine 2 than 3 weeks have fallen out of favor. After scle-
rotherapy, compression stockings should be worn
Sodium morrhuate 5
continuously during the recommended period. In
>5 mm Polidocanol 3–5 general, graduated compression of 15–18 mmHg
Perforators for 1–2 weeks should be worn following sclero-
Sodium tetradecyl 2–3
sulfate therapy of telangiectases and reticular veins of
Saphenopopliteal Polyiodide iodine 3–12
up to 3 mm in diameter. Larger reticular veins
and measuring 4–6 mm or minor varicose veins less
saphenofemoral than 6 mm in diameter should be compressed
junction with hose of 20–30 mmHg for 2 weeks. Gradu-
Modified from Goldman MP, ed. Sclerotherapy Treatment of Varicose and
ated compression hose of 30–40 mmHg should
Telangiectatic Leg Veins. St Louis: Mosby Year Book, 1991. be worn for 2 weeks or more after sclerotherapy
of varicose veins greater than 6 mm in diameter.
Adequate immediate compression therapy (with
with the clear sclerosant (Fig. 18-� 7), then subse- either stockings or foam pads) is essential to suc-
quently become inflamed and edematous (Fig. cessful sclerotherapy as it provides direct contact
18-�8). Compression should be applied to the of the inner walls of the veins to facilitate effec-
site ­ immediately after ­ injection. Massaging the tive fibrosis, reduces the risk of thrombus forma-
injected area, ­ immediately upon withdrawal of tion, decreases the incidence of ­ pigmentation,
the ­needle, away from the puncture site into the decreases the risk of new telangiectatic matting
smallest branches of the ­ telangiectases may de- in treated areas, more rapidly dilutes the scle-
crease the risk of bruising,­ reflux, and extravasa- rosing agent, and ultimately provides a better
tion of the sclerosant. long-term outcome of treated vessels. Adequate
Adequate compression immediately after scle- ambulation following sclerotherapy is also essen-
rotherapy is recommended. Consensus on the tial. See Box 18-� 8 for complications following
duration for which compression stockings should sclerotherapy.

ERRNVPHGLFRVRUJ
 18

Chapter
Sclerotherapy of varicose and telangiectatic leg veins 227

B ox 1 8 - 7
Preoperative and postoperative guidelines
for sclerotherapy
Preoperative instructions
Avoid shaving legs for 2 days prior to the scheduled procedure.
Avoid blood-thinning drugs (such as aspirin, ibuprofen, vitamin E,
etc.) for 7–10 days prior to the scheduled procedure.
Bring loose-fitting shorts to wear during the procedure.
Bring the medical-grade support pantyhose recommended by
the physician.
A light breakfast or lunch is recommended 1 h prior to the
procedure.
Postoperative instructions
Normal activity may be resumed, but avoid strenuous physical
activity (such as aerobics, jogging, heavy lifting) for the first
2–3 days after the procedure.
Avoid hot baths or showers for 24 h after the procedure.
Avoid prolonged standing in one position. If necessary, move
your feet or toes frequently, or support one foot on a small
stool or box.
Wear the medical-grade support pantyhose for the first 24 h
and during the day for 7 days.
Do not apply creams or lotions to the legs for the first 24 h after
the procedure.
If swelling occurs over an injection site, elevate and apply ice
to the affected extremity.
Small dark clots may develop in the treated veins. If so, let the
physician know when the area becomes painful or red. This
area may be removed by making a small incision over the top
of the clot.
A small, superficial ulceration of the skin may occur over
an injected vein. Contact the physician should this happen.
Meticulous wound care with hydrogen peroxide and a healing
ointment will help expedite its healing and prevent a scar from
forming.
Irritation of the injected vein (superficial thrombophlebitis)
rarely occurs. This can be treated with compression stockings
and anti-inflammatory medications, such as aspirin and
ibuprofen.
Repeat treatments may be performed after 6–8 weeks, as
needed.
If the underlying cause of the varicosities/­
telangiectases is addressed and proper technique
with adequate postsclerotherapy compression is
maintained, the risk of recanalization will de-
crease due to permanent vessel fibrosis.
Laser treatment of spider veins
The development of new lasers over the past
20 years has led to increased efficacy and safety
when using laser technology to treat telangiecta­
ses. Laser or light therapy is used primarily to treat
B ox 1 8 - 8
Complications of sclerotherapy
• Pain during and following injections (mainly with hypertonic
saline and glycerin solutions)
• Urticaria directly following injections but typically resolves
within 30 min
• Hyperpigmentation
• Telangiectatic matting
• Superficial thrombophlebitis
• Edema
• Necrosis or ulceration (typically due to extravasation or high
concentrations of sclerosant)
• Deep venous thrombosis
• Anaphylaxis (rare)
• Blistering
• Recurrence of treated vessels
B ox 1 8 - 9
Indications for laser therapy
• Small-caliber isolated telangiectases without varicosities
• Adjunctive treatment
• Matted telangiectases
• Fine telangiectases
• Allergy to sclerosant
• Patients with needle phobia
• Patients who have failed sclerotherapy or had unacceptable
side-effects
small-caliber telangiectases without ­ underlying
varicosities or as an adjunctive ­ treatment for
telangiectases after using another method to treat
the varicosities (Box 18-� 9). Typically more than
one session is needed, at 6–12-week ­ intervals.
­Patients must be advised strongly against tanning
prior to and following the procedure to avoid the
risk of dyschromia. Side-effects of ­ laser therapy
include pain, bruising, blistering, dyschromia,
transient hemosiderin staining, and rarely ­scarring.
See Chapter 19 for an in-depth discussion of laser
treatments of ­spider veins.
A number of surgical approaches for varicose veins
are available including saphenous vein stripping,­
ligation of the saphenofemoral or sapheno-
popliteal junction, short stripping of the greater
saphenous vein in the thigh, ambulatory phlebec-
tomy, endovenous laser or radiofrequency­ abla-
tion, and transilluminated power ­ phlebectomy.

ERRNVPHGLFRVRUJ
228 Dermatologic Surgery
Sclerotherapy may be performed after the larger
varicosities have been addressed with one or more
of these approaches.
Further reading
Bergan J. Surgical management of primary and
recurrent varicose veins. In: Gloviczki P, Yao J,
eds. Handbook of Venous Disorders: Guidelines
of the American Venous Forum, 2nd edn. London:
Arnold Press, 2001:287–302.
Bergan JJ, Sparks SR, Owens EL, et al. Growing the
vascular surgical practice: venous disorders. Cardio-
vasc Surg 2001;9:431–4318.
Bradbury A, Evans C, Allan P, et al. What are the
symptoms of varicose veins? Edinburgh vein
study cross sectional population survey. BMJ
1999;318:353–356.
Coon WW, Willis PW, Keller JB. Venous thrombo­
embolism and other venous disease in the
Tecumseh Community Health Study. Circulation
1973;48:839–846.
Dover JS, Sadick NS, Goldman MP. The role of
lasers and light sources in the treatment of leg
veins. Dermatol Surg 1999;25:328–336.
Fedor L, Kistner RL, Eklof B. Surgical manage-
ment of deep venous reflux. Semin Vasc Surg
2002;15:50–56.
Fowkes FGR, Evans CJ, Lee AJ. Prevalence and risk
factors of chronic venous insufficiency. Angiology
2001;52(Suppl):S5–S118.
Fronek HS. Noninvasive examination of the venous
system in the leg: presclerotherapy evaluation.
J Dermatol Surg Oncol 1989;15:170–173.
Fronek HS. Noninvasive examination of the patient
before sclerotherapy. In: Goldman MP, ed. Sclero-
therapy: Treatment of Varicose and Telangiectatic
Leg Veins. St Louis: Mosby Year Book, 1991:
108–157.
Goldman MP. Polidocanol (Aethoxyskerol) for sclero­
therapy of superficial venules and telangiectases. J
Dermatol Surg Oncol 1989;15:204–209.
Goldman MP. Anatomy and histology of the venous
system of the leg. In: Goldman MP, ed. Sclerother-
apy: Treatment of Varicose and Telangiectatic Leg
Veins. St Louis: Mosby Year Book, 1991:7–31.
Goldman MP. Pathophysiology of varicose veins. In:
Goldman MP, ed. Sclerotherapy: Treatment of
Varicose and Telangiectatic Leg Veins. St Louis:
Mosby Year Book, 1991:61–818.
Goldman MP. Mechanism of action of sclerotherapy.
In: Goldman MP, ed. Sclerotherapy: Treatment of
Varicose and Telangiectatic Leg Veins. St Louis:
Mosby Year Book, 1991:183–218.
ERRNVPHGLFRVRUJ
Goldman MP. Complications and adverse sequelae of
sclerotherapy. In: Goldman MP, ed. Sclerotherapy:
Treatment of Varicose and Telangiectatic Leg Veins.
St Louis: Mosby Year Book, 1991: 219–2618.
Goldman MP, Bennett RG. Treatment of telangiecta-
sia: a review. J Am Acad Dermatol 1987;17:
167–182.
Goldman MP, Kaplan RP, Oki LN, Cavender PA,
Strick RA, Bennett RG. Sclerosing agents in the
treatment of telangiectasia: comparison of the
clinical and histological effects of intravascular
polidocanol, sodium tetradecyl sulfate, and hyper-
tonic saline in the dorsal rabbit ear vein model.
Arch Dermatol 1987;123:1196–1201.
Goldman MP, Weiss R, Bergen J. Diagnosis and
treatment of varicose veins: a review. J Am Acad
Dermatol 1994;31:393–413.
London NJM, Nash R. Varicose veins. BMJ
2000;320:1391–1394.
Neumann HAM. Compression therapy with medical
elastic stockings for venous diseases. Dermatol
Surg 1998;24:765–770.
Nicolaides AN. Investigation of chronic venous
insufficiency: a consensus statement. Circulation
2000;102(20):e126–e163.
Sadick NS. Treatment of varicose and telangiectatic
leg veins with hypertonic saline: a comparative
study of heparin and saline. J Dermatol Surg Oncol
1990;16:24–28.
Sadick NS. Sclerotherapy of varicose and telangiec-
tatic leg veins: minimal sclerosant concentrations
of hypertonic saline and its relationship to vessel
diameter. J Dermatol Surg Oncol 1991;17:65–70.
Somjen GM, Ziegenbein R, Johnston AH, Royle JP.
Anatomical examination of leg telangiectases
with duplex scanning. J Dermatol Surg Oncol
1993;19:940–9418.
Thibault P, Bray A, Wlodarczyk J, Lewis W. Cosmetic
leg veins: evaluation using duplex venous imaging.
J Dermatol Surg Oncol 1990;16:612–618.
Weiss RA, Weiss MA. Resolution of pain associ-
ated with varicose and telangiectatic veins after
compression sclerotherapy. J Dermatol Surg Oncol
1990;16:333–336.
Weiss RA, Weiss MA. Doppler ultrasound findings
in reticular veins of the thigh subdermic lateral
venous system and implications for sclerotherapy.
J Dermatol Surg Oncol 1993;19:947–951.
Weiss RA, Weiss MA, Goldman MP. How minor
varicosities cause leg pain. Contemp Ob Gyn
1991;36(8):113–1218.
Weiss RA, Weiss MA. Sclerotherapeutic agents used
for treatment of spider and varicose veins: update
2002. J Drugs Dermatol 2002;1(1):53–59.

Lasers: physics
and medical indications
Theresa Dressler Conologue
Clinical overview
Key Points
• Lasers and their use in dermatology have
advanced significantly over the past 20 years.
• Lasers is an acronym for Light Amplification by
the Stimulated Emission of Radiation.
Laser use in dermatology has made significant
­advances over the past 20 years. With the im-
provement in laser technology, the demand for
laser surgery has grown. Increasing numbers of
patients and physicians are interested in laser sur-
gery due to the ease of use, lower risk of compli-
cations, and successful treatment of a wide variety
of cutaneous concerns (Table 19-1).
Lasers (Light Amplification by the ­Stimulated
Emission of Radiation) were first developed
based on the principles using stimulated emis-
sions of microwave radiation. After demonstra-
tion in 1954 of the ‘maser’ principle, systems
based on visible light were developed. The first
laser was built in 1960 by Theodore Maiman,
using a synthetic ruby rod stimulated with
high-intensity flashlamps generating millisec-
ond pulses of coherent 694-nm red light. A few
years later, Dr Leon Goldman began research
on interaction of laser light in skin, including
early human studies. Early on lasers came with
a significant number of side-effects. Scar forma-
tion and pigment alteration were common side-
effects due to excess thermal injury to the skin.
However, in 1980 the theory of “selective pho-
tothermolysis” was born. Anderson and Parrish’s
landmark article demonstrated the concept of
a pulsed laser beam. This allowed specific de-
struction of a target, with minimal unwanted
thermal injury, while sparing the surrounding
normal tissue.
Laser physics
Key Points
• Lasing mediums determine the wavelength of operation. This allows much higher peak ­powers
a particular system and may be solid, liquid, than are available in true continuous opera-
or gas.
ERRNVPHGLFRVRUJ
19
Chapter
• Laser light is coherent, collimated, and
monochromatic.
• Laser output can be continuous wave or pulsed.
• Laser systems can be long pulsed (LP), with
pulse duration ranging from 450 ms to 40 ms, or
quality switched (QS), creating a very short pulse
of 5–100 ns.
• The key measurements that determine the laser
output are: energy, power, fluence, spot size,
irradiance, and exposure time.
• Based on selective photothermolysis, lasers can
target a particular chromophore while sparing the
surrounding tissue.
• The main target chromophores are: water,
hemoglobin, and melanin.
The basic components of laser systems are lasing
medium, source of excitation for that medium,
and mirrors to reflect the excited photons back
to the cavity containing the medium. Lasing me-
diums vary and may be solid (e.g. ruby), liquid
(e.g. dye), or gas (carbon dioxide); they determine
the wavelength of a particular system. Laser light
itself is unlike ordinary light. It is coherent, colli-
mated, and monochromatic. Coherence is defined
by the laser’s ability to travel in a synchronized
phase. The collimation of laser light refers to the
parallel nature of the beam in which the narrow
intense beam of light can propagate across long
distances without light divergence. Collimated
light can be focused into small spots, allowing for
precision. Laser light is monochromatic, referring
to the single wavelength of the beam determined
by the lasing medium; this property allows laser
light to deliver energy to specific tissues.
Laser output can be continuous wave (CW)
or pulsed. CW lasers emit a constant energy out-
put. Lasers such as the CW carbon dioxide or the
original argon lasers emitted a constant beam of
energy, measured as power in watts (W), resulting
in nonselective tissue injury. Quasi-CW lasers op-
erate by emitting fast, short, repetitive bursts of
pulses of light, producing an interrupted emission
of constant laser energy, simulating continuous
tion and permits the use of ­scanners to ­separate ­
230 Dermatologic Surgery

Table 19-1  Lasers used to treat vascular and melanocytic lesions

Wavelength (nm) Laser type Chromophore Cutaneous application
532 (green) Potassium–titanyl-phosphate (KTP) Hemoglobin Pigmented and vascular lesions
Q-switched Nd:YAG Tattoo ink (red) Pigmented lesions, red/orange/
yellow tattoos
585–600 (yellow) Pulsed dye Hemoglobin Vascular lesions, scars, striae,
verrucae, nonablative remodeling
Hematoporphyrins
694 (red) Ruby
• QS Tattoo ink (black/blue) Pigmented lesions, blue/black/
green tattoos
• Normal mode Melanin Hair removal
755 (infrared) Alexandrite
• QS Tattoo ink (black/blue/ Pigmented lesions, blue/black/
green) green tattoos
• Normal mode Melanin Hair removal, leg veins
800–810 (infrared) Diode Melanin Hair removal, leg veins
1064 (infrared) Nd:YAG

• QS Tattoo ink (black/blue) Pigmented lesions, blue/black

tattoos
• Normal mode Melanin Hair removal, leg veins,
nonablative dermal remodeling

adjacent pulses, reducing the ­ potential for
­thermal damage. Pulsed lasers emit a high-energy
laser light with ultrashort pulse ­ durations and a
long intervening time (0.1–1 s) between pulses.
Laser systems can be long pulsed (LP), with pulse
duration ranging from 450 ms to 40 ms, or qual-
ity switched (QS), creating a very short pulse
of 5–100 ns. QS lasers use shutters to build up
laser energy maximally, permitting the release
of ­ ultrashort high-energy bursts that cause ex-
tremely rapid heating of the target. The ­resulting
shockwaves cause a photomechanical disruption
of the target.
There are key measurements that determine
the laser output. Energy, the amount of work of
a laser, is measured in joules. Power, or rate at
which the laser expends energy, is measured in
joules per second. Fluence, the energy density, is
measured in joules per square centimeter. Spot
size is determined by the cross-sectional area of
the laser beam and directly affects the fluence
and irradiance. Irradiance, the power divided by
the spot size, is expressed in watts per square
centimeter. The ability to manipulate the differ-
ent measurements – fluence, irradiance, spot size,
exposure time, power, and energy – allows differ-
ent parameters to be adjusted for specific clinical
applications.
Selective photothermolysis is the principle of
a laser’s ability selectively to target a particu-
lar chromophore while sparing the surrounding
t­ issue. For this to be effective, the laser must
first be able to produce an appropriate wave-
length that is absorbed by the key chromophore
in the particular lesion being treated. Second,
the exposure time or the pulse duration of the
laser beam must be shorter than the time it
takes for a chromophore to cool to one half of
its peak temperature, defined as the thermal re-
laxation time. This allows heating of the target
chromophore while preventing heat diffusion to
the surrounding tissue (Table 19-2). Finally, the
energy density or fluence must be strong enough
to destroy the target within the allotted pulse
duration. Putting it all together allows one to
tailor a specific wavelength, pulse duration, and
fluence to target cutaneous lesions selectively
without nonselective damage to surrounding
tissues (Table 19-3).
Table 19-2  Target chromophores and thermal
relaxation times for vascular and pigment lasers
Target Size Thermal relaxation time
Melanosome 1 mm 1 ms
Erythrocyte 7 mm 20 ms
Blood vessel 50 mm 1 ms
Ectatic blood 100 mm 15 ms
vessel

ERRNVPHGLFRVRUJ
 19

Chapter
Lasers: physics and medical indications 231

Table 19-3  Side-effects of lasers and light sources (blue–green light), argon-pumped tunable dye, kryp-
ton 568 nm, copper vapor/bromide 578 nm, potas-
Pulsed-dye laser Purpura, swelling, sium–titanyl-phosphate (KTP) 532 nm, pulsed-dye
hypopigmentation (tanned
laser (PDL) 577–600 nm, neodymium:yttrium–alu-
and darker skin types more
at risk), postinflammatory minum–garnet (Nd:YAG) 532 nm and Nd:YAG
hyperpigmentation, crusting, 1064 nm.
urticaria papules The introduction of the flashlamp-pumped
PDL changed the way we treat vascular lesions.
KTP lasers Erythema, urticaria edema
lasting up to 36 h, crusting,
Some of the early PDL systems used a wave-
scarring length of 577 nm, which was later increased to
585 nm to allow for deeper tissue penetration.
LP Nd:YAG lasers Scarring, crusting, Second-generation PDLs have been developed
erythema, urticarial edema,
with longer wavelengths (595 and 600 nm) and
swelling, postinflammatory
hyperpigmentation, blisters pulse durations ranging from 0.45 to 40 ms. This
longer pulse duration allows for reduced inten-
IPL Sunburn-like erythema, sity and duration of purpura, as well as the use
edema, burning, scarring
of higher fluence for treating larger vessels. In ad-
Tattoo/pigment lasers Hypopigmentation, scarring, dition, dynamic cooling devices have been incor-
pinpoint bleeding, crusting, porated into the laser system to increase patient
blisters, paradoxical comfort while protecting the epidermis from
darkening of flesh-colored thermal injury.
tattoos, chrysiasis, allergic
The Nd:YAG laser uses a KTP crystal to halve
reaction to tattoo pigment
the 1064-nm wavelength (frequency doubling) so
that it emits a 532-nm wavelength in the green
Medical treatment options: spectrum. The light is absorbed by hemoglobin
about the same as the 585-nm light, with a slightly
vascular laser systems shorter depth of penetration. An advantage of the
Key Points KTP system is that pulse durations are extended
to the 1–200-nm range, providing slow heating
• Vascular laser systems target intravascular of the vessels and thereby avoiding purpura. The
oxyhemoglobin.
disadvantage is the increased risk in dark-skinned
• Oxyhemoglobin has three primary peaks at 418,
518, and 577 nm.
individuals as a result of increased absorption of
• There is a broad oxyhemoglobin absorption band melanin at the lower wavelength.
in the 800–1000-nm range Near-infrared lasers are useful in treatment
• Absorption of melanin decreases as wavelength of vascular lesions owing to their greater depth
increases. of penetration and the broad oxyhemoglobin
• Longer wavelengths have greater depth of ­absorption band in the 800–1000-nm range.
penetration and can be used to target deep Intense pulsed-light (IPL) systems, although
vascular lesions. not a laser, use a high-intensity flashlamp to emit a
• Intense pulsed-light systems, although not a broad spectrum of noncoherent light ranging from
laser, use a high-intensity flashlamp to emit a
500 to 1200 nm. This includes green, yellow, red,
broad spectrum of light ranging from 500 to
1200 nm. and infrared light, thereby delivering hundreds or
thousands of colors of light at a time. Pulsed-light
machines use “cut off” filters selectively to deliver
The key element in all vascular laser systems is the desired wavelengths. These wavelengths can
the ability to target intravascular oxyhemoglobin. be customized to reach the specific target chromo-
This relies on the absorption peaks of oxyhemo- phore, or skin component, being treated, and can
globin, which lie in the visible light range, with be modified with each pulse. As longer wave-
three primary peaks at 418, 518, and 577 nm. In lengths penetrate deeper into the target, filters can
the infrared region there is a broad oxyhemo- be used to block out shorter visible wavelengths,
globin band, beyond 900 nm. As the absorption of resulting in the ability to target deeper or larger-
melanin decreases over the range of wavelength diameter blood vessels while avoiding superficial
from 200 to 2000 nm, lasers in the infrared region parts of the skin. IPL sources have multiple pulse
have an advantage of targeting hemoglobin with modes, fluences ranging from 3 to 90 J/cm2, and a
minimal interference of melanin. In addition, the large rectangular footprint. Prior to treatment, a
longer wavelength has a greater depth of penetra- thick layer (1–2 mm) of water-based gel is applied
tion and can be used to target deep vascular le- to protect the skin. It is recommended to perform
sions. In the past few decades a number of laser multiple test spots carefully with increasing en-
systems have been developed to target specific ergy until a faint erythema is achieved. The pulses
vascular lesions, including the argon 488–514 nm should be applied with ­minimal overlap. A major

ERRNVPHGLFRVRUJ
232 Dermatologic Surgery

advantage of IPL systems is that they can be used

to treat a broad spectrum of disorders with mini-
mal side-effects (Box 19-1).

B ox 1 9 - 1
Intense pulsed light sources: clinical
applications

• Hair removal
• Rosacea
• Facial erythema
• Port-wine stain
• Hemangioma Figure 19-1  Port-wine stain
• Ephelids
• Photorejuvenation
• Rhytids
• Scars
• Acne
• Tattoo

Comparative outcomes
Port-wine stains
Key Points
• Port-wine stain (PWS) is a progressive vascular
malformations that occurs in 0.03% of newborns.
• They begin as pink macules, becoming
thickened and even nodular by adulthood.
• Treatment should begin as early as possible.
• Pulsed-dye lasers remain the “gold standard” of
laser treatment.
• Most patients require a series of treatments,
ranging from 5 to 12, with average treatment
intervals of 4–6 weeks.
• Approximately 80% fading is usually seen after 10
treatments.
• PWS of the centrofacial regions (medial aspect
of the cheek, upper cutaneous lip, and nose) and
V2 dermatome responds less favorably.
Port-wine stains (PWSs) are progressive vascular
malformations (Fig. 19-1). They occur in 0.03%
of newborns and are a congenital malformation of
small-caliber vessels. They can occur anywhere on
the body, but nearly two-thirds are found on the
face. The natural progression of the lesions is to
begin as a pink macule, becoming thickened and
even nodular by adulthood. Given the natural
history of these lesions, it is recommended to start
treatment as early as possible. Children whose
treatments begin at less than 1 year of age show a
marked reduction in the lesion. PDLs remain the
“gold standard” of laser treatment of PWS. Most
Figure 19-2  Treated port-wine stain
patients require a series of treatments, ­ ranging
from 5 to 12, with gradual clearing at each suc-
cessive treatment. Average treatment intervals
range from 4 to 6 weeks. Approximately 80% fad-
ing is usually seen after 10 treatments. Clearance
rates depend on a number of factors, including
anatomic location and size of the lesion. In one
study, PWS of the centrofacial regions (medial as-
pect of the cheek, upper cutaneous lip, and nose)
responded less favorably than other grouped re-
gions (periorbital, forehead/temple, lateral aspect
of the cheek, neck, and chin). In addition, evalu-
ation by dermatomal distribution revealed that
dermatome V2 showed a good response (mean
lightening 73.8%), combined dermatomes V1,
V3, and C2/C3 showed an excellent response
(mean lightening 82.4%), and midline lesions had
an excellent response rate in adults and children,
with mean lightening of 92.4%.
The most common side-effect is purpura,
which may occur during the procedure and can
persist for up to 2 weeks (Fig. 19-2). Hyperpig-
mentation has been reported in darker-skinned
patients, but is not permanent. Vascular blanch-
ing and atrophic scaring is a rare but a significant
complication, especially in younger patients.
Although not considered a side-effect, patients

ERRNVPHGLFRVRUJ

Lasers: physics and medical indications
Figure 19-3  Hypertrophic port-wine stain
should be informed about the possibility of re-
darkening of PWS at long-term follow-up.
Optimal treatment parameters have yet to be
defined in the literature. Typical settings for children
receiving the 585-nm laser are: 7.0-mm spot size,
0.45 ms, 6.0 J/cm2, or 10.0-mm spot size, 0.45 ms,
5.0–6.0 J/cm2. Settings for the 595-nm laser are:
7.0 mm spot size, 1.5 ms, 8.0–11.0 J/cm2, and 10.0-
mm spot size, 1.5 ms, 5.0–9.5 J/cm2. In general, a
lower fluence is used in children, and in areas with
an increased risk for scarring such as around the eyes,
upper lip, and neck. Hypertrophic PWS (Fig. 19-3)
requires a large spot size and high fluence. Typical
settings with a 7-mm spot size can be up to 13 J/
cm2, and at 10.0 mm 7.5 J/cm2 (Table 19-4). Multi-
ple pass treatments in hypertrophic PWS have been
shown to be effective. The technique uses longer
wavelength to target deeper vessels, with a second
pass using a shorter (585 nm) wavelength to hit the
smaller, more superficial, vessels. An overlap of up
to 35% has been suggested to avoid an unwanted
speckled appearance that can occur in treated PWS.
­Patients need to be informed that overlapping may
increase or cause more severe side-effects.
Other lasers have been shown to be effective in
treatment of PWS. The KTP laser has been shown
to be effective in treating PWSs that were refracto-
ry to PDL. One study showed significant lightening
of PWS at settings of 18–24 J/cm2 with a pulse du-
ration ranging from 9 to 14 ms. Although patients
preferred the treatment over PDL, scarring (10%)
and hyperpigmentation (7%) was ­ noted. Longer
wavelengths such as the Alexandrite (755 nm) and
Nd:YAG (1064 nm) can be beneficial in the treat-
ment of hypertrophic and resistant PWS. Similar
clearance rates were found when a 595-nm PDL
was compared with the long-pulsed Nd:YAG in
the treatment of PWS. These near-infrared lasers
ERRNVPHGLFRVRUJ
19
Chapter
233
Table 19-4  Recommendations for pulse durations
based on target size
Target size (mm) Pulse duration (ms)
100 1
300 10
500–1000 20–100
In general, pulse duration should increase as the target size increases. Adapted
from Zelickson B. Laser treatment of leg veins. In: Pearls from the 10th
International Symposium on Cosmetic Laser Surgery, Las Vegas, April 2001.
penetrate deeper when used at a higher fluence.
Care must be taken to assure epidermal cooling.
IPL has recently been studied in the treatment
of PWS. In a multicenter study of 37 adults, the
PhotoDerm VL showed good results in ­treatment-
resistant PWS, as well as in purple and ­hypertrophic
PWS. Complete clearance of pink lesions was
shown after an average of four sessions, and red le-
sions after an average of 1.5 sessions. Dark purple
PWS lightened 70–99% after an average of four
sessions. Another study in PDL-resistant PWS
showed improvement in 7 of 15 patients, with 6
showing 75–100% ­improvement.
Pearls
Treatment of port-wine stains with pulse-dye laser
Color: Purple is good, gray is bad. Start with
a test site to assess the best fluence. Graying
indicates epidermal injury and can result in
necrosis and scarring. Avoid overtreatment.
Crusting: Be prepared for crusting and instruct
patients to use topical ointment daily.
Contour: Begin treatment by outlining the lesion
to avoid treating unaffected areas.
Clean: Clean the treatment area with
nonflammable soap and water prior to treatment
to avoid interference of the laser light
The darker the skin, the longer the wait time
between treatments (8–16 weeks).
Begin treatment with the largest available spot size.
The target vessel size can be increased by plac-
ing the area in a dependent position or by the
application of heat.
Hemangiomas
Key Points
• Laser treatment of uncomplicated hemangiomas
remains controversial.
• PDL treatment in ulcerated hemangiomas has
been shown to be effective.
• Laser treatment should be at low fluence with a
short pulse duration, to trigger an active process
of regression, rather than ablation.
• Postinvolution residua responds well to laser
treatment.
234 Dermatologic Surgery
The treatment of hemangiomas remains contro-
versial owing to the self-resolving nature of these
lesions. One study of 121 patients showed that
the percentage of completely cleared hemangi-
omas at 1-year follow-up was significantly higher
in the group treated with PDL. However, when
looked at in terms of complete clearance or mini-
mal residual signs, there was no significant differ-
ence between the treated and untreated group.
The authors concluded that PDL should not be
used to treat uncomplicated hemangiomas. It
is important to recognize the laser used in this
study was an older model with no cooling device.
A more recent study looked at 52 Asian infants,
aged 1–3 months, with early hemangiomas. These
infants were assigned to PDL (585 nm) treatment
at 0.45 ms and 7 J/cm2 without epidermal cool-
ing or LPD laser (595 nm) treatment at 10–20 ms
and fluence of 9–15 J/cm2 with cryogen sprayed
cooling. At 1 year of age, outcome measures such
as clearance rate, time period of maximum pro-
liferation, and complications were assessed. A
higher clearance was found with the LPD laser:
65% compared with 54% in the PDL group.
Compared with the LPD laser, PDL-treated
children had more hypopigmentation (3 [12%]
versus 8 [31%]; P = 0.001), more hyperpigmen-
tation (2 [8%] versus 4 [15%]; P = 0.005), and
more textural changes (1 [4%] versus 6 [23%];
P = 0.001). It is important to keep in mind that
the PDL was not designed to treat hemangiomas
and, given the shallow depth of penetration
(1.2 mm), has little effect on thick tumors. The
fluences used for PWS treatment may become
treacherous ­because there is so ­little dermis be-
tween the ­target vessels. One author has recom-
mended low ­ fluence at 3–6 J/cm2 and a short
pulse duration, with the aim of triggering an ac-
tive process of regression, rather than ­ablation of
some ­abnormal vessels.
On the other hand, PDL treatment of ­ulcerated
hemangiomas has been shown to be effective.
Reports vary, but several have shown increased
healing, decreased pain, and an acceleration of
­involution. In one study 71 of 78 patients re-
sponded to laser therapy alone, with a mean of 2.0
treatments. Six patients with very large heman-
giomas required oral steroids (2–3 mg/kg ­ daily)
in combination with the PDL. After failing to
­improve on steroid therapy, two patients required
the addition of interferon to their treatment pro-
tocol. At a mean follow-up of 15 months there
was no sign of recurrence.
Before starting laser therapy it is important
to rule out other vascular lesions, such as venous
malformation, which can look similar to a hem­
angioma. Further, deep lesions will not respond
to PDL treatment. Magnetic resonance imaging
with gadolinium can be helpful in the diagnosis
of difficult cases.
ERRNVPHGLFRVRUJ
Most studies have used PDL lasers at a wave-
length of 585–595 nm with a pulse duration of
0.45–1.5 ms. Currently we use the long pulsed
tunable dye laser (LPTDL) with cryogen cooling
at a 7.0-mm spot size with a 0.45–1.5-ms pulse
duration and 3–7 J/cm2. In some cases intralesional
triamcinolone (Kenalog) at doses of 10–20 mg/mL
is used directly after the laser treatment.
Laser treatment of postinvolution residua is
generally accepted. The debate remains on how
long to wait to treat. Not only PDL but other la-
sers such as KTP and Nd:YAG can have benefit
in treating residual vascular lesions. Fatty atrophic
residual and scars can be improved with the car-
bon dioxide laser or Er:YAG. IPL may play a role
in treatment of posthemangioma residua, but it is
still too early to tell.
Facial telangiectases
Key Points
• Lasers are an excellent treatment choice for facial
telangiectases.
• Longer pulse durations can be used at
subpurpuric doses with little or no down time.
• An effective endpoint is observed vessel spasm.
• Evaluate the vessel size and depth; many larger-
caliber or deeper vessels require purpuric dosing
or deeper penetrating lasers.
Lasers are an excellent treatment choice for facial
telangiectases. Newer, tunable systems can give
dramatic results with little or no down time. In
the past, PDL treatments with short pulse dura-
tions resulted in significant purpura which lasted
for up to 2 weeks. Technologic advances allow
for longer pulse durations which can be used at
subpurpuric doses. Effective treatment requires
pulse stacking or multiple pulses to an endpoint
of observed vessel spasm. Flash darkening of the
vessel is seen with each pulse; the goal endpoint is
an observed transient oxidation and in some cases
blanching of the vessel.
In a study that compared pulse stacking with
lower fluence to a single pulse of higher fluence,
mean vessel clearing 1 week after treatment was
74.3% for the pulse stacked side and 58.5% for the
single pulsed side. Mean vessel clearing 6 weeks
after treatment was 87.6% for the pulse stacked
side and 67.4% for the single pulsed side. Another
study compared a single purpuric pass with four
subpurpuric passes, and showed that purpuric
fluences produced a greater reduction in ves-
sel diameter and arborization, whereas the sub-
purpuric doses were more effective in ­ reducing
background erythema. Of note, ­purpuric fluence
produced more significant edema and transient
hyperpigmentation in one patient.
Most patients prefer the subpurpuric ­approach,
and the use of pulse stacking enables treatment
with PDL that is cosmetically acceptable and

Lasers: physics and medical indications
e­ ffective. It important to evaluate the vessel size
and depth; many larger-caliber or deeper vessels
require purpuric dosing or deeper penetrating la-
sers. Typical settings with a 10-mm spot size range
from 6.5 to 7.5 J/cm2 with a pulse duration of
6–10 ms, and those for a 7-mm spot size range from
8.0 to 14 J/cm2 with pulse duration of 6–10 ms.
KTP lasers are also an effective and safe treat-
ment for facial telangiectases. The treated vessels
are drawn out with pulses applied directly over
the vessel to the endpoint of visible vessel blanch-
ing. It is important to have epidermal cooling, and
newer KTP systems are equipped with a cooled
sapphire tip, used with cold gel applied to the skin.
Typical fluence ranges from 9 to 14 J/cm2 at 2–
4-mm spot sizes. Limitations with KTP lasers are
in treating tanned or pigmented skin, due to com-
petitive melanin absorption. A recent split-faced
comparison of the 532-nm KTP and 595-nm
PDL demonstrated more effective treatment
­using the KTP, but more swelling and ­erythema.
Long-pulsed Nd:YAG is useful in treating
deeper reticulated facial veins, prominent vessels
around the nose, and facial telangiectases. Caution
must be taken to assure proper epidermal cooling
using both before and after cooling, and avoid-
ance of pulse stacking. Given the lower absorp-
tion spectrum of the wavelength, high fluences
are needed for effective absorption by the vessel.
Typical parameters range from 100 to 150 J/cm2,
with spot sizes of 2–6 mm and pulse widths of
25–100 ms depending on the size of the vessel.
Leg veins
Key Points
• Sclerotherapy remains the “gold standard.”
• Treat the deep incompetent feeder vessels first.
• Lasers are an effective tool for patients who
are needle phobic, have contraindications
to sclerotherapy, small vessels, or have
telangiectatic matting following sclerotherapy.
• Consider vessel size, depth, and patient skin type
in order to select the best modality for treatment.
• Shorter wavelengths work well for superficial
reddish telangiectases but are limited because of
melanin absorption.
• Longer wavelengths penetrate deeply and can
be used in darker skin tones with proper cooling
techniques.
• In general, pulse duration should increase as the
target size increases.
Laser therapy for leg veins has made significant
advancements over the past decade. Sclerother-
apy remains the “gold standard,” but lasers can
be used in patients who are needle phobic, have
contraindications to sclerotherapy, or have vessels
that are too small for effective treatment. Even
after successful sclerotherapy of leg veins, some
patients will require laser treatment for residual
ERRNVPHGLFRVRUJ
19
Chapter
235
t­ elangiectatic matting. In the author’s experi-
ence, most patients present with a wide variety of
­vascular ectasias and achieve the best results us-
ing a combination of techniques. It is important to
consider vessel size, depth, and patient skin type
in order to select the best modality for treatment.
Superficial reddish telangiectases have more
oxygenated blood flow and are better target-
ed with shorter wavelength visible light lasers
(500–600 nm). The drawback is the limited depth
of penetration and risk of hypopigmentation due
to the considerable melanin absorption. A study
comparing the 532-nm Nd:YAG with the 595-nm
pulsed dye laser showed that both were effective
in minimizing the appearance of leg telangiecta-
sias smaller than 1.0 mm.
Vessels that are deep blue, owing to their depth
and size, require longer wavelengths (800–1100 nm)
to penetrate deeply and selectively destroy the tar-
get chromophore. In particular, the 1064-nm Nd:
YAG laser has been shown to be effective in treat-
ing leg veins. With regard to skin type, the 1064-nm
wavelength has been shown to be safe for type V
skin, the 810-nm wavelength at super-long pulse
widths of 400–1000 ms is safe for type IV and mar-
ginal for type V skin, and the 755-nm wavelength
is limited to nontanned type I–III skin.
More recently, IPL has been used in the treat-
ment of leg veins. In one study patients with tel-
angiectases, cherry angiomas, or leg veins smaller
than 1 mm were more satisfied after IPL, whereas
patients with leg veins greater than 1 mm were
more satisfied after Nd:YAG therapy. Overall, sat-
isfaction with treatment of vascular lesions was
greater with Nd:YAG, although this method was
more painful.
Of the two primary clearance mechanisms, ves-
sel contraction and thrombosis, vessel contraction is
favored. Most side-effects occur with vessel throm-
bosis. To achieve constriction of the vessel, the use
of parameters that induce “slow” vessel heating
(longer pulses with long wavelengths) has been
suggested to decrease side-effects when using lasers
to treat leg veins of 0.2–2 mm in diameter, with the
exception of very small vessels (0.1–0.6 mm) in fair
skin, where an equal response to green and yellow
light short-wavelength lasers can be achieved with
much less pain and lower side-effect potential. This
is consistent with the extended theory of selective
photothermolysis where nonuniformly absorbing
structures, such as blood vessels, require longer
pulse durations for selective destruction. For vessel
closure to occur, the vessel wall, with resultant col-
lagen shrinkage, must be heated by diffusion from
the blood; this requires a significantly longer pulse
duration (see Table 19-4).
When using the 1064-nm Nd:YAG laser,
high fluences (350–600 J/cm2), small spot sizes
(<2 mm), and short pulse durations (15–30 ms)
are most effective for small red vessels (<1 mm),
236 Dermatologic Surgery
which are usually superficial, red, and have a high
oxyhemoglobin saturation. For larger blue ­vessels
(1–4 mm) that are deeper and have a lower oxy-
genated hemoglobin content, larger spot sizes
(2–8 mm), moderate fluences (100–350 J/cm2),
and extended pulse durations (30–50 ms) are
most efficacious. In general, pulse duration
should increase as the target size increases (Table
19-5). In a study that investigated the optimal
treatment parameters for vessel ablation in vivo
using the 1064-nm Nd:YAG laser and a 6.0-mm
spot size, for a vessel diameter of 0.2–1.0 mm
the ideal pulse width range was found to be 15–
60 ms with an optimal fluence of 80–110 J/cm2.
Improved cooling technologies in laser therapy
have not only improved results in the treatment
of leg veins while minimizing side-effects, but also
provides greater patient comfort. This is particu-
larly important when using higher wavelengths,
which have an increased risk of epidermal damage
and are generally more painful. The use of proper
cooling allows the delivery of higher energies
while maintaining epidermal protection. Several
types of cooling device have been incorporated
to provide direct cooling: copper-cooled plates or
water-cooled sapphire tips applied directly to the
skin, cooling gels, air-blowing cooling devices, and
cryogen-cooled spray devices.
There are some interesting but still limited
data on the use of two-pulsed visible and near-
­infrared lasers to treat leg veins. The theory is
based on a phenomenon called green light -
­ induced ­infrared absorption, whereby a pulse of
Table 19-5  Laser treatment of deep vascular lesions
using constant wavelength of 1064 nm
Increase with
Pulse duration Large-diameter
vessels
Higher vascular
volume
Spot size Deep vessels
Large-diameter
vessels
Fluence Pink or red
vessels
Small-diameter
vessels
Deep vessels
Small spot sizes
High-pressure
vessels
Adapted from Groot D, Rao J, Johnston P, Nakatsui T. Algorithm for using
a long-pulsed Nd:YAG laser in the treatment of deep cutaneous vascular
lesions. Dermatol Surg 2003;20(1):35–42.
green light ­changes the chemical constituents of
blood to met-­hemoglobin and results in enhanced
infrared ­absorption. Another approach to leg vein
treatment is the use of a bimodal approach in
which shorter wavelengths (500–600 nm) are uti-
lized to treat oxygenated red telangiectasias, and
longer wavelengths (800–1100 nm) to treat de-
oxygenated blue venulectasias and reticular veins.
However, this approach requires the utilization of
two lasers, or a laser plus an intense pulsed light
source, in order to achieve the desired effects
(Table 19-6).
The endovenous laser is fast approaching the
mainstream for the treatment of incompetent
veins. One of the first published studies in 2001
showed short-term safe results using fiberoptic
insertion and photocoagulation of the greater
saphenous vein with a diode 810-nm laser. Vari-
ous wavelengths, including 810, 940, 980 nm
(all target hemoglobin) and 1320 nm (targets
water), have been used to produce intravascular
destruction of varicose veins. In 2002, the US
Food and Drug Administration (FDA) approved
endovenous laser treatment as a minimally inva-
sive method for ablating incompetent saphenous
veins. The procedure is performed in the office
under local anesthesia using a form of directed
laser energy from the inside to shrink and seal the
targeted vein. Tumescent anesthesia is used, not
only as a safe alternative to general anesthesia, but
because it protects perivascular tissues from the
thermal effects of the intravascular energy. It also
provides greater efficacy by collapsing the treated
vein, allowing for better absorption of energy by
the target chromophore. The 1320-nm water-
­targeting device appears to be associated with
less pain and bruising than 810-, 940-, or 980-nm
Decrease with
hemoglobin-targeting endovenous devices.
Small-diameter Treatment of varicose veins should follow a
vessels logical and algorithmic approach:
Lower vascular
volume 1 Diagnose and treat the deep incompetent
feeder vessels.
Superficial
vessels 2 Perform sclerotherapy, proceeding from the
largest to the smallest vessels – 80–90% of
Small-diameter vessels respond to a single treatment.
vessels
Purple or blue able 19-6  Recommended light and laser systems
T
vessels based on vessel size
Large-diameter Size of vessel (mm) Recommended system
vessels
0.1–0.4 585/595-nm PDL, 532-nm
Superficial KTP, 500–1200-nm
vessels (noncoherent) IPL
Large spot sizes 0.4–1.0 585/595-nm long pulse
Flaccid vessels PDL, intense pulsed light,
755-nm pulsed alexandrite,
800–940-nm diode, 1064-nm
long pulsed Nd:YAG
1.0–3.0 Diode, Nd:YAG
ERRNVPHGLFRVRUJ

Lasers: physics and medical indications
3 Employ lasers and IPL sources for residual
vessels that do not respond to sclerotherapy,
are too small to be injected, or remain after
feeding vessels have been treated.
Pearls
Leg vein treatment
 Treat incompetent feeder vessels first.
Sclerotherapy remains the first-line treatment.
Assess the residual vessel for size and depth to
guide treatment.
Use hydrostatic forces to help distend vessels
and provide a bigger target.
Superficial red vessels require higher fluence
and shorter pulse durations.
Large blue vessels require moderate fluences
and extended pulse durations.
Proper cooling is needed for epidermal
protection.
Medical treatment options: pigmented
lesions
Key Points
• There are two broad categories of laser options:
pigment selective and pigment nonselective.
• QS lasers (quality switched) are pigment-
selective lasers designed to target melanosomes
based on their short thermal relaxation time using
nanosecond pulse durations.
• Nonselective lasers are absorbed by water,
producing heat in the epidermis and dermis, but
do not specifically target pigment.
• Absorption of melanin decreases as the
wavelength increases from 200 to 2000 nm.
Laser treatment options for pigmented lesions
can be broken down into two broad categories:
pigment selective and pigment nonselective.
Pigment-selective lasers are designed to tar-
get melanosomes based on their short thermal
relaxation time using nanosecond pulse dura-
tions. This short pulse duration causes a local
shockwave, termed a photoacoustic or photo-
mechanical effect, resulting in damage to the
target. As described above, absorption of mela-
nin decreases as the wavelength increases from
200 to 2000 nm. A variety of lasers and light
sources have been developed using these princi-
ples ­(Table 19-7).
Green light lasers are useful in treating su-
perficial pigmented lesions. Examples are the
PDL 510 nm, with a 300-ns pulse of energy, and
the QS frequency-doubled 532-nm Nd:YAG
laser, with a 5–10-ns pulse duration. Because
of the wavelength, these lasers also target he-
moglobin and are useful in the treatment of
superficial ­ vascular lesions. The side-effect of
ERRNVPHGLFRVRUJ
19
Chapter
237
Table 19-7  Selective and nonselective pigment lasers
Nonselective pigment CO2, Erb:YAG, fractional
lasers
Selective: epidermal QS 532-nm frequency-
doubled Nd:YAG
QS 694-nm ruby
QS 755-nm alexandrite
Selective: dermal QS 800-nm diode
QS 1064-nm Nd:YAG
Other IPL 500–1200 nm
purpura ­ following laser irradiation is common.
Unwanted vascular damage can be avoided by
applying firm pressure during treatment to re-
move hemoglobin through compression of the
dermal vessels. QS red light lasers have longer
wavelengths and allow deeper penetration into
the dermis. Examples of red light lasers are the
Q-switched ruby 694-nm laser, the Q-switched
755-nm laser, and the near-infrared Q-switched
1064-nm laser. The 1064-nm near-infrared laser
has decreased absorption of melanin, but al-
lows for deep penetration into the skin (up to
6 mm).
Nonselective lasers are absorbed by water, pro-
ducing heat in the epidermis and dermis, but do
not specifically target pigment. The 10 600-nm
carbon dioxide laser and the 2940-nm Er:YAG
laser are useful in treating superficial and some
dermal pigmented lesions. A new concept in re-
surfacing is becoming popular; fractional resurfac-
ing uses a mid-infrared laser in which microbeams
are used to create millions of microscopic thermal
treatment zones. This approach pixilates the skin,
leaving areas of intact skin between each treat-
ment zone and allowing for faster healing. Frac-
tional resurfacing can be useful in treating a host
of pigment disorders.
IPL can be used to target pigment through
the use of proper filters. Given the wide range of
wavelengths (500–1200 nm), IPL has been show
to be versatile in treatment of epidermal pigment.
The mechanism by which IPL removes pigmenta-
tion is not completely understood. In one study
reflectance-mode confocal microscopy and op-
tical coherence tomography showed IPL to be
­effective in removing melanosomes by promoting
a rapid differentiation of keratinocytes, accompa-
nied by an upward transfer of melanosomes along
with necrotic keratino­cytes; this resulted in the
elimination of melanosomes as the microcrusts
were removed from the skin.
All patients treated with lasers should be rou-
tinely screened for previous parenteral or oral
gold therapy, as QS lasers are associated with a
risk of laser-induced chrysiasis.
238 Dermatologic Surgery
Pearls
Treatment of pigmented lesions
Recognize the depth of pigment to determine the
best laser options.
Wood’s lamp evaluation can help determine
depth of pigment with more superficial pigment
accentuation.
Longer wavelengths are needed to treat deeper
pigmented lesions.
Avoid pulse stacking or overtreatment
because of the high risk of postinflammatory
hyperpigmentation.
Transient epidermal whitening after laser
irradiation is a useful clinical endpoint.
Vigilon or Second Skin occlusive dressing can
be used during treatment or directly afterwards
to provide pain relief and assist in healing.
Vigilon or Second Skin used during treatments
with QS lasers eliminates the risk of blood or
tissue splatter, but requires a slightly higher
fluence.
When using the 532-nm laser, purpura can
be minimized by treating through a firmly
applied glass microscope slide to compress
blood vessels, thereby eliminating the vascular
component.
Comparative outcomes
Lentigines and freckles
Key Points
• Shorter wavelength lasers are useful to treat
superficial lesions given the high rate of melanin
absorption and shorter depth of penetration.
• IPL systems and 532-nm pulsed lasers have
a unique advantage when treating combined
vascular and pigmented disorders.
Superficial lentigines and freckles are easily and per-
manently removed by any of the QS lasers or IPL
systems. Shorter wavelength lasers are ideal ­given
the high rate of melanin absorption and shorter
depth of penetration. IPL systems and 532-nm
pulsed lasers have a unique advantage when treat-
ing combined vascular and pigment alterations as
seen in photodamage. In a study that compared
the QS 755-nm alexandrite laser with IPL in treat-
ment of lentigines and freckles in Asian skin, both
were found to be effective. QS alexandrite was su-
perior to IPL in the treatment of freckles, but had
a higher risk of postinflammatory hyperpigmenta-
tion in patients with lentigines; thus, IPL should be
considered first in the treatment of lentigines and
in patients who do not want downtime. It is im-
portant for patients to understand that when lack
of downtime is desired, they will usually require
more treatments to obtain the desired effect.
ERRNVPHGLFRVRUJ
Postinflammatory hyperpigmentation caused
by QS lasers has led some authors to look at
alternative ways to treat lentigines. One study
­recommended a test spot using the LP 532-
nm Nd:YAG laser (pulse duration 2 ms, fluence
6.5 J/cm2, spot size 2 mm); in patients who did
not wish to have downtime, or those who devel-
oped postinflammatory hyperpigmentation after
the test, IPL treatment was offered. Another
study of long pulsed lasers showed that applying
pressure with a glass window on a long pulsed
pulsed-dye laser (LPDL) handpiece provided
a safe and effective treatment of lentigines. Al-
though the LPDL is commonly used for vascu-
lar lesions, this modification using firm pressure
blanches the skin blood vessels, minimizing ab-
sorption by hemoglobin. The authors compared
the LPDL with compression and the QS ruby
laser in the treatment of facial lentigines; they
found similar results, but decreased side-effects
with the LPDL owing to optimal pulse duration
for targeting the basal cell layer with minimal
mechanical effects.
Labial lentigines have been successfully treated
with the QS ruby laser, the ruby laser, and the
frequency-doubled QS Nd:YAG laser.
Nevus of Ota
Key Points
• This lesion presents as a blue–gray
hyperpigmented lesion in the periorbital region.
• Similar lesions in the cervical or thoracic region
can occur and are referred to as nevus of Ito.
• Dermal depth of the pigment in these lesions
requires a longer wavelength for effective
treatment.
• The most frequently used pulsed lasers are the
QS Nd:YAG, QS ruby, and QS alexandrite lasers.
• Lightening of the lesion may take months
because of residual melanin in the dermis long
after the nevus cells have been removed.
• It has been suggested that treatment in children
can result in complete clearance with fewer
sessions and fewer complications.
Nevus of Ota is often present at birth or by the
second decade of life, presenting as a blue–gray
hyperpigmented lesion in the periorbital region.
It is characterized by dermal melanocytosis in-
nervated by the first and second branches of the
trigeminal nerve, and is typically seen in Asians. A
similar lesion in the cervical or thoracic region can
occur and is referred to as nevus of Ito. The der-
mal depth of the pigment in these lesions requires
a longer wavelength for effective ­treatment. The
most commonly used pulsed lasers are the QS
Nd:YAG (1064 nm), the QS ruby laser (694 nm),
and the QS alexandrite (755 nm) ­lasers.
A study comparing the tolerability of treat-
ments between QS alexandrite and QS Nd:YAG

Lasers: physics and medical indications
lasers found that both had a similar short-term
morbidity, but patients felt the QS alexandrite
was more tolerable. Hypopigmentation can occur
with any of the QS laser treatments, but appears
to be more common with combined treatments,
such as in patients who receive alternating treat-
ments with QS alexandrite and QS Nd:YAG.
Alternatively, when comparing efficacy, the Nd:
YAG has been shown to be more effective in
lightening nevi of Ota, with no differences in
complications.
Recommendations of treatment intervals vary.
One study found that clinical response in the
20–27-week treatment interval group was signifi-
cantly better than that in the 12–19-week interval
group, but showed no significant difference when
compared to both the 28–35- and the ≥36-week
interval group. This study also indicated that
zygomatic, buccal, and frontal areas had a better
response than ocular and temporal areas. Light-
ening of the lesion can take months due to re-
sidual melanin in the dermis long after the nevus
cells have been removed, leading many to suggest
treatment intervals of 3–6 months. In one study,
three treatments were applied at 1-month inter-
vals, with follow-up at 6–8 months; the lesion
had usually disappeared by the follow-up. It is
unclear what is the best age to start treatment.
One study showed that children had complete
clearance with fewer sessions and a lower com-
plication rate when the QS ruby laser was used
for nevi of Ota.
Hori’s nevus (acquired bilateral nevus of Ota-
like macules) is a common condition of dermal
melanocytic hyperpigmentation. The QS Nd:
YAG laser can be used for treatment, but the re-
sults do not appear to be as good as those seen
with nevus of Ota. A retrospective study showed
effective treatment of Hori’s nevus with QS
­alexandrite. Postoperative pigmentary changes
were frequent and the use of topical bleaching
agents was necessary to achieve a satisfactory
result. A transient hypopigmentation risk oc-
curred in up to 50% of the patients. A recent
study showed that concurrent use of the QS
532-nm Nd:YAG laser in combination with the
1064-nm laser was more effective in pigment
clearance than using the QS 1064-nm Nd:YAG
laser alone.
Congenital nevi
Key Points
• Laser treatment should be reserved for lesions
that are disfiguring and cannot be excised
surgically.
• Many congenital nevi are resistant to laser
treatment, and even successfully removed
lesions have a high rate of repigmentation.
• Congenital nevi of the palms and soles tend to
respond better.
ERRNVPHGLFRVRUJ
19
Chapter
239
• Early treatment has been argued, based on the
smaller size of early lesions, better tolerance, and
cosmetic benefit prior to school years.
• Benefit of early treatment with regard to
decreasing recurrence or malignant potential has
yet to be proven.
Laser treatment for congenital nevi should be
­reserved for lesions that are disfiguring and can-
not be excised surgically. For such patients, lasers
that have been used successfully include pigment-
specific lasers, resurfacing lasers, or a combina-
tion of both. Many congenital nevi are resistant
to laser treatment; even successfully removed
lesions have a high rate of repigmentation. One
of the key issues of removal is that lesions con-
sist of both superficial and deeper components,
and can extend deep into the dermis and adnexal
structures. There have been reports of extension
into the fat and muscle. The most likely cause of
­repigmentation is remnant deep dermal melano-
cytes that, over time, lead to ­repigmentation.
The QS ruby laser has been reported to light-
en small and medium congenital nevi effectively
without scarring. The initial lightening was not
permanent, leading the authors to conclude that
the QS ruby laser is a viable alternative for cos-
metic improvement of irresectable lesions, but
should not be considered definitive treatment. A
combination of treatments to target the superfi-
cial aspect first, followed by QS Nd:YAG treat-
ment for further removal of residual pigment, has
been shown to be effective. One study that em-
ployed a combined laser treatment (abrading the
surface epithelium with a carbon dioxide laser,
then treating with a QS alexandrite laser) found
a favorable clinical outcome with safer, less pain-
ful treatments, and relative nonscarring. Patients
had a short recovery period and required fewer
sessions compared with conventional treatments.
Early treatment has been argued, based on the
smaller size of early lesions, better tolerance of
treatment by younger patients, and cosmetic ben-
efit prior to school years, but the benefit of early
treatment with regard to decreasing ­recurrence or
malignant potential has yet to be proven. Con-
genital nevi of the palms and soles tend to re-
spond better to laser treatment, perhaps because
of the absence of hair follicles.
Café-au-lait macules
Key Points
• The success of laser treatment is highly variable,
with high recurrence rates.
• QS frequency-doubled Nd:YAG, QS ruby, and
QS alexandrite lasers are useful, with a low risk of
side-effects.
• Patients should be instructed to avoid sun
exposure because of the increased risk of
repigmentation of the lesion.
240 Dermatologic Surgery
• Multiple treatment sessions and a relatively low
fluence should be used.
• In general, lesions that remain clear at 12 months
have long-lasting results.
Café-au-lait macules (CALMs) occur in up to
20% of the population, with an increased prev-
alence during infancy decreasing into adult life.
­Lesions present with light or dark brown, uni-
form melanin pigmentation. The success rate of
laser treatment is highly variable, with recurrence
rates of up to 50%. Review of the literature shows
variable results with different laser systems, with
no one system standing out from the others. QS
frequency-doubled 532-nm Nd:YAG, QS ruby,
or QS alexandrite lasers are useful for treating
CALMs, with a low risk of side-effects. Many le-
sions lighten or clear after treatment only to recur
a few months later; other lesions have transient
darkening; and others show no change at all. A
retrospective study in Japan showed that the QS
alexandrite laser was not very efficient for ­nevus
spilus/café-au-lait spots, especially when the
pigmentation had appeared after 1 year of age,
was treated after 5 years of age, was located on
the face, was oval with a smooth border, and the
patient was male. Success has been reported us-
ing the 510-nm short-pulsed dye laser to remove
CALMs completely in childhood, and in type V
skin. The erbium (Erb):YAG 2940-nm laser has
been reported to be successful without repigmen-
tation for a year in treating CALMs.
Long-term follow-up is needed but, consider-
ing that most repigmentation occurs within 1 year,
CALMs may respond well to resurfacing. Patients
should be instructed to avoid sun exposure, owing
to an increased risk of repigmentation of the le-
sion. CALMs require multiple treatment sessions
at 6–8-week intervals, and a relatively low fluence
should be used. In general, lesions that remain
clear at 12 months have long-lasting results.
Melasma
Key Points
• The underlying etiology must be addressed first.
• All patients should be placed on bleaching creams
and high skin protection factor (SPF) sunscreens,
with instructions for strict sun avoidance.
• Epidermal melasma responds well to topical
bleaching creams, retinoids, azaleic acid, and a
host of procedural treatments such as chemical
peels, IPL, and laser treatments.
• There is a variable response to pigment-specific
QS lasers in the treatment of deeper mixed
melasma.
• Effective treatment has been reported using a
combination of the QS alexandrite laser with
carbon dioxide resurfacing.
• The Fraxel laser has recently been shown to be
effective in treating melasma.
ERRNVPHGLFRVRUJ
Melasma is a common condition presenting to
the dermatologist. Multiple medical therapies
exist to treat the epidermal hyperpigmentation
of melasma, but many patients appear to have a
mixed degree of epidermal and dermal pigmenta-
tion. Epidermal melasma responds well to topi-
cal bleaching creams, retinoids, azaleic acid, and
a host of procedural treatments such as chemical
peels, IPL, and laser treatments.
IPL has been shown to provide 76–100%
clearance for epidermal melasma after two pulses.
Deeper mixed melasma had poor clearance after
four pulses and a high risk of postinflammatory
hyperpigmentation. IPL works best as an adju-
vant to topical therapy and sunscreens in resistant
cases. One study showed a 39.8% improvement
in the IPL group when compared to the control
group who received hydroquinone and sunscreens
alone.
Melasma appears to have a variable response to
pigment-specific QS laser treatment. One study
compared the Nd:YAG and the QS ruby laser, re-
porting that neither was effective. The QS ruby
laser has been shown to be effective, especially in
patients with a fair complexion, but recurrence
is common.
The outcomes of combined modalities to
treat melasma have also been variable. One study
demonstrated effective treatment using a com-
bination of QS alexandrite laser with carbon
dioxide resurfacing. A split-faced study of re-
fractory melasma also found better results with
a combined protocol using ultrapulse carbon
dioxide and QS alexandrite, but with more fre-
quent ­ adverse effects such as postinflammatory
­hyperpigmentation.
More recently, fractionated technology has
been applied to the treatment of melasma. Ten
patients who were unresponsive to previous
therapy were treated at 1- to 2-week intervals
with the Fraxel laser (Reliant Technologies,
Palo Alto, CA, USA). Wavelengths of 1535 and
1550 nm were used, with treatment parameters
of 6–12 mJ per microthermal zone with 2000–
3500 MTZ/cm2. After four to six treatment
sessions, 60% of patients achieved 75–100% clear-
ance and 30% had less than 25% improvement.
Patients required no downtime; one ­patient had
post­inflammatory hyperpigmentation and there
were no cases of hypopigmentation. According
to the authors, patients with melasma should be
treated monthly with low energies of 6–8 mJ at
1000–2000 MTZ/cm2. Patients can expect to
have two or three treatments in total, with a
“touch-up” at 6 months.
Prior to any laser treatment, the underlying
etiology must be addressed. In addition, all pa-
tients should be given bleaching creams and high
SPF sunscreens, with instructions for strict sun
avoidance.

Lasers: physics and medical indications
Controversies
Questions about the increased risk of malignant
transformation due to laser treatment have yet
to be answered, and questions have been raised
over the biologic effect of continued nonlethal
low-energy laser irradiation and heating on ­tissue
and melanocytes. Melanocyte proliferation and
migration has been observed following exposure
to low-energy helium–neon laser irradiation.
One study described the effect of sublethal laser
damage from the QS 755-nm alexandrite laser
in melanoma cell lines, reporting an increase in
p16 expression, which implies damage to the
cellular DNA. To date there has been no direct
evidence that laser treatment causes melanoma.
A case of metastatic malignant melanoma occur-
ring 2 years after carbon dioxide laser treatment
of a pigmented lesion has been reported. Another
case report demonstrated melanoma occurring in
the periphery of a giant congenital melanocytic
nevus that had been incompletely treated by ar-
gon laser. Such reports demonstrate the need for
continued monitoring of these lesions after treat-
ment. Of interest, there have been a number of
reports of pseudo-melanoma after laser therapy.
These pigmented lesions histologically resemble
superficial spreading malignant melanoma and
typically occur after incomplete treatment.
Another concern is the possibility of inadvert-
ent treatment of dysplastic lesions by unaware,
untrained technicians and aestheticians when
performing laser or pulsed light treatments. The
growing number of spas that offer these treat-
ments has opened the door to a host of medico-
legal risks and controversies. Although many of
the professional societies have issued a variety of
guidelines on who should operate various lasers,
physicians should be aware that state laws always
supersede these guidelines, even when the society
guidelines are stricter.
Recently, recurrence of port-wine stain years
after completion of treatment has been a topic of
discussion. It appears that PWS has a tendency to
recur at a rate approaching 50% between 3 and
4 years after completion of treatment. Although
lesions may recur, it should be noted that patients
respond well to retreatment; further studies are
needed to determine whether recurrence is due
to residual vascular ectasia or just the natural pro-
gression of the lesion.
Laser treatment of hemangiomas remains a
topic for debate. Although laser treatment of
ulcerated hemangiomas is the most accepted
indication, the treatment of uncomplicated he-
mangiomas with the PDL continues to be con-
troversial. Superficial lesions appear responsive
to PDL treatment, but with the limited depth of
penetration there is theoretically little effect on
deeper tissue.
ERRNVPHGLFRVRUJ
19
Chapter
241
There is no argument that ocular safety is
important when working with lasers. However,
there is concern that inadequate goggles may be
used when treating lesions around the eyes, es-
pecially when working with 1064- and 810-nm
diode lasers. The depth of penetration of these
near-infrared lasers can result in unexpected cor-
neal damage. Protective lenses should be placed
behind the lids and be of sufficient size to provide
adequate protection of the globe.
Another concern with regard to laser hazards
is the protection against possible disease trans-
mission through laser plume. Specific protection
against hazards of laser plume remains unclear. As
laser plume has been shown to transmit viral dis-
ease, standard precautions are recommended. The
use of smoke evacuators in combination with ­laser
masks is recommended when treating any lesion
that has the potential to produce laser plume.
Strict care must be maintained by practitioners
and time spent on proper education of staff.
Another area of controversy is the FDA approv-
al of medical devices. The market boom for lasers
and laser treatments has led to a large number of
laser and light devices that are FDA approved. It
is important to recognize that FDA approval of
medical devices differs from that for medications.
A seal of approval by the FDA does not always
mean that the safety and efficacy of the system
has been demonstrated by clinical trial. The tra-
ditional 510(k) approval process does not require
companies to perform clinical trials for devices
that are similar to systems already approved and
legally marketed in the USA. Before buying any
new device, ask the manufacturer what data was
used for the FDA approval and whether there are
specific clinical studies demonstrating safe and
­effective treatment for that device.
Finally, the internet and glamour magazines
have created a savvy and sometimes unrealistic
patient. Spend time talking with patients to de-
termine their precise expectations of a particular
procedure. Realize that you are better off with a
patient who decides not to have a procedure, than
dealing with an unhappy patient whose unobtain-
able and unrealistic goals cannot be met.
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Yang MU, Yaroslavsky AN, Farinelli WA, et al. Long-
pulsed neodymium: yttrium–aluminum–garnet
laser treatment for port wine stains. J Am Acad
Dermatol 2005;52:480–490.
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Photodynamic therapy
Christopher Charles Gasbarre and Edward V. Maytin
Clinical overview
Key Points
• Photodynamic therapy requires a photosensitizer,
activating light, and oxygen.
• Absorption of light energy by the photosensitizer
leads to generation of reactive oxygen species.
• Singlet oxygen is the primary effector molecule,
leading to cell necrosis, apoptosis, or induction
of inflammatory signaling cascades.
• Protoporphyrin IX (PpIX) is the photosensitizer
utilized in most dermatologic applications of PDT.
• Topically applied δ-aminolevulinic acid (ALA) or
methyl aminolevulinate (MAL) are precursors of
PpIX. Intracellular accumulation and conversion
via the heme synthesis pathway produce PpIX.
• ALA and MAL accumulate preferentially inside
dysplastic or rapidly proliferating cells.
• The light source chosen must be able to deliver
light of sufficient energy and appropriate
wavelength to the tissue of interest to be
absorbed by the photosensitizer.
Mechanism
The goal of photodynamic therapy (PDT) is to
deliver a treatment effect preferentially to a par-
ticular tissue via a photochemical reaction. This is
accomplished through the simultaneous delivery
of three key components to the target tissue:
1 a photosensitizer
2 activating light of the proper wavelength
3 oxygen.
A photosensitizer is chosen that will accumu-
late in the cells of interest. Light is absorbed by
the photosensitizer and energy is transferred to
molecular oxygen, creating reactive oxygen spe-
cies, which are the primary mediators of cell and
tissue damage through necrosis, apoptosis, and
induction of inflammatory cascades. Specifically,
the photosensitizer molecule absorbs light energy
(photon), thereby promoting it to the first excited­
ERRNVPHGLFRVRUJ
20
Chapter
singlet state (S1). From this state, the molecule
may relax to its ground state (S0), generating heat
or fluorescence, or it may cross to a triplet state
(T1). Triplet state molecules activate ground state
oxygen, creating singlet oxygen (1O2), or initiat-
ing direct photochemical effects. The majority of
the effect of PDT is derived from the action of
singlet oxygen (Fig. 20-1).
The fluorescence emitted by the photosensi-
tizer when decaying to the ground state may be
used to delineate tumor margins via a procedure
called fluorescence detection. This is an area of
current investigation.
Photosensitizer
The first “photodynamic reaction” was described
more than 100 years ago when it was noted that
light potentiated the cytotoxicity of acridine orange
against protozoa. Since then, a variety of photo-
sensitizers have been investigated in the treatment
of infection and malignancy. Chlorine derivatives,
phthalocyanines, and hematoporphyrin derivatives
(HPDs) have received the most ­ attention. Der-
matologic use has centered on the HPDs, though
recent investigations have been made into the use
of the silicon phthalocyanine Pc4.
The HPDs used in dermatologic applications
of PDT are δ-aminolevulinic acid (ALA) and
methyl aminolevulinate (MAL) (Table 20-1). These
two molecules are small enough to pass through
the epidermis. ALA has been developed in the
USA, whereas MAL is used primarily in Europe
and abroad. MAL is approved in Europe for the
treatment of actinic keratosis, basal cell carcinoma
(BCC), and in-situ squamous cell carcinoma (SCC).
Currently, it is not readily available in the USA.
After topical application, ALA and MAL are
preferentially absorbed by damaged skin and taken
up by dysplastic, metabolically active, cells. Be-
cause these molecules are precursors that bypass
the rate-limiting enzyme of the heme synthesis
pathway (ALA synthase), feedback inhibition of
the pathway does not occur and protoporphyrin
246 Dermatologic Surgery

Photodynamic therapy

Electron excited state (S1 ) Triplet state (T1 ) Singlet oxygen ( 1O2 )

Phosphorescence

Absorption Tumor diagnosis

Fluorescence

Photosensitizer (PpIX) Oxygen ( 3 O2)

Electron ground state (S0)

Light
Figure 20-1  Diagram showing energy levels of photosensitizer excitation (adapted from Hasan et al 2006)

Table 20-1  FDA-approved systems for PDT

Topical agent Brand name Manufacturer Light source Indication Available in USA
δ-Aminolevulinic Levulan Kerastick DUSA, USA Blu-U, 417 nm Actinic keratosis Yes
acid HCl, 20% (approx.), (nonhyperkeratotic,
solution noncoherent fluorescent on head
and scalp), 2000
Methyl Metvix PhotoCure ASA, Aktilite, 634 nm Actinic keratosis, No
aminolevulinate, Norway (approx), light- 2004
16% cream emitting diode,
noncoherent

IX (PpIX) rapidly accumulates in these cells (Fig.

20-2). Some dysplastic cells also exhibit decreased
ferrochelatase activity and lower the ferric ion con-
centration, which promotes further accumulation
of PpIX.
Dermatology is an ideal arena for the devel-
opment of PDT because photosensitizers can
be applied topically, avoiding some potential
adverse events such as the generalized photo-
sensitivity associated with the systemic delivery
of photosensitizers. PDT of the skin also adds
a second degree of selectivity. In addition to
preferentially increased ALA uptake and PpIX
production by malignant or damaged cells, light
delivery can be easily directed to encompass
only involved sites.
Light source
In choosing a light source for PDT, three key
­criteria need to be considered.
1. Light must be able to penetrate the
tissue containing the photosensitizer
Light energy must be able to be delivered mecha-
nistically to the tissue of interest. In cutaneous
applications, this is usually accomplished easily.
However, careful considerations must be made
regarding the depth of penetration of these light
sources. Generally, longer wavelengths penetrate
more deeply into tissue. This may be of impor-
tance when considering the condition being
­treated (see Controversies – Light source).

ERRNVPHGLFRVRUJ
 20

Chapter
Photodynamic therapy 247

Cytosol

Heme Mitochondrion

Fe ferrochelatase

Protoporphyrin IX Glycine + Succinyl CoA

protoporphyrinogen IX ALA synthase

oxidase

Protoporphyrinogen δ-Aminolevulinic acid

coproporphyrinogen III
oxidase

Coproporphyrinogen III

Coproporphyrinogen III δ-Aminolevulinic acid

uroporphyrinogen ALA dehydratase

decarboxylase

Uroporphyrinogen III Porphobilinogen

Hydroxymethylbilane
Figure 20-2  Heme synthesis pathway

4.0
Blu-U 417 nm
2. The wavelength must be sufficiently 3.5
absorbed by the photosensitizer used 3.0
Absorption

Each photosensitizer has a specific absorption 2.5

spectrum. The ideal wavelength used should be 2.0
well absorbed by PpIX but not by other endog- 1.5
enous chromophores. While PpIX readily absorbs 1.0
light in the Soret band (414 nm), so too do other 0.5
compounds. Laser sources used in PDT protocols
0
typically are chosen to lie within secondary ab- 300 400 500 600 700 800
sorption peaks of PpIX, such as those at approxi-
Wavelength (nm)
mately 630 and 570–580 nm.
Figure 20-3  PpIX spectrum from 300 to 800 nm. Blu-U,
3. Light must be delivered in sufficient noncoherent (blue) light source
energy to activate the photosensitizer
The light source chosen must have a sufficiently 0.60
IPL 515–1200 nm
0.55
high energy output to make the delivery of suf- KTP 532 nm
0.50
ficient light doses clinically feasible. Numerous PDL 585 nm
0.45
such sources have been reported, and do not PDL 595 nm
Absorption

0.40
necessarily have to be fancy or expensive. In fact, 0.35
early topical PDT experiments were conducted 0.30
using a slide projector bulb. The absorption spec- 0.25
trum of PpIX with an overlay of a few of the 0.20
more commonly used light sources can be seen in 0.15
Figures 20-3 & 20-� 4. 0.10
450 500 550 600 650 700 750
Oxygen Wavelength (nm)
Oxygen is critical to the generation of singlet oxy- Figure 20-4  PpIX spectrum above 450 nm. IPL, intense
gen species. This may be of clinical relevance in pulsed light; KTP, potassium titanyl phosphate (green) light
hypoxic tissues. source; PDL, pulsed dye laser

ERRNVPHGLFRVRUJ
248 Dermatologic Surgery

Medical treatment options B ox 2 0 - 2

A variety of dermatologic conditions amenable to Medical treatment options other than PDT
medical therapies have been treated with topical
Actinic keratoses
PDT (Box 20-1). To date in the USA, only treat-
ment of nonhypertrophic actinic keratoses of the Topical 5-fluorouracil
head and scalp is Food and Drug ­Administration Topical imiquimod
Topical diclofenac
Topical retinoids (tretinoin, adapalene, tazarotene)
B ox 2 0 - 1
Squamous cell carcinoma in situ (Bowen’s disease,
Dermatologic uses for photodynamic therapy erythroplasia of Queyrat)
FDA approved Topical 5-fluorouracil
Actinic keratoses (approval is for nonhypertrophic actinic Topical imiquimod
keratosis of head and scalp)
Oral acitretin (chemoprevention)
Commonly used in North America or Europe
Superficial basal cell carcinoma
Squamous cell carcinoma (SCC) in situ
Topical imiquimod
Basal cell carcinoma (superficial or nodular subtypes)
Photorejuvenation
Acne vulgaris
Small case series, anecdotal reports, or investigational (FDA) approved. Current international consen-
sus guidelines support the use of topical PDT
Acne inversa (hidradenitis suppurativa) for the treatment of actinic keratoses, SCC in
Verrucae vulgaris situ (Bowen’s disease), and superficial BCC.
Chemoprevention of nonmelanoma skin cancer Specifically MAL-PDT is recommended for the
treatment of nodular BCC. Medical treatment
Cutaneous T-cell lymphoma
alternatives to the afore-mentioned are listed in
Cutaneous B-cell lymphoma Box 20-2.
Keratoacanthoma
Rosacea/rhinophyma Surgical approach
Molluscum contagiosum There is a great deal of variation in published
Actinic cheilitis ALA-PDT treatment protocols. Variations in tis-
Morphea/lichen sclerosus
sue pretreatment (e.g. mild chemical peels or cu-
rettage), ALA formulation, ALA application time,
Scleroderma light source, light dose, or treatment frequency
Psoriasis may have significant effects on outcome. How-
Lichen planus ever, general consensus guidelines have been pub-
lished for topical ALA-PDT and are listed below.
Gorlin’s syndrome (basal cell nevus syndrome)
Perioral dermatitis
Sebaceous hyperplasia Topical ALA-PDT treatment algorithm
Melasma
(Fig. 20-5)
Alopecia areata Pretreatment
Darier’s disease • Continue current topical and systemic
medications.
Hailey–Hailey disease
• Consider pretreatment of hypertrophic
Infected leg ulcers actinic keratoses or severe photodamage with
Dermatophytoses a short course of 5-fluorouracil or imiquimod.
Cutaneous leishmaniasis Light sources
Extramammary Paget’s disease • Commonly used light sources are listed in
Nevus sebaceous Table 20-2.
Disseminated superficial actinic porokeratosis • Blue light: 15 min when used as single light
source, 5–8 min when used in addition
Port wine stain to intense pulsed light (IPL) or laser for
increased photobleaching.

ERRNVPHGLFRVRUJ

• Avoid purpuric settings with pulsed dye laser
(PDL).
• Double pulsing of PDL may be used in the
treatment of sebaceous skin, rhinophyma, or
rosacea.
Post-treatment
• Titanium dioxide or zinc oxide sunblock
• Patient to avoid direct sun exposure for
48–72 h
• Apply moisturizers as needed
• Patient education should include expectation
of desquamation and mild to moderate
erythema for 48–72 h.
Timing of treatments
• Two to five treatments, 2–4 weeks apart
• Vary incubation time and light dose on
follow-up treatments to optimize therapeutic
effect.
Pearls
• Superficial crust and/or scale may be removed
via curettage prior to application of ALA to permit
increased and more uniform tissue absorption.
• Though adequate for the treatment of actinic
keratoses, acne, and photodamage, short ALA
incubation/contact times (30–60 min) may not be
adequate for the treatment of other conditions.
• The most common adverse event is patient
­ iscomfort during light exposure and for a few
d Studies vary significantly in the degree of pretreat-
hours post-treatment. Most patients describe
­stinging, burning, and/or pruritus.
• Pain seems to increase with the amount of
­surface area treated.
• Ice and cooling devices may help with pain
during and immediately after treatment. Topical
­anesthetics seem to provide little, if any, benefit
(see Controversies). Furthermore, ALA is unsta-
ble at basic pH. The use of topical anesthetics
such as EMLA (pH 9) should be avoided.
• Avoid sun exposure post-treatment for 24–48 h.
­ atients should wear sunscreen/sunblock,
P treating tumors as described in the next section.
­preferably titanium dioxide or zinc oxide.
• Newer PDT protocols, aimed at increased PDT
efficacy, tolerability, or convenience, include
intralesional injection of ALA, fractionated light
dosing, induction of keratinocyte differentiation,
and “ambulatory PDT” in which patients wear a
battery-operated light source at home.
Comparative outcomes
Variation in treatment parameters makes a ­direct
comparison of most PDT trials difficult at best.
Despite this, consistent success demonstrated with
ALA-PDT in the treatment of actinic ­keratosis and
ERRNVPHGLFRVRUJ
20
Chapter
Photodynamic therapy 249
Wash with soap and water or alcohol swab
Microdermabrasion (single pass) or acetone scrub
(enhances uniform penetration of ALA)
Prepare 20% ALA
Crush ampules and shake Kerastick for 3 min
Apply ALA evenly with firm pressure
30–60-min incubation time
Photoprotection
Remove ALA with soap and water
Wipe with alcohol
Figure 20-5  Treatment algorithm for topical ALA-PDT
nonmelanoma skin cancer (in-situ SCC, superfi-
cial BCC, nodular BCC) has prompted recent in-
ternational consensus support for the use of PDT
for the treatment of these entities. Representative
studies using topical ALA are listed in Table 20-3,
with a comparison of respective clearance rates.
ment to respective lesions prior to the application
of photosensitizer (i.e. curettage). Additionally,
different follow-up periods make a true assess-
ment of tumor clearance rates difficult. The reader
is referred to the original reports to make their
own judgments regarding these issues. Finally, we
have omitted a large number of the trials for non-
melanoma skin cancer conducted in Europe using
topical MAL-PDT, which is not currently avail-
able in the USA. There may be potential benefits
for MAL-PDT compared with ALA-PDT when
Controversies
Vehicle
As mentioned above, numerous formulations of
topical photosensitizers have been reported in
the literature. The only currently FDA-approved
formulation of topical PDT available in the USA
is Levulan Kerastick (DUSA Pharmaceuticals).
Methylation of ALA (MAL) appears to increase
absorption of the molecule, presumably leading
to increased PpIX production. For this reason,
some advocate MAL-PDT over ALA-PDT for the
treatment of nonmelanoma skin cancer. It is un-
clear, however, whether this leads to ­ substantial
250 Dermatologic Surgery

Table 20-2  Light sources used for PDT

Condition Preferred Alternate Other
Actinic keratosis Blue light PDL, IPL Green, yellow, red
Superficial BCC
Photodamage IPL Blue, PDL Green, yellow
Blue for type VI skin
Acne PDL + blue (5 min) Blue (8 min) Green, red, yellow, IPL
Sebaceous skin PDL, blue IPL Green, yellow, red
Rosacea
Rhinophyma
Blue, noncoherent light source with main peak at 417 nm (Blu-U); IPL, intense pulsed light; PDL, pulsed dye laser (585, 595 nm).

Table 20-3  Reported topical PDT regimens using 20% δ-ALAa

No. of patients/ Application Light source
Indication lesions time and dose Results Reference
AK 36/70 14–18 h Blue light (417 66% CR (88% with Jeffes et al (2001)
nm), 2–10 J/cm2, 2nd treatment)
3–10 mW/cm2
243/1909 14–18 h Blue light (417 83% CR Piacquadio et al
nm), 10 mW/cm2 (2004)
41/3622 14–18 h open, or FL-PDL (595 nm) 65–100% CR Alexiades-
3–4 h occluded laser, 7.5 J/cm2 Armenakas &
Geronemus (2003)
24/>4 lesions per 1h Blue light (417 50% CR Smith et al (2003)
patient nm), 1000 s
FL-PDL (595 nm),
7.5 J/cm2
32/multiple 15–20 h Blue light (417 94% CR Goldman & Atkin
nm), 1000 s (2003)
18/>4 lesions per 1–3 h (± 40% Blue light (417 94% CR at 2 h, Touma et al (2004)
patient urea for 7 days) nm), 10 J/cm2 87% CR at 1 h
50 lesions 6–8 h 630-nm argon- 84% CR Calzavara-Pinton
pumped dye laser (1995)
(repeated qod)
17 1h IPL, 560-nm filter, 68% CR Avram & Goldman
28–32 J/cm2 (2004)
SCC in situ 19/20 4h Xenon arc lamp 75% after 1 Morton et al
(Bowen’s) (300 W), 125 treatment, 100% (1996)
J/cm2, 70 mW/cm2 after 2 treatments
16/61 4h Xenon arc lamp Morton et al
(300 W) (2000)
540 ± 15-nm filter 72% CR, 48%
(green) 12 months
630 ±15-nm filter 94% CR, 88%
(red) 12 months
20/33 4h Xenon arc lamp 88% CR, 6 weeks Salim et al (2003)
(300 W), 630
±15-nm filter,
100 J/cm2, 50–90
mW/cm2
Continued

ERRNVPHGLFRVRUJ
 20

Chapter
Photodynamic therapy 251

Table 20-3  Reported topical PDT regimens using 20% δ-ALAa—cont’d

No. of patients/ Application Light source
Indication lesions time and dose Results Reference
BCC, superficial 80 lesions 90% CR, 2–3 Kennedy et al
months (1990)
21/80 4–6 h Nd:YAG pumped 100% CR, 3 weeks Svanberg, et al
dye laser (630 nm), (1994)
55/80 superficial
60 J/cm2, <110
37/55 recurrent mW/cm2
23 lesions 6–8 h 630-nm argon 87% CR, 1 month Calzavara-Pinton
pumped dye laser, (histologic or (1995)
60–80 J/cm2, 100 clinical response)
mW/ cm2 (repeated
qod)
32/34 20 h Halogen lamp, red 88% CR with 1 Fijan et al (1995)
filter, 300 J/cm2, treatment, 97% CR
150–250 mW/cm2 with 2 treatments ,
up to 20 months
37/190 3h Xenon lamp, 92% CR, 6 months Wennberg et al
620–670-nm band (1996)
pass filter, 70–100
J/cm2, 125–166
mW/cm2
47/95 4h 250-W slide 86% CR, 2–4 Fink-Puches et al
projector lamp, weeks, 56% CR, (1998)
broad spectrum, median 19 months
510-, 570-, or
610-nm filters,
18–131 (median
60) J/cm2, or UVA,
1.1 J/cm2
6/26 3–4 h Paterson 96% CR, Haller et al (2000)
light source, 16 months
noncoherent, 630 (2 treatments)
± 15 nm, 120–134
J/cm2, 50–100
mW/cm2
22/22 6h Nd:YAG, 635-nm 62% CR, 3 months Wang, et al (2001)
laser, 60 J/cm2, 80
± 20 mW/cm2
aAlthough all above studies utilized 20% ALA, there was variation in the delivery vehicle. CR, complete response; qod, every other day; FL-PDL, flashlamp

pulsed-dye laser.

treatment benefit. Of note, DUSA currently
holds US patents related to the use of ALA in
topical PDT regimens. Pharmacies compounding
other formulations of ALA in the USA have lost
lawsuits brought by DUSA for patent infringe-
ment. Pretreatment of the skin with agents such
as 40% urea to improve tissue penetration has
demonstrated little to no treatment benefit for
actinic keratoses.
Application time
FDA-approved use of Levulan Kerastick for the
treatment of actinic keratoses of the face or scalp
specified a 14–18-h application. However, since
the approval of Levulan in 1999, authors have re-
ported similar efficacy with improved tolerability
using abbreviated contact times of approximately
1–3 h. There is some evidence to suggest that time
to optimal ALA uptake and PpIX production
varies depending on the condition being treated.
Therefore, these short contact times may not be
ideal for the treatment of conditions other than
actinic keratoses.
Light source
As demonstrated above, numerous light sources
are capable of delivering an appropriate wave-
length and energy to activate PpIX. Advocates of
different light sources suggest improved efficacy
or tolerability. In general, the use of lasers does not
seem to be necessary, as similar efficacy and toler-
ability have been noted with noncoherent light
sources. Some contend that greater tolerability can
be achieved by utilizing laser sources rather than

ERRNVPHGLFRVRUJ
252 Dermatologic Surgery
broadband noncoherent light, but this has been
an inconsistent finding. Longer wavelengths (red
and green light) have greater tissue penetration
than blue light, leading to a general ­ conclusion
that blue light sources, although appropriate for
the treatment of actinic keratoses, are inferior to
red or green wavelengths for the treatment of
other conditions, such as cutaneous malignancies.
The flashlamp PDL (585 or 595 nm) has shown
promise as a light source in PDT protocols for the
treatment of actinic keratoses and acne. However,
it is controversial whether this is due to the direct
photoactivation of PpIX or vascular damage.
Pain control
Tolerability of topical PDT regimens varies from
study to study, but most patients achieving the
desired treatment effect will experience at least
some discomfort (burning sensation) during, and
immediately after, the administration of light. This
can usually be managed with the use of cooling
devices and fans. The use of topical or injectable
anesthetics has unfortunately been of little ben-
efit. More recently, some authors have reported
improved tolerability utilizing lower fluence rates
during light delivery.
References
Alexiades-Armenakas MR, Geronemus RG. Laser-
mediated photodynamic therapy of actinic kera-
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Avram DK, Goldman MP. Effectiveness and safety of
ALA-IPL in treating actinic keratoses and photodam-
age. J Drugs Dermatol 2004;3(1 Suppl):S36–S39.
Calzavara-Pinton PG. Repetitive photodynamic
therapy with topical delta-aminolaevulinic acid as
an appropriate approach to the routine treatment
of superficial non-melanoma skin tumours.
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Fijan S, Honigsmann H, Ortel B. Photodynamic
therapy of epithelial skin tumours using delta-
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Dermatol 1995;133(2):282–288.
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Haller JC, Cairnduff F, Slack G, et al. Routine double
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Morton CA, Whitehurst C, Moore JV, MacKie RM.
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Further reading
Braathen LR, Szeimies RM, Basset-Seguin N, et al.
Guidelines on the use of photodynamic therapy
for nonmelanoma skin cancer: an international
consensus. International Society for Photodynamic
Therapy in Dermatology, 2005. J Am Acad Der-
matol 2007;56(1):125–143.
Fink-Puches R, Soyer HP, Hofer A, Kerl H, Wolf P.
Long-term follow-up and histological changes of
superficial nonmelanoma skin cancers treated with
topical delta-aminolevulinic acid photodynamic
therapy. Arch Dermatol 1998;134(7):821–826.

Fotinos N, Campo MA, Popowycz F, Gurny R,
Lange N. δ-Aminolevulinic acid derivatives
in photomedicine: characteristics, ­application
and perspectives. Photochem Photobiol
2006;82(4):994–1015.
Gold MH. Aminolevulinic acid photodynamic
therapy: medical evidence for its expanded use.
Expert Rev Med Devices 2006;3(3):357–371.
Morton CA, Brown SB, Collins S, et al. Guidelines
for topical photodynamic therapy: report of a
workshop of the British Photodermatology Group.
Br J Dermatol 2002;146(4):552–567.
Moseley H, Ibbotson S, Woods J, et al. Clinical and
research applications of photodynamic therapy
in dermatology: experience of the Scottish PDT
Centre. Lasers Surg Med 2006;38(5):403–416.
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Photodynamic therapy 253
Nestor MS, Gold MH, Kauvar AN, et al. The use
of photodynamic therapy in dermatology: results
of a consensus conference. J Drugs Dermatol
2006;5(2):140–154.
Sato N, Moore B, Keevey S, Drazba J, Hasan T,
Maytin EV. Vitamin D enhances ALA-mediated
protoporphyrin IX production and photodynamic
cell death in 3-D organotypic cultures of keratino-
cytes. J Invest Dermatol 2007;127:925–934.
Strasswimmer J, Grande DJ. Do pulsed lasers pro-
duce an effective photodynamic therapy response?
Lasers Surg Med 2006;38(1):22–25.
 Index

actinic keratoses beta-adrenergic blockers 77

ALA-PDT 248, 250–1 biopsy instruments 59–61, 119–20
topical regimens 250 biopsy specimens 122
adhesives, true allergic reactions 77 biopsy techniques 117–22
Adson forceps 65 elliptical 121–2
alar notching 214 incisional vs excisional 118
alcohol preparations (antisepsis) 44–5 nail unit 194–5
alginate dressings 93 pigmented lesions 118–19
algorithms punch 122
complications of surgery 207 punch biopsy instruments 59–60
flaps for defect closure 165 shave 119–21
topical ALA-PDT 249 Bishop—Harmon forceps 66
treatment of infections 213 bolster dressings 182, 184
wound closure 164–5 bone chisel and hammer 70
allergic contact dermatitis, caused by antibacterials 213 Bowen’s disease, photodynamic therapy (PDT) 248
allergic reactions 76–7, 213 Brodie—Trendelenburg test 222
Allis forceps or clamp 67 Brown—Adson forceps 65
allografts, cultured allografts 94 buccinator muscle 7
aluminum chloride 191, 192 Burow’s wedge advancement flap (BWAF) 166–7,
delta-aminolevulinic acid (ALA) 245, 248–51 170, 179
application time 251 Burrow’s triangles 131–2
light source 251
anaphylaxis 216 cadexomer iodine 92–3
anatomy cadherins 82
head and neck 1–40 café-au-lait macules, laser therapy 239–40
nail unit 189–90 candidal infection 212–13
scalp 27–9, 37–9 capillary bed stimulant, epithelialization and
anesthesia see local anesthesia healing 94
angina and ischemic heart disease 74 cardiac pacemakers 75, 105
antibacterials, allergic contact dermatitis 213 minimizing interference from electrosurgery 105
antibiotic prophylaxis 74–5, 89 cardiovascular disease 74
regimens 75 carotid system 25–6
antibiotics arteries of ECA and ICA system 35
ointments 88–9 Castroviejo needle holders 68
true allergic reactions 77 Castroviejo scissors 64
wound dressings 94 cephalosporin, hematoma 209
anticoagulation therapy 77–8 cervical plexus 22
antiseptic agents 43–5, 87–8 sensory nerves 27
arrhythmias 216 chalazion clamps 69
arterial insufficiency ulcers 99 chlorhexidine 44–5, 88
atrophie blanche 221 chlorodifluoromethane 108–9
auriculotemporal nerve 3 chloroxylenol 45
autoclave 47 chronic venous insufficiency 219
chronic wounds 86–90
bacitracin 88–9 assessment 90
bacterial skin flora 42, 87 etiology 88
basal cell carcinoma 123 classification, surgical wounds 43
bathing routine 96 clotting cascade 82–3
Baumgartner needle holder 68 Cockcroft—Gault equation 76
Beaver blades (miniblade system) 61 collagenase (MMP-1) 84
benign lesions, treatment with cryosurgery 110 complications of surgery 207–18
benzoyl peroxide 108 abnormal scarring/wound appearance 213–14

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256 Index

complications of surgery (Continued) ecchymosis 209–10

algorithm 207 ectropion 214
composite skin grafts 186–7 electricity, principles of 102
cryosurgical techniques 114 electrocoagulation (deep skin ablation) 104–5
dehiscence and epidermolysis 210–11 electrosection 104–5
excisional surgery 134–6 vs conventional scalpel surgery 103–4
full-thickness skin grafts 182 electrosurgery 101–5
infections and mimickers 212–14 electrocautery 103–4
life-threatening surgical complications 216 electrodessication 103, 105
nail surgery 197 electrofulguration 103, 105
necrosis 182, 211–12 indications 105
scarring 215–16 monoterminal vs biterminal 101
sclerotherapy 227 problems and their management 104, 105
seroma 210 endocarditis, and prosthesis infection 75
see also hematoma endothelial cells, in wound healing 83–6
compression therapy 223–4 epidermolysis, post surgery 210–11
indications and contraindications 223–4 epilating forceps 66–7
consultation area 73 epinephrine 53–4
contour lines and cosmetic units 4, 7, 126 adverse effects 54
cosmetic subunit junction lines 124 causing malignant hypertension 77
Crile—Wood needle holders 68 contraindications 54
cryogens, boiling points 108 drug reactions 55
cryosurgical techniques 107–16 Erb’s point 21, 26
benign lesions 110, 113 ethanolamine oleate 225–6
closed technique 112 ethylene oxide 47
cold instrument technique 112–13 excisional surgery 123–38
complications 114 anesthetizing a planned excision 126
cone spray technique 112 closing the surgical wound 131–6
depth of freeze and spraying factors 109 complications 134–6
factors affecting freezing of tissue 108 crescentic excision 127–8
indications and contraindications 109–10 hemostasis 130–2
key events during freezing 109 margins of excision 124
open spray technique 112 orienting the ellipse 123–4
postoperative course and care 114 performing the excision 124–6
premalignant/malignant lesions 110, 113–15 planes of undermining 130
treatment guidelines 113 planned excision 124, 126
curette biopsy 121 postoperative care 133–4
curettes 61–2 removal of sutures 134
cutaneous microbiology 42, 87 S-plasty and M-plasty excision 127–8
cyclosporine 77 specimen removal and undermining 128–30
cysts, management 137 wound care 133–5
cytochrome P450, inhibiting medications 52 eyelid biopsy 118–19

Dakin’s solution 88 face

debridement arterial pulses and danger zones 35
enzymatic debriders 94 arterial supply 23–5, 29–30
surgical and medical alternatives 91 contour lines and cosmetic units 4, 7
deep vascular lesions, laser therapy 236 H zone (indicating areas of tumor recurrence) 201
deep venous thrombosis (DVT) 221 muscles of facial expression 9–15
defibrillators 75 skin tension lines (STLs) 8–9
minimizing interference from electrosurgery 105 veins 35
dehiscence and epidermolysis, post surgery 210–11 venous supply 25–7
DeJardin forceps 68 facemasks with eye shields 46
diabetes mellitus 74 facial artery
diabetic ulcers 98 with angular artery 31
increased risk of Pseudomonas sp infections 42 branches (external carotid system) 30
digital nerve block 57 facial nerve
disease transmission, through laser plume 241 areas susceptible to injury 12, 13
‘dog ears’ 131–2 branches 10–11
Duffy—Goldman classification, abnormal veins 223 and parotid gland 5–6, 10
muscles and glands innervated 12, 19
ear zygomatic branch 18
regional sensory innervation 23 facial telangiectases 234–5
sensory innervation 29 FDA
superficial temporal artery, and auriculotemporal approval of medical devices 241
nerve 3 approved systems for PDT 246

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 Index 257

fetal wound healing 85–6 grafts (Continued)

fibroblasts, in wound healing 83–6 full-thickness, indications and contraindications 181
fish mouth scar 214 full-thickness grafts 181–3
flaps 163–80 complications 182
advancement flaps 164 donor site selection 181–2
A—T advancement flap 171 postgraft cosmetic considerations 182–3
bilateral crescenteric advancement flap 172 pincushioning/scarring 182
crescenteric advancement flap 171 postoperative graft physiology 182
Kite or V—Y advancement flaps 167 prevention of hematoma 182
algorithm for defect closure 165 split-thickness grafts 184–7
biomechanics and design 165–7 donor site selection 184
cheek to nose staged random pattern indications and contraindications 184
flap 178 granulation tissue 84
classification 164–5, 167 great auricular nerve, and external jugular
complications, necrosis 211–12 vein 28
defined 163
flap delay and flap inset 168, 179 H zone of face (indicating areas of tumor
island pedicle flaps (IPFs) 167, 172 recurrence) 201
movement hair cover (surgeon) 46
advancement versus rotation 168 hair removal by shaving 46–7
inherent, vertical and lateral restraints 165–7 Halstead mosquito hemostat 70
operative technique 173–9 hand scrub 45
pivotal restraint 165, 170 head and neck
postoperative care 179 surgical anatomy 1–40
preoperative planning 170–2 topographical landmarks 1–2
rotation flaps 164, 167 hemangiomas, laser therapy 233–4, 241
cervicofacial rotation flap 173 hematoma
cheek 173 prevention and treatment 207–9
dorsal nasal rotation flap (Rieger) 174 skin grafts 182
O—Z bilateral rotation on scalp 175 hematoporphyrin derivatives (HPDs) 245
staged axial flaps 177 heme, synthesis pathway 247
staged flaps 168 hemostasis
transposition flaps 164, 167 during nail surgery 191–2
bilobe transposition flap 176 in wound healing 81, 84
melolabial transposition flap 175 hemostatic agents 89
rhombic transposition flap 169 hemostats 69–70
trilobe transposition flap 177 herpes simplex virus (HSV) infection 76
Webster, bilobe, trilobe 167–8 Hori’s nevus, QS alexandrite laser 239
trap-dooring 215 Hutchinson’s sign 16
U-plasty advancement flap design 171 hyaluronan 82
vascular supply 164–5 hyaluronic acid (HA) 84–5
random vs axial pattern flap 169 hydrocolloids 93
foramina of skull, bony landmarks 2 hydrogels 93
forceps 65–7 hydrogen peroxide 47
formaldehyde 47 hypertension 74
freckles, laser therapy 238
Freer septum elevator 191 immunosuppressants 77
freezing see cryosurgical techniques infections 41–8
full-thickness skin graft (FTSG) 165 and mimickers 212–14
treatment algorithm 213
galea aponeurotica 27–8 inflammatory phase, in wound healing 82–6
gelatinases (MMP-2and MMP-9) 84 informed consent 79
glossopharyngeal nerve 29 infraorbital foramen, and related structures 22
glucocorticoids 77 infraorbital muscles 16
glutaraldehyde 47 infraorbital nerve block 18, 56
glycerin with chromium potassium alum 225–6 injection, reducing pain of 52
glycomer-631 160 instrument sterilization 47
glycosaminoglycans 82 instrument tie (square knot) 140–2
Gradle scissors 63 iodine, cadexomer iodine 92–3
grafts 181–8 iodophores 92
classification 181 iris forceps 67
complications, necrosis 182, 211–12 iris scissors 63–4
composite grafts 185–6 isopropyl and ethyl alcohols 44–5
complications 186–7
donor site selection 185 Jacobsen hemostat 70
defined 181 jeweler’s (splinter) forceps 66

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258 Index
keratinocytes 83
expansion in culture 94
Klippel—Trenaunay syndrome 219
labial artery and related structures
lower lip and chin 32
upper lip and cheek 33
lactation, local anesthesia 54
Lagrange scissors 64
laser physics 229–30
types and chromophores 230
laser plume, disease transmission 241
laser therapy 231–43
applications 230
café-au-lait macules 239–40
congenital nevi 239
controversies 241
deep vascular lesions 236
facial telangiectases 234–5
freckles 238
hemangiomas 233–4, 241
Hori’s nevus 239
leg veins 235–7
lentigines 238
medical indications 231–43
melasma 240
nevus of Ota 238–9
pigmented lesions 237
port-wine stains 232–5
recurrence 241
side-effects 231
spider veins 227
vascular laser systems 231–5
laser types
argon 488-514 nm/ argon-pumped tunable
dye 231
intense pulsed-light (IPL) systems 231
long pulsed tunable dye laser (LPTDL) 234
near-infrared 231
neodymium:yttrium—aluminum—-garnet (Nd:
YAG) 231, 233
potassium—titanyl-phosphate (KTP) 231,
233, 235
pulsed-dye laser (PDL) 231
QS red light lasers 237–8
latex, true allergic reactions 77
leg veins, laser therapy 235–7
lentigines, laser therapy 238
leukocyte adhesion molecules (integrins) 82
levator palpebrae superioris (LPS) 19
lidocaine 49–58
with epinephrine (1:100 000) 202
maximum recommended dose 52
mechanism of action 49
pKa and onset of action 50
toxicity 216
lipodermatosclerosis 221
lipomas, management 137
lipoxins 83
liquid nitrogen 110–11
liver disease 76
local anesthesia 49–58
acid—base equilibrium around nerve cell
­membrane 50
adverse cardiovascular effects 52–3
ERRNVPHGLFRVRUJ
local anesthesia (Continued)
allergic reactions 53
alternatives 54
brand names and properties 51
chemical structure 49
classification 50–1
CNS toxicity 54
history 49
mechanism of action 49
mucous membranes 55
nail surgery 190–1
pKa and onset of action 50
planned excision 126
in pregnancy and lactation 54
systemic/local adverse effects 51
differential diagnosis 53
techniques 55–6
true allergic reactions 77
lower limb, major veins 220
lymphatic system
deep lateral cervical nodes 37
facial group of lymph nodes 37
head and neck 27, 36
superficial collecting nodes 37
maggot therapy 94
Phaenicia sericata (green bottle fly) 91
malignant hypertension, epinephrine 77
malignant lesions
cryosurgery 107–16
Mohs micrographic surgery 199–206
treatment overview 199–200
malvosid 81
matrix metalloproteinases (MMPs) 84–6
matrixectomy, nail 193–4
maxillary artery branches (ECA system) 34
medical devices, FDA approval 241
medical history 73
melanoma
biopsy technique 118
post argon laser treatment 241
post carbon dioxide laser treatment 241
melasma, laser therapy 240
mental foramen, and related structures 24
mental nerve block 56
methemoglobinemia (hematologic) 53
methicillin-resistant S. aureus (MRSA) 89
methyl aminolevulinate (MAL) 245–6
Metzenbaum scissors 64
microbiology, skin flora 42, 87
modiolus, elevators, and depressors 17
Mohs micrographic surgery 199–206
concepts 199–200
management of postoperative defects 205
Mohs map 203–4
preoperative evaluation 201, 202
tissue processing and interpretation 204
treatment overview 199–200
tumors (list) 202
monocyte/macrophages, in wound healing 82–6
motor nerve, transection 217
motor nerve deficits 215
mucous membranes, topical anesthetics 55
mupirocin 89
myocardial infarction 216
 Index 259

nail avulsion, proximal/distal 192–3 photosensitizers (Continued)

nail matrixectomy 193–4 light source choice 247, 248, 250
nail surgery 189–98 methyl aminolevulinate (MAL) 245–6
anesthesia 190–1 physical examination 78
complications 197 pigmented lesions
hemostasis 191–2 biopsy techniques 118–19
medical history 190 laser therapy 237
postoperative management 196–7 pincushioning 182, 215
nail unit placement 139–50
anatomy 189–90 platelet-derived growth factor [PDGF] 82
biopsy techniques 194–6 platelets
en bloc excision 196 activation in wound healing 81–6
needle holders or drivers 67–8 function 83
needles 157–9 polidocanol 225–6
nomenclature 157 poliglecaprone-25 160
nerve blocks 56–7 polybutester 10
digital nerve block 57 polydioxanone 160
infraorbital nerve block 18, 56 polyglactin 159
mental nerve block 56 polyglycolic acid 159
reducing pain of injection 52 polyiodide iodine 225–6
ring or digital block 57 polymyxin B sulfate 89
supraorbital/supratrochlear nerve block 18, 56 polytrimethylene carbonate 160
nerve cell membrane, acid—base equilibrium around port-wine stains
nerve cell membrane 50 laser therapy 232–3
nerve deficits 215 recurrence 241
nerve fibers, size and conduction velocity 50 posterior triangle of the neck 21–2, 24–6
neuroischemic ulcers 99 potassium alum 225–6
neutrophil elastases 86 povidone—iodine 44–5
neutrophils, in wound healing 82–3 pregnancy 76
nevi, congenital, laser therapy 239 pregnancy and lactation, local anesthesia 54
nevus of Ota, laser therapy 238–9 preoperative assessment 73–80
nitrogen, liquid 110–11 pressure ulcers 97–8
nonsteroidal anti-inflammatory agents (NSAIDs) 77 primary/secondary standing cone 166
Northbent scissors 64 proliferative phase, re-epithelialization 84
nose, nerves innervating 22 prosthesis infection 75
protoporphyrin IX (PpIX), photosensitizer in
Olsen—Hegar needle holder 68 PDT 245
ophthalmic artery, branches (ICA system) 34 psychiatric/psychological impairment 76
ophthalmic nerve 16–17 punch biopsy 121
orbicularis oculi muscle, and zygomatic branch of punch biopsy instruments 59–60
facial nerve 18
orbital rim 1–2 reconstructive surgery see flaps; grafts
ortho-phthalaldehyde (OPA) 47 regional sensory innervation, trigeminal nerve 23
renal disease 76
pacemakers 75, 105 ring or digital block 57
para-aminobenzoic acid (PABA) 49
para-chlorometaxylenol (PCMX, chloroxylenol) 45 saline and dextrose 225–6
parotid gland and duct 4–7 saphenous vein insufficiency/reflux 224
percussion test 222 scalp
periosteal elevators 70 anatomy 27–9, 37–9
peripheral artery occlusive disease (PAOD) 99 arterial supply 29–31, 39
Phaenicia sericata (green bottle fly) 91 borders 38
photodynamic therapy (PDT) 245–54 four areas 1, 27–9
actinic keratoses 248 layers 37–8
alternatives to PDT 248 muscles 38
Bowen’s disease 248 nerves 39
dermatologic uses 248 scalpel biopsy 119–20
light source for PDT 246 scalpels 60–1
pain control 252 scars
photosensitizers 245 complications of scarring 215–16
absorption spectra 247–8 hypertrophic 214–15
delta-aminolevulinic acid (ALA) 245, 248–50 Schwartz test 222
algorithm for topical ALA-PDT 249 scissors 62–3
topical regimens 250 sclerosing agents 224
controversies 249–50 important characteristics 225–6
excitation, energy levels 246 relative potency 226

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260 Index

sclerotherapy sutures (Continued)

complications 227 combination running simple and vertical mattress
contraindications 226 suture 146
indications 224–5 general guidelines for suture placement 139–45
preoperative/postoperative guidelines 227 granuloma 214
varicose and telangiectatic leg veins 219–28 halfburied vertical mattress suture 143–4
secondary defect closure 166 horizontal mattress suture 144–5
secondary standing cone 166 instrument tie (square knot) 140–2
seizures 216 interrupted buried stitch 153
selectins 82–3 modified buried vertical mattress 154
sensory nerve deficits 215 nonabsorbable 158, 160–1
seroma 210 properties 159
shave biopsy 59, 120 pulley suture 144, 145
shaving (hair removal) 46–7 purse-string suture 150, 155
silicone nonadherent mesh 94 removal of sutures 134, 150
skin cancer see malignant lesions running combination simple and vertical
skin grafts see grafts mattress 152
skin hooks 69–70 running cuticular stitch 149
skin substitutes 92–5 running horizontal mattress 151
composite skin substitutes 95 running locked suture 146
dermal grafts 95 running subcuticular suture 147–8, 155
epidermal tissue culture 94–5 simple interrupted suture 140, 143
skin tension lines 123–4 site for, recommendations 161
face 8–9 strip suture method 137
face; trunk; extremities 125 three- and four-point corner (tip) sutures 145–7
skull and foramina, bony landmarks 2 vertical mattress suture 140, 143–4
smoking 78 near—far adaptation 145–6
effect on wounds 96
and necrosis 211 telangiectases, facial 234–5
social and family history 78 telangiectatic leg veins
sodium morrhuate 225–6 Duffy—Goldman classification 223
sodium tetradecyl sulfate 224–6 laser therapy 227, 235–7
spider veins 221 sclerotherapy 219–28
laser therapy 227 treatment options 224
spinal accessory nerve 3, 22, 26 temple 1–2
split-thickness skin grafts (STSGs) 165 borders 2
‘stair-casing’, wound margins 127 temporal artery
standing cone deformity 131–2 and auriculotemporal nerve 3
Staphylococcus aureus infections 42 branches (ECA system) 34
stasis dermatitis 221 superficial 3
sterile field 46 tetanus status 89
sternocleidomastoid muscle 4 thrombophlebitis 221
anterior and posterior triangles 1 tissue-derived inhibitors of metalloproteinases
stromelysin (MMP-3) 84 (TIMPs) 85
superficial musculoaponeurotic system topical anesthesia
(SMAS) 6–8 mucous membranes 55
supraorbital/supratrochlear nerve block 18, 56 see also local anesthesia
supraorbital/supratrochlear neurovascular transection, major motor nerve 217
structures 21 transforming growth factor beta 82
surgeon’s apparel 46 trigeminal nerve 12–17, 20
surgical gut 159 divisions and branches 20
surgical instruments 59–72 tumescent technique for liposuction 57
sterilization 47 tumors
surgical site list potentially treated with Mohs 202
infections 41–8 see also malignant lesions
preparation 45–6
surgical wounds see wounds ulcers
sutures 139–56, 157–62 arterial insufficiency ulcers 99
absorbable 158–60 diabetic ulcers 98
allergic reactions 213 neuroischemic ulcers 99
basting sutures 182, 184 pressure ulcers 97–8
braided sutures 158 venous ulcers 86, 96–8
buried sutures 146–7
buried vertical mattress suture 147, 153 varicose veins
canal suture 145–7 clinical presentation and diagnosis 221
closure material alternatives 162 laser therapy 227

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 Index 261

varicose veins (Continued) wound infections (Continued)

pathophysiology 219–20 and hair removal by shaving 46–7
risk factors 222 increase in rate 42
sclerotherapy 219–28 risk factors 42–4
treatment options 224 wounds
vascular endothelial growth factor (VEGF) 82 acute wounds 89–90
vascular endothelial receptors (selectins, cadherins) 82 analysis and characteristics 164
vasovagal reactions 216 care 133–5
veins care guidelines 95–9
compression therapy 223–4 chronic wounds 86–90
Duffy—Goldman classification 223 classification 43, 87, 89, 212
venous ulcers 96–8 surgical wounds 43
wound epithelialization 86 closure algorithm 164–5
debridement 90–1
waveforms, factors 102 healing 81–100
Webster (Halsey) needle holders 68 fetal wound healing 85–6
wedge advancement flap, Burow’s (BWAF) 166–7, maturation and remodeling 84–5
170, 179 phases and time course of events 82
Westcott scissors 64 normal closure rates 89
wound dressings 91–9 remodeling and wound strength 85
list 93 skin substitutes 92–5
skin substitutes 92–3 and smoking 96
wound infections 41–8, 90
differential diagnosis 43–4 zygomatic branch, facial nerve 18

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