scar revision.pdf
Post on 11-Nov-2014
75 Views
Preview:
DESCRIPTION
TRANSCRIPT
Oral Maxillofacial Surg C
Secondary Procedures in Maxillofacial Dermatology
James M. Henderson, DDS, MDa,b,c,*,
Bruce B. Horswell, DDS, MD, FACSa,b,c,d
aDepartment of Surgery, West Virginia University School of Medicine-Charleston Campus, 3110 MacCorkle Avenue,
Charleston, WV 25304, USAbDepartment of Oral and Maxillofacial Surgery, West Virginia University School of Dentistry, Morgantown, WV 26506, USA
cPrivate Practice, Facial Surgery Center/FACES, 415 Morris Street, Suite 309 Charleston, WV 25302, USAdFirst Appalachian Craniofacial Deformity Specialists, 830 Pennsylvania Avenue, Suite 302, Charleston, WV 25302, USA
The main surgical goal in managing cutaneous
carcinomas is eradication of the primary lesion
with disease-free margins. Once this goal has been
achieved, attention can be turned to reconstruction of
the surgical defect with favorable esthetic results.
Many of the factors that ultimately lead to an es-
thetically favorable outcome begin with a critical
evaluation of the anatomic subunit involved, primary
repair versus secondary repair, choice of flap used for
reconstruction, tissue handling, and various host
factors (ie, tobacco use, comorbid disease). Some of
these factors have been discussed in previous articles
and receive only cursory review in this article. This
article focuses on secondary procedures used to im-
prove the esthetic outcome of surgical resection. Man-
agement of flaps and scars is discussed, including
the immediate postoperative period and the late
(secondary) period. Various adjunctive measures are
discussed, including scar revision, resurfacing proce-
dures, silicone, dressings, and topical agents.
Numerous treatments are available for the man-
agement of facial scars. Each modality can partially
improve the outcome in various ways, and a com-
bination of treatments is often required to achieve
optimal results. It is imperative to evaluate patient
expectations before excision of facial lesions and
1042-3699/05/$ – see front matter D 2005 Elsevier Inc. All rights
doi:10.1016/j.coms.2005.02.006
* Corresponding author. FACES/Facial Surgery Cen-
ter, 830 Pennsylvania Avenue, Suite 302, Charleston,
WV 25302.
E-mail address: james.henderson@camc.org
(J.M. Henderson).
throughout the postoperative period, because patients
often have unrealistic expectations about the reso-
lution of their wound and the eventual esthetic out-
come. Physicians must emphasize that no therapeutic
modality can bring about complete resolution of
scarring and that multiple treatments and treatment
modalities are often required [1].
Wound healing
To fully appreciate the role of secondary proce-
dures in improving the esthetic outcome of surgical
resection, one first must have a basic understanding
of wound healing. This understanding helps guide
the reconstructive surgeon in choosing a mode of
therapy best suited to achieve the desired result.
Wound healing represents a complex series of events
that until recently have been understood poorly.
The complex interaction of events in wound
healing has been divided into phases, including in-
flammation, migration, proliferation, and remodeling
(contraction). Inflammation begins when a site is
injured (surgical incision) and results in a cascade of
events that involves vasoconstriction, platelet activa-
tion, and eventual clot formation [2–9]. Exaggeration
of the inflammatory phase increases the concentration
of various growth factors, including transforming
growth factor beta, platelet-derived growth factor,
interleukin-1, and insulin-like growth factor. Neutro-
phils predominate initially, followed by macrophages
several days later. In the migratory phase, angiogenic
factors and fibroblasts increase, while excess amounts
lin N Am 17 (2005) 173 – 189
reserved.
oralmaxsurgery.theclinics.com
henderson & horswell174
of collagen and extracellular matrix are produced
[8,10]. The proliferative phase is characterized by an
increase in collagen production and epithelial cell
migration and regeneration. Granulation tissue also
becomes evident during this phase. Scar contracture
and collagen reorganization are observed in the
remodeling (late) phase of wound healing. Wound
contraction is characterized by a decrease in fibro-
blasts, macrophages, and wound vascularity and is
believed to be the result of myofibroblasts [8]. Col-
lagen cross-linking and alignment characterize the
mature wound; epithelial architecture is stable, al-
though it never returns to its preinjured state [11].
The phases of wound healing seem to act in con-
cert to various degrees. As a result, any disruption
of a specific component leads to an imbalance in
the process that may lead to excessive wound con-
tracture, hypertrophic scar formation, keloids, or pig-
mentary changes, which lead to a compromised
esthetic result. Numerous factors can affect the deli-
cate balance of wound healing and lead to scar for-
mation, including infection, foreign body, systemic
toxins, hematoma, tissue hypoxia, prolonged healing
by secondary intention, improper tissue handling, and
wound tension (traction) [11]. Various growth, hor-
monal, immunologic, and genetic factors also may
be altered during the phases of wound healing, con-
tributing to an imbalance in the process and eventual
scar formation.
Any of the agents typically used to improve
healing, including topical and systemic agents, can be
used inappropriately and disrupt the normal mecha-
nism of wound healing. Ultimately, any of the factors
listed previously increase metabolic and cellular
activity within the wound leading to an excessive
deposition of tissue collagen, water, fibronectin, and
glycosaminoglycans [2–9,12].
With regard to scar management, numerous tech-
niques and therapies have been advocated in the
literature. Many therapies have been shown to be
effective in small-scale studies and anecdotal reports;
however, few of these modalities have been sup-
ported by prospective studies with adequate control
groups and long-term follow-up. Care must be exer-
cised when applying information from these studies
and extrapolating it to the treatment of facial scars,
because many studies are based on dermatologic
wound healing in other body regions. Facial skin is
thinner, has more appendages, and may be affected
adversely by some scar treatment modalities [1].
Mustoe et al [13] gathered international recom-
mendations on prevention and management of
abnormal scarring and provided evidence-based rec-
ommendations for treatment. The consensus of this
international group of experts emphasizes the primary
role of silicone gel sheeting and intralesional cortico-
steroids in scar management, and it is based on large-
scale, prospective, evidence-based trials. Throughout
the remainder of this article, the authors attempt to
highlight treatments supported by large-scale, pro-
spective studies and point out therapies based on
small-scale reviews or anecdotal reports.
Host and local factors
Systemic health of the patient who undergoes
surgery or dermatologic corrective measures has long
been recognized as a key component in achieving
a good result. Numerous host factors play a critical
role in normal wound healing, including nutrition,
oxygenation, coexisting disease, and existing derma-
tologic disease [14]. This is particularly relevant in
oncologic patients who also may have undergone
radiation treatment for their disease. The healthier a
patient, the more accelerated and predictable the
healing process and the less susceptible a wound is to
adverse microbial and local environmental influ-
ences. Numerous studies have shown that scarring is
minimized when a patient’s health status has been op-
timized. A review of the literature indicates that two
or more comorbid systemic diseases significantly
affect surgical outcome, which is compounded by
increasing age, poor nutritional status, and substance
abuse [11,14,15]. Patient selection for a particular
procedure is paramount (some patients may not be
good candidates for revision surgery, unless there are
adverse functional concerns). Reducing or controlling
smoking (particularly in the perioperative period),
improving nutritional status if malnourishment is
suspected, and optimizing the general medical con-
dition improve outcomes after surgery for even minor
procedures [11]. Nutrition should be optimized to
provide an intact immune system and the building
blocks needed for normal healing. Vitamins A and C
and ferrous iron are needed for normal collagen
synthesis. Reduced levels of zinc lead to decreased
protein production and delayed epithelialization.
Local host factors also play a key role in normal
healing. The more involved the planned procedure
(ie, deeper and more extensive flaps or grafts), the
more one can anticipate problems—and possibly
failure—in a compromised patient. Surgeons should
consider options carefully for dermatologic revision
or correction, with patients and their health in mind.
A wide and deep excision to bone or scar that ne-
cessitates local flap advancement in a smoker with
poorly controlled diabetes may invite disaster and
Fig. 1. Hyperpigmentation of scars in Fitzpatrick
V individual.
secondary procedures in maxillofacial dermatology 175
more problems. Scars located over convex surfaces
can be difficult to revise because of unfavorable forces
and high surface tension. Surgical defects located in
areas of function may be prone to widened and
deformed scars for similar reasons. Tissue type is also
critical, with thick sebaceous skin being more prone
to milia formation, acneiform eruption, and pro-
longed inflammation [16–19].
In the postablative patient, it is critical to review
any history of radiation therapy. For patients who are
otherwise healthy and have received less than 50 Gy,
successful secondary procedures can be performed in
an effort to reduce scarring. Regions of the head and
neck that have received more than 50 Gy generally
have compromised cutaneous characteristics of basi-
lar fibrosis, dermal plexus obliteration, atrophy of the
subcutaneous and surface epithelium, and some loss
of dermal appendages. These conditions lead to
delayed healing and an increased risk of wound com-
plications that may contribute to a poor esthetic out-
come [15].
Sun exposure is another host factor that is often
overlooked when discussing postoperative secondary
procedures and the prevention of scarring. Many
patients who have undergone resection of skin ma-
lignancies have had an extensive sun exposure
history and may continue to work outdoors or engage
in outdoor recreational activities. Not only can con-
tinued sun exposure lead to further solar damage to
the skin and risk of malignancy but it also can lead to
significant pigmentary changes in postsurgical scars
[16]. Even minimal sun exposure within the first
60 days of repair can lead to hyperpigmentation. A
broad-brimmed hat and sunblock should be recom-
mended to every patient to prevent these changes [14].
Dermatologic conditions
Inherent ethnic and skin characteristics affect
results. Darkly pigmented individuals (Fitzpatrick IV,
V, and VI) are prone to prolonged, unpredictable,
and often less desirable results (Fig. 1) [16]. Persons
with darker skin have a tendency to unpredictable
dyschromia caused by melanocytic dysfunction that
results in either hypo- or hyperpigmentation. This
situation must be discussed carefully with patients
before treatment. Judicious use of perioperative
steroids and 4% hydroquinone may assist in modu-
lating abnormal melanocytic responses [17].
Patients with active acne, rosacea, eczema, or
other inflammatory dermatoses should have secon-
dary revision surgery deferred until the condition
is controlled or in remission [18,19]. A patient with
active acne lesions in the midst of a wound have
worse wound healing and increased scarring (Fig. 2).
Active acne is usually treated with a combination of
antibiotics, surface exfoliating adjuncts (eg, salicylic
and azeleic acids, benzoyl peroxide), and, in severe
cases, retinoic acid derivatives [19]. Preoperative
mechanical or chemical resurfacing procedures may
need to be planned before more extensive dermato-
logic surgery to optimize local skin conditions.
Surgical management
The most critical time to prevent scar formation
is at the time of injury or surgical resection. It is
important to briefly review several factors involved in
the surgical planning and resection of skin lesions and
scars that have a profound impact on the eventual
esthetic result.
Skin preparation
Optimizing a patient’s skin condition is paramount
for revision surgery success. Preoperative adjuncts
include resurfacing procedures (eg, chemical, laser, or
dermabrasion techniques) that improve skin metabo-
lism, vasularity, orderliness of skin cell maturation,
and collagen or elastin components in the dermis
[20]. Generally, the skin should be prepared approxi-
mately 4 weeks before revision surgery to allow
some maturation of the skin layers, especially the
epidermis. The more extensive the resurfacing
procedure, the longer the healing period until final
secondary procedures can be performed. Some
clinicians believe that preoperative administration of
multivitamins, particularly vitamins C and E, one or
two weeks before surgery enhances healing and
Fig. 2. Active acne and increased inflammation in scars.
henderson & horswell176
improves surgical results, although this has not been
proven [21,22].
Fig. 3. RSTLs of the facial region with lines of maximal
extensibility that run perpendicular.
Scar revision
Several types of excisional designs are available
to the surgeon. Limberg’s excellent treatise on scar
revision is foundational to our understanding and
practice in dermatologic surgery [23]. He designed
many flaps based on mathematical configurations,
which are useful for reconstructing defects with local
tissue. These flaps are discussed later; however, sev-
eral factors must be considered before planning re-
excision of scar tissue or lesions.
Timing
It is never too late to perform a scar revision;
however, scar revision can be done too early [24]. As
a general rule, scar modification surgery should be
deferred 6 to 12 months. This is the time when mature
collagen makes up most of the wound bed. Wounds
in the inflammatory and proliferative phases of heal-
ing are more prone to exaggerated and prolonged
inflammation and, consequently, increased scarring
[1,15,24,25]. Adults typically have less wound heal-
ing vigor, and planning for surgery may take place
earlier. For wounds with poor scar orientation or
wound alignment, surgery can be considered earlier
[26]. Children heal quickly but with longer periods
of vascularity and more collagen depot; deferment
for 1 or 2 years may be prudent [27]. This time pe-
riod results in some improvement in appearance of
the scar and diminution of scar size and bulk. No
amount of time improves a scar or defect that has
resulted in tissue mismatch in the vermilion border or
eyelid margins or in a disfiguring avulsion defect
with foreign body inflammation. These scars may
need to be revised much sooner than anticipated.
Scars in regions that restrict function, such as the
eyelid, neck, and oral cavity, may need earlier inter-
vention. Factors such as harassment and social
alienation by other children and parental anxieties
also may lead to earlier intervention [24].
Scar location
It is important to understand that the goal of scar
modification surgery is not to eliminate scars but
to hide them and make them as inconspicuous as
possible [15,25]. One also must take into account
how the scar appears and may be accentuated during
animation. A scar with favorable characteristics is flat
(level with surrounding tissue), has similar color and
texture to the surrounding tissues, is oriented within
or along resting skin tension lines (RSTLs), and may
have a geometric design that is less detectable to the
naked eye [12,15,28].
Incorporation and deformation of normal sur-
rounding tissue must be minimized as much as pos-
sible. The practicality of this concept is limited by
scar maturity, width, and location. Wide, hyper-
trophied scars may be better suited to intralesional
excision or resurfacing [24,29].
Scars ideally should lie within the relaxed skin
tension lines (Fig. 3). Planning for scar or defect
revision with local flaps should incorporate this
objective so that healing proceeds without excessive
Fig. 4. Triamcinolone injection of keloid before revi-
sion surgery.
secondary procedures in maxillofacial dermatology 177
tension [28]. Scars that cross RSTLs typically widen
and become hypertrophic, particularly over convex
surfaces [30]. Earlier reorientation of the scar or
placement of a free graft (not as ideal as local tissue)
to avoid tension may be indicated.
Nature of injury or procedure
Areas of tissue loss, such as those seen after
Mohs’ surgery or excision of facial skin lesions, are at
high risk for widened scar formation [24,29]. Tissue
loss connotes increased skin tension during primary
and secondary closure. Normal skin texture is not
obtained with re-epithelialization, and the resultant
dermis is characteristically thin and atrophic [24].
Meticulous handling of the tissues, evacuation of
blood from the wound, accurate wound alignment,
and careful suture placement reduce inflammation and
subsequent scarring [8,9,15,24,31].
Avulsive wounds and heavily contaminated
wounds require judicious management to preserve
viability and reduce bacterial load to prepare the bed
for reconstruction. Some surgeons culture the tissue
to confirm reduced bacterial load (<105 organisms/
gram of tissue) before repair [11].
Wound healing history (hypertrophic scars, keloids)
Patients with a history of keloid formation should
be approached with caution. Time usually does not
improve a keloid, and use of adjunctive preoperative
agents is important before revision surgery (Table 1)
[29]. Preoperative triamcinolone injection two or
three times before planned excision helps prepare
Table 1
Dosage of Kenalog (triamcinalone acetonide) for adults and
children
Adults
Lesion size (cm2) Dosage (mg)
1–2 20–40
2–6 40–80
6–10 80–100
>10 100–120
Children
Age (y) Dosage (mg)
1–2 20
3–5 40
6–10 80
Adapted from Chowdri NA, Mattoo MM, Darzi MA.
Keloids and hypertrophic scars: results with intra-operative
and serial postoperative corticosteroid injection therapy.
Aust N Z J Surg 1999;69:656.
a keloid for more ordered and controlled healing
(Fig. 4). A frank, honest discussion with patients
before surgery is mandatory, with the expectation that
some amount of keloid scarring will recur.
Scar morphology
Scars that are raised and high profile are more
difficult to camouflage than depressed scars hidden in
RSTLs or under anatomic borders (eg, the ala or
lower lip) [30,31]. More staged revision is required
for the former type of scar, and patients must be in-
formed of possible protracted treatment. Selection of
excisional and reconstructive techniques follows a
simple to more complex design algorithm. Fig. 5
(an algorithm for dermatologic secondary procedures)
represents a decision-making tree on which the sur-
geon can add or modify adjunctive treatments, such
as skin preparation, resurfacing, and postopera-
tive modalities.
Simple excision
Fusiform and Z-plasty techniques
Unsightly scars can be re-excised with a fusiform
or geometric design (Fig. 6). Generally, fusiform
excision is performed for smaller scars or lesions that
lie parallel to the RSTLs, which places the repair in a
favorable and esthetic position after healing (Fig. 7).
Scars that run across RSTLs need some reorienta-
tion, which can be achieved through Z-plasties of
varying lengths, number, and angles. Typically, the
more acute the angle of the limb, the less the gain in
length of repair and reorientation of the scar [31,32].
Fig. 5. Algorithm for decision making in dermatologic revision surgery. (From Horswell BB. Scar modification: techniques for revision and camouflage. Atlas Oral Maxillofac Surg Clin
North Am 1998;6:55–72; with permission.)
henderson
&horswell
178
secondary procedures in maxillofacial dermatology 179
Fig. 8 illustrates a Z-plasty design for a scar band in
the cheek that runs perpendicular to the RSTLs. It
correctly reorients the incision and limbs in the
direction of the RSTL and allows the retracted lip
and cheek to displace inferiorly. Multiple Z-plasties
also may be constructed to lengthen scar and de-
crease tension across the revised tissue plane
[28,32,33]. Vigorous, yet judicious, undermining of
the triangle bases must be performed to effect ease
in transposition.
A variant of Z-plasty is an S-plasty design, which
results in a softer, less obvious linear arrangement.
The S-plasty is indicated in higher profile or convex
surfaces, as in over-the-cheek, nasal tip, and chin
Fig. 6. Diagram of various facial scar excisions. (A) Fusi-
form. (B) H-flap. (C) W-plasty. (D) Z-plasty. (E) Elliptical
and Z-plasty combined. (F) geometric design. Stippled areas
of (E) and (F) represent simultaneous dermabrasion. (Image
n Bill Winn; with permission.)
Fig. 7. Diagram of closed scar excisions of Fig. 6. (Image nBill Winn; with permission.)
areas. Because of a broader tip, there is less distal
ischemia and necrosis than in Z-plasty [33].
Geometric designs
A long linear scar over the cheek, upper jaw line,
or forehead can be improved through incorporating
multiple segmental Z-plasties or a ‘‘W-plasty’’ con-
figuration (Fig. 9) [32,34]. This design favorably
realigns the scar that runs across RSTLs into one that
is more parallel or more easily hidden. The tips can
be designed with pointed, round, or squared ends to
help break up the scar profile. Often, the tips become
edematous and may heal with some element of
hypertrophy, which can be dermabraded for a final
smooth appearance after initial healing. For U-shaped
scars on a convex surface, the inner arch of W-plasties
Fig. 8. Release of retracted lip and cheek with Z-plasty technique. (A) Preoperative. X indicates subcutaneous scar band.
(B) Intraoperative Z-plasty incision. (C) Postoperative closure of Z-plasty with inferior rotation of lip.
henderson & horswell180
should have less length and angle (approximately
45�) than the outer W-plasties (approximately 60�),so that the advanced tissue runs radially in direction
with and easily incorporate into the outer arc of tissue
(Fig. 10) [35].
Fig. 9. W-plasty revision of cheek and lip scar followed by posto
Flaps
After excision of scar or a lesion, the defect may
be too large for simple closure. Larger local flaps may
need to be designed that can move tissue from the
perative dermabrasion. (A) Preoperative. (B) Postoperative.
Fig. 10. U-shaped W-plasty excision of scar. (A) W-plasty excision (white lines indicate radial advancement of arc). (B) Closure
of W-plasty excision.
secondary procedures in maxillofacial dermatology 181
surrounding region into the defect. These flaps have
various geometric designs, most notably the rhom-
boid flap.
Rhomboid flaps are the workhorse facial flaps for
reconstructing defects not amenable to local closure
[36,37]. They are particularly useful over the cheek
and in nasal sidewalls, where the incision limbs can
align with anatomic margins or RSTLs. Every defect
has four possible rhomboid flaps, of which one is
more ideal for tissue transfer and final limb orienta-
tion (Fig. 11) [37]. Final closure should provide a
limb that aligns with the RSTLs, and allows tissue
to rotate easily as the flap extends from lax tissue
(perpendicular to the RSTLs). Surgeons should re-
member that greatest tension is at the leading edge of
the flap; secure, permanent subcuticular sutures may
be helpful in this area [38].
A variation of rhomboid flaps is the lobed flap,
which may have several lobed components. The less
Fig. 11. Four possible rhomboid flaps for a nasal lesion, one
(X) of which is ideal because of final position of the
incisional limbs and direction of tissue transfer.
the lobed flap must rotate (less arc of rotation), the
less tissue distortion and vascular compromise will
occur [38]. Lobed flaps are useful for smaller defects
or lesions in the nasal region.
Rotation flaps may be used to reconstruct large
defects or lesions. Larger cheek or lower eyelid de-
fects can be closed with a random-pattern cheek flap
that is rotated anteriorly (Fig. 12). Flaps also can be
raised on a vascular pedicle (axial-pattern) and ro-
tated to a defect. Flaps based on the infratrochlear
(glabellar), supratrochlear (forehead), and superior
labial (nasolabial) vascular branches are useful for
reconstructing nasal region defects (Fig. 13).
Tissue expansion
At times, large avulsion or resection defects may
require reconstruction through tissue recruitment via
expansion. This technique is particularly useful for
scalp, forehead, and some cheek and neck defects
(Fig. 14) [39]. The area to be reconstructed must
be mature, with no recent incisions, dehiscence, or
inflammation. The tissue reservoir to be expanded
also should be uninvolved and distant enough to
allow generous expansion without defect distortion;
however, it should be close enough to afford local
tissue matching and ease of transfer. Temporary dis-
tortion of cosmetic units may occur; care should be
taken to avoid overexpansion and tissue transfer,
which move the ears, brows, and lips [40]. Semi-rigid
(reinforced) expander bases can be used in areas of
underlying soft tissue (eg, cheeks, neck) to ensure
overlying skin expansion without deeper structure
distortion. Tissue expansion requires good knowl-
edge of tissue mechanics, expander instrumenta-
Fig. 12. Advancement cheek flap (rotational) into infraorbital defect. (A) Diagram of cheek advancement flap to repair
infraorbital defect. (B) Clinical photo of advanced cheek flap. (C) Postoperative view.
henderson & horswell182
tion, and skill with placement. Experience is the key
to success.
Immediate postoperative wound management
The incidence of hypertrophic scarring after sur-
gery is approximately 40% to 70%. The rate is
considerably higher in burn injuries [9]. Recent
evidence from the literature suggests that hydration
is the most important external factor responsible for
optimal wound healing and an esthetically pleasing
scar [7,11,12,27]. Wound support with microporous
tape is also critical in the immediate postsurgical
phase. By 3 weeks, wounds have attained only 20%
of their final strength. Interventions too early in the
healing process can weaken the closure and lead to an
unaesthetic scar [12,41]. Scar support, however, is
critical during this period to prevent increased tension
across the scar, which can lead to exaggerated
scarring. The vector of tension is also important.
Excess tension along a single axis may result in a
widened or stretched scar, whereas multidirectional
tension or intermittent tension leads to hypertrophic
scarring [12,34,42].
With open wounds, an occlusive dressing is rec-
ommended in the immediate postoperative phase.
Scab formation should be prevented. Scabs consist of
necrotic cells, fibrin, and blood products that retard
healing through inhibition of epithelial migration.
Occlusive dressings prevent scab formation, allow
rapid epithelialization, and reduce wound pain,
fibrosis, and infection, which produce a better cos-
metic result [11]. Appropriate dressings include poly-
urethane films, hydrogels, and perforated plastic films
[14,41].
Antibiotic ointments may serve as effective topi-
cal dressings during the exudative postoperative pe-
riod; however, cleaning the wound daily to remove
the film and reapplying the ointment are imperative.
Topical antibiotics are usually not necessary beyond
day 5 for closed facial wounds. Dermatitis, allergy,
and development of resistant organisms are all con-
cerns associated with prolonged antibiotic ointment
use. Neomycin is particularly prone to cause skin
sensitivity. Ointments with multiple antibiotics are
available to broaden the spectrum of coverage [14].
Fig. 13. Forehead and nasolabial flaps for reconstruction of a large, full-thickness (skin, bone, mucosa) postradiation defect
of the nasal-canthal region. (A) Full-thickness defect of nasal-canthal area with forehead (F) and nasolabial (N) flaps outlined
for incision. (B) The nasolabial flap is de-epithelialized and advanced superiorly to line nasal cavity and the forehead flap
is turned down over it (top right). (C) Final result 6 months after division of forehead flap.
secondary procedures in maxillofacial dermatology 183
The skin is exquisitely sensitive to adverse envi-
ronmental influences, particularly during early wound
healing. It is important to remove or reduce excessive
wetting and drying and protect the skin in extreme
climatic conditions. Patients whose employment or
hobbies include exposure to potential biohazards,
heat, smoke, dust, and other irritants should be care-
Fig. 14. Tissue expanders for scar excision and scalp reconstruction
tissue fields lateral to defect. Note: care must be taken not to encr
ful to protect surgical sites or defer surgery until such
time that initial healing can be guaranteed. It is well
known that potentially harmful biofilms colonize
chronically exposed or challenged skin and render
the revised wound more susceptible to inflammation,
breakdown, infection, and increased scarring [11].
At least 2 weeks should be allowed for healing after
. (A) Large scar and forehead defect. (B) After expansion of
oach on the brow region or overexpand the scar defect.
henderson & horswell184
simple or local skin flap surgery, and up to 6 weeks
should be allowed after advanced procedures that
involve regional flaps, grafts, or tissue expansion in
susceptible patients whose activities or work may
compromise healing.
Late postoperative wound management
The choice of treatment modality for the manage-
ment of existing scars depends on a careful evaluation
of scar characteristics, age of the scar, and healing
properties of patients. It is important to assess how
patients have healed previously and whether they
have a propensity toward hypertrophic scar produc-
tion or the development of keloids. Distinguishing
between hypertrophic scars and keloid formation is
critical in planning intervention and choosing an
appropriate therapeutic modality. Clinical character-
istics of hypertrophic scars include confinement to
original wound, spontaneous regression, onset within
3 months of injury, and improvement with surgery.
Keloids, however, extend beyond the original wound
margins, persist over time, have an onset of months to
years after injury, have a familial tendency, and may
worsen with surgery [8,34,42]. Prolonged adjunctive
therapy for keloid scar revision includes periodic
steroid injections—if not performed preoperatively—
and pressure therapy up to 1 year after revision.
Several modalities are available to for surgeons to
use in conjunction with, or after, scar revision
procedures and are discussed in the following section.
Preoperative management may include staged skin
preparation with glycolic acid peels or microderm-
abrasion. Glycolic acid peels are a predictable way to
prepare skin for revision procedures, but one must be
careful not to overinflame the skin just before
surgery. After initial healing (2–3 weeks), the revised
scar and surrounding tissues can be re-treated with
peels or microdermabrasion to enhance epithelial
leveling, but one must ensure that no excessive
inflammation or dehiscence is present. By relying on
subcutaneous sutures and little surface sutures for
tissue support and approximation, a surgeon can
expect less surface irritation. One should defer greater
depth peels until the skin has matured.
Resurfacing (dermabrasion, laser therapy)
Dermabrasion may play a role in the management
of postablative scarring and treatment of certain be-
nign lesions, including actinic and seborrheic kera-
toses, epidermal nevi, syringomas, angiofibromas,
trichoepitheliomas, lentigines, cysts, milia, and mol-
luscum. Dermabrasion can be performed safely with
simultaneous scar revision procedures (Fig. 15) [43].
Potential complications of dermabrasion include
milia formation, acne flares, viral and bacterial infec-
tions, pigmentary changes, and contact dermatitis.
Acne flares are temporary and may persist for 6 to
12 weeks. These flares are treated the same as any
other acne flare and usually do not lead to new acne
scars. Most viral infections can be prevented with
proper prophylaxis. Antiviral agents should be ad-
ministered preoperatively and during the process of
re-epithelialization (7–10 days). Patients with break-
through viral infections or a predisposition to herpetic
outbreaks should be treated with a zoster dose of
antiviral medication. Prophylactic antibiotics are not
typically warranted, except in patients with a history
of rosacea or impetigo. The most common compli-
cation of dermabrasion is pigmentary alteration [16].
Permanent hypopigmentation can occur in 10% to
20% of patients and is more common in persons with
Fitzpatrick skin types IV, V, and VI. Postinflamma-
tory hyperpigmentation is the most common pig-
mentary alteration encountered after dermabrasion.
Typically, changes begin 3 to 4 weeks after surgery
and can be reversed with topical steroids, hydro-
quinone (4%–8%), and sun avoidance [17,43].
Late or persistent erythema heralds the onset of
scar formation and must be aggressively diagnosed
and managed. Topical steroids may be useful during
the initial phase, but intralesional steroids are used
once any papular quality or induration develops [43].
The flashlamp-pumped pulse-dye laser was devel-
oped as a means to obliterate underlying vasculature
believed to play a role in blood-borne tissue factors
and growth factors that stimulate fibroblast activity
[41,42]. Scars treated with the pulse-dye laser have
shown a decrease in erythema and improved scar
texture, height, and pruritis [10,41]. Typical treatment
regimens involve fluences of 6.5 to 7.5 J/cm2 using a
spot size of 5 mm, with treatments repeated at 6- to
8-week intervals until the desired result is achieved or
no further improvement is noted. The effects are not
as effective in patients with Fitzpatrick types IV, V,
and VI skin [41]. Laser resurfacing of new surgical
scars 6 to 8 weeks postoperatively produces results
similar to those achieved with dermabrasion [1,20].
One area that shows promise for using laser resur-
facing immediately after Mohs’ surgery is the nose.
The predictability of secondary intention healing of
defects on convex nasal surfaces is not reliable. For
surgical defects of concave nasal surfaces, however,
secondary intention healing can equal or surpass sur-
gical reconstruction. In a retrospective review by
Fig. 15. Simultaneous scar revision and dermabrasion. (A) Preoperative view of multiple uneven, hyperpigmented scars.
(B) Clinical photo of planned areas for excision and dermabrasion. (C) Postoperative view at 6 months.
secondary procedures in maxillofacial dermatology 185
Ammirati et al [44], 74 patients underwent immediate
postoperative laser resurfacing of convex nasal sur-
faces after Mohs’ surgery using a scanned carbon di-
oxide or long-pulsed Er:YAG laser. All of the patients
in their series were satisfied with the result, and an
independent panel of nine physicians who reviewed
postoperative photographs of 30 patients in the series
deemed the results acceptable or excellent.
Medications
Steroids
Steroid preparations commonly used in the man-
agement of hypertrophic scars and keloids include
triamcinolone acetonide (Kenalog) and triamcinolone
diacetate (Aristocort). Mechanisms of action include
reduced angiogenesis, decreased fibroblast prolifera-
tion, decreased cytokine production, inhibition of
collagen and extracellular matrix protein synthesis,
and disruption of fibrosis [1,9,10,41,42]. Steroids can
be used at various times during therapy. For early pre-
excisional treatment and early postsurgical treatment,
a low concentration is used (Kenalog, 10–20 mg/mL).
After scar maturation and in persons with a predis-
position to excessive scarring, higher concentrations
are used (Kenalog, 40 mg/mL). Treatment is usu-
ally administered with multiple injections given 4 to
6 weeks apart (Table 1) [1,15,41].
Complications of steroid administration include
skin atrophy, granulomas, pigmentary changes, and
development of telangiectasias [1,9,41]. To reduce
the risk of these complications, Grossman [1] recom-
mends starting with lower concentrations and slowly
increasing the dose over several sessions. For the
treatment of facial lesions, he begins with a dose of
3 mg/mL and increases this to 10 mg/mL.
Topical agents
Many topical agents are available for use in the
management of scars. Many of these agents are
vitamin based or contain herbal extracts. Topical
Fig. 16. Silicone gel sheets to reduce keloid tendencies
in scars.
henderson & horswell186
vitamin E has been advocated by medical profes-
sionals and lay people alike for the treatment of scars.
The mechanism of action seems to be related to
reduction of oxygen radicals, which alter collagen and
glycosaminoglycan production and decrease heal-
ing by damaging DNA, cellular membranes, proteins,
and lipids [41,45]. Systemic use of vitamin E seems
to slow early wound healing by downregulating the
inflammatory response and may lead to decreased
tensile strength. Topical administration of vitamin E
has shown mixed results in the literature [12,17,
22,45]. Despite having widespread anecdotal support,
a double-blind study by Bauman and Spencer [45]
using topical vitamin E showed no improvement
in the cosmetic appearance of surgical scars [45].
Topical vitamin E also has been observed to have
mild deleterious effects on the esthetic outcome of
some wounds if administered too early in the healing
process by reducing tensile strength of the wound
[12,41]. Topical use of vitamin E later in the wound
healing process (4–6 weeks) may contribute to a
flatter scar but also may result in a stretched and
weakened scar [12].
Topical vitamins A, C, and K also have been used
in the perioperative management of dermatologic
wounds [21,22]. Their antioxidant properties are be-
lieved to soften and flatten scars, decrease pruritus,
and prevent capillary leakage. Systemic use of vita-
min A has shown a modest improvement in the ap-
pearance of some hypertrophic scars and keloids [41].
Antimetabolites
Another scar treatment that shows promise is intra-
lesional injection of bleomycin and 5-fluorouracil
[41]. Bleomycin is available in 15-U vials, and
5-fluorouracil is available in 50-mg/mL vials. Some
authors recommend combining 5-fluorouracil with
triamcinalone, 1 mg/mL, with frequent injections to
maximize scar tissue resolution. 5-fluorouracil is
converted into its active substrate, which is incorpo-
rated into DNA and inhibits DNA synthesis. Cells
that synthesize increased amounts of DNA, such as
fibroblasts, are targeted, which leads to decreased
proliferation. A single application in the first few days
after wound closure seems to be effective. Wound
healing amid actinic conditions has been shown to be
improved with limited use of 5-fluorouracil and
glycolic acid peels in the perioperative period. One
advantage of the use of antimitotic agents is that
steroid atrophy can be avoided [1]. Contraindications
to the use of 5-fluorouracil include existing bone
marrow depression, infection, pregnancy, and lacta-
tion [1,9,46].
Other agents
Calcium channel blockers may play a role in the
management of existing hypertrophic scars by induc-
ing collagenase production, which leads to scar tissue
degradation. Verapamil or other calcium channel
blockers can be injected into the lesions in a manner
similar to that for corticosteroids. Alternatively, 4% to
5% verapamil in a cream base can be applied topi-
cally. This application often can be alternated with ste-
roid injections to achieve a reasonable response [9].
Silicone gel sheeting
Numerous randomized, controlled trials and a
meta study of 27 trials have demonstrated that
silicone gel sheeting is a safe and effective therapeu-
tic technique in the prevention and management of
hypertrophic scars and keloids (Fig. 16) [13]. Silicone
gels have been shown to be effective in reducing scar
size and erythema through steady-state oxygen and
hydration maintenance. Hydration has been shown to
inhibit the production of collagen and glycosamino-
glycans by fibroblasts [41]. Silicone gel seems to
function like the stratum corneum by reducing water
loss and restoring homeostasis to the scar, which re-
sults in decreased capillary hyperemia, collagen de-
position, and hypertrophic scar formation [1,12,42].
Use should begin when the incision has epithe-
lialized fully. Silicone gel sheets should be worn 12 to
24 hours per day for at least a month; thereafter they
should be continued on a weaning basis over the next
3 months until maturation is complete. Silicone
ointments may be useful, particularly in the head
and neck region; however, their use is not supported
secondary procedures in maxillofacial dermatology 187
by controlled trials. When used, silicone gels are
typically applied two times per day after the removal
of sutures [1,10,12,13,41,42].
Fig. 17. Subdermal placement of temporalis fascia to
‘‘plump’’ depressed scar at the commissure and cheek.
Pressure therapy
Pressure therapy is often used as first-line therapy
in the management and prevention of scarring and
has been used since the 1970s. In general, pressure of
24 to 30 mm Hg must be maintained for several hours
per day over a period of 6 to 12 months [10,13,14].
The beneficial effects of compression seem to be
related to local tissue hypoxia, reduced scar blood
flow, decreased protein deposition, decreased edema,
and a reduction in the population of mast cells, which
may affect fibroblast growth [10,41,42].
Soft-tissue augmentation
Various materials can be used to augment atrophic
and depressed scars. These techniques are more suc-
cessful in scars that are distensible and not exces-
sively bound down [41]. The first material to become
available for injection was bovine collagen. Several
forms are available, with various studies showing
degradation after 6 to 9 months. The major drawback
to using bovine collagen injections is allergy. Three
percent to 3.5% of the population have a localized
hypersensitivity reaction. Other adverse reactions to
bovine collagen injection include bruising, herpes
reactivation, and bacterial superinfection [1,47].
Collagen should not be injected into patients with a
history of autoimmune diseases or patients with
hypersensitivity to lidocaine [1]. Allogeneic collagen
has intact collagen fibers, which give it greater lon-
gevity. Allogeneic collagen is derived from donated
human skin from donors who have been screened
carefully for infectious diseases, such as HIV, hepa-
titis B, hepatitis C, and syphilis [41]. In addition to
being used in an injectable form, Alloderm can be
used to elevate depressed scars and prevent recur-
rence of the contracted scar tissue bands. After the
scar is excised, Alloderm is cut to the shape of the
defect and the wound edges are approximated and
closed over the defect [48].
Autologous fat and fascia also have been advo-
cated for soft-tissue augmentation. Delicate tissue
handling is paramount to successful transfer of viable
cells. Large-bore, low-pressure harvesting and inject-
ing devices should be used to maintain cell integrity.
Longevity of 6 months to years has been documented
when cells are atraumatically harvested and placed
[41]. Sites for fat harvest include the abdomen,
thighs, and buttocks. Fat is collected and centrifuged
at 3000 rpm for 5 minutes. The lower layer of fat is
used for transplantation. Cannulas 4 to 5 mm in
diameter are used to transplant the autologous fat.
The endpoint of injection is when the depressed scar
is obliterated and approximately 20% to 30% over-
correction is achieved. The amount of fat needed for
transplantation is approximately 3 cm3/cm of scar
length [49]. Fascia similarly can be used to plump
and fill depressed scars (Fig. 17). Fascia is easily
harvested from the temporalis or fascia lata of the
thigh and has no immune rejection phenomena.
Camouflage therapy
For patients who have local or systemic factors
that contraindicate secondary procedures or for pa-
tients who do not wish to undergo any surgical
revisions, camouflage therapy may represent a viable
option for improved cosmesis. Camouflage therapy
can conceal postoperative bruising and erythema and
can normalize the skin’s appearance, providing a
psychological lift to a patient. Camouflage also can
be used as an interim measure to allow scars to
mature or local/systemic factors to improve before
definitive secondary procedures [50]. Water-based
cosmetics can be applied as soon as sutures are
removed (5–7 days) or after re-epithelialization is
complete (10–14 days) [15,50].
Another form of camouflage therapy is placement
of color by micropigmentation or cosmetic tattooing.
White scars can be improved by placing skin-colored
pigment into the mature scar tissue. The pigment
henderson & horswell188
typically lasts 3 to 5 years. Several treatments may be
required to obtain an optimal color match [1].
Consultation with an esthetician who is experienced
in medical-grade pigmentation procedures can be a
valuable asset to the reconstructive facial surgeon.
Summary
Secondary dermatologic procedures for revision
of scar or re-excising a lesion must take into account
many factors. A patient’s health and habitus, local
tissue characteristics and health, previous treatments
to the area of concern, and location of the lesion are
some factors that influence the outcome of second-
ary procedures. A thorough understanding of wound
healing and how to intervene appropriately during
healing, if necessary, is important for clinicians. It has
become clear in the literature that proper preparation
of the site through elimination of inflammatory
conditions and increasing tissue integrity and health
provide the foundation for satisfactory and predict-
able results. Surgeons also must consider which
surgical (eg, excision, flaps, dermabrasion) and non-
surgical (eg, resurfacing techniques, medications,
dressings, pressure therapy) modalities optimally will
correct the condition and continue to improve on its
healing state through the postoperative period until
tissue maturity.
References
[1] Grossman KL. Facial scars. Clin Plast Surg 2000;
27(4):627–42.
[2] Brissett AE, Sherris DA. Scar contractures, hyper-
trophic scars, and keloids. Facial Plast Surg 2001;17:
263–71.
[3] Atiyeh BS, Ioannovich J, Al-Amm CA, et al. Improv-
ing scar quality: a prospective clinical study. Aesthetic
Plast Surg 2002;26:470–6.
[4] Giglio JA, Abubaker AO, Diegelmann RF. Physiology
of wound healing of skin and mucosa. Oral Maxillofac
Surg Clin North Am 1996;8(4):457–65.
[5] Stucki-McCormick SU, Santiago PE. The metabolic
and physiologic aspects of wound healing. Oral
Maxillofac Surg Clin North Am 1996;8(4):467–76.
[6] Beldon P. Management of scarring. J Wound Care
1999;8(10):509–12.
[7] Atiyeh BS, Amm CA, El-Musa KA. Improved scar
quality following primary and secondary healing of cu-
taneous wounds. Aesthetic Plast Surg 2003;27:411–7.
[8] Su CW, Alizadeh K, Boddie A, et al. The problem scar.
Clin Plast Surg 1998;25(3):451–65.
[9] Roseborough I, Grevious M, Lee R. Prevention and
treatment of excessive dermal scarring. J Natl Med
Assoc 2004;96(1):108–16.
[10] Demling R, DeSanti L. Scar management strategies
in wound care. Rehab Manag 2001;14(6):26–30.
[11] Lawrence WT, Bevin AG, Sheldon GF. Acute wound
care. In: Wilmore DW, Cheung LY, Harken AH,
Holcroft JW, Meakins JL, Soper NJ, editors. ACS sur-
gery: principles and practice. New York7 Web MD
Corp.; 2002. p. 131–4.
[12] Widgerow AD, Chait LA, Stals R, et al. New
innovations in scar management. Aesthetic Plast Surg
2000;24:227–34.
[13] Mustoe TA, Cooter RD, Gold MH, et al. International
clinical recommendations on scar management. Plast
Reconstr Surg 2002;110:560–71.
[14] Leach J. Proper handling of soft tissue in the acute
phase. Facial Plast Surg 2001;17(4):227–38.
[15] Horswell BB. Scar modification: techniques for revi-
sion and camouflage. Atlas Oral Maxillofac Clin North
Am 1998;6(2):55–72.
[16] Rendon MI. Melasma and postinflammatory hyperpig-
mentation. Cosmetic Dermatology 2003;16(4):9–17.
[17] Pandya AG. Pharmacological sgents in skin of color.
Cosmetic Dermatology 2003;16(4):49–52.
[18] Koopmann Jr CF. Cutaneous wound healing. Otolar-
yngol Clin North Am 1995;28(5):835–45.
[19] Thiboutot OM. Acne and rosacea: new and emerging
therapies. Dermatol Clin 2000;18:63.
[20] Lowe NJ, Lask G, Griffin ME. Laser skin resurfac-
ing: pre- and post-treatment guidelines. Dermatol Surg
1995;21:1017.
[21] Fitzpatrick RE, Roston EF. Double-blind, half-face
study comparing topical vitamin C and vehicle for
photodamage. Dermatol Surg 2002;28:231.
[22] Hayakawa R, Ueda H, Nozaki T, et al. Effects
of combination treatment with vitamins E and C on
chloasma and contact dermatitis: a double-blind con-
trolled clinical trial. Acta Vitaminol Enzymol 1981;
3:31.
[23] Limberg AA. The planning of local plastic operations
on the body surface: theory and practice. Lexington
(MA)7 DC Heath and Co.; 1984.
[24] Schweinfurth JM, Fedok F. Avoiding pitfalls and
unfavorable outcomes in scar revision. Facial Plast
Surg 2001;17(4):273–7.
[25] Bradley DT, Park SS. Scar revision via resurfacing.
Facial Plast Surg 2001;17(4):253–61.
[26] Borges AF. Timing of scar revision techniques. Clin
Plast Surg 1990;17:71–6.
[27] Krummel TM, Blewett C. Wound healing. In: Ziegler
MM, Azizkhan RG, Weber TR, editors. Operative
pediatric surgery. New York7 McGraw-Hill; 2003.
p. 179–80.
[28] Borges AF. Relaxed skin tension lines (RSTL) versus
other skin lines. Plast Reconstr Surg 1984;73:144.
[29] Murray JC. Keloids and hypertrophic scars. Clin
Dermatol 1994;12:27.
[30] Borges AF. Elective incisions and scar revision.
Boston7 Little Brown and Co.; 1973. p. 1–14.
secondary procedures in maxillofacial dermatology 189
[31] Rudolph R, Schneider G. Scar revision. In: Georgiade
GS, Riefkahl R, Levin LS, editors. Plastic, maxillo-
facial, and reconstructive surgery. Baltimore7 Williams
and Wilkins; 1997. p. 114–21.
[32] Gustafson J, Gustafson J, Larrabee WF, et al. Ex-
perimental analysis of the adjunctive Z-plasty in the
closure of fusiform defects. Arch Otolaryngol 1984;
110:41–4.
[33] Kaplan B, Potter T, Moy RL. Scar revision. Dermatol
Surg 1997;23:435–42.
[34] Rudolph R. Wide spread scars, hypertrophic scars, and
keloids. Clin Plast Surg 1987;14:247–53.
[35] Borges AF. W-plasty. In: Thomas JR, Holt GR, editors.
Facial scars: incision, revision, and camouflage. St.
Louis7 CV Mosby; 1989. p. 150–9.
[36] Bray OA. Clinical applications of the rhomboid flap.
Arch Otolaryngol 1983;109:37–42.
[37] Borges AF. Choosing the correct Limberg flap. Plast
Reconstr Surg 1978;62:542–5.
[38] Larrabee Jr WF, Sutton D. Biomechanics of advance-
ment and rotation flaps. Laryngoscope 1981;91:726.
[39] Wiselander JB. Tissue expansion in the head and neck.
Scand J Plast Reconstr Surg 1991;25:47–56.
[40] Cheney ML. Tissue expansion in the repair of facial
defects. In: Cheney ML, editor. Facial surgery. Bal-
timore7 Williams and Wilkins; 1997. p. 259–67.
[41] Chang CWD, Ries WR. Nonoperative techniques for
scar management and revision. Facial Plast Surg
2001;17(4):283–7.
[42] Tsao SS, Dover JS, Arndt KA, et al. Scar management:
keloid, hypertrophic, atrophic, and acne scars. Semin
Cutan Med Surg 2002;21(1):46–75.
[43] Harmon CB. Dermabrasion. Dermatol Clin 2001;
19(3):439–42.
[44] Ammirati CT, Cottingham TJ, Hruza GJ. Immediate
postoperative laser resurfacing improves second inten-
tion healing on the nose: 5-year experience. Dermatol
Surg 2001;27:147–52.
[45] Baumann LS, Spencer J. The effect of topical vitamin
E on the cosmetic appearance of scars. Dermatol Surg
1999;25:311–5.
[46] Apikian M, Goodman G. Intralesional 5-fluorouracil in
the treatment of keloid scars. Aust J Dermatol 2004;
45:140–3.
[47] Ashinoff R. Overview: soft tissue augmentation. Clin
Plast Surg 2000;27(4):479–87.
[48] Terino EO. Alloderm acellular dermal graft: applica-
tion is aesthetic soft-tissue augmentation. Clin Plast
Surg 2001;28(1):83–99.
[49] Benito J, Fernandez I, Nanda V. Treatment of de-
pressed scars with a dissecting cannula and an autolo-
gous fat graft. Aesthetic Plast Surg 1999;23:367–70.
[50] LeRoy L. Camouflage therapy. Dermatol Nurs 2000;
12(6):415–6.
top related