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146 / Complications of Local Flaps: Prevention and Management
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ABC
Figure 13-4. Ischemic cheek fl ap. (A) Initial defect. (B) Immediate postoperative appearance showing early
signs of ischemia. (C) Postoperative result with scattered tissue loss.
infi ltrative, or morpheaform tumors. Associated
parasethesias or neural symptoms should raise suspicion for perineural invasion. Whereas standard
hospital frozen sections are often unreliable, Mohs
micrographic excision minimizes tissue loss and
maximizes the prospects for successful tumor clearance. If fl ap reconstruction is undertaken and a positive margin later identifi ed, reresection may prove
diffi cult. Furthermore, subsequent reconstructive
options are limited due to the prior procedure.
Ischemia and Flap Loss
Flap ischemia refers to impaired delivery of blood,
oxygen, and nutrients to tissues. Most tissues can
ABC
survive with only a fraction of the usual blood fl ow,
provided that neovascularization occurs to reduce
dependency on the pedicle blood supply. However,
sustained ischemia leads to tissue necrosis (Figures
13-4–13-6). Several factors conspire to increase the
risk of ischemia in the local fl aps—transection of
small feeding vessels, torsion of vessels along the
pedicle of the fl ap, and tension across suture lines.
Transection of small sympathetic nerve branches
induces release of catecholamines with resulting
vasoconstriction. Thromboxane A is also released
from small-platelet thrombi. The collective effect of
these vasoactive substances is to decrease perfusion
and increase the risk of fl ap loss. Overzealous fl ap
Figure 13-5. Ischemic nasal sidewall reconstruction with V-to-Y advancement. (A) Initial defect. (B) Immediate
postoperative appearance showing ischemia. (C) Postoperative result with fl ap necrosis.
ABC
Figure 13-6. Ischemic nasal tip reconstruction based on nasalis. (A) Initial defect. (B) Immediate postoperative
appearance with ischemia. (C) Partial local fl ap loss.
Complications of Local Flaps: Prevention and Management / 147
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thinning, charring of tissues, and excessive tension
across the wound closure all impair wound healing
potential. Minimizing the impact of these factors
during fl ap design and dissection will markedly diminish ischemic stress.
The signs of ischemia are easily recognizable.
Reduced fl ap temperature, coupled with slow or
absent bleeding on pinprick, is indicative of arterial insuffi ciency. Purple discoloration and bloated
appearance to the fl ap with immediate bleeding on
pinprick indicates venous congestion. Venous congestion is tolerated more poorly than arterial insuffi ciency, although either may cause fl ap demise. For
arterial insuffi ciency, release of overly tight sutures
may allow for salvage of the fl ap. Arterial insuffi ciency due to kinking of the fl ap pedicle or tight dressing
is reversible, provided the diagnosis is made early. A
fl ap showing arterial insuffi ciency may be returned
to the donor bed for delay before performing the repair at a future time. This allows for enhanced blood
supply to the fl ap, so that it may be more resistant to
ischemia when reelevated. For venous insuffi ciency,
suture release or medicinal leeching may allow for
salvage. Antibiotic coverage with fl uoroquinolones
(ciprofl oxacin) is recommended as a prophylaxis
against Aeromonas infection if leeches are used. The
same features of a hostile bed that predispose to
local fl ap loss may also be associated with poor take
of skin or composite grafts (Figure 13-7).
Whenever possible, it is preferable to salvage
as much of a threatened fl ap as possible. Once the
extent of ischemia has demarcated, debridement
should be performed. Removal of nonvital tissue
decreases the risk of infection and allows for granulation. Devitalized tissue is removed with sharp dissection until bleeding tissue is encountered. Tissue
that has good adherence to the underlying surgical
bed is usually viable. If there is only partial-thickness
loss, a debrided surgical bed can be left to granulate
in preparation for secondary skin grafting. Inset of
a new fl ap is likely to be necessary, however. Meticulous wound care, including use of moistening ointments, and either wet-to-dry dressings or peroxide
promotes favorable healing.
Unsightly and Malpositioned Scars
Full-thickness incisions invariably result in visible
scars, but skillful placement of incisions and meticulous surgical technique minimize the incidence
of unacceptable scars. Hypertrophic or keloid scars
often benefi t from steroid injection. In other cases,
an abnormal appearance results from poor placement of incisions. Failure to respect facial aesthetic
units invariably results in more conspicuous scars
and abnormal appearance. One common example
is blunting the crease of the alar sulcus, which forms
a boundary between the nose, cheek, and upper lip.
The use of interpolated cheek fl aps for this area is
preferred to advancement or transposition fl aps,
which tend to efface this aesthetic border (Figure
13-8). It may be preferable to use separate fl aps or
a combination of a fl ap and skin graft to preserve
normal boundaries and optimize cosmesis. For example, defects extending from the nose to the adjacent cheek are often best repaired with separate
fl aps. This approach allows for camoufl age of the
scar within a shadowed area while also preserving
the normal concavity of the sulcus between the nose
and cheek.
Patient-related factors also infl uence fl ap selection. Incisions that are made in thick, sebaceous skin
are more likely to widen or leave depressed scars.
Broader fl aps, rather than intricate fl ap designs,
minimize risk of unfavorable scars in such patients.
Young patients heal differently than older patients.
Although the risk of wound dehiscence is lower in
young patients, younger patients have less tissue
laxity and also often develop exaggerated erythema
and hypertrophy. Applying sunscreen over a newly
ABC
Figure 13-7. Necrosis of composite graft. (A) Initial defect. (B) Immediate postoperative result. (C) Necrotic
graft at follow-up.
148 / Complications of Local Flaps: Prevention and Management
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ABC
Figure 13-8. Blunting of melolabial sulcus with fl ap reconstruction. (A) Melolabial fl ap. (B) Cheek fl ap.
(C) Cheek fl ap.
epithelialized surface minimizes postinfl ammatory
hyperpigmentation. Due to the signifi cant remodeling of scars in younger patients, it is preferable to
delay revision in children for a year to allow time for
spontaneous improvement. Patients with hyperfl exibility possess more elastin and are therefore more
likely to have widened scars. Gorlin’s sign refers to
the ability to touch the tongue to the nasal tip, and
Beighton’s sign refers to the capability to bend the
thumb back to the fl exor aspect of the forearm; both
are signs of excessive or abnormal fl exibility. These
individuals are more prone to suboptimal scarring.
Trap Door Deformity
Trap door deformity refers to the tendency of a fl ap
to mushroom up or pincushion in its center, leaving
a depressed scar around its periphery (Figure 13-9).
It results from persistent edema, poor lymphatic
drainage, and accumulation of serum and hematoma deep to the fl ap. Flaps that have curved borders are particularly susceptible to this deformity.
The cicatricial contraction of the edges of the fl ap
results in central bulging. The scar sheet beneath the
fl ap is thought to contribute to this deformity. Some
degree of trap door is inevitable with most bilobed
fl aps due to the combination of dependent edema
coupled with the curved shape of these fl aps, especially when performed in patients with very sebaceous and thick skin. Generous undermining of the
skin and soft tissues can reduce the tendency toward
scar contracture. Superiorly based fl aps are more
prone to this problem due to venous congestion and
disrupted lymphatic channels.
Although trap door deformity does tend to im-
prove with the passage of time, a number of interventions may be helpful. Dermabrasion is useful for
smoothing irregularities in nasal bilobe fl aps and
improves the blending of skin texture and contour.
For more prominent trap door deformities, asteroid injection to the subcutaneous tissue may be
performed initially. Usually low concentration triamcinolone acetonide (10 mg/mL) is preferred to
minimize the risk of tissue atrophy. Not uncommonly, surgical revision proves necessary. In this case,
correction involves incising the borders of the fl ap,
removing subcutaneous fat and scar, and generous
undermining followed by redraping with placement
of Z-plasties, to minimize the risk of recurrence.
Distortion of Mobile Structures
Distortion of mobile structures is another important consideration in a local fl ap reconstruction.
ABC
Figure 13-9. Trap door deformities, demonstrating pincushioning and dependent-fl ap lymphedema with venous
stasis. (A) Cheek transposition fl ap. (B) Note fl ap (modifi ed rhomboid fl ap). (C) Island melolabial fl ap.
Complications of Local Flaps: Prevention and Management / 149
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Mobile structures include the eyelids, lips, earlobes,
and nasal alar rim. Although such distortion may
occur at time of initial reconstruction, it is more
commonly observed as a late effect of healing. Because tissues heal by scar contraction, it is not uncommon for contractural forces to exert themselves
on structures that are not rigidly anchored. Therefore, the potential for future tissue distortion is best
identifi ed at the time of initial surgery.
Eyelid malposition is a common—but generally
preventable—problem after local fl aps in the periorbital region. Distortion of the lower eyelid is more
frequent than the upper eyelid due to the effect of
gravity and senile laxity of the lower lid. Among the
more common eyelid complications associated with
local fl aps are symptomatic dry eyes, lagophthalmos, lacrimal duct obstruction or avulsion, impairment of visual fi elds, or visual loss. Excessive tension
on closure in the vertical dimension will predispose to eyelid retraction, with secondary effects on
hydration of the cornea and risk for exposure keratitis. The ability of the eye to adequately generate a
tear fi lm is impaired with malposition of the puncta
as well. Direct injury to the lid may also occur with
surgery; therefore, it is important to be familiar with
the cross-sectional anatomy of the upper and lower
eyelids.
The lip, earlobes, and nose are also prone to distortion that creates a variety of functional and cosmetic diffi culties. Distortion of the lip may include
blunting of the lateral commissure, lip ectropion,
or lip entropion. Distortion of the lips can result in
cosmetic deformity, with an unacceptable appearance; but it may also have functional consequences.
Abnormal distortion of the lip may interfere with
speech, facial expression, and control of salivation.
Excessive desiccation and aberrant salivation can
also predispose to dental caries. Alar retraction is a
signifi cant risk when repairing nasal defects within a
few millimeters of the alar rim with a local fl ap. Use
of structural grafting and careful fl ap selection can
avoid a vector of tension that is directed superiorly.
Excessive tension on the earlobe may result in “pixie
ear” where the earlobe is abnormally elongated.
to resurface the nasal interior will doom an otherwise well-conceived nasal reconstruction due to late
effects of scar contracture. The initial result of such
a repair may be quite satisfactory, but the repair
does not withstand the test of time. The undersurface of covering fl aps contract as raw tissue surfaces
heal secondarily, distorting the external shape of
the nose and narrowing the nasal airway. Nasal lining fl aps that are too thick, insuffi ciently pliable, or
poorly vascularized yield poor results. Use of thin,
vascularized fl aps, usually vestibular skin or mucoperichondrium, avoids such distortion.
Nasal lining defects are also predisposed to
chronic infection. Infections related to a hole in the
nasal lining often present weeks after the original
reconstruction and are usually heralded by drainage with erythema, edema, and warmth. With lining
fl aps that are torn or not fully viable, blood supply
to the overlying cartilage may be tenuous. Fulminant infections may cause extensive lining necrosis
with cartilage exposure and loss, but chronic smoldering infections are more common and tend to be
more localized. Empiric antibiotics and a culture
and sensitivity are helpful in decreasing the risk of
loss of free grafts, but resurfacing of exposed tissue
may be needed. If the response to antibiotics is not
brisk, the wound should be explored and debrided
as necessary. A few months thereafter, subsequent
graft placement may be considered.
Conclusion
The preponderance of complications in local fl aps
can be mitigated or prevented with careful planning
and meticulous technique. If the surgeon ensures
that blood is delivered to the tissues, the tissues will
live and the risk of infection and unfavorable healing are dramatically reduced. Detailed knowledge of
the relevant anatomy minimizes the risk of injury
to adjacent structures and of distortion of mobile
landmarks. Additional consideration of the nuances
of aesthetic units and anticipation of late effects in
wound healing helps ensure favorable healing.
Nasal Lining Defects and
Smoldering Infections
One of the more common oversights in nasal reconstruction is failure to adequately restore nasal
lining. Because the nasal lining is diffi cult to visualize, inadequate reconstruction of this layer might
seem to be a minor transgression. However, failure
References
1. Angel MF, Ramasastry SS, Swartz WM, et al. The
critical relationship between free radicals and degrees
of ischemia: Evidence for tissue intolerance of marginal
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239.
2. Cutting C. Critical closing and perfusion pressures in
fl ap survival. Ann Plast Surg Dec 1982;9(6), 524.
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3. Diaz DD, Freeman SB, Wilson JF, Parker GS.
Hematoma-induced fl ap necrosis and free radical
scavengers. Arch Otolaryngol Head Neck Surg May
1992;118(5), 516–518.
4. Forrest CR, Pang CY, Lindsay WK. Dose and time
effects of nicotine treatment on the capillary blood
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rat. Br J Plast Surg May 1987;40(3), 295–299.
5. Gideroglu K, Yildirim S, Akan M, Akoz T. Immediate
use of medicinal leeches to salvage venous congested
reverse pedicled neurocutaneous fl aps. Scand J
Plast Reconstr Surg Hand Surg 2003;37(5), 277–
282.
6. Jewett BS. Complications of local fl aps. In: Baker SR,
ed. Local Flaps in Facial Reconstruction. 2nd ed. New
York: Mosby; 2007, 691–722.
7. Kaufman AJ, Kiene KL, Moy RL. Role of tissue
undermining in the trapdoor effect of transposition
fl aps. J Dermatol Surg Oncol Feb 1993;19(2), 128–
132.
8. Kinsella JB, Rassekh CH, Wassmuth ZD, Hokanson
JA, Calhoun KH. Smoking increases facial skin
fl ap complications. Ann Otol Rhinol Laryngol Feb
1999;108(2), 139–142.
9. Polk HC, Jr., Miles AA. Enhancement of bacterial
infection by ferric iron: kinetics, mechanisms, and
surgical signifi cance. Surgery Jul 1971;70(1), 71–77.
10. Salasche SJ. Acute surgical complications: cause,
prevention, and treatment. J Am Acad Dermatol. Dec
11. Salasche SJ, Grabski WJ. Complications of fl aps.
J Dermatol Surg Oncol Feb 1991;17(2), 132–140.
12. Sebben JE. Sterile technique and the prevention of
wound infection in offi ce surgery—Part I. J Dermatol
Surg Oncol Dec 1988;14(12), 1364–1371.
13. Sebben JE. Sterile technique and the prevention
of wound infection in offi ce surgery—Part II.
J Dermatol Surg Oncol Jan 1989;15(1), 38–48.
14. Utley DS, Koch RJ, Goode RL. The failing fl ap in
facial plastic and reconstructive surgery: Role of the
medicinal leech. Laryngoscope Aug 1998;108(8 Pt 1),
1129–1135.
15. Vural E, Key JM. Complications, salvage, and
enhancement of local fl aps in facial reconstruction.
Otolaryngol Clin North Am Aug 2001;34(4), 739–751.
Index
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Information in fi gures and tables is indicated by f and t.
A
Abbe fl ap, for lip/perioral defects, 85–86, 85f
aberrant wound healing, 18–19
absorbable sutures, 30, 31f
adhesives, tissue, 31–32, 138–139
advancement fl aps, 37, 37f, 38–43, 40f–43f
for cheek defects, 101
for eyelid defects, 110, 110f
for lip/perioral defects, 81–82, 82f
for scalp, 125, 125f
age, healing and, 10
ala, nasal, 71, 72f
amides, 24, 24t
anatomy
of cheek, 98, 98f
neural, 98–99, 99f, 100f
vascular, 98, 99f
of eyelids, 105–108
of forehead and brow, 89–91, 89f–91f
neural, 91–93, 92f–93f
vascular, 91, 91f
of lips, 79–80, 79f
nasal, 59–61, 59f–61f
periocular, 105–108
of scalp, 117–121, 118f–120f
of skin, 1–11
neural, 2–3, 4f
vascular, 2, 3f
anesthesia/anesthetics
local, 24–25, 24t, 25t, 26t
topical, 25
tumescent, 25–26
angular artery, 34f
apocrine sweat gland, 2f, 4f
arrector pili, 2f, 4f
ascending pharyngeal artery, 34f
auricular composite grafts, 72–73
auriculotemporal nerve, 99
axial pattern fl aps, 5–6, 6f, 38, 39f
B
basal cell layer, histology of, 1
basement membrane, 1
benzocaine, 24t, 25t
bilateral advancement fl ap, 41f
for lip/perioral defects, 82, 82f
for scalp, 125, 125f
bilateral rotation fl ap, 46f
bilobed fl ap, 49, 50f, 51
for nasal defects, 67, 67f, 68f
for nasal tip defects, 71
bipedicle vestibular skin advancement fl ap, for nose, 73,
74f
brow, 95–96. see also forehead and brow
Brown-Adson forceps, 21, 22f
buccal nerve, 99
bupivacaine, 24t, 25t
C
camoufl age, scar, 139–140
canthal malposition, 113–114
canthal tendons, 106f, 107f
canthi, 107
canthus defects, 111
capillary perfusion pressure, fl ap necrosis and, 40f
cardiovascular disease, wound healing and, 10
cervicofacial rotation fl ap, 44, 45f
for cheek defects, 101, 102f
cheek
anatomy, 98, 98f
anterior, 101–102, 102f
central, 102–103
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cheek (Continued)
cervicofacial rotation fl ap for, 101, 102f
choice of reconstructive technique for, 100–101
defect analysis in, 99–100
defect preparation in, 100
esthetic subunits of, 97, 97f
grafts for, 101
inferior, 102–103
local fl ap alternatives for, 101
in men vs. women, 97
neural anatomy of, 98–99, 99f, 100f
posterior, 101
superior, 103
tension lines in, 97–98
transposition fl aps for, 101
vascular supply, 98, 99f
cheek advancement fl ap, 41f
chloroprocaine, 24t, 25t
clear margins, 145–146
closure techniques, 27–29, 28f, 29f
cocaine, 25t
columella defects, 71–72
common carotid artery, 34f
comorbid disease, wound healing and, 9–11, 10f, 10t
complications, of local fl aps
clear margins and, 145–146
dissection plane and, 143
fl ap design and, 145–149, 145f–148f
hemostasis and, 143–144
ischemia, 146–147, 146f–147f
mobile structure distortion, 148–149
nerve injury and, 144
overview of, 141
patient factors in, 141–142
scars, 147–148, 148f
structural elements and, respect for, 144
surgical technique and, 142–144
tissue handling and, 143
wound infection and, 142–143
conjunctivodacryocystorhinostomy, 112
connective tissue growth factor (CTGF), 9t
continuous sutures, 28, 29f, 30f
controlled tissue expansion, for scalp, 133–134
corrugator, 90f, 92, 106f
CTGF. see connective tissue growth factor (CTGF)
cutaneous tissue adhesives, 31–32, 138–139
D
debridement, healing and, 17
Dermabond, 31–32, 138–139
dermal regeneration templates, 134–135
dermatome, 55, 56, 56f
dermis, histology of, 1–2, 2f
design, fl ap, complications and, 145–149, 145f–148f
diabetes, wound healing and, 9–10, 18
dorsal nasal fl ap, 69, 70f, 71f
dressings, 135–136
Dufourmental fl ap, 46f
E
ectropion, 113
EGF. see epidermal growth factor (EGF)
endocrine sweat gland, 2f
epidermal growth factor (EGF), 9t
epidermis, histology of, 1, 2f
epinephrine, 24
epithelial turn-in fl ap, for nasal defects, 77, 78f
esters, 24, 24t
esthetic units, of face, 26, 27f, 34–35, 35f
etidocaine, 25t
exposure keratitis, 113
external carotid artery, 33, 34, 34f
eyelid and periocular area
advancement fl aps for, 110, 110f
anatomic considerations, 105–108
canthal malposition with, 113–114
dry eye and, 112–113
ectropion with, 113
esthetic units in, 107–108
exposure keratitis with, 113
eyelid reconstruction, 108–112
lower eyelid marginal defects, 109–111, 109f,
110f
mobile structure distortion in, 148–149
ocular issues with, 112–113
postoperative care, 112
prominent scarring in, 114–115
restrictive strabismus with, 113
revision surgery in, 113
skin types in, 107–108
upper eyelid defects, 111
eyelid malpositions, 113–115
eyelid retraction, 113
F
face, esthetic units of, 26, 27f, 34–35, 35f
facial artery, 33–34, 34f, 98, 99f, 118f
facial nerve, 92, 92f, 93, 93f, 99, 100f, 120, 121f
FGFs. see fi broblast growth factors (FGFs)
fi broblast growth factors (FGFs), at wound sites, 9t
fl aps
advancement, 37, 37f, 38–43, 40f–43f
for cheek defects, 101
for lip/perioral defects, 81–82, 82f
for scalp, 125, 125f
axial pattern, 5–6, 6f, 38, 39f
bilobed, 49, 50f, 51
for nasal defects, 67, 67f, 68f
for nasal tip defects, 71
bipedicle vestibular skin advancement, 73, 74f
classifi cation of, 33t
design of, complications and, 145–149, 145f–148f
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Dufourmental, 46f
facial esthetic units and, 34–35, 35f
Gilles fan, 86, 86f
Hughes transconjunctival, 111
infl ammatory phase and, 6–9, 7f, 8f, 9t
injury response, 6, 7f
island, 47, 48f, 49
Karpandzic, 84–85, 85f
latissimus dorsi free, 132–133, 132f
lip-switch, 85–86, 85f
local, 36–38, 37f, 38f
loss of, 146–147, 146f–147f
melolabial, 45
for nasal sidewall defects, 68–69, 69f
musculocutaneous, 38, 39f
for nasal defects, 62
paramedian forehead, 48f, 63f
for nasal defects, 63–64, 63f, 65f, 66f
proliferative phase and, 9, 10f
random pattern, 3, 5, 5f, 38, 39f
rhomboid, 44, 46f
Limberg, 114f
for temporal region, 96, 96f
rotation, 37f, 43–44, 44f–46f
cervicofacial, 44, 45f
for cheek defects, 101, 102f
for lip/perioral defects, 82–83
for scalp, 125–126, 126f–127f
septal composite chondromucosal pivotal, 76, 77f
septal mucoperichondrial hinge, 73–76, 74f–75f
superfi cial temporal artery-based, 126, 128, 129f–
130f
survival factors, 6
transposition, 38, 38f, 44–51, 47f–50f
for cheek defects, 101
for glabellar defects, 94–95
for lip/perioral defects, 83, 83f
for scalp, 128–129, 130f–131f
tubed interpolation, 47, 48f
vascular supply of, 33–34, 34f
Webster, 46f
Z-plasty, 49, 49f
forceps, 21, 22f
forehead and brow
alternatives to local fl aps for, 94
anatomy of, 89–91, 89f–91f
choice of reconstructive technique for, 94
defect analysis in, 93
defect preparation in, 93–94
glabella, 94–95, 95f
importance of symmetry in, 95
in men vs. women, 89
neural anatomy of, 91–93, 92f–93f
relaxed skin tension lines in, 89, 91f
secondary intention healing in, 95
temporal region, 96, 96f
vascular supply, 91, 92f
forehead fl ap, paramedian, 48f, 63f
for nasal defects, 63–64, 63f, 65f, 66f, 76–77
frontalis, 90f, 91, 106f, 119f
frontal nerve, 92
G
galeal relaxing incisions, 126f
gender, forehead/brow anatomy and, 89
Gilles fan fl ap, 86, 86f
glabella, 94–95, 95f
gland(s)
apocrine sweat, 2f, 4f
exocrine sweat, 2f
lacrimal, 106f
sebaceous, 2f
grafts
for cheek defects, 101
defi nition of, 53
donor sites for, 54, 56, 57f
dressings for, 135
for eyelid defects, 109–110
harvesting of, 54–56, 55f
healing of, 56–57, 57t
for nasal ala defects, 71, 72f
for nasal defects, 62
overview of, 53
placement of, 56, 56f
planning for, 53–54, 54t
postoperative care for, 57–58
preoperative analysis for, 53–54, 54t
recipient site for, 54
for scalp, 123–124, 124f
great auricular nerve, 118f
greater occipital nerve, 118f
growth factors, at wound sites, 9t
H
hair
pilosebaceous units and, 3, 4f
transplants, 134
hairline, 89, 91
harvesting, graft, 54–56, 55f
healing
aberrant, 18–19
age and, 10
cardiovascular disease and, 10
comorbid disease and, 9–11, 10f,
debridement and, 17
desiccation and, 17
diabetes and, 9–10, 18
factors affecting, 17–18, 17t
hemostasis in, 13, 16f
hypertrophic scars in, 18–19
infl ammatory phase, 6–9, 7f, 8f, 9t, 13–14, 14f
keloids and, 18–19
10t
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healing (Continued)
local factors affecting, 17–18, 17t
malnutrition and, 18
maturation phase of, 15–17, 16f
medications and, 18
moisture and, 17
phases of, 13–17
proliferative phase, 9, 10f, 14–15, 15f, 16f
of skin grafts, 56–57, 57t
smoking and, 10
systemic factors affecting, 18
tensile strength and, 17
timeline, 7f, 16f
vitamins and, 18
hemostasis
complications and, 143–144
in wound healing, 13, 16f
Henle’s layer, 4f
histology, of skin, 1–2, 2f
hooks, 22, 23f
horizontal advancement fl ap, 40f
for lip/perioral defects, 83
horizontal mattress sutures, 28, 29f, 30f
Hughes transconjunctival fl ap, 111
Huxley’s layer, 4f
I
IGF-1. see insulin-like growth factor 1 (IGF-1)
incision planning, 26, 26f, 27f
infection
complications and, 142–143, 149
smoldering, 149
inferior alveolar artery, 34, 34f
inferior labial artery, 34f
inferior turbinate fl ap, 76, 76f
infl ammatory phase, of wound healing, 6–9, 7f,
8f, 9t, 13–14, 14f
infraorbital artery, 34f
infraorbital nerve, 98–99
infundibulum, 4f
injury response, 6, 7f. see also healing
instrumentation, 19f–21f, 21–24
insulin-like growth factor 1 (IGF-1), 9t
interleukins, at wound sites, 9t
internal carotid artery, 34f, 91, 117
interpolation fl ap, tubed, 47, 48f
intraoperative tissue expansion, for scalp, 134
inverted Burrow’s triangle excision, 43f
ischemia, as complication, 146–147, 146f–147f
island fl ap, 47, 48f, 49
isthmus, 4f
K
Karpandzic fl ap, for lip/perioral defects, 84–85,
85f
keloids, 18–19
keratitis, exposure, 113
knife handles, 21
L
lacrimal canaliculi, 108f
lacrimal drainage system, 107, 108f, 111–112
lacrimal gland, 106f
lateral canthus defects, 111
latissimus dorsi free fl ap, 132–133, 132f
lesser occipital nerve, 118f
levator aponeurosis, 106f
levobupivacaine, 25t
lidocaine, 24–25, 24t, 25t
Limberg rhomboid fl ap, 114f
lines, relaxed skin tension, 26, 26f, 27f
in cheek, 97–98
in forehead, 89, 91f
nose and, 35–36, 36f
lingual artery, 34f
lips
Abbe fl ap for, 85–86, 85f
advancement fl aps for, 81–82, 82f
anatomy of, 79–80, 79f
choice of reconstructive techniques for, 81
complications with, 87
defect considerations with, 81–87
facial analysis for, 79–80, 79f
Gilles fan fl ap for, 86, 86f
Karpandzic fl aps for, 84–85, 85f
mobile structure distortion and, 149
mucosal restoration for, 84
overview of, 79
postoperative care for, 87
preoperative considerations with, 80–81
rotational fl aps for, 82–83
total reconstruction, 86–87
transpositional fl aps for, 83, 83f
lip-switch fl aps, 85–86, 85f
local anesthesia, 24–25, 24t, 25t, 26t
local fl aps, 36–38, 37f, 38f
long-term scar care, 139
M
malnutrition, wound healing and, 18
mandibular nerve, 99
margins, clear, 145–146
mattress sutures, 28, 29f, 30f
maturation phase, of wound healing, 15–17, 16f
maxillary artery, 34, 34f
medial canthus defects, 111
medications, wound healing and, 18
Meissner’s corpuscles, 3, 4f
melanocyte, 2f
melolabial fl ap, 45
for nasal sidewall defects, 68–69, 69f
mental artery, 34f
Index / 155
https://t.me/medicina_free
mepivacaine, 24t, 25t
Merkel cell-nurite complex, 4f
microsurgical tissue transfer, for scalp, 132–133, 132f
middle meningeal artery, 34
mobile structure distortion, 148–149
mucosal restoration, for lip/perioral defects, 84
musculocutaneous fl aps, 38, 39f
musculocutaneous perforators, 6f
N
needle holders, 22, 22f
nerve injury, 144
neural anatomy
of cheek, 98–99, 99f, 100f
of forehead and brow
neural, 91–93, 92f–93f
of scalp, 118f, 120–121, 121f
of skin, 2–3, 4f
nose
ala defects, 71, 72f
anatomy of, 59–61, 59f–61f
auricular composite grafts for, 72–73
bilobed fl ap for, 67, 67f, 68f
bipedicle vestibular skin advancement fl ap,
73, 74f
choice of reconstructive technique for, 62
columella defects, 71–72
defect analysis, 61, 61f
defect preparation, 62
dorsal nasal fl ap for, 69, 70f, 71f
dorsum reconstruction, 66
epithelial turn-in fl ap for, 77, 78f
as esthetic unit, 35, 35f, 61, 61f
inferior turbinate fl ap for, 76, 76f
innervation of, 61
lining defects, 149
lining restoration, 72, 73t
local fl ap alternatives for, 62
melolabial fl ap for, 68–69, 69f
paramedian forehead fl ap for, 63–64, 63f, 65f, 66f
septal composite chondromucosal pivotal fl ap for,
76, 77f
septal mucoperichondrial hinge fl aps for, 73–76,
74f–75f
sidewall defects, 67–69, 68f–71f
skeleton of, 60–61, 61f
subtotal dorsal defects, 66–67, 67f, 68f
tip defects, 70–71
total nasal defects, 63–65, 63f
vascular anatomy of, 59–60, 60f
O
occipital artery, 34, 34f, 119f
occipital muscle, 119f
ophthalmic artery, 91
orbicularis, 90f, 92, 105, 106f
–65f
orbicularis oris, 80
O-to-T closure, 42, 42f
O-to-Y closure, 39, 41f
P
Pacinian corpuscles, 3, 4f
paramedian forehead fl ap, 48f, 63f
for nasal defects, 63–64, 63f, 65f, 66f, 76–77
pattern fl aps
axial, 5–6, 6f, 38, 39f
random, 3, 5, 5f, 38, 39f
PDGF. see platelet-derived growth factor (PDGF)
pedicled interpolation fl ap, 47, 48f
perioral. see lips
permanent sutures, 30–31, 32f
physiology, of skin, 1–11
pilosebaceous units, 3, 4f
platelet-derived growth factor (PDGF), 9t
postauricular artery, 119f
posterior auricular artery, 34f
postoperative care
dressings, 135–136
eyelid and periocular area, 112
grafts, 57–58
lips, 87
scalp, 135
tissue adhesives, 138–139
prickle cell layer, histology of, 1
prilocaine, 24t, 25t
procaine, 24t, 25t
procerus, 90f, 92, 106f
proliferative phase, of wound healing, 9, 10f, 14–15,
15f, 16f
pulse dye laser (PDL), for keloids, 19
R
random pattern fl aps, 3, 5, 5f, 38, 39f
relaxed skin tension lines (RSTLs), 26, 26f, 27f
in cheek, 97–98
in forehead, 89, 91f
nose and, 35–36, 36f
remodeling, in wound healing, 15–17, 16
restrictive strabismus, 113
reticular dermis, 1
rhomboid fl ap, 44, 46f
Limberg, 114f
for temporal region, 96, 96f
ropivacaine, 25t
rotation fl ap, 37f, 43–44, 44f–46f
cervicofacial, 44, 45f
for cheek defects, 101, 102f
for lip/perioral defects, 82–83
multiple, for scalp, 126, 127f–128f
for scalp, 125–126, 126f–127f
RSTLs. see relaxed skin tension lines (RSTLs)
running suture, 28, 29f, 30f
f
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