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SECTION IV: BREAST AND BODY
RECONSTRUCTION
Section Editor: Sherry Tang
47 Breast Augmentation, Mastopexy, and Augmentation
Mastopexy
Sarah Hart Kennedy
48 Reduction Mammoplasty, Top Surgery, and Gynecomastia
Sherry Tang
49 Breast Disease
Emily Barrett
50 Breast Reconstruction
Sherry Tang
51 Thoracic Reconstruction
Megan Lane and Paige L. Myers
52 Abdominal Reconstruction
Brigit Baglien
53 Perineal, Penile, and Vaginal Reconstruction
Kyle R. Latack and Widya Adidharma
54 Gender-Affirming Pelvic Surgery
Caleb Haley
55 Pressure-Induced Skin and Soft Tissue Injuries
Humza N. Mirza and Geoffrey E. Hespe
56 Lower Extremity Reconstruction
Connor Mullen
SECTION V: AESTHETICS
Section Editor: Rami D. Sherif
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57 Evaluation of Facial Aging
Jaclyn T. Mauch
58 Nonoperative Facial Rejuvenation
Galina G. Primeau
59 Periocular Rejuvenation: Blepharoplasty, Eyelid Ptosis, and
Brow Lift
Peter M. Kally and Jane S. Kim
60 Rhinoplasty
Johnny Yanjun Xie and Rami D. Sherif
61 Face-lift and Neck Lift
Christopher J. Breuler and Rami D. Sherif
62 Genioplasty
Rami D. Sherif
63 Gender-Affirming Facial Surgery
Megan Lane
64 Liposuction, Panniculectomy, and Abdominoplasty
Christopher J. Breuler
65 Brachioplasty and Thighplasty
Geoffrey E. Hespe
SECTION VI: OTHER
66 How to Excel During Your Plastic Surgery Sub-Internship
Geoffrey E. Hespe and Widya Adidharma
Index
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1
Complex Wound Care
Brigit Baglien
ANATOMY
Collagen: most abundant connective tissue protein in mammals
Twenty types of collagen; most abundant types are as
follows
*Type I: skin, tendon, bone, and mature scar; have
a 4:1 ratio of type I:III
Type II: cartilage and cornea
Type III: blood vessels and immature scar
Type IV: basement membrane
Composed of high concentration of hydroxyproline and
hydroxylysine amino acids.
Skin Layers and Structures (Fig. 1-1A and B): ordered from
superficial to deep layers
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Figure 1-1 Cross section of the skin.
(From Chung KC, ed. Grabb and Smith’s
Plastic Surgery. 8th ed. Wolters Kluwer;
2020. Figure 45.1)
Epidermis: derived from ectoderm—stratified, keratinized,
and avascular layer
Stratum corneum: acellular layer of keratin.
Stratum lucidum: dead cells without nuclei.
Stratum granulosum: cytoplasmic granules contribute
to keratin formation.
Stratum spinosum: desmosomes connect cells and
create a shiny appearance.
Stratum basale (aka germinativum): melanocytes
produce melanin, which is taken up by the predominant
keratinocytes.
Dermis: derived from mesoderm
Papillary: loose vascular tissue
Reticular: dense, more vascular layer
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Contains fibroblasts, adipocytes, macrophages,
collagen, and ground substance
Adnexa: sources of reepithelialization in partial-thickness
wounds
Hair follicles (ectodermal origin)
Ingrowth of epidermis into dermis and
subcutaneous tissue
Associated sebaceous glands secrete into the hair
follicle
Remains intact when harvesting split-thickness
skin grafts
Eccrine sweat glands (ectodermal origin)
Coiled structures located throughout the body with
high concentrations in the palms and soles that
secrete primarily water and salt via a single duct
into the epidermis
Not present in split-thickness skin grafts
Apocrine sweat glands (ectodermal origin)
Located in axillary, inguinal, and areolar regions,
secrete watery fluid higher in protein into hair
follicles. Associated with malodorous sweating
Muscle: derived from paraxial mesoderm; classified as smooth,
skeletal, and cardiac muscles
Microscopic: sarcomere unit—bundles of myofibers
(composed of actin and myosin filaments) form muscle
fibers.
Macroscopic: organized groups of muscle fibers form
fascicles; bundles of fascicles form muscles.
Neuromuscular junction: “motor endplate” consists of
sarcolemmal folds within which acetylcholine receptors
reside.
Bone: derived from lateral plate mesoderm (except for skull
bones derived from neural crest)
Cross-sectional anatomy
Outer layer: fibrous periosteum and osteogenic
periosteum
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Mature compact (cortical) bone: 80% of total bone
mass; lamellar structure that is permeated by elaborate
interconnecting vascular canals (haversian canals)
Immature compact (cortical) bone: woven structure of
collagen fibrils that is replaced by mature bone through
remodeling
Trabecular (cancellous) bone: 20% of total bone mass,
but much greater surface area due to lower density;
bony matrix organized into a matrix (trabeculae) along
lines of stress. Develops into compact bone via
osteoblasts along the trabeculae
Tendon: derived from lateral plate mesoderm
Organizational anatomy
Collagen is arranged longitudinally into fibrils.
Fibrils and fibroblasts are organized into fascicles,
which are grouped into tendons.
Cartilage: derived from lateral plate mesoderm, the cartilage
consists of extracellular matrix (ECM) composed of collagen
fibers, ground substance, and elastin, and is classified into
elastic cartilage, hyaline cartilage, and fibrocartilage, depending
on the proportion of each component.
Nerve: peripheral nerves have neural crest origin.
Organizational anatomy
A nerve describes a bundle of axons traveling together
peripherally.
The nerve is covered by the epineurium.
Bundles of axons are called fascicles and are wrapped
in the perineurium.
The majority of axons are myelinated, and individual
axons are enveloped in the endoneurium.
WOUND HEALING
NORMAL WOUND HEALING
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Skin and Subcutaneous Tissue
Wound healing categories
Primary intention
*Immediate primary closure of a surgical
incision (epithelialization occurs in ~24 hours).
Delayed closure of a surgical incision (usually to
either allow clearance of infection or resolution of
edema) is known as “delayed primary closure.”
Secondary intention
Full-thickness wound healing by a combination of
migration of fibroblasts and keratinocytes from the
wound periphery leading to wound contraction
Phases of wound healing
Inflammatory phase (first minutes to first week)
Vasoconstriction of vessels: occurs for first 10
minutes following injury.
*Coagulation: Platelets arrive and degranulate,
releasing thromboxane A2 that causes
transient vasoconstriction to facilitate
hemostasis with thrombus formation. Plateletderived growth factor (PDGF) is released,
acting as a potent chemotaxin and mitogen for
fibroblasts and macrophages.
Vasodilation and increased permeability: small
vessels dilate in response to prostaglandins to
allow white blood cells (WBCs) (neutrophils,
plasma cells, and monocytes) attracted by the
leukotrienes, complement, and cytokines
(interleukin-1 [IL-1], tumor necrosis factor-α [TNFα], TGF-β, epidermal growth factor (EGF), and
platelet factor 4 [PF4]) to enter.
Cellular response.
Neutrophils
*Dominant cell type at 24 hours, first
to respond
Approach injury site by chemoattractants
via circulatory system
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Undergo margination and diapedesis
Migrate through interstitium by
chemotaxis to injury site
*Macrophages (transformed monocytes)
are the dominant cell type at 2-3 days,
most important for releasing cytokines to
attract fibroblasts and releasing growth
factors (PDGF and TGF-β1).
Proliferative phase (aka “fibroblastic phase,”
approximately days 3-21)
*Fibroblasts are the predominant cell
population at 3-5 days and transform into
myofibroblasts to promote wound contraction.
High rate of collagen type III and I synthesis from
days 5 to 21.
Tensile strength begins at days 4-5.
Fibroblasts form ECM by synthesizing
proteoglycan and fibronectin.
*Keratinocytes migrate into the wound due to
loss of contact inhibition secondary to wound.
*Neovascularization occurs under the
influence of vascular endothelial growth factor
(VEGF) expression.
Remodeling (maturation) phase (approximately week
3 to 1 year)
Collagen replaces proteoglycan/fibronectin and
reorganizes creating stronger cross-links.
*Equilibrium between collagen breakdown and
synthesis by weeks 3-5.
Matrix metalloproteinases (MMPs) and tissue
inhibitors of metalloproteinases (TIMPs) remodel
the collagen matrix.
The wound achieves 5% of its tensile strength at 1
week, 20% at 3 weeks, 50% at 4 weeks, and 80%
after 6 weeks to a year after repair. Maximum
tensile strength of a wound reaches only
approximately 80% of noninjured skin.
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*Final ratio of type I:type III collagen is 4:1.
Epithelialization
Mobilization: due to loss of contact inhibition in
keratinocytes.
Migration: cells migrate across the wound until
contact inhibition is reestablished when touch cells
of opposite wound edge.
Mitosis: cells further back from wound edge
proliferate to bridge wound.
Differentiation: after migration ceases, epithelial
layers are reestablished from basal layer to
stratum corneum.
Contraction (occurs with full-thickness injury through
dermis)
Fibroblasts differentiate into myofibroblasts and
are present throughout granulating wound.
Myofibroblasts appear at day 3 and reach the
maximum level at days 10-21.
Amount of secondary contraction is dependent
upon the amount of dermis within the wound; more
dermis equals less secondary contraction.
Muscle Healing
Phases of muscle healing (phases overlap with each
other)
Destructive phase (days 0-7 following injury)
Myoblasts join with each other to form myotubes,
which then fuse to form new myofibers.
Analogous to inflammatory phase of skin healing
with cytokine release and initial response with
neutrophils followed by macrophages.
Repair phase (starting at day 3 and lasting up to
several weeks)
Regeneration of disrupted myofibers
Production of connective tissue scar
Remodeling phase (occurs concomitantly with repair
phase)
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Vascular ingrowth (to feed the upregulated
metabolism of regeneration).
Regeneration of intramuscular nerves is necessary
for functional regeneration.
Adhesion of myofibers to ECM.
Bone Healing
Bone healing categories
Primary (direct) bone healing in the setting of absolute
stability created by rigid surgical fixation
Minimal callus formation (bypasses the stage of
woven bone formation)
Lamellar bone formation parallel to the long axis of
the bone
Secondary (indirect) bone healing by external
splint/cast fixation (nonrigid fixation)
Healing with callus formation; amount of callus
correlates with the amount of instability
encountered during healing.
Immobilization is important to allow for healing.
Phases of bone healing
Inflammatory phase (from time of fracture to start of
bone formation at 7-10 days)
Initial platelet degranulation and contained
hematoma aids in healing.
Inflammatory response as detailed in previous
section; osteoclasts break down necrotic bone
edges, releasing osteogenic cytokines.
Reparative phase (starting during the first week and
lasting up to several months)
Inflammatory debris is cleared by macrophages.
Acid tide—acidic local environment stimulates
osteoclasts.
Vascular ingrowth from periosteum and
endosteum.
pH rises at approximately day 10 with the
presence of increased alkaline phosphatase,
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