Review of Plastic Surgery – Donal W. Buck II

Syndromic Craniosynostosis
39
5
2. Saethre-Chotzen syndrome (acrocephalosyndactyly)
• Autosomal dominant
• TWIST-1 gene mutation
• Characterized by bicoronal craniosynostosis, eyelid ptosis,
low hairline, proptosis, antimongoloid slanting of palpebral
fissures, and syndactyly of the hands and/or feet
3. Pfeiffer syndrome (acrocephalosyndactyly; see Figure 5.6)
• Autosomal dominant
• FGFR-1 or FGFR-2 gene mutation
• Characterized by bicoronal craniosynostosis, enlarged
thumbs and halluces, and mild partial syndactyly of the
hands and feet
Figure 5.5.  Apert syndrome. A, Lateral view of a child with Apert
syndrome. B, Syndactyly of the hand. (Reprinted from Zitelli, B.J.,
McIntire, S.C., Nowalk, A.J. [Eds.], 2012. Atlas of Pediatric Physical Diagnosis,
6th ed. Elsevier, 889–912.)
A
B
Figure 5.6.  Pfeiffer syndrome. A, Lateral view. B, Great toe
anomalies. (Reprinted from Zitelli, B.J., McIntire, S.C., Nowalk, A.J. [Eds.],
2012. Atlas of Pediatric Physical Diagnosis, 6th ed. Elsevier, 889–912.)
A
B
4. Crouzon syndrome (craniofacial dysostosis; see Figure 5.7)
• Autosomal dominant
• FGFR-2 and/or FGFR-3 gene mutation
• Characterized by bicoronal craniosynostosis (occasionally
turribrachycephaly), midface hypoplasia, exorbitism, and
normal hands and feet
• Increased chance of ocular herniation due to hypolastia of
the greater wing of the sphenoid

Craniosynostosis and Craniofacial Syndromes
40
condyle, chin deviation to the affected side, and an
occlusal cant upward on the affected side (see
Figure 5.8).
■ Maxillary hypoplasia: Hypoplasia of the ipsilateral
maxillary dentoalveolar process (contributes to the
occlusal cant)
• Cranial nerve abnormalities are also common and most
frequently involve the facial nerve.
■ The most common finding is dysfunction of the
marginal mandibular nerve on the affected side (see
Table 5.3).
• Treatment
■ Commissuroplasty for macrostomia repair:
Reconstruction of the orbicularis oris and layered
closure is paramount for successful commissuroplasty.
■ Mandibular distraction: Useful for patients with
Type-IIA or -IIB mandibular deformity
■ Rib or iliac crest bone grafts are useful in the absence of
the ramus and condyle (Type-III mandibular defects as
above); the cartilaginous portion should be removed on
rib grafts to reduce the risk for overgrowth.
■ Microtia/ear reconstruction: Typically performed when a
child is 6 to 7 years of age or 10 years of age (if using the
Nagata technique)
■ Orthognathic surgery: Reserved for skeletally mature
patients when indicated
2. Goldenhar syndrome (OAV dysplasia/sequence)
• A variant of craniofacial microsomia
• Characterized by
■ Epibulbar dermoids
■ Preauricular skin tags
■ Spinal anomalies
■ Hypoplasia of the ear, mandible, and maxilla
• Occasionally associated with cleft lip and palate
3. Treacher Collins syndrome (“mandibulofacial dysostosis”)
• Autosomal dominant; always bilateral and almost always
symmetric
• TCOF1 gene mutation
• Characterized by
■ Normal intelligence
■ Lower lid colobomas with absence of cilia
■ Downward slanting of the palpebral fissures
■ Hypoplasia of the maxilla and zygoma, with absence of
the zygomatic arch
■ Tessier 6, 7, or 8 orofacial cleft
■ Conductive hearing loss
■ Mandibular hypoplasia and retrognathia
• Other associated anomalies: Cleft palate and
velopharyngeal insufficiency (in 33% of cases) (see
Figure 5.9)
• Treatment: Staged reconstruction. Example:
■ Within first year, macrostomia repair, tracheostomy
■ At 12 months, cleft palate repair
■ At 2 to 3 years, staged eyelid reconstruction (e.g., wedge
resection of coloboma vs. tripier flap vs. graft),
mandibular distraction
5. Carpenter syndrome
• Autosomal recessive
• Characterized by mutlisutural craniosynostosis (e.g.,
sagittal, lambdoid, coronal), preaxial polydactyly of the feet,
sympbrachydactyly (shortness) of the hands, developmental
delay, and ocular findings
6. Muenke syndrome
• Autosomal dominant
• FGFR-3 gene mutation
• Characterized by unicoronal or bicoronal craniosynostosis,
midface hypoplasia, carpal or tarsal fusions, sensorineural
hearing loss
7. Waardenburg Syndrome
• Autosomal dominant with variable penetrance
• PAX3 or MITF gene mutations
• Characterized by
■ Sensorineural hearing loss
■ Telecanthus
■ White forelock of hair
■ Craniosynostosis
■ Broad nasal bridge and high-arched cleft palate
■ Congenital heart disease, neural tube defects
Nonsynostotic Syndromes
1. Craniofacial microsomia (oculoauriculovertebral [OAV]
spectrum disorder)
• Second most common craniofacial anomaly after cleft lip
and palate
• Exact etiology is unknown, although some postulate that it
may be related to a defect of the stapedial artery.
• Highly variable presentation affecting structures of the first
and second branchial arches; more commonly unilateral
• Three main features
■ Auricular hypoplasia: May include small ears, auricular
skin tags, and/or microtia
■ Mandibular hypoplasia: Typical presentation includes
hypoplasia or absence of the mandibular ramus and/or
Figure 5.7.  Crouzon syndrome. Frontal view. (Reprinted from Zitelli,
B.J., McIntire, S.C., Nowalk, A.J. [Eds.], 2012. Atlas of Pediatric Physical
Diagnosis, 6th ed. Elsevier, 889–912.)

Nonsynostotic Syndromes
41
5
■ At 7 to 10 years, bone grafting for zygoma
reconstruction, ear reconstruction
■ Skeletal maturity: Orthognathic surgery, genioplasty,
rhinoplasty
4. Nager syndrome (acrofacial dysostosis)
• Autosomal recessive; extremely rare
• Craniofacial features similar to Treacher Collins syndrome
Figure 5.8.  Pruzansky classification of the mandibular deformity, as modified by Kaban et al. A, Type I: Mandibular deficiency is only mild.
B, Type IIA: Condyle and ramus are small, but condyle and glenoid fossa are anatomically oriented. Note that a flattened condyle can be
hinged on a flat, often hypoplastic, infratemporal surface, and the coronoid process may be absent. C, Type IIB: Similar to type IIA except
that the vertical or superoinferior plane of the condyle ramus is medially displaced. There is no functioning glenoid fossa. D, Type III:
Absence of the ramus, condyle, and coronoid process. (Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, 3rd ed. Elsevier, 761–791.)
Type I
Type IIA
Type IIB
Type III
A
B
C
D
• Characterized by
■ Hypoplasia of the zygoma, maxilla, and
mandible
■ Pierre Robin sequence with cleft palate and
velopharyngeal insufficiency (VPI)
■ Radial hand deformities: Thumb and/or radial
hypoplasia, camptodactyly, syndactyly, clinodactyly

Craniosynostosis and Craniofacial Syndromes
42
• Treatment: Orthognathic surgery (LeFort I or II osteotomy
advancement) followed by dorsal nose augmentation
6. Mobius syndrome
• Often sporadic, but autosomal dominant and recessive
familial patterns have been reported.
• Characterized by
■ Bilateral congenital abducens and facial nerve palsies
■ Other cranial nerve involvement (e.g., hypoglossal,
vagus)
■ Musculoskeletal abnormalities (e.g., clubfoot)
■ Congenital heart defects
5. Binder syndrome (nasomaxillary dysplasia)
• Autosomal recessive, with incomplete penetrance
• Exact etiology unknown, although some postulate that this
is related to an underdevelopment of the nasomaxillary
spine.
• Characterized by
■ Absent or reduced anterior nasal spine, leading to a short
nose, short columella, and flat nasal bridge
■ Acute nasolabial angle
■ Class-III malocclusion
■ Concave facial profile (“dish face”)
Table 5.3  Spectrum and Incidence of Associated Extracranial Malformations in Craniofacial Microsomia
PRINCIPAL ANOMALIES
ASSOCIATED ANOMALIES
Mandibular
Mandibular hypoplasia (89-100%),
malformed glenoid fossa (24-27%)
Craniofaical
VPI (35-55%), palatal deviation (39-50%), orbital dystopia (15-43%),
ocular motility disorders (19-22%), epibulbar dermoids (4-35%), cranial
base anomalies (9-30%), cleft lip and/or palate (15-22%), eyelid defects
(12-25%), hypodontia/dental hypoplasia (8-25%), lacrimal drainage
abnormalities (11-14%), frontal plagiocephaly (10-12%), sensorineural
hearing loss (6-16%), preauricular sinus (6-9%), parotid gland hypoplasia,
other cranial nerve defects (e.g., V, IX, XII)
Ear
Microtia (66-99%), preauricular
tags (34-61%), conductive hearing
loss (50-66%), middle-ear (ossicle)
defects
General
Vertebral/rib defects (16-60%), cervical spine anomalies (24-42%),
scoliosis (11-26%), cardiac anomalies (4-33%), pigmentation changes
(13-14%), extremity defects (3-21%), central nervous system defects
(5-18%), genitourinary defects (4-15%), pulmonary anomalies (1-15%),
gastrointestinal defects (2-12%)
Midfacial
Maxillary and zygomatic hypoplasia,
occlusal canting
Soft-Tissue
Masticatory muscles hypoplasia
(85-95%), macrostomia (17-62%),
seventh-nerve palsy (10-45%)
The prevalence rates were summarized from 19 reports that appeared in the literature from 1983 to 1996. Studies based on selected samples
were omitted to minimize selection bias. The authors recognized that the prevalence rate may be falsely elevated because the reporting tertiary
centers may have a referral bias of more severely affected patients.
VPI, Velopharyngeal insufficiency.
Adapted from Cousley, R.R., Calvert, M.L. 1997. Current concepts in the understanding and management of hemifacial microsomia. Br. J.
Plast. Surg. 50, 536–551.
Figure 5.9.  A, A 7-year-old boy with Treacher Collins syndrome presenting with severe coloboma of the lower eyelids, hypoplastic maxilla,
and underprojected and narrow maxilla. There is bilateral microtia and macrostomia. The mandible shows severe hypoplasia, including at
the menton. B, 3D-CT scan showing absence of the zygoma and malar bone and lack of inferolateral orbital floor. The mandible has a very
short ascending ramus and the posterior aspect of the maxilla is also very short vertically. (Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013.
Plastic Surgery, 3rd ed. Elsevier, 828.)
A
B

Nonsynostotic Syndromes
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■ Myopia
■ Micrognathia and Pierre Robin sequence
■ Midface hypoplasia and malar bridge depression
■ Bifid uvula and submucous cleft palate
■ Early-onset degenerative joint disease
Suggested Readings
Buchanan, E.P., Xue, A.S., Hollier, L.H., 2014. Craniofacial syndromes. Plast.
Reconstr. Surg. 134 (1), 128e–153e.
Campbell, C.A., Yu, J.C., Lin, K.Y., 2010. Chapter 38: Craniofacial
microsomia. In: Weinzweig, J. (Ed.), Plastic Surgery Secrets Plus, 2nd ed.
Mosby, pp. 253–256.
Fearon, J., 2013. Chapter 35: Syndromic craniosynostosis. In: Neligan, P.C.,
Losee, J. (Eds.), Plastic Surgery, 3rd ed. Elsevier, pp. 749–760.
Forrest, C.R., Hopper, R.A., 2013. Craniofacial syndromes and surgery. Plast.
Reconstr. Surg. 131 (1), 86e–109e.
Jones, K.L., Jones, M.C., Casanelles Del Campo, M., 2013. Craniosynostosis
syndromes. In: Smith’s Recognizable Patterns of Human Malformation, 7th
ed. Saunders Elsevier, Philadelphia, pp. 530–559.
Kirmi, O., Lo, S.J., Johnson, D., et al., 2009. Craniosynostosis: a radiological
and surgical perspective. Sem. Ultrasound CT MRI 30 (6), 492–512.
Kirschner, R.E., Nah, H.D., 2009. Chapter 28: Craniofacial growth: Genetic
and morpholical processes in craniosynostosis. In: Guyuron, B., Eriksson, E.,
Persing, J.A., et al. (Eds.), Plastic Surgery: Indications and Practice, 1st ed.
Elsevier, pp. 317–330.
Lin, A.Y., Losee, J.E., 2012. Chapter 22: Pediatric plastic surgery. In: Zitelli,
B.J., McIntire, S.C., Nowalk, A.J. (Eds.), Atlas of Pediatric Physical Diagnosis,
6th ed. Elsevier, pp. 889–912.
McCarthy, J.G., Grayson, B.H., Hopper, R.A., et al., 2013. Chapter 36:
Craniofacial microsomia. In: Neligan, P.C., Losee, J. (Eds.), Plastic Surgery,
3rd ed. Elsevier, pp. 761–791.
Molina, F., 2013. Chapter 39: Treacher-Collins syndrome. In: Neligan, P.C.,
Losee, J. (Eds.), Plastic Surgery, 3rd ed. Elsevier, p. 828.
Persing, J.A., Knoll, B., Duncan, C.C., 2009. Chapter 33: Non-syndromic
craniosynostosis. In: Guyuron, B., Eriksson, E., Persing, J.A., et al. (Eds.),
Plastic Surgery: Indications and Practice, 1st ed. Elsevier, pp. 389–404.
Steinbacher, D.M., Bartlett, S.P., 2013. Chapter 34: Nonsyndromic
craniosynostosis. In: Neligan, P.C., Losee, J. (Eds.), Plastic Surgery, 3rd ed.
Elsevier, pp. 726–748.
Taub, P.J., Silver, L., Torok, K.S., 2013. Chapter 37: Hemifacial atrophy. In:
Neligan, P.C., Losee, J. (Eds.), Plastic Surgery, 3rd ed. Elsevier, pp. 792–802.
Tewfik, T.L. Manifestations of Craniofacial Syndromes. Meyers, A.D., Ed.
Emedicine.com. Available at: <
article/844209-overview.> Accessed on: November 20, 2014.
Weinzwieg, J., Whitaker, L.A., 2010. Chapter 30: Craniosynostosis. In:
Weinzweig, J. (Ed.), Plastic Surgery Secrets Plus, 2nd ed. Mosby,
pp. 196–211.
• Occasionally associated with cleft palate, retrogenia, and
microstomia
• Treatment: Eye protection, facial reanimation with free
functioning muscle transfer after the age of 5
■ For bilateral cases, operations are often spaced 3 to 6
months apart.
7. Parry-Romberg syndrome/disease (progressive hemifacial
atrophy)
• Etiology unknown, although some postulate that it may be
related to an autoimmune disorder or a variant of
scleroderma.
• Characterized by progressive hemifacial atrophy beginning
between 5 and 15 years of age and involves skin, soft
tissue, muscle, and bone within the trigeminal nerve
dermatomes
■ Classic sign: Linear indentation along the forehead
(“coup de sabre”)
• Patients have normal facial appearance until the disease
occurs.
• Can be associated with seizures or other neurologic
symptoms
• Treatment: Fat grafting or microvascular fasciocutaneous
flaps (e.g., parascapular or scapular flaps) to restore
facial contour; immunosuppression in combination
with methotrexate has been shown to stop progression
of disease.
■ Should be delayed until disease progression has stopped
8. Stickler syndrome (hereditary arthro-ophthalmopathy)
• Autosomal dominant
• Collagen production gene mutations (e.g., COL2A1,
COL11A1, COL11A2)
• Characterized by deficits of the eyes, craniofacial skeleton,
ears, and joints, including
■ Cataract
■ Retinal detachment

Clefts and
Orthognathic Surgery
Chapter
6 
Embryology
1. The formation of the face occurs between the 4th and 10th
weeks of human development, secondary to fusion of the
midline frontonasal prominence and the paired maxillary,
lateral nasal, and mandibular prominences (see Figure 6.1).
• Frontonasal prominence
■ Forms the forehead, midline of the nose, philtrum,
middle portion of the upper lip, and the primary palate
■ Gives rise to the lateral and medial nasal processes
• Lateral nasal prominence/process
■ Forms the nasal alae
• Maxillary prominence
■ Forms the upper jaw, sides of the face, sides of the upper
lip, and the secondary palate
• Mandibular prominence
■ Forms the lower jaw and lip
2. Cleft lip deformities
• From disruptions occurring during the 3rd to 7th weeks of
gestation
• Unilateral cleft lip: Failure of fusion of the medial nasal
process and the maxillary prominence on one side
• Bilateral cleft lip: Failure of fusion of the merged medial
nasal processes with the maxillary prominences bilaterally
3. Cleft palate deformities
• From disruptions occurring during the 5th to 12th weeks of
gestation
• Cleft of the primary palate (anterior to the incisive
foramen): Failure of fusion of the frontonasal prominence
(median palatine process) and maxillary prominences
(lateral palatine process)
• Cleft of the secondary palate (posterior to the incisive
foramen): Failure of fusion of the maxillary prominences
(lateral palatine processes)
• Fusion of the palate proceeds from anterior to posterior as
the tongue drops and the lateral palatal shelves rotate from a
vertical to horizontal orientation (~7 to 8 weeks gestation).
Epidemiology
1. Isolated cleft palate and cleft lip with or without cleft palate
are thought to be two genetically distinct deformities (see
Table 6.1).
• The incidence of cleft lip/palate differs among ethnicities
and is approximately 1:1000 in those of Caucasian descent,
1:2000 of African, and 1:500 of Asian.
• The incidence of isolated cleft palate is approximately
1:2000 in Caucasians.
Figure 6.1.  Prominences of vertebrate face. Frontonasal
prominence (FNP), which contributes to forehead, middle of the
nose, philtrum, and primary palate; maxillary prominence (MXP),
which contributes to sides of face, lip, and secondary palate;
lateral nasal prominence (LNP), which forms sides of nose; and
mandibular prominence (MNP), which produces lower jaw. (Reprinted
from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed.
Elsevier, 503–516.)
FNP
MXP
LNP
MNP

General Anatomy
45
6
■ One affected parent and one affected child: Recurrence
risk of 17%
• Cleft palate
■ Unaffected parents with one affected child: Recurrence
risk of 2%
■ Unaffected parents with two affected children:
Recurrence risk of 1%
■ One affected parent and no affected children: Recurrence
risk of 6%
■ One affected parent and one affected child: Recurrence
risk of 15%
General Anatomy
1. Unilateral cleft lip
• Orbicularis abnormally inserts onto the columella on the
noncleft side and the ala on the cleft side
• Complete: Cleft includes the nasal sill.
• Incomplete: Nasal sill contains some soft-tissue elements
(“Simonart’s band”).
2. Bilateral cleft lip (see Figure 6.2)
• Orbicularis oris abnormally inserts onto the ala bilaterally.
• Prolabium is void of any orbicularis muscle and is often
protruded forward.
• Severe deficiency of columellar height
• Wide alar bases
• Cleft lip/palate is more common in boys.
• Isolated cleft palate is more common in girls.
• Cleft lip/palate affects the left side more often.
2. Isolated cleft palate is associated with a craniofacial syndrome
in as many as 50% of patients, whereas only 30% of cleft lip/
palate patients have an associated syndrome.
• Van der Woude syndrome
■ One of the most common syndromes associated with
clefts
■ Autosomal dominant
■ Characterized by lower lip sinus tracts (“pits”), cleft lip/
palate, or cleft palate
• 22q chromosomal deletion (“velocardiofacial syndrome”)
■ Common syndrome associated with clefts (particularly,
cleft palate)
■ Characterized by “bird-like” facial appearance, soft-
palate dysfunction, developmental delay, congenital
heart disease, B-cell immune dysfunction, and
medialization of the carotid arteries
• Pierre Robin sequence
■ Characterized by the triad of micrognathia, glossoptosis,
and respiratory distress
■ 60-90% have associated cleft palate, which is typically of
the soft palate and is U shaped or wide
■ Associated with Stickler syndrome (autosomal dominant
inheritance, myopia, and joint problems), craniofacial
microsomia, and Treacher Collins syndrome
■ Initial treatment is conservative and focused on airway
protection including prone positioning and/or tongue-
lip adhesion. In cases that have failed conservative
measures, mandibular distraction or tracheostomy
should be considered.
3. Inheritance of clefts
• Cleft lip/palate
■ Unaffected parents with one affected child: Recurrence
risk of 4%
■ Unaffected parents with two affected children:
Recurrence risk of 9%
■ One affected parent and no affected children: Recurrence
risk of 4%
Table 6.1  Incidence of Cleft Lip/Palate in Differing
Ethnic Groups
ETHNICITY
INCIDENCE PER 1000 BIRTHS
Amerindian
3.6
Japanese
2.1
Chinese
1.7
White
1.0
African-American
0.3
Data from Wyszynski, D.F., Beaty, T.H., Maestri, N.E., 1996.
Genetics of nonsyndromic oral clefts revisited. Cleft Palate Craniofac.
J. 33, 406–417; Vieira, A.R., Orioli, I.M., 2001. Candidate genes for
nonsyndromic cleft lip and palate. ASDC J. Dent. Child. 68 (229),
272–279.
Figure 6.2.  Bilateral cleft nose deformity involves bilateral
displacement and distortion of osseocartilaginous skeleton of
nose. Shortened columella plays prominent role in bilateral
deformity and must be lengthened in subsequent procedures.
(Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3,
3rd ed. Elsevier, 631–654.)
Web alar rim
Flaring alae
Wide nostril
Short columella
Obtuse angle
Dislocation and separation
3. Cleft palate
• Levator palatini abnormally inserts onto the hard palate
instead of decussating in the midline.
■ Affects speech
■ Leads to severe Eustachian tube dysfunction; chronic
otitis media found in 96% to 100% of patients (see
Figure 6.3)
• Classification
■ Kernahan Y classification (see Figure 6.4)
■ Veau classification (see Figure 6.5)

Clefts and Orthognathic Surgery
46
Figure 6.3.  A, Normal anatomy: Levator veli palatini muscle can be seen forming a sling across soft palate; tensor veli palatini is shown
coming around hamulus to fuse with levator. B, Cleft palate: Muscles are seen running more or less parallel with cleft margin. (Reprinted
from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 569–583.)
Aponeurosis
Hamulus
Tensor muscle
Levator muscle
Uvulus muscle
Aponeurosis
Hamulus
Tensor muscle
Accessory muscle
Levator muscle
A
B
Figure 6.4.  Kernahan’s classification of clefts allows for
standardized reporting of severity of both cleft lip and palate.
(Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3,
3rd ed. Elsevier, 569–583.)
9
10
11
Hard
palate
Soft
palate
Nose
1
2
3
5
6
7
4
8
Lip
Nasal floor
Alveolus
Hard palate
• Submucous cleft palate
■ Occurs when the palate has mucosal continuity but
levator palatini muscle is discontinuous and abnormally
oriented.
■ Characterized by Calnan’s triad: Midline clear zone
(“zona pellucida”), bifid uvula, palpable notch of the
posterior hard palate
■ Requires speech evaluation to determine
symptomatology.
■ If asymptomatic, submucous cleft palate requires no
treatment. In symptomatic patients (~33% of cases),
palatoplasty is required. A common technique includes
the Furlow double-opposing Z plasty.
4. Unilateral cleft nasal deformity
• Septum is deviated toward the cleft side.
• Anterior nasal spine and nasal tip are deviated toward the
noncleft side.
• Piriform and alveolus on the cleft side are displaced
posteriorly.
• Ala on the cleft side is flattened and displaced inferior,
posterior, and lateral
• Columella is deficient (see Figure 6.6).

General Anatomy
47
6
Figure 6.5.  Veau classification system. A, Veau I cleft of soft palate. B, Veau II cleft of soft and hard palates. C, Veau III unilateral cleft.
D, Veau IV bilateral cleft. (Reprinted from Butler, C.E. [Ed.], 2009. Head and Neck Reconstruction, Elsevier, 271–294.)
A
B
C
D
Figure 6.6.  Key aspects of cleft nose deformity involve abnormalities of osseocartilaginous skeleton. AP, Anteroposterior. (Reprinted from
Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 631–654.)
Deviated septum
Normal alar cartilage
AP
Worm’s eye
Displaced nasal
spine
Lowered nostril sill
Displaced alar base
Cleft side alar cartilage
Depressed dome on cleft side
Slanted
columella

Clefts and Orthognathic Surgery
48
Cleft Care
1. Requires multidisciplinary team care.
2. Initial treatment should focus on parental reassurance and
counseling, feeding, and infant growth.
3. General sequence and timing of repair (see Table 6.2).
Table 6.2  Surgical Protocol
3 months
Primary cleft lip and nose
8 months
Two-flap palatoplasty
5 years (35%)
Secondary minor lip–nose
7-9 years (100%)
Cancellous iliac bone graft to alveolar cleft
7 years (full growth)
Distraction osteogenesis >12 mm, occlusal
class III
Full growth (25-30%)
Orthognathic surgery
12-18 years
Rhinoplasty; other secondary soft tissue
Reprinted from Guyuron, B., Eriksson, E., Persing, J.A., et al. (Eds.),
2009. Plastic Surgery: Indications and Practice, 1st ed. Elsevier,
473–492.
4. Presurgical orthopedics
• Useful in wide clefts to align lip/alveolar segments, reduce
overall cleft width, and improve cleft nasal deformity (e.g.,
lengthen columella in bilateral cases).
• Several techniques available, including passive devices
(nasoalveolar molding [NAM]), active devices (Latham
appliance), lip adhesion, and taping.
5. Unilateral cleft lip repair (see Figures 6.7 and 6.8)
• Often performed at 3 months of age, following the “rule of
10s”: 10 weeks, 10 g hemoglobin, 10 kg.
• Several techniques have been described and all are
variations of the Millard rotation-advancement technique.
• Many current techniques involve some component of early
cleft nasal repair via release of abnormal alar cartilage and
suture techniques.
• Noncleft side is the rotational component and the cleft
side/lateral lip element is the advancement component of
the repair.
• Full release of the abnormally inserted orbicularis oris
muscle with meticulous layered closure is critical to a
successful repair.
• L flap is taken from the residual mucosa of the lateral lip
element and used when necessary to assist with nasal
lining.
• C flap is created on noncleft side and used to lengthen the
columella.
Figure 6.7.  Preoperative markings. (Reprinted from Guyuron, B.,
Eriksson, E., Persing, J.A., et al., [Eds.], 2009. Plastic Surgery: Indications and
Practice, 1st ed. Elsevier, 473–492.)
Figure 6.8.  Preoperative incisions (dotted lines). (Reprinted from
Guyuron, B., Eriksson, E., Persing, J.A., et al., [Eds.], 2009. Plastic Surgery:
Indications and Practice, 1st ed. Elsevier, 473–492.)

Cleft Care
49
6
• Complications of bilateral cleft lip repair
■ Dehiscence: As above for unilateral cleft lip repair
■ Poor scarring
■ Tight lip: May require scar release and Abbe flap for
correction.
7. Cleft palate repair
• Often performed at 9 to 12 months of age
• Palate repair surgery is often a balance between obtaining a
closed functioning velum and limiting future maxillary
growth disturbances.
• Several techniques are available for primary cleft palate
repair
■ Furlow double-opposing Z plasty (see Figure 6.11)
■ Two-flap palatoplasty (see Figure 6.12)
■ Von Langenbeck repair (see Figure 6.13)
■ Veau-Wardill-Kilner (VWK) repair (see Figure 6.14)
• Complications after cleft palate repair
■ Dehiscence: If early, re-repair can be performed.
■ Fistula: See below
■ Velopharyngeal dysfunction (VPD): See below
8. Palatal fistula repair
• Symptomatic fistulas require repair.
• First option in fistula repair is often local random-pattern
tissue flaps or reelevation of tissues and layered closure.
• If local random pattern flaps are not possible or reelevation
fails, then more advanced techniques include
■ Acellular dermis interposition with mucosal reelevation
and layered closure
■ Facial artery myomucosal (FAMM) flap: Based off
buccal branch of the facial artery; includes buccinator
muscle (see Figure 6.15).
• Complications of unilateral cleft lip repair include
■ Dehiscence: If early, perform re-repair with adequate
soft-tissue release to allow tension-free closure.
■ Poor scarring: Treat early scar contracture conservatively
because most will settle.
■ Whistle deformity: May require surgical correction with
dermal fat grafts, vermillion lip-switch flaps, or re-repair.
■ Inadequate rotation: May perform re-repair with
rotation-advancement flap technique.
6. Bilateral cleft lip repair (see Figures 6.9 and 6.10)
• Prolabial skin is used to create a philtrum.
• Prolabial mucosa is discarded or used to provide lining to
the upper labial sulcus.
• Lateral lip vermillion is used to create the median tubercle.
• Orbicularis oris must be reapproximated at the midline
beneath the prolabial skin flap.
• Length of philtral flap is typically set at 6 to 7 mm, with a
width of 2 mm at columellar-labial junction, and 3.5 to
4 mm between Cupid’s bow peaks.
Figure 6.9.  Markings for synchronous repair of bilateral cleft lip
and nasal deformity. (White circles) Tattooed dots. Anthropometric
points: Pronasale (prn); highest point of columella nasi (c);
subnasale (sn); ala nasi (al); crista philtri superior (cphs); crista
philtri inferior (cphi); labiale superius (ls); stomion (sto). (Reprinted
from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed.
Elsevier, 550–568.)
prn
c
sn
cphs
cphi
ls
sto
al
Figure 6.10.  Using cautery Colorado needle dissection in
preperiosteal plane for additional exposure. (Reprinted from Neligan,
P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 550–568.)
prn
c
sn
cphs
cphi
ls
al
sto

Clefts and Orthognathic Surgery
50
Figure 6.11.  Furlow double-opposing Z
plasty. A, Oral flap design shown with
posteriorly based flap on left side. If
necessary, relaxing incisions can be
continued up to cleft margin behind
alveolus, similar to two-flap palatoplasty
for hard palate closure. B, Left-sided oral
flap is raised with levator muscle, the
right-sided flap above muscle. Reverse
pattern is planned for oral side. Vomer flap
is shown closing nasal mucosa anteriorly.
C, Nasal flaps transposed and anterior oral
mucosa closed. D, Final appearance after
transposition of oral flaps. (Reprinted from
Neligan, P.C., Buck, D.W. [Eds.], 2013. Core
Procedures in Plastic Surgery, Elsevier, 156–165.)
A
B
C
D
Figure 6.12.  Two-flap palatoplasty.
A, Incisions similar to von Langenbeck
repair but they meet cleft margin just
behind alveolar ridge. B, Mucoperiosteal
flaps developed on both sides with
preservation of greater palatine vessels.
C, Levator veli palatini muscle is freed from
posterior border of hard palate and sutured
across midline. D, Final closure. It is often
possible to close much of lateral incision
and minimize raw areas. (Reprinted from
Neligan, P.C., Buck, D.W. [Eds.], 2013. Core
Procedures in Plastic Surgery, Elsevier, 156–165.)
A
B
C
D

Cleft Care
51
6
Figure 6.13.  von Langenbeck repair. A, Relaxing incisions made behind alveolar ridge, creating bilateral bipedicle flaps for midline closure.
Greater palatine vessels must be preserved. B, Cleft margins incised in a manner to leave adequate nasal mucosa for complete closure.
C, Closure of nasal mucosa and muscle repair. D, Final appearance. (Reprinted from Neligan, P.C., Buck, D.W. [Eds.], 2013. Core Procedures in Plastic
Surgery, Elsevier, 156–165.)
A
B
C
D
Figure 6.14.  A, Buccal mucosal flap. Kaplan advocated use of this flap to elongate nasal mucosa. B, Flap transposed into nasal surface.
In some situations, bilateral flaps can be used with second flap lining oral surface. (Reprinted from Neligan PC, Buck, D.W. [Eds.], 2013. Core
Procedures in Plastic Surgery, Elsevier, 156–165.)
A
B

Clefts and Orthognathic Surgery
52
Figure 6.15.  A-D, Buccal tissue can be harvested via axial pattern flap based off facial artery. FAMM, Facial artery myomucosal. (Reprinted
from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 631–654.)
Mucosa
Buccinator
Cross section through cheek
Muscles of facial expression
Skin
Buccal fat pad
Submucosa
Buccal branch
of facial artery
Buccal branch
of facial artery
FAMM flap
A
B
C
D

Velopharyngeal Dysfunction
53
6
■ Tongue flap: Based off lingual artery; often used as last
resort because tongue must be tethered for 2 to 3 weeks
(see Figure 6.16).
Figure 6.16.  The tongue offers another regional option for palatal
fistula repair. (Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic
Surgery, vol. 3, 3rd ed. Elsevier, 631–654.)
Velopharyngeal Dysfunction
1. Borders of the velopharyngeal port
• Soft palate (anterior)
• Lateral pharyngeal walls
• Posterior pharyngeal wall
2. Muscles involved in velopharyngeal port function
• Levator veli palatini
• Palatoglossus (anterior tonsillar pillar)
• Palatopharyngeus (posterior tonsillar pillar)
• Musculus uvulae
• Superior pharyngeal constrictor
3. All muscles of the velopharynx are innervated by the
pharyngeal plexus (cranial nerves IX, X, and XI) except the
tensor veli palatini, which is innervated by the mandibular
branch of the trigeminal nerve (cranial nerve V3).
4. Levator veli palatini is primary muscle responsible for
velopharyngeal closure.
5. Velopharyngeal insufficiency: Inadequate closure of
velopharyngeal port secondary to anatomic or structural
defects (e.g., clefts, postsurgical cicatrix, etc.)
6. Velopharyngeal incompetence: Inability to close
velopharyngeal port secondary to neuromuscular or
neurologic deficits
7. Diagnosis of VPD
• Speech assessment (see Box 6.1)
Reprinted from Neligan, P.C., Losee, J. (Eds.), 2013. Plastic Surgery,
vol. 3, 3rd ed. Elsevier, 614–630.
BOX 6.1  COMMON SPEECH PATHOLOGY TERMINOLOGY
Intelligibility: Perceived amount of speech (i.e., number of
words) understood
Resonance: Perceptual balance of oral and nasal sound
energy in speech. Speakers with VPD have an abnormal
escape of excessive nasal sound energy through
velopharyngeal port and into nasal cavity, referred to as
hypernasality.
Hypernasality: Perception of excessive nasal sound energy
in speech, typically on vowels, glides (W, Y), and liquid
sounds (L, R).
Hyponasality: Perception of decreased nasal sound energy
in speech, typically on nasal sounds M and N, and
usually due to structural obstruction (e.g., enlarged
adenoid pad, nasal congestion).
Mixed resonance: Combination of hypernasality and
hyponasality perceived by listener. Cul-de-sac resonance
is sometimes considered a form of mixed resonance, in
which sound energy escapes to anterior nasal cavity and
becomes trapped by some form of nasal obstruction or
constriction, such as a deviated septum.
Nasal emission: Abnormal escape of airflow through nose
during consonant production (audible or inaudible).
When audible, may also be referred to as nasal
turbulence.
Compensatory articulation errors: Category of articulation
errors typically observed in populations with cleft palate
or VPD, believed to result from an active strategy to
regulate pressure and airflow for speech. Typically
includes a pattern of producing sounds in a posterior
place of vocal tract, such as pharynx or larynx, where
pressure and airflow can be “valved” before their escape
to level of velopharynx or oral cavity.
Glottal stop substitutions: Most common type of
compensatory articulation errors seen in children with
cleft palate or history of VPD, produced by adducting
vocal folds together and abruptly releasing pressure
beneath to create sound of an oral pressure consonant.
Often used as a replacement (substitution) for pressure
consonants such as P, B, T, D, K, and G.
Nasal substitutions: Active replacement of oral sounds P,
B, T, and D with nasal sounds M and N.
Active nasal fricative: Learned articulatory behavior in
which oral sound (usually S, SH, CH) is replaced with
voiceless nasal sound (i.e., all airflow is emitted through
the nose); sometimes accompanied by nasal grimace.
Weak pressure consonants: Perception of decreased
pressure in oral consonants such as P, B, T, D, and F,
resulting from fistula or velopharyngeal gap, causing
these sounds to take on nasalization (e.g., B sound is
perceived as an M; D perceived as an N), even though
speaker is accurately attempting to produce correct
sound. Often co-occurs with nasal emission.
Sibilant distortions: Incorrect tongue placement resulting
from faulty learning or malocclusion, resulting in
imprecise production of sounds S and Z.

Clefts and Orthognathic Surgery
54
• Videofluoroscopy
• Nasopharyngoscopy
8. Surgical treatments: Treatment is often directed by the
motion or lack thereof detected on videofluoroscopy and
nasopharyngoscopy.
• Furlow palatoplasty
■ Useful to lengthen a velum that is too short to contact
the posterior pharyngeal wall.
• Posterior pharyngeal flap (see Figure 6.17)
Figure 6.17.  A,B, Posterior pharyngeal flap. (Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 614–630.)
Suture in
uvula
Transverse
incision in
soft palate
Posterior
pharyngeal
flap
Posterior
pharyngeal flap
A
B
■ Useful when there is good lateral wall motion and poor
posterior wall motion.
■ Flap is often superiorly based, and donor site closed
primarily.
■ Take care when dissecting the flap in patients with
velocardiofacial syndrome because of risk for
medialization of carotid vessels.
■ A flap that is too wide can cause severe airway
obstruction and/or obstructive sleep apnea.
• Sphincter pharyngoplasty
■ Useful when there is good posterior wall motion, and
poor lateral wall motion
■ The palatopharyngeus muscles/posterior tonsillar pillars
are elevated bilaterally and interdigitated to create a
sphincter.
■ Similar risks to pharyngeal flaps (see Figure 6.18).
• Posterior pharyngeal wall augmentation
■ Useful in patients who have good overall velar motion
with a small gap, in which augmentation may reduce the
overall port size.
■ Typically used as a secondary option for VPD
■ Possible materials used for augmentation can include
autologous fat, calcium hydroxyapatite, or other
soft-tissue fillers.
9. Nonsurgical treatments: Often used if surgery is not possible
or desired.
• Prostheses: Palatal lift and speech bulb
• Behavioral speech therapy
Orthognathic Surgery
1. Orthognathic surgery: Surgical movement of the maxilla and
mandible to optimize facial harmony and occlusion
2. Orthognathic surgery should not be performed until skeletal
maturity is reached.
3. Patient selection and planning rely on history, physical exam,
and cephalometric analysis (see Figure 6.19).
• Sella-nasion-subspinale (SNA) angle
■ Provides information regarding position of maxilla in
the anteroposterior plane.

Orthognathic Surgery
55
6
■ Normal SNA is 82 degrees (Caucasian) and 85 degrees
(African-American).
■ If less than normal, maxilla is in abnormal posterior
position with respect to cranial base and vice versa.
• Sella-nasion-supramentale (SNB) angle
■ Provides information regarding position of mandible in
the anteroposterior plane.
■ Normal SNB is 80 degrees (Caucasian) and 81 degrees
(African-American).
■ If less than normal, mandible is in abnormal
posterior position with respect to cranial base and
vice versa.
• Subspinale-nasion-supramentale (ANB) angle
■ Provides information on relationship of maxilla to
mandible in the anteroposterior plane.
■ Normal ANB is 2 degrees (i.e., maxilla protrudes 2
degrees more anterior than mandible with respect to
cranial base.).
• Frankfurt horizontal plane: Line from porion (midpoint of
upper contour of external auditory canal) to orbitale
(lowest point on inferior margin of bony orbit)
Figure 6.18.  Sphincter pharyngoplasty. (Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 614–630.)
Palatoglossal arch
Soft palate
Palatopharyngeal arch
Palatopharyngeus flaps
Flaps interdigitated
Posterior adenoid pad
Posterior pharynx
• Ricketts’ esthetic plane
■ In a patient with normal proportions, a line extending
from nasal tip toward soft tissues of chin should touch
lower lip, with upper lip 2 mm behind it.
■ If chin is retruded, it will be behind this line.
4. Occlusion
• Often described according to the Angle classification
■ Class-II malocclusion: ANB less than normal;
retrognathic mandible, increased overjet
■ Class-III malocclusion: SNA less than normal or ANB
greater than normal; retruded maxilla or prognathic
mandible, negative overjet (see Figure 6.20).
• Overbite: Vertical overlap between upper and lower incisal
edges with the teeth in occlusion
• Overjet: Horizontal between labial surface of upper incisor
and lower incisor with the teeth in occlusion
5. LeFort I osteotomy
• Developed to provide segmental movements of maxilla
• Maxilla can be advanced, impacted, set back, or moved
in multiple planes with multipiece osteotomies (see
Figure 6.21).

Clefts and Orthognathic Surgery
56
Figure 6.19.  Cephalometric radiograph identifies skeletal landmarks used in determining lines and angles that reflect facial development.
These measurements aid in determining extent to which each jaw contributes to dentofacial deformity. S, Sella turcica, midpoint of sella
turcica; N, nasion, anterior point of intersection between nasal and frontal bones; A, “A point,” innermost point in depth of concavity of
maxillary alveolar process; Ar, articulare; B, “B point,” innermost point on contour of mandible between incisor tooth and bony chin;
Ba, basale, most inferior point of skull base; Pog, pogonion, most anterior point on contour of chin; Go, gonion, most inferior and posterior
point at angle formed by ramus and body of mandible; Po, porion, uppermost lateral point on roof of external auditory meatus; Or, orbitale,
lowest point on inferior margin of orbit; PNS, posterior nasal spine, most posterior point on maxilla; Ptm, pterygomaxillary fissure;
ANS, anterior nasal spine, most anterior point on maxilla; Gn, gnathion, center of inferior contour of chin; Me, menton, most inferior point
on mandibular symphysis; MP, mandibular plane, line connecting Go and Gn; OP, occlusal plane. (Reprinted from Neligan, P.C., Losee, J. [Eds.],
2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 655–670.)
MP
Go
Me
Gn
Pog
OP
B
A
ANS
PNS
Or
Ptm
Ar
Ba
Pg
S
N
Figure 6.20.  Angle’s classification may be used to describe anterior-posterior relationship of maxillary and mandibular dental arches. In
class-I relationship, mesial buccal cusp of upper first molar articulates in buccal groove of mandibular molar. In class-II relationship, mesial
buccal cusp of upper first molar articulates between mandibular first molar and second premolar. In class-III relationship, mesial buccal
cusp of upper first molar articulates between first and second mandibular molar teeth; mandible is said to be prognathic (more anterior)
when compared with maxilla. (Reprinted from Neligan, P.C. [Ed.], 2013. Plastic Surgery, 3rd ed. Elsevier, 354–372.)
Class II
Class I
Class III

Craniofacial Clefts
57
6
8. Genioplasty
• Chin position can be evaluated by measuring the
sella-nasion-pogonion (SNPg) angle or using Ricketts’
esthetic line.
• When manipulating mandible or maxilla, may be necessary
to adjust chin position to account for unnecessary changes.
• Chin segment can be advanced, impacted, reduced, or
angled inferiorly and fixed into place.
• Make transverse osteotomy at least 3 mm below mental
foramen (located between first and second premolar) to
avoid injury to mental nerve.
• Resuspend mentalis muscle during closure to prevent lower
lip ptosis and/or “witch’s chin” deformity.
Craniofacial Clefts
9. Rare deformities of face and cranium that occur in many
patterns and degrees of severity
10. Classification system of cleft patterns established by Tessier
(see Figure 6.23).
11. Tessier 3 cleft involves alar base and medial canthus.
12. The Tessier 4 cleft spares the nose and is often referred to as
“oro-ocular.”
13. Tessier 7 cleft is the most common craniofacial cleft and is
frequently associated with craniofacial microsomia first and
second branchial arch syndrome, Goldenhar syndrome, and
Treacher Collins syndrome.
• Treatment of Tessier 7 cleft involves a full-thickness
incision with meticulous layered closure involving
reorientation and restoration of orbicular oris muscle at
commissure.
• In patients with history of cleft lip/palate, there is a
concern that VPD will develop after advancement.
• Many advocate limiting movements to less than 1 cm to
reduce risk of relapse, nonunion, and/or instability.
■ In situations requiring movements greater than 1 cm,
distraction should be considered.
• In patients with narrow alveolar arches, perform palatal
expansion before LeFort I osteotomies.
• LeFort I osteotomy with impaction is the most common
method for treating patients with “long face syndrome.”
■ Long face syndrome is characterized by increased vertical
maxillary height, increased gingival show, and lip
incompetence.
■ Impaction of maxilla can lead to decreased nasolabial
angle, widened alar base, and anterior positioning of the
chin.
• Take care to cauterize or clip descending palatine arteries
during downfracture of maxilla to prevent significant
postoperative bleeding.
6. Bilateral sagittal split osteotomy
• Developed to provide segmental movements of mandible
• Mandible can be advanced, impacted, and/or rotated.
• Take care to avoid injury to the inferior alveolar nerve.
• Lower lip paresthesias extremely common postoperatively,
with most resolving over time (see Figure 6.22).
7. “Double jaw” surgery
• Movement of maxilla and mandible in one procedure may
be necessary in select patients.
• In general, maxillary osteotomies are completed first;
maxilla is placed into its new position and plated; and then
the mandibular osteotomies are completed.
Figure 6.21.  A-E, LeFort I osteotomies demonstrating maxillary advancement, impaction, setback, and multipiece LeFort. (Reprinted from
Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed. Elsevier, 655–670.)
A
B
C
D
E

Clefts and Orthognathic Surgery
58
Figure 6.22.  Mandibular sagittal split osteotomies demonstrating
mandibular advancement (middle) and setback (bottom). (Reprinted
from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3, 3rd ed.
Elsevier, 655–670.)
Figure 6.23.  Tessier classification of craniofacial clefts.
A,B, Illustrations of Tessier clefts: Skeletal locations of numeric
clefts are depicted on right side of face (left half of drawings).
Soft-tissue landmarks are outlined on left side of face (right half
of drawings). Facial clefts are numbered 0 through 7 and cranial
clefts 8 through 14. Mandibular midline facial cleft is number 30.
(Reprinted from Neligan, P.C., Losee, J. [Eds.], 2013. Plastic Surgery, vol. 3,
3rd ed. Elsevier, 701–725.)
14 1312
11
10
9
8
7
6
5
4
1
1
0
2 3
1 2
3
0
30
1
23
4
5
6
7
7
8
9
10
11
12
13
14
0
A
B
14. Tessier 8 cleft is located at lateral canthus and is called the
“equator of the Tessier craniofacial time zones.” It divides
facial clefts from cranial clefts.
15. Treacher Collins syndrome has a combination of Tessier 6, 7,
and 8 clefts.
16. Tessier 0-14 clefts occur in midline forehead and cranium and
may represent encephaloceles.
Suggested Readings
Afshar, M., Brugmann, S.A., Helms, J.A., 2013. Chapter 22: Embryology of
the craniofacial complex. In: Neligan, P.C., Losee, J. (Eds.), Plastic Surgery,
vol. 3, 3rd ed. Elsevier, pp. 503–516.
Bradley, J.P., Kawamoto, H.K., 2013. Chapter 33: Craniofacial clefts. In:
Neligan, P.C., Losee, J. (Eds.), Plastic Surgery, vol. 3, 3rd ed. Elsevier,
pp. 701–725.
Chen, K.-T.C., Noordhoff, S.M., Fisher, D.M., et al., 2013. Chapter 8: Cleft lip
repair. In: Neligan, P.C., Buck, D.W. (Eds.), Core Procedures in Plastic
Surgery, Elsevier, pp. 134–155.
Chen, P.K.T., Noordhoff, M.S., Kane, A., 2013. Chapter 23: Repair of the
unilateral cleft lip. In: Neligan, P.C., Losee, J. (Eds.), Plastic Surgery, vol. 3,
3rd ed. Elsevier, pp. 517–549.
Cole, P.D., Stal, S., 2009. Chapter 13: Cleft lip repair: Evaluation, planning,
and surgical approach to single and bilateral defects. In: Butler, C.E. (Ed.),
Head and Neck Reconstruction, Elsevier, pp. 295–307.
Feldman, E.M., Koshy, J.C., Hollier, L.H., et al., 2013. Chapter 29: Secondary
deformities of the cleft lip, nose, and palate. In: Neligan, P.C., Losee, J. (Eds.),
Plastic Surgery, vol. 3, 3rd ed. Elsevier, pp. 631–654.
Goldstein, J.A., Bakter, S.B., 2013. Chapter 30: Cleft and craniofacial
orthognathic surgery. In: Neligan, P.C., Losee, J. (Eds.), Plastic Surgery, vol. 3,
3rd ed. Elsevier, pp. 655–670.

Craniofacial Clefts
59
6
Mulliken, J.B., 2013. Chapter 24: Repair of bilateral cleft lip. In: Neligan, P.C.,
Losee, J. (Eds.), Plastic Surgery, vol. 3, 3rd ed. Elsevier, pp. 550–568.
Neligan, P.C., Buck, D.W. 2013. Chapter 9: Cleft palate repair. In: Neligan,
P.C., Buck, D.W. (Eds.), Core Procedures in Plastic Surgery, Elsevier,
pp. 156–165.
Parker, T.H., 2007. Chapter 21: Velopharyngeal incompetence. In: Janis, J.E.
(Ed.), Essentials of Plastic Surgery, 1st ed. QMP, pp. 197–203.
Shivapuja, P.K., Spolyar, J.L., 2010. Chapter 27: Cephalometrics. In:
Weinzweig, J. (Ed.), Plastic Surgery Secrets Plus, 2nd ed. Mosby,
pp. 179–186.
Sommerlad, B.C. 2009. Chapter 40: Cleft palate. In: Guyuron, B., Eriksson, E.,
Persing, J.A., et al. (Eds.), Plastic Surgery: Indications and Practice, 1st ed.
Elsevier, pp. 505–520.
Taub, D.I., Jacobs, J.M.S., Jacobs, J.S., 2013. Chapter 16: Anthropometry,
cephalometry, and orthognathic surgery. In: Neligan, P.C. (Ed.), Plastic
Surgery, 3rd ed. Elsevier, pp. 354–372.
Gosman, A.A., 2007. Chapter 19: Cleft lip. In: Janis, J.E. (Ed.), Essentials of
Plastic Surgery, 1st ed. QMP, pp. 176–182.
Gosman, A.A., 2007. Chapter 20: Cleft palate. In: Janis, J.E. (Ed.), Essentials of
Plastic Surgery, 1st ed. QMP, pp. 183–196.
Hoffman, W.Y., 2013. Chapter 25: Cleft palate. In: Neligan, P.C., Losee, J.
(Eds.), Plastic Surgery, vol. 3, 3rd ed. Elsevier, pp. 569–583.
Kirschner, R.E., Baylis, A.L., 2013. Chapter 28: Velopharyngeal dysfunction.
In: Neligan, P.C., Losee, J. (Eds.), Plastic Surgery, vol. 3, 3rd ed. Elsevier,
pp. 614–630.
Lam, A., Koudela, C.L., 2010. Chapter 25: Dental basics. In: Weinzweig, J.
(Ed.), Plastic Surgery Secrets Plus, 2nd ed. Mosby, pp. 165–170.
Losee, J.E., Smith, D., 2009. Chapter 12: Cleft palate repair. In: Butler, C.E.
(Ed.), Head and Neck Reconstruction, Elsevier, pp. 271–294.
Marchac, A.C., Cheng, M.S., Michienzi, J.W., et al., 2009. Chapter 38:
Unilateral cleft lip repair. In: Guyuron, B., Eriksson, E., Persing, J.A., et al.
(Eds.), Plastic Surgery: Indications and Practice, 1st ed. Elsevier, pp. 473–492.

Ear Reconstruction
Chapter
7 
1. Embryology (see Figure 7.1)
• The 6 branchial arches: At the 4th week of gestation,
develop within the walls of the anterior foregut with
subsequent branchial clefts/grooves (externally) and
pharyngeal pouches (internally)
• The ear arises from the 1st (mandibular) and 2nd (hyoid)
branchial arches, which are further defined by the
development of six hillocks, appearing during 6th week.
■ 1st arch: Anterior hillocks (1 to 3) form tragus, root of
the helix, and superior helix; Meckel’s cartilage ossifies
to become malleus and incus.
■ 2nd arch: Posterior hillocks (4 to 6) form posterior helix,
antihelix, antitragus, and lobule; Reichert’s cartilage
ossifies to form stapes.
• The external acoustic meatus develops from the first
branchial groove.
• The middle ear and eustachian tube are formed from the
first pharyngeal pouch.
• The second, third, and fourth branchial grooves are
obliterated within the cervical sinus during the later stages
of development.
• The lymphatic drainage of the ear follows embryologic
development.
■ 1st arch structures drain to the parotid lymph nodes.
■ 2nd arch structures drain to cervical lymph nodes.
2. Anatomy
• The external ear: A three-tiered cartilaginous framework
with skin on its anterior surface
■ The complete ear includes the scapha, concha, helix,
antihelix, tragus, and lobule as shown in Figure 7.2.
Figure 7.1.  Stages in the development of the external ear. (From Carlson, B.M., 2009. Human Embryology and Developmental Biology, 4th ed. Mosby,
Philadelphia.)
3
2
1
4
5
6
3
2
1
6
5
4
3
2
1
6
5
4
A
B
C
D
E
Figure 7.2.  Anatomical structure of the ear. (Reprinted with permission
from Janis, J.E., Rohrich, R.J., Gutowski, K.A., 2005. Otoplasty. Plast. Reconstr.
Surg. 115 [4], 60e–72e.)
Crura of antihelix
Crus of helix
Anterior
incisure
Tubercle
of tragus
Tragus
External
meatus
Intertragal
incisure
Lobe
Antitragus
Posterior sulcus
Antihelix
Helix
Concha
Scapha
Tubercle
of helix
Triangular fossa

Ear Reconstruction
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7
• Blood supply: Primary supply to ear is via posterior
auricular artery; multiple perforators pierce cartilage to
supply anterior ear (see Figures 7.3 and 7.4).
■ The superficial temporal artery supplies only a small
portion of the auricle and the triangular fossa.
■ The occipital artery supplies minor contribution to
posterior ear.
Figure 7.3.  Vascular anatomy of the face and neck. (Reprinted from Drake, R.L., Vogl, A.W., Mitchell, A.V.M. [Eds.], 2015. Gray’s Anatomy for Students.
Elsevier, 835–1135.)
Zygomaticotemporal artery and vein
Zygomaticofacial artery and vein
Transverse facial artery and vein
Superficial temporal artery and vein
Posterior auricular vein
Posterior auricular artery
Occipital artery
Occipital vein
External jugular vein
External carotid artery
Internal jugular vein
Facial vein
Facial artery
Inferior labial
artery and vein
Superior labial
artery and vein
Lateral nasal
artery and vein
Angular artery and vein
Dorsal nasal artery and vein
Supratrochlear
artery and vein
Supraorbital artery and vein
Figure 7.4.  Perforating sites of the posterior auricular artery.
Left, Anterior surface; right, posterior surface. CaC, cavum
conchae; Cyc, cymba conchae; HR, helical root; Lb, earlobe;
PAA, posterior auricular artery; Tr, Triangular fossa. (Adapted from
Park, C., Lineaweaver, W.C., Rumly, T.O., et al., 1992. Plast. Reconstr. Surg. 90,
38–44.)
Lb
PAA
Lb
CaC
CaC
HR
HR
Cyc
Tr
Tr

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62
• Sensory innervation of the external ear
■ Great auricular nerve (C2, C3) ascends from Erb’s point,
6.5 cm below the level of the tragus on the midpoint of
the sternocleidomastoid (SCM) and travels just slightly
posterior to the external jugular vein (EJV)
○ Supplies sensory to lower half of ear (anterior and
posterior)
■ Auriculotemporal nerve (V3) ascends with superficial
temporal vessels.
○ Supplies the tragus and the anterior/superior portions
of auricle and external auditory canal
■ Lesser occipital nerve (C2, C3) emerges higher than the
greater auricular nerve (GAN) and travels along the
posterior border of SCM
○ Supplies the posterosuperior aspect of auricle
■ Arnold’s nerve (auricular branch of vagus; cranial nerve
10 [CN X]) travels along the ear canal.
○ Supplies the concha and posterior auditory canal
■ External ear block: Place a ring of local anesthetic
around the ear.
○ Exception: The concha and posterior auditory canal
are innervated by Arnold’s nerve (the auricular
branch of the vagus nerve (X), which travels along
the ear canal).
3. The normal ear (see Figures 7.5 and 7.6)
• 85% to 90% of normal ear development is largely complete
by 5 to 6 years of age, although the width of the ear and its
distance from the scalp will increase until 10 years of age.
The superior level of the ear is at the same height as the
lateral brow, whereas the inferior aspect of the ear is at the
same height as the nasal base.
• On frontal view, the helical rim should be seen more lateral
than the antihelical rim.
• The vertical axis of the ear is tilted posteriorly (when
relating the apex of the helix to the lobule) ~15 to 20
degrees, which roughly correlates with the angle of the
nasal dorsum.
• The vertical height of the ear is roughly equal to the
distance from the lateral orbital rim to the helical root at
the level of the brow.
• Ideal ear size
■ Male: 63 mm × 35 mm
■ Female: 59 mm × 32 mm
■ Width of ear is 55% of height.
• Normal helical rim-to-head measurements for each third
of the ear are 10 to 12 mm at the helical apex, 16 to 18 mm
at the midpoint, and 20 to 22 mm at the lobule.
• Projection of the helical rim is 1 to 2.5 cm from the
mastoid skin, with a normal scapha-conchal angle of 90
degrees and a normal auriculocephalic (AC) angle of 20 to
30 degrees.
■ Projection >20 mm or 45 degrees corresponds to a
prominent ear.
Figure 7.5.  Anatomical relationships of the normal ear. (Reprinted
with permission from Bauer, B.S., 1998. Congenital anomalies of the ear. In:
Bentz, M.L. [Ed.], Pediatric Plastic Surgery. Appleton & Lange, Stamford,
359–392.)
8°
37°
.10
.5
.5
.23
.43
.33
15°–20°
Figure 7.6.  Proportional analyses of an ideal auricle, as described
by Tolleth. (Reprinted from Guyuron, B., Eriksson, E., Persing, J.A., et al. [Eds.],
2009. Plastic Surgery: Indications and Practice, 1st ed. Elsevier, 671–699.)
33%
20˚
8˚
37˚
10%
43%
23%
A
50%
50%
55%
B

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7
4. Prominent ear
• Increased conchoscaphal angle, deepened conchal bowl,
and prominent lobule
• The superior and middle thirds of the ear are most likely to
be affected.
■ The most likely cause of a prominent superior third:
Absence or effacement of the superior crus of the
antihelix.
○ The conchoscaphal angle is >90 degrees and the helix
is positioned >12 to 15 mm from the temporal region.
○ The cephaloauricular angle is also increased and
typically measures >25 degrees.
■ Prominence of the middle third of the ear is most likely
caused by hypertrophy of the concha cavum.
○ The concha cavum has a depth of >1.5 cm.
○ The middle third of the ear is located >16 to 18 mm
from the mastoid region.
• Various corrective methods have been described, including
rasping of the anterior surface of the antihelix (Stenstrom),
placement of retention sutures to recreate the antihelical
fold (Mustarde), conchal bowl resection, and suturing of
the conchal bowl to the mastoid fascia (Furnas).
• At birth, the neonate’s ears are soft and pliable, which
makes molding therapy of ear deformities more successful.
■ Due to maternal estrogen, which increases cartilage
content of hyaluronic acid
■ After 6 weeks, infant’s estrogen levels begin to fall and
ears become less malleable. Breastfed babies have higher
levels of estrogen for a longer time; thus, their ears may
be moldable for a longer period.
■ Molding is most effective in infants <3 months.
■ Custom-made mold can be fashioned out of soft putty
and affixed into the ear with surgical tape or Steri-Strips.
○ Depending on severity, molding can be continued for
several weeks to a few months.
• The top two causes of prominent ears are (1) inadequate
formation of the antihelical fold and (2) conchal
hypertrophy.
■ An antihelical fold can be created by a posterior
approach and suturing techniques.
■ Conchal reduction can be performed via an anterior
approach (reduction of skin and cartilage) or a posterior
approach (reduction of cartilage only).
• Surgical repair of deformational or prominent ears are
reserved for older children with residual deformities.
5. Ear deformations/congenital malformations
• Lop ear/cup ear/constricted ear (see Figure 7.7)
■ Deformity that involves a constricted helical rim with
the superior portion of the helix often folding over the
scapha
■ Acquired in utero and related to softened cartilage of the
upper helix from circulating maternal estrogens. This
cartilage lacks sufficient stiffness to support the upper
helix.
○ Infants: Respond to shaping with a molding splint
formed to match the normal helix
○ Recurrent or older child: Cartilage rasping or surgical
options work, including detaching the helix from the
scapha and resuturing it to the scapha at a proper
angle (see Figure 7.8).
Figure 7.7.  Moderately constricted ear. (Reprinted from Brent, B., 1980.
The correction of microtia with autogenous cartilage grafts. II. Atypical and
complex deformities. Plast. Reconstr. Surg. 66, 13.)
• Cryptotia
■ An adherence of the superior portion of the helix to the
temporal skin with varying degrees of severity.
■ In some cases, the helix can be “pulled” out to normal
position.
○ Surgical correction involves release of this abnormal
connection and frequently requires skin grafting, or
posterior auricular flaps, depending on the severity of
the deformity (see Figure 7.9).
• Stahl’s ear
■ A hereditary auricular deformity caused by an abnormal
cartilaginous pleat that extends from the crus antihelix
to the edge of the helix, deforming the regular curvature
of the ear
■ Primarily includes a “third antihelical crus”
○ One method of treatment is wedge excision of the
third crus (see Figure 7.10).
• Microtia (see Figure 7.11)
■ Congenital malformation with abnormal/rudimentary
development and/or absence of ear structures
○ Occurs in 1 in 7000 births; more males than females;
more in right ear than left; highest incidence in
Asian/Hispanics; 15% family history (hx)
50% associated with other craniofacial (CF)
syndromes/disorders involving 1st or 2nd
branchial arch
◆ Orbital auricular vertebral syndrome (Goldenhar)
◆ CF microsomia
◆ Tessier 7 cleft
◆ Treacher Collins syndrome (more common)
○ Inner ear not typically involved (not derived from
1st/2nd branchial arch)

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64
■ In children, treatment is frequently performed with
autologous cartilage grafts when the patient is 6 to 7
years of age (sufficient cartilage present for adequate
reconstruction; Nagata technique waits until 10 years of
age or chest circumference of 60 cm).
■ Reconstruction is not an option for infants or younger
children, although surgery to place bone-conduction
hearing aids will improve hearing on the affected side
and can be placed at 6 to 12 months of age.
■ In patients with unilateral microtia, creation of an ear
canal or insertion of bone-anchored hearing aids
(BAHAs) should be delayed until after ear reconstruction
Figure 7.8.  Neonate with lop ear. (Reprinted from Tan, S.T., Abramson, D.L., MacDonald, D.M., et al., 1997. Molding therapy for infants with deformational
auricular anomalies. Ann. Plast. Surg. 38, 263.)
B
C
A
Figure 7.10.  Correction of Stahl’s ear. (Redrawn from Kaplan, H.M.,
Hudson, D.A., 1999. A novel surgical method of repair for Stahl’s ear: a case
report and review of current treatment modalities. Plast. Reconstr. Surg. 103,
566–569.)
B
A
C
D
Figure 7.9.  Cryptotia. (Reprinted from Neligan, P.C., 2013. Plastic Surgery.
Elsevier, 187–225.)

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65
7
6. Total auricular reconstruction
• Goal: Restore the cosmesis of the auricle and the function
of the superior helical rim to provide support for
eyeglasses
■ The most difficult problem in elderly patients:
Fabrication of cartilage framework from calcified and
extremely brittle costal cartilage; therefore, prosthetics or
osseointegration (OI) is probably best.
■ In younger patients, the major difficulty is attainment of
sufficient skin surface area to cover the fabricated
cartilage frame without resorting to skin grafts.
• Autogenous reconstruction most often requires 2 to 4
stages. If perichondrium is kept intact, construct should
grow with child.
■ Stage 1: Creation of a cartilage framework and placement
under vascularized tissue (usually temporoparietal fascia
[TPF] if lack posterior auricular skin)
■ Stage 2: Elevation of the framework
■ Stage 3: Lobule transposition
■ Stage 4: Conchal excavation (see Figures 7.12 and 7.13)
• Medpor (porous polyethylene)/prosthetic reconstruction
■ Rate of extrusion can be reduced with TPF flap
coverage.
■ Can have some soft-tissue incorporation/ingrowth.
○ Small areas of exposure/extrusion can be treated
initially with dressing changes and topicals.
○ Contraindicated in infected wound beds or areas
without adequate soft-tissue coverage
• Autogenous versus prosthetic techniques
■ Pediatric microtia patients: Autogenous reconstruction
■ Traumatic or ablative defects in adults: Prosthetic
reconstruction
■ Patients with severe soft-tissue hypoplasia, low or
unfavorable hairline, and failed autogenous
reconstruction: Prosthetic reconstruction
• Indications for osseointegrated implants: Major cancer
extirpation, poor local tissue, absence of the lower half of
the ear, salvage following unsuccessful surgery, and
poor-operative-risk patients (see Figure 7.14)
7. Traumatic reconstruction
• Upper third: Defects of helix/antihelix
■ In an older patient, a partial middle ear defect can be
treated by wedge resection and direct closure.
○ In a younger patient, the cupping of the ear resulting
from this approach would be esthetically
unacceptable; therefore, a more complete
reconstruction is required.
■ Partial-thickness injuries involving the upper third
of the ear with exposed perichondrium are best
approached with conservative debridement and topical
treatment to prevent dessication until devitalized tissues
demarcate.
• Postoperative management is imperative in total auricular
reconstruction.
■ Skin coaptation to the carved cartilage construct is best
provided by continuous closed suction drainage for the
first 5 postoperative days. The reported complication
rate is <1%.
■ The quantity and quality of drainage can be monitored,
and any potential hematoma should be removed before
it obscures the framework details.
■ Pressure dressings risk skin necrosis over the new
cartilage framework and are not preferred over closed
suction drainage.
■ If early cellulitis/infection is suspected, aggressive
incision and drainage, placement of irrigating drains,
and antibiotics are first-line therapies made in an
attempt to preserve the cartilage construct.
○ If fever and cellulitis do not improve quickly, the
construct must be removed.
(13 to 19 years of age) to minimize scarring and avoid
interference with reconstruction.
■ Alloplastic frameworks, such as porous polyethylene, can
be placed in younger patients. However, they have a
greater incidence of extrusion and infection.
Figure 7.11.  Lobule-type microtia. (Reprinted from Guyuron, B., Eriksson,
E., Persing, J.A., et al. [Eds.], 2009. Plastic Surgery: Indications and Practice,
1st ed. Elsevier, 671–699.)

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66
■ A full-thickness loss of rim, antihelical fold, and/or
variable amount of concha can be reconstructed only
with a flap.
○ The postauricular transposition skin flap is the best
solution for large defects (>2 to 2.5 cm).
◆ The flap is based at the edge of the hairline, and
the width of the flap is equal to that of the defect.
➔ After 10 days, the base of the flap is divided and
the remainder of the flap is used to resurface
the posterior part of the ear.
➔ The donor area, if small, will heal spontaneously
or a skin graft may be used.
Figure 7.12.  Rib cartilage harvest for ear framework fabrication. Note that the upper border of the sixth cartilage is preserved; this will
help prevent subsequent chest deformity as the child grows. The entire “floating cartilage” will be used to create the helix. To produce the
acute flexion necessary to form the helix, the cartilage is deliberately warped in a favorable direction by thinning it on its outer, convex
surface. The thinned helix is affixed to the main sculptural block with horizontal mattress sutures of 4-0 clear nylon; the knots are placed
on the framework’s undersurface. (Reprinted from Neligan, P.C. [Ed.], 2013. Plastic Surgery, 3rd ed. Elsevier, 187–225.)
Rim preserved
Bank
Figure 7.13.  Nagata three-dimensional framework for microtia
reconstruction. (Reprinted from Guyuron, B., Erikkson, E., Persing, J., et al.
[Eds.], 2009. Plastic Surgery: Indications and Practice. Elsevier, 671–699.)

Ear Reconstruction
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7
○ A rim-only defect <1.5 cm can be treated with a small
triangular kite flap or a rim advancement flap
(Antia-Buch; see Figure 7.15).
◆ Antia-Buch flap: A local chondrocutaneous flap
that uses tissue from the helical rim based on the
postauricular skin to reconstruct the helical margin
Figure 7.14.  Osseointegrated implants with ear prosthesis. (Courtesy Gregory G. Gion, M.M.S, C.C.A.)
A
B
C

Ear Reconstruction
68
○ The postauricular revolving door island flap is ideal
for defects of the conchal area.
◆ Design: Partially on posterior ear and partially on
the mastoid area
➔ A skin incision is made around the island and
the flap is raised posteriorly and anteriorly.
➔ The skin is incised through the anterior surface
of the ear, and the posterior skin elevation stops
at the ear/mastoid groove.
Figure 7.15.  Antia-Buch advancement flap. A, A 1.5-cm defect and proposed incisions. B, The two segments of the helical rim are
advanced. C, Final result with an overall reduction in size of the ear. (Modified from Thorne, C.H., 2006. The external ear. In: McCarthy, J.G., Galiano,
R.D., Boutros, S.G. [Eds.], Current Therapy in Plastic Surgery. Elsevier, Philadelphia, 103.)
1.5cm
A
B
C
➔ This vertical attachment becomes the pedicle or
hinge of the flap.
➔ The posterior skin island can be rotated like a
revolving door into the interior conchal defect,
the conchal defect is reconstructed, and the
posterior defect is closed primarily.
○ For larger/more complex lesions
◆ Geometric wedge resection (see Figure 7.16)
Figure 7.16.  Techniques for reducing the auricular circumference and decreasing tension at the suture line in primary closure of helical
defects of the upper or middle thirds. A-F, Various patterns of excision. (Modified from Converse, J.M. [Ed.], 1977. Reconstructive Plastic Surgery, 2nd
ed. WB Saunders, 1671–1719.)
A
B
C
D
E
F

Ear Reconstruction
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7
Figure 7.17.  Repair of posterosuperior auricular defect by the tunnel procedure of Converse. (Reprinted from Converse, J.M., 1958. Reconstruction
of the auricle. Plast. Reconstr. Surg. 22, 150–230.)
A
B
C
D
E
F
G
H
I
J
◆ Cartilage graft with posterior auricular tunnel
procedure of Converse (see Figure 7.17).
◆ Orticochea chondrocutaneous flap: A full-
thickness incision is made outlining the entire
Figure 7.18.  Orticochea procedure of conchal rotation for the repair of upper- and middle-third auricular defects. (Adapted from Ha, R.Y., Trovato,
M.J. Plastic Surgery of the Ear, Selected Readings in Plastic Surgery, 11 [R3], 2013.)
C
B
A
concha. The flap is pedicled off of the helical rim,
which must be at least 1 cm wide. The flap is
rotated to fill the defect and the donor site is
closed primarily (see Figure 7.18).

Ear Reconstruction
70
Figure 7.19.  Dieffenbach’s technique for reconstruction of the middle third of the auricle, drawn from his description (1829-1834). (A) The
defect and outline of the flap. (B) The flap advanced over the defect. (C,D) In a second stage, the base of the flap is divided and the flap
is folded around the posteromedial aspect of the auricle. A skin graft covers the scalp donor site. (Reprinted from Neligan, P.C., 2013. Plastic
Surgery, 3rd ed. Elsevier, 187–225.)
Graft
A
B
C
D
• Middle-third defects
■ Many of the same techniques described above, including
wedge excision and Antia-Buch flaps, can be used for
small defects.
Figure 7.20.  Repair of a defect of the middle third of the auricle: The tunnel procedure. (A) Carved costal cartilage graft. (B) The defect.
(C) Incisions through the margins of the defect. (D) Incisions through the edge of the defect are extended backward through the skin of the
mastoid area. (E) The skin of the mastoid area is undermined between the two incisions. (F) The medial edge of the incision at the border
of the auricular defect is sutured to the edge of the postauricular incision. A similar type of suture is placed at the lower edge of the
defect. (G) The cartilage graft is placed under the skin of the mastoid area and anchored to the auricular cartilage with sutures. (H) Suture
of the skin incision. (Reprinted from Converse, J.M., 1958. Reconstruction of the auricle. Plast. Reconstr. Surg. 22, 150–230. Copyright © 1958, The Williams &
Wilkins Company, Baltimore.)
A
E
F
G
H
B
C
D
■ For larger composite defects involving variable portions
of the antihelix and concha, a conchal cartilage or rib
graft with retroauricular skin flap coverage is useful
(see Figures 7.19 and 7.20).

Ear Reconstruction
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7
• Lower-third defects
■ Involve the lobule only, which is a skin-only
reconstruction (see Figure 7.21)
○ Reconstructive plan depends on size of defect
○ Wedge excision and closure
○ Staged reconstruction with septal cartilage
○ Multiflap techniques
Figure 7.21.  Reconstruction of the earlobe. A, The curved line abc outlines the proposed earlobe as measured on the unaffected
contralateral auricle. A vertical flap is outlined; line bd is equal in length to line ab, and cd is equal to ca. B, Incisions are made through
the outlined skin and subcutaneous tissue. C, The vertical flap is raised from the underlying tissue as far upward as the horizontal line ac,
and the apex of the flap is sutured to point a. D, The operation completed. (Modified from Alanis, S.Z., 1970. A new method for earlobe reconstruction.
Plast. Reconstr. Surg. 45, 254.)
A
B
C
D
8. Ear replantation
• Microsurgical ear replantation provides best esthetic result
in select cases of ear amputation.
■ Venous congestion occurs to some extent in nearly every
case and is the most common cause of postreplantation
complications.
■ There have been several case reports of successful ear
replantation without a venous anastomosis, although
venous anastomosis is recommended whenever possible.
○ Postoperative congestion can be managed with leech
therapy for vascular compromise.
○ Arterial compromise demands reexploration, whereas
venous compromise can be managed nonoperatively.
• Because the large arteries to the ear enter on the posterior
aspect, anastomosis is most appropriate on the posterior
surface (recipient vessels include branches of the external
carotid artery, the anterior auricular branch of the
superficial temporal artery, and a branch of the occipital
artery).
• Despite reports of banking amputated cartilage pieces in
abdomen and/or forearm, later retrieval often yields
warped cartilage that has lost its strength.
■ Because of these disadvantages, microvascular
replantation should be used, when possible, to give the
best chance for preserving the native auricular
architecture.
9. Complications of otoplasty/ear reconstruction/trauma
• The most common complication is recurrence
• Persistent prominence of the lobule after otoplasty results
from inadequate cavum concham reduction before Furnas
suture placement in cases with significant conchal
hypertophy.
• Pinned-back appearance results from overtightening of
scapha-mastoid sutures.
• Auricular chondritis and perichondritis: A serious surgical
infection requiring immediate surgical intervention as the
primary course of treatment in traumatic cases
■ Culture swabs will guide antibiotic therapy.
■ Chondritis complicating elective otoplasty: Intravenous
antibiotics, removing a few sutures to allow drainage/
insertion of irrigating drains
○ If no response, open incision and drainage (I&D),
remove all sutures, and plan for a delayed otoplasty.
• Hematoma can cause cauliflower ear deformity (fibrosis of
cartilage; see Figures 7.22 and 7.23).
■ Presents as severe, acute ear pain
■ Most appropriate management is complete evacuation
via a small incision, with application of a bolster
dressing to prevent reaccumulation of the fluid or blood.
■ Resection of the posterior cartilage and sculpting of the
anterior cartilage is the treatment option for chronic
calcification or cauliflower ear deformity.

Ear Reconstruction
72
10. Burned ear reconstruction
• Conchal transposition flap (orticochea) has minimal donor
site morbidity, low complication rate, and can allow
eyeglass wear.
■ Auricular osteointegrated prostheses have a high
complication rate in burn patients.
■ Silastic prostheses with temporoparietal flap coverage
have very high exposure and infection rates.
11. Chondrodermatitis nodularis helicis (see Figure 7.24)
• A benign condition commonly found in older men often
associated with trauma from sleeping. It begins as an area
of cartilage inflammation and then ulcerates through the
skin. On exam, patient presents with a painful, scabby area
with a central crater.
■ Treatment is excision of the cartilage and closure of the
skin.
■ Can mimic a skin cancer on physical examination
■ Recurrence rate is high.
○ Preventive measures to decrease the recurrence rate
include avoidance of sleeping on the affected ear.
Figure 7.22.  An auricular hematoma. (Reprinted from Neligan, P.C.,
Plastic Surgery, 3rd ed., 23–48.)
Figure 7.23.  After evacuation of an auricular hematoma. (Reprinted
from Neligan, P.C., Plastic Surgery, 3rd ed. 23–48.)
Figure 7.24.  This firm nodule with a central crater is seen on the
antihelix of an elderly woman with chondrodermatitis nodularis
helicis; antihelical lesions are more common in women. (Reprinted
from Thompson, L.D.R., Goldblum, J.R. [Eds.], 2013. Head and Neck Pathology,
2nd ed. Elsevier, 399–420. Courtesy Dr. S.A. Norton.)
12. Auricular composite grafts
• Unlike skin grafts, composite grafts only interface with the
recipient bed along their perimeter; therefore, graft size
should be no larger than 1.5 cm in diameter, so the center
of the graft is never more than 5 to 8 mm from a blood
supply.
• The clinical appearance of a healing composite graft
follows a reproducible pattern.
■ 6 to 8 hours: Very white
■ 8 to 24 hours: Slight pink tinge signaling
revascularization
■ 24 hours to 1 week: Cyanosis 2/2 venous congestion
■ After 1 week: Graft ultimately becomes pink and then
redder as revascularization intensifies.
■ 6 months to 1 year: Redness will fade, and the tissue
acquires its final tone.
○ A lingering whitish area in the center of a cyanotic
graft most likely represents impending necrosis.
◆ However, even if eschar develops, it should not be
debrided.
➔ Removing the eschar may dislodge the surviving
portion of the graft and also places it at
increased risk for infection.
➔ Observation is the most prudent initial step in
management.

Ear Reconstruction
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7
• Postoperative cooling is recommended to decrease the
metabolic rate of the grafted tissue until secondary
revascularization has taken place.
13. Otoplasty
• Commonly calls for a combination of procedures
■ Create an antihelical fold.
○ Stenstrom cartilage abrasion
◆ Partial-thickness scoring, scratching, or abraiding
of anterior surface of antihelix causing cartilage to
bend away from the scoring (relieves internal
stress)
○ Mustarde sutures
◆ Mattress sutures on posterior aspect of ear
cartilage to create an antihelical fold (see
Figure 7.25)
■ To reduce conchal hypertrophy: Cartilage reduction
■ To reduce conchal bowl projection: Furnas sutures
(see Figure 7.26)
○ Only method known for placement of conchomastoid
sutures
○ Designed to correct ears with deep conchae (>2.5 cm)
○ Mattress sutures from conchal cartilage to mastoid
periosteum
Figure 7.25.  Placement of Mustarde sutures. (Reprinted with
permission from Janis, J.E., Rohrich, R.J., Gutowski, K.A., 2005. Otoplasty. Plast.
Reconstr. Surg. 115 [4], 60e–72e.)
Fossa triangularis
Concha
Scapha
Figure 7.26.  Placement of Furnas conchomastoid sutures. Note that suture placement too close to the external auditory canal can
constrict the canal (far right). (Reprinted with permission from Janis, J.E., Rohrich, R.J., Gutowski, K.A., 2005. Otoplasty. Plast. Reconstr. Surg. 115 [4],
60e–72e.)
A
B
C
14. Cleft lobe repair (see Figure 7.27)
• Extremely common, usually a traumatic etiology (pulling)
or slow stretch over time (may be caused by heavy
earrings)
• Many techniques including straight line wedge excision
and layered closure versus incorporation of Z plasty
• Refrain from repiercing until 6 weeks (if remote from scar
line) or 12 weeks (if within scar line)
■ Alternatively, techniques have been described for repair
and preservation of a perforation for an earring.
• Key is approximation of lower lobule skin to prevent
notching (most common complaint)

Ear Reconstruction
74
Figure 7.27.  Repair of an earlobe cleft with preservation of the perforation for an earring. A, A flap is prepared by a parallel incision on
one side of the cleft; the other side is “freshened” by excision of the margin. B, The flap is rolled in to provide a lining for preservation
of the earring track. C, Closure is completed; a small Z plasty may be incorporated. (Modified from Pardue, A.M., 1973. Repair of torn earlobe with
preservation of the perforation for an earring. Plast. Reconstr. Surg. 51, 472.)
A
B
C
Suggested Readings
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M.L. (Ed.), Pediatric Plastic Surgery. Appleton & Lange, Stamford, CT, pp.
359–392.
Beahm, E.K., Walton, R.L., 2002. Auricular reconstruction for microtia: part I.
Anatomy, embryology, and clinical evaluation. Plast. Reconstr. Surg. 109,
2473–2482.
Brent, B., 2002. Microtia repair with rib cartilage grafts: a review of personal
experience with 1000 cases. Clin. Plast. Surg. 29 (2), 257–271, vii.
Brent, B., 1999. Technical advances in ear reconstruction with autogenous rib
cartilage grafts: personal experience with 1200 cases. Plast. Reconstr. Surg.
104, 319–334.
Brent, B.D., 2013. Reconstruction of the ear. In: Neligan, P.C. (Ed.), Plastic
Surgery, 3rd ed. Elsevier, pp. 187–225.
Byrd, H.S., Langevin, C.J., Ghidoni, L.A., 2010. Ear molding in newborn
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Cho, B.H., Ahn, H.B., 1999. Microsurgical replantation of an ear, with leech
therapy. Ann. Plast. Surg. 43, 427–429.
Dancey, A., Jeynes, P., Nishikawa, H., 2005. Acrylic ear splints for treatment
of cryptotia. Plast. Reconstr. Surg. 115 (7), 2150–2152.
Donelan, M.B., 1989. Conchal transposition flap for postburn ear deformities.
Plast. Reconstr. Surg. 83, 641–654.
Elsahy, N.I., 2002. Acquired ear defects. Clin. Plast. Surg. 29, 175–186.
Elsahy, N.I., 2002. Reconstruction of the ear after skin and cartilage loss. Clin.
Plast. Surg. 29, 201–212.
Eppley, B.L., 1999. Alloplastic implantation. Plast. Reconstr. Surg. 104, 1761.
Furnas, D.W., 2002. Otoplasty for prominent ears. Clin. Plast. Surg. 29 (2),
273–288, viii.
Furnas, D.W., 2000. Otoplasty for protruding ears, cryptotia, or Stahl’s ear. In:
Evans, G.R.D. (Ed.), Operative Plastic Surgery. McGraw-Hill, New York, pp.
417–448.
Ha, R.Y., Trovato, M.J., 2013. Plastic surgery of the ear. In: Selected Readings
in Plastic Surgery, vol. 11. (R3), pp. 1–52.
Hackney, F.L., 2001. Plastic surgery of the ear. In: Selected Readings in Plastic
Surgery, vol. 9. pp. 1–26.
Jackson, I.T., 2002. Ear reconstruction. In: Jackson, I.T. (Ed.), Local Flaps in
Head and Neck Reconstruction. Quality Medical Publishing, St. Louis,
pp. 251–271.
Janis, J.E., Rohrich, R.J., Gutowski, K.A., 2005. Otoplasty. Plast. Reconstr.
Surg. 115 (4), 60e–72e.
Janz, B.A., Cole, P., Hollier, L.H. Jr., et al., 2009. Treatment of prominent and
constricted ear anomalies. Plast. Reconstr. Surg. 124 (1 Suppl.), 27e–37e.
Kind, G.M., 2002. Microvascular ear replantation. Clin. Plast. Surg. 29,
233–248.
Nagata, S., 2000. Microtia: auricular reconstruction. In: Achauer, B.M.,
Eriksson, E., Guyuron, B., et al. (Eds.), Plastic Surgery: Indications, Operations
and Outcomes. Mosby, St. Louis, pp. 1023–1056.
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auricle: parts I-IV. Plast. Reconstr. Surg. 93 (2), 221–266.
Park, C., Lew, D.H., Yoo, W.M., 1999. An analysis of 123 temporoparietal
fascial flaps: anatomic and clinical considerations in total auricular
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Plast. Reconstr. Aesthet. Surg. 62 (6), 727–736.
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Plastic Surgery, 5th ed. Lippincott & Raven, Philadelphia, pp. 141–148.

SECTION 2: Breast
Breast Anatomy, Embryology,
and Congenital Defects
Chapter
8 
1. Breast embryology/development
• Embryologic development
■ Ectodermal breast bud develops during the 5th to 6th
week of gestation.
■ Ectodermal thickening from the axilla to the pelvis
forms the milk line or “milk streak” (see Figure 8.1)
○ Most of this atrophies by the 9th week except in the
pectoral region, which forms the mammary ridge.
Figure 8.1.  The milk lines. (Reprinted with permission from Standring, S.
[Ed.], 2008. Gray’s Anatomy, 40th ed. Churchill Livingstone, London, 1712.)
■ Basal cells within the mammary ridge proliferate to form
the nipple bud during the 9th week of gestation.
■ Mammary ducts and lobular buds are formed by the
12th week of gestation.
■ The lactiferous ducts form by 16 to 24 weeks.
2. Breast anatomy (see Figures 8.2 and 8.3)
• General
■ Coopers suspensory ligaments support the breast
parenchyma.
○ Attenuation of these ligaments leads to breast ptosis.
■ Breast lobule
■ Up to 50% of the breast is fat.
■ Lymphatic drainage occurs via the axillary and
parasternal nodes.
Figure 8.2.  Tangential and sagittal view of the breast. The breast
lies in the superficial fascia just deep to the dermis, attached to
the skin by the suspensory ligaments of Cooper. The retromammary
bursa separates it from the investing fascia of the pectoralis major
muscle. Cooper’s ligaments form fibrosepta in the stroma that
provide support for the breast parenchyma. From 15 to 20
lactiferous ducts extend from lobules comprised of glandular
epithelium to openings located on the nipple. Subcutaneous fat
and tissue are distributed around the lobules of the gland and
account for much of its mass. (Reprinted from Copeland, E.M. III, Bland,
K.I., 2004. The Breast, 4th ed. WB Saunders, Philadelphia, 21–38.)
Pectoralis major muscle
Pectoralis major fascia
Intercostal muscles
Parietal pleura
Visceral pleura
Stroma
Cooper's ligament
Lactiferous sinus
Lactiferous duct
Retromammary bursa
Lobule of gland
Internal mammary lymph nodes
Lymphatic vessels
Subcutaneous
fatty tissue

Breast Anatomy, Embryology, and Congenital Defects
76
• Sensory innervation
■ Multiple contributions from cutaneous nerves
■ Sensitivity decreased with increased age, breast size/
volume, and breast ptosis
○ Superior pole: Supraclavicular branches of the
cervical plexus
◆ Most sensitive area to light pressure
○ Lateral breast: Anterior rami of lateral cutaneous
branches of 3rd to 6th intercostal n.
○ Medial breast: Anterior cutaneous branches of 2nd to
6th intercostal n.
○ NAC
◆ Dominant innervation: Lateral cutaneous branch
of 4th intercostal n. (T4)
➔ Danger zone: Nerves perforate the fascia just
lateral to the pectoralis major m. border
through interdigitation of the serratus anterior
muscle.
 Blunt dissection recommended in this region
to reduce the risk for nerve injury and NAC
sensory disturbance.
◆ Also contributions from 5th lateral cutaneous n.
and 3rd to 4th medial cutaneous n.
➔ Dominant innervation with medially based
pedicles is T3-T4 intercostal n.
◆ NAC most sensitive to vibration (areola) and least
sensitive to light pressure (nipple).
• Arterial supply of the breast (see Figures 8.4-8.6)
■ Dominant supply via the 2nd and 3rd internal mammary
artery (IMA) perforators
○ Nipple-areolar complex (NAC): Perforators from the
two IMA vessels
○ Superior/superomedial pedicle: 2nd and 3rd
intercostal IMA perforators
○ Medial pedicle: 3rd intercostal IMA perforators
○ Inferior pedicle: Intercostal a. perforators
○ Central mound pedicle
■ Other sources: Perforators from intercostal
arteries, lateral thoracic a., thoracodorsal a., and
thoracoacromial a.
Figure 8.3.  Statistical standards for the dimensions of the breast.
(Reprinted from Neligan, P.C. [Ed.], 2013. Plastic Surgery, 3rd ed. Elsevier,
1–12.)
19 to 21 cm
19 to 21 cm
19 to 21 cm
5 to 6 cm
5 to 6 cm
9 to
11 cm
2 cm
Figure 8.4.  Blood supply to the breast. (Reprinted from Neligan, P.C.
[Ed.], 2013. Plastic Surgery, 3rd ed. Elsevier, 1–12.)
Lateral intercostal
perforator
Intercostal
artery
Lateral thoracic artery
Internal mammary
artery
Anterior intercostal perforator
Figure 8.5.  Blood supply to the breast; cross-sectional view.
(Reprinted from Neligan, P.C. [Ed.], 2013. Plastic Surgery, 3rd ed. Elsevier,
1–12.)
Lateral thoracic artery
Thoracodorsal
artery
Anteromedial intercostal perforators
Anterolateral intercostal
perforators
Internal mammary
perforators

Breast Anatomy, Embryology, and Congenital Defects
77
8
• Innervation of the pectoralis m.
■ Medial pectoral nerve
○ From medial cord of brachial plexus and innervates
lateral and inferior portion of pectoralis major (after
passing up through pectoralis minor)
■ Lateral pectoral nerve: From lateral cord of brachial
plexus and innervates the medial and superior portions
of pectoralis major
• Pubertal development (see Figure 8.7)
■ Tanner stages
○ Stage I: No breast development or pubic hair
○ Stage II: Onset of breast development (thelarche);
pubic hair appears.
◆ Darkening and widening of the areola
◆ Areola forms a mound that is elevated from the
underlying palpable breast bud.
Figure 8.6.  Comprehensive breast anatomy. (Reprinted from Drake, R.L., Vogl, A.W., Mitchell, A.V.M. [Eds.], 2015. Gray’s Atlas of Anatomy. Elsevier, 61–131.)
Internal thoracic artery
Pectoral branch of
thoracoacromial artery
Axillary artery
Lateral thoracic artery
Pectoralis major
Axillary process
2nd thoracic
intercostal nerve
4th thoracic
intercostal nerve
6th thoracic intercostal nerve
Areola
Arteries and innervation of breast
Mammary branches of
internal thoracic artery
Lymphatic drainage of breast
Parasternal nodes
Drains into abdominal
lymphatics
Drains to opposite side
Pectoral axillary nodes
Subscapular axillary
nodes
Lateral axillary
nodes
Central axillary nodes
Apical axillary nodes
Left subclavian (lymphatic) trunk
Left parasternal lymphatic vessel
○ Stage III: Breast bud enlarges beyond areola; darker,
coarser, and wider distribution of pubic hair
○ Stage IV: Areola/nipple for a secondary mound
projecting above the underlying breast mound;
adult-like pubic hair sparing the medial thighs
○ Stage V: Recession of secondary mound to create a
mature adult breast with projection of the nipple;
adult-like pubic hair
■ Menarche can begin at Tanner stages II-V
■ Benign premature thelarche: Breast development before
pubic hair development or menarche

Breast Anatomy, Embryology, and Congenital Defects
78
3. Congenital breast/chest wall abnormalities
• Amastia
■ Absence of glandular tissue and the nipple
• Amazia
■ Absence of the glandular tissue only
■ Can result from surgical removal of the breast bud,
radiation, or congenital absence (e.g., Jeune syndrome)
• Athelia
■ Absence of the nipple only
• Ectopic breast tissue
■ Breast tissue found outside of the milk line
○ For example, scalp, ear, back, shoulder, epigastrium,
and posterior thigh
• Accessory breast tissue (polymastia)
■ Extra breast tissue found along the milk line
(polymastia)
○ Most localized to the chest region, although may also
involve the axilla, groin, vulva, and medial thigh
○ Can cause pain, restrict arm movement, affect
cosmesis, and develop malignancy
■ Treatment recommendation is for surgical removal.
• Polythelia
■ Extra nipple tissue due to failure of complete regression
of the milk line
• Tuberous breast deformity (see Figure 8.8)
■ Classic signs: Narrowed breast base, high and constricted
inframammary fold (IMF), hypertrophy, and herniation
of the NAC
■ Treatment recommendation is augmentation with radial
gland scoring and areola reduction.
Figure 8.7.  Stages of breast development at puberty. A, Breast
bud elevation; B, growth and protrusion of the nipple; C, elevation
of the secondary areolar mound; D, regression of the areolar
mound to the level of the general breast contour. (Reprinted from
Mansel, R.E., Webster, D.J.T., Sweetland, H.M., et al. [Eds.], 2009. Hughes,
Mansel, & Webster’s Benign Disorders and Diseases of the Breast, 3rd ed.
Elsevier, 25–40.)
A
B
C
D
Figure 8.8.  Preoperative appearance of a 19-year-old woman with
a fully developed “classic” tuberous breast deformity. The breast
is hypoplastic in general and whatever parenchyma is present is
located mainly under the NAC. There does not appear to be normal
peripheral expansion of the breast mound. As a result, growth of
the constricted breast bud projects through the elastic areolar skin,
creating an areolar “pseudoherniation.” Along with this is seen
a concomitant enlargement of the areolar diameter. As a result
of the failure of the breast bud to expand peripherally, the
surrounding breast skin remains tight and the IMF that does form
is malpositioned superiorly. (Reprinted from Hammond, D.C. [Ed.], 2009.
Atlas of Aesthetic Breast Surgery. Elsevier, 183–194.)
A
B
• Juvenile breast hypertrophy
■ Severe diffuse breast enlargement (unilateral or bilateral)
without mass or nodularity
■ Occurs early in puberty and rarely regresses
spontaneously
○ Etiology: Abnormal end-organ responsiveness to
estrogen, with normal levels of hormone and
hormone receptors
■ Treatment recommendation is observation until size has
stabilized (1 year or more), followed by reduction
mammaplasty
○ Reduction mammaplasty can be performed even if
patient is younger than 18 years of age.
• Fibroadenoma (see Figure 8.9)
■ Most common breast neoplasm in adolescent females
■ Differentiated from juvenile hypertrophy by presence of
palpable mass

Breast Anatomy, Embryology, and Congenital Defects
79
8
• Anterior thoracic hypoplasia
■ Anterior chest wall depression from posteriorly displaced
ribs
■ Hypoplasia of ipsilateral breast with a superiorly
displaced NAC and a normal sternum and pectoralis
major muscle
• Pectus excavatum
■ Most common congenital chest wall abnormality
■ A concave anterior chest wall defect from abnormal
formation of the ribs and sternum
■ Most commonly involves the lower third of the sternum
• Pectus carinatum
■ A convex or anteriorly projecting sternum and ribs
■ Often creates the appearance of a “pigeon’s chest”
• Poland syndrome (see Figure 8.10)
■ Often unilateral
■ Classic signs: Absence of the sternal head of the
pectoralis major, hypoplasia or aplasia of the breast or
nipple, deficiency of subcutaneous fat and axillary hair,
abnormalities of the rib cage, and upper extremity
anomalies
■ Complex presentations include hypoplasia or aplasia of
the chest wall musculature or total absence of the
anterolateral ribs with herniation of the lung.
Figure 8.9  Benign giant fibroadenoma of adolescence. Rapid
growth, vascularity, and pressure skin necrosis raised the question
of malignancy. (Reprinted from Mansel, R.E., Webster, D.J.T., Sweetland, H.M.,
et al., 2009. Hughes, Mansel, & Webster’s Benighn Disorders and Diseases of
the Breast, 3rd ed. Elsevier, 81–106.)
Figure 8.10.  A, A 17-year-old female patient with Poland syndrome. B, Custom silicone chest wall implant made from moulage. C, Chest
wall implant placed through inframammary incision. D, Breast implant placed in front of chest wall implant at separate stage. (Reprinted from
Neligan, P.C., 2013. Plastic Surgery, 3rd ed. Elsevier, 548–557.)
A
B
C
D
■ Classic signs of giant fibroadenoma: Rapid asymmetric
breast enlargement just after onset of puberty, with
prominent overlying veins, a palpable mass >5 cm in
size, and occasional pressure-induced skin ulceration
■ Treatment recommendation is enucleation using
reduction mammoplasty techniques to obtain symmetry
with contralateral breast.

Breast Anatomy, Embryology, and Congenital Defects
80
4. Gynecomastia
• Abnormal benign enlargement of the male breast that
correlates with hormonal changes
■ Infancy: Secondary to circulating maternal estrogens
■ Adolescence: Secondary to transient increase of estradiol
at the onset of puberty
○ Reported to affect up to 65% of adolescent males
■ Increasing age: Results from decreased testosterone
production with age and increased peripheral conversion
of testosterone to estrogen
• Conditions associated with gynecomastia (see Box 8.1)
• Drugs associated with gynecomastia (see Box 8.2)
■ Reconstructive options include the insertion of
subcutaneous tissue expanders in young patients,
followed by latissimus flap reconstruction with
permanent implants once breast development is
completed.
• Sternal cleft
■ Failure of midline fusion of the sternum
■ Potential for the lack of protection to the heart and great
vessels
■ Not associated with aplasia or hypoplasia of the breast
Reprinted from Guyuron, B., Eriksson, E., Persing, J.A., et al. (Eds.), 2009. Plastic Surgery: Indications and Practice, 1st ed. Elsevier, 727–736.
BOX 8.1  ETIOLOGY OF GYNECOMASTIA
Physiologic
Neonatal period
Puberty
Advanced age
States of androgen deficiency
Hypogonadism
Primary
Klinefelter syndrome
Kallman syndrome
Congenital anorchia
Adrenocorticotropic hormone (ACTH) deficiency
Defects in synthesis of androgens
Secondary
Trauma
Orchitis
Cryptorchidism
Irradiation
Hydrocele
Spermatocele
Varicocele
Renal failure
Androgen insensitivity syndrome
States of estrogen excess
Testicular sources
Germ cell tumor
Choriocarcinoma
Seminoma
Teratoma
Non–germ cell tumor
Leydig cell tumor
Granulosa-theca tumor
Sertoli cell tumor
True hemaphroditism
Liver disease
Cirrhosis
Malnutrition
Protein deficiency
Fat deficiency
Infectious sources
Sparganum or plerocercoid larva of the tapeworm
Neoplastic
Breast carcinomas
Adrenal cortical carcinomas
Lung carcinomas
Liver carcinomas
Systemic diseases with idiopathic mechanisms
Non-neoplastic conditions of the lung
Trauma
Obesity
AIDS
Familial
Reprinted from Guyuron, B., Eriksson, E., Persing, J.A., et al. (Eds.), 2009. Plastic Surgery: Indications and Practice, 1st ed. Elsevier, 727–736.
BOX 8.2  PHARMACOLOGIC SOURCES OF GYNECOMASTIA
Estrogen-like activity
Estrogens
Heroin
Marijuana
Digitalis
Digoxin
Digitoxin
Anabolic steroids
Inhibit testosterone
Cimetidine
Ketoconazole
Phenytoin
Spironolactone
Antineoplastic agents
Diazepam
Cytoproterone
Flutamide
Gonadotropins
Human chorionic gonadotropin
Central nervous system agents
Phenothiazines
Amphetamines
Sympathetic modifiers
Idiopathic mechanisms
Reserpine
Theophylline
Verapamil
Tricyclic antidepressants
Fuorosemide
Methyldopa

Breast Anatomy, Embryology, and Congenital Defects
81
8
Figure 8.11.  Rohrich algorithm. CT, Computed tomography; DHEAS, dehydroepiandrosterone; FSH, follicle-stimulating hormone;
LH, luteinizing hormone; US, ultrasound. (Adapted from Rohrich, R.J., Ha, R.Y., Kenkel, J.M., et al., 2003. Classification and management of gynecomastia:
defining the role of ultrasound-assisted liposuction. Plast. Reconstr. Surg. 111, 909.)
Detailed patient history and physical exam
Negative history and normal
physical exam
Normal after workup
Persistent gynecomastia
>12 months
Surgical management
Observation
<12 months
Positive history
Abnormal physical exam
Drug history: Discontinue drug
Systemic disease: Correct underlying
disease
Klinefelter syndrome: Karyotype,
bilateral mastectomy
Prepubertal, bilateral disease:
Testicular ultrasound
Testicular mass: Testicular US; serum testosterone, LH,
estradiol, and DHEAS; urology and endocrine consultation
Thyroid mass: Thyroid function tests; endocrine consultation
Breast mass: Mammography, US, biopsy, surgical
oncology consultation
Hypogonadism: Serum LH/FSH, estradiol, testosterone,
and DHEAS + karyotype; +/– adrenal CT scan; endocrine
consultation
Abdominal masses/hepatomegaly: Liver function tests;
serum LH/FSH, estradiol, testosterone, and DHEAS; +/–
abdominal CT; endocrine consultation
• Diagnosis (see Figure 8.11)
■ Thorough history and physical examination
○ Testicular examination and/or ultrasound
◆ Especially in adolescents
○ Persistence of symptoms
■ Labs
○ Estrogen/androgen ratio
◆ Increased in testicular tumors, Klinefelter syndrome
○ Thyroid function tests
○ Luteinizing hormone (LH)/follicle-stimulating
hormone (FSH)
○ Karyotyping
◆ Klinefelter Syndrome
➔ Rare, XXY chromosomal abnormality
➔ Increased risk of breast cancer (elevated FSH,
LH, estrogen receptor [ER], progesterone
receptor [PR] and decreased testosterone)
➔ 50% to 65% of patients will develop
gynecomastia.
➔ Bilateral mastectomy may be recommended in
symptomatic patients.
• Classification: Based on degree of skin excess and glandular
excess
■ Simon’s classification (see Table 8.1)
Table 8.1  Classification of Gynecomastia
GRADE
BREAST ENLARGEMENT
SKIN EXCESS
I
Small
Absent
IIA
Moderate
Absent
IIB
Moderate
Present
III
Large
Present
Reprinted from Guyuron, B., Eriksson, E., Persing, J.A., et al. (Eds.),
2009. Plastic Surgery: Indications and Practice, 1st ed. Elsevier,
727–736.
• Treatment options include ultrasound-assisted liposuction,
traditional suction lipectomy, concentric circumareolar
resection, periareolar resection with adjunctive suction
lipectomy, and breast amputation with free nipple grafting.
■ Treatment reserved for symptoms present for >12
months.
■ For resection techniques, a Wise pattern reduction is not
recommended because it will produce a conical,
projecting breast.
■ The decision between liposuction and resection largely
depends on the degree of skin excess.
○ Liposuction for gynecomastia requires disruption of
the IMF for best results.
■ In severe gynecomastia with significant ptosis, skin
excision is often necessary. In these cases, the ideal
configuration and location of the male nipple is within
the 4th or 5th intercostal space, 3 cm in diameter, and
oval in shape.

Breast Anatomy, Embryology, and Congenital Defects
82
5. Galactorrhea
• Abnormal breast/nipple discharge
■ Rare in regularly menstruating women who have never
been pregnant; however, reportedly can occur in 25% of
women with prior pregnancies.
• Etiology
■ History of pregnancy
■ Hypothyroidism
■ Pituitary tumor (prolactinoma)
■ Medications: Tricyclic antidepressants, fluoxetine
• Diagnosis
■ Thorough history and physical examination
■ Labs
○ Prolactin
○ Thyroid function tests (hypothyroidism) and a
history of all medications, including tricyclic
antidepressants and fluoxetine
■ Imaging
○ Magnetic resonance imaging (MRI) of brain to rule
out a pituitary tumor in women with elevated
prolactin levels
• Treatment recommendations: Bromocriptine to suppress
prolactin secretion
Suggested Readings
Beer, G.M., Budi, S., Seifert, B., et al., 2001. Configuration and localization of
the nipple-areola complex in men. Plast. Reconstr. Surg. 108 (7), 1947–1952.
Berrino, P., Berrino, V., 2013. Chapter 23: Poland syndrome. In: Neligan, P.C.
(Ed.), Plastic Surgery, 3rd ed. Elsevier, pp. 548–557.
Cederna, P.S., 2009. Chapter 54: Gynecomastia. In: Guyuron, B., Eriksson, E.,
Persing, J.A., et al. (Eds.), Plastic Surgery: Indications and Practice, 1st ed.
Elsevier, pp. 727–736.
De La Torre, J., Davis, M.R., 2013. Chapter 1: Anatomy for plastic surgery of
the breast. In: Neligan, P.C. (Ed.), Plastic Surgery, 3rd ed. Elsevier, pp. 1–12.
Ferri, F.F., 2014. Gynecomastia. In: Ferri, F. (Ed.), Ferri’s Clinical Advisor
2014. Mosby, pp. 511.
Mansel, R.E., 2009. Chapter 3. In: Mansel, R.E., Webster, D.J.T., Sweetland,
H.M., et al. (Eds.), Hughes, Mansel, & Webster’s Benign Disorders and
Diseases of the Breast, 3rd ed. Elsevier, pp. 25–40.
Muti, E., 2013. Chapter 23: Congenital anomalies of the breast. In: Neligan,
P.C. (Ed.), Plastic Surgery, 3rd ed. Elsevier, pp. 521–547.
Rohrich, R.J., Ha, R.Y., Kenkel, J.M., et al., 2003. Classification and
management of gynecomastia: defining the role of ultrasound-assisted
liposuction. Plast. Reconstr. Surg. 111, 909.
Sabel, M.S., 2009. Chapter 1: Anatomy and physiology of the breast. In:
Sabel, M.S. (Ed.), Essentials of Breast Surgery: A Volume in the Surgical
Foundations Series, 1st ed. Mosby, pp. 1–17.
Weinzweig, J., 2010. Chapter 90: Chest wall reconstruction. In: Weinzweig, J.
(Ed.), Plastic Surgery Secrets Plus, 2nd ed. Mosby, pp. 587–593.

Breast Cancer and
Breast Reconstruction
Chapter
9 
1. Breast cancer epidemiology
• Most common noncutaneous malignancy among women
■ Affects 1 : 8 women
• Independent risk factors
■ Exposure to estrogen
○ Early age at menarche
○ Late menopause
○ First full-term pregnancy after 30 years of age (yo)
■ Personal history of breast cancer or benign proliferative
breast disease
■ BRCA mutation (occurs in <1% of women; accounts for
5% of breast cancers; 60% to 80% lifetime risk)
○ BRCA1 mutation associated with the following
malignancies: Breast (85%), ovarian (62%), male
breast, pancreatic, testicular, and early-onset prostate
cancers
○ BRCA2 associated with the following malignancies:
Breast (85%), ovarian (25%), male breast (7%),
pancreatic, and prostate cancers
■ Breast cancer in a first-degree relative
○ Age of affected <50 yo → Risk ratio (RR) 2.3
○ Age of affected >50 yo → RR 1.8
○ Bilateral breast cancer → RR 5.5
2. Breast cancer diagnosis
• Clinical breast exam
• Mammography
■ Radiographic imaging of the breast that is an excellent
screening tool for abnormal masses or calcifications
○ Linear or branching calcifications may suggest
malignancy.
○ Pleomorphic/granular calcifications may suggest
malignancy.
○ Popcorn-like calcifications suggest fibroadenoma.
○ Large rod-like calcifications suggest secretory ducts.
○ Round eggshell calcifications suggest oil cysts.
○ Dystrophic/coarse calcifications suggest fat necrosis.
◆ Calcifications can be found in ~25% of women
who have had inferior pedicle breast reductions.
■ Patients with implants may get mammograms; however,
they require a special view called the Eklund view, where
the prosthesis is pushed against the chest wall and the
breast parenchyma is pulled anteriorly around and away
from the implant.
○ Implant position, capsular contracture, and small
native breasts can compromise the reliability of
mammography.
◆ Implant size has not been shown to affect
mammography.
• Magnetic resonance imaging (MRI)
■ Newer tool for evaluating the breast for breast cancer
■ Especially useful for screening high-risk patients
■ May have high false-positive rate, resulting in increased
secondary procedures such as biopsy and mastectomy
• Ultrasound
■ Widely used as a diagnostic modality; often used as a
secondary study to work up a mass
■ Useful in women with dense breasts (i.e., younger
women)
■ Ultrasound findings can help differentiate between
malignant and benign lesions.
○ The following ultrasound findings suggest
malignancy: Spiculations, asymmetric mass,
calcifications, angular margins, hypoechoic lesion
with posterior shadowing, heterogenous
• Histologic diagnostic modalities
■ Core biopsy
○ Image guided
■ Fine-needle aspiration
○ Disadvantages
◆ Does not provide structural information to
determine invasive from in situ
◆ High false-negative rates from sampling error (2%
to 22%)
■ Excisional biopsy
○ Indications: Disagreement between mammography
and histology, atypical ductal hyperplasia on
percutaneous biopsy, radial scar on mammography,
or percutaneous biopsy
3. Breast cancer types
• Ductal carcinoma in situ (DCIS)
• Lobular carcinoma in situ (LCIS)
• Invasive ductal carcinoma (IDC)
• Invasive lobular carcinoma (ILC)

Breast Cancer and Breast Reconstruction
84
• Inflammatory breast carcinoma
■ Can often involve chest wall, requiring a modified
radical mastectomy with wide skin defect
○ Treatment options include a rectus abdominal
myocutaneous flap (preferred choice, especially if
breast reconstruction desired), latissimus (lat) flap
+/− split thickness skin graft, omental flap + split
thickness skin graft.
4. Breast cancer staging (see Tables 9.1 and 9.2)
Table 9.1  Staging of Breast Cancer: TNM System
Tumor Size: T (Largest Diameter)
TX
Primary tumor cannot be assessed
T0
No evidence of primary tumor
Tis
Carcinoma in situ
Tis (DCIS)
Ductal carcinoma in situ
Tis (LCIS)
Lobular carcinoma in situ
Tis (Paget’s)
Paget’s disease of the nipple not associated with invasive carcinoma and/or carcinoma in situ (DCIS and/or LCIS) in the
underlying breast parenchyma. Carcinomas in the breast parenchyma associated with Paget’s disease are categorized based
on the size and characteristics of the parenchymal disease, although the presence of Paget’s disease should still be noted.
T1
Tumor ≤20 mm in greatest dimension
T1mi
Tumor ≤1 mm in greatest dimension
T1a
Tumor >1 mm but ≤5 mm in greatest dimension
T1b
Tumor >5 mm but ≤10 mm in greatest dimension
T1c
Tumor >10 mm but ≤20 mm in greatest dimension
T2
Tumor >20 mm but not ≤50 mm in greatest dimension
T3
Tumor >50 mm in greatest dimension
T4
Tumor of any size with direct extension to chest wall or skin (includes inflammatory carcinoma)
Nodal Involvement: N (Nodal Status)
NX
Regional lymph nodes cannot be assessed (e.g., previously removed, not removed).
N0
No regional lymph node metastases histologically
N1
Metastases to movable ipsilateral level-I, -II axillary lymph node(s)
N2
Metastases in ipsilateral level-I, -II axillary lymph nodes that are clinically fixed or matted or in clinically detected* ipsilateral
internal mammary nodes in the absence of clinically evident axillary lymph node metastases
N3
Metastases in ipsilateral infraclavicular (level-III axillary) lymph node(s) with or without level-I, -II axillary lymph node
involvement, clinically detected* ipsilateral internal mammary lymph node(s) with clinically evident level-I, -II axillary lymph
node metastases, or ipsilateral supraclavicular lymph node(s) with or without axillary or internal mammary lymph node
involvement
N3a
Metastases in ipsilateral infraclavicular lymph node(s)
N3b
Metastases in ipsilateral internal mammary lymph node(s) and axillary lymph node(s)
N3c
Metastases in ipsilateral supraclavicular lymph node(s)
Metastases: M
M0
No clinical or radiographic evidence of distant metastases
cM0(i+)
No clinical or radiographic evidence of distant metastases, but deposits of molecularly or microscopically detected tumor cells
that are no larger than 0.2 mm in circulating blood, bone marrow, or other nonregional nodal tissue in a patient without
symptoms or signs of metastases
M1
Distant detectable metastases as determined by classic clinical and radiographic means and/or histologically proven larger
than 0.2 mm
From 2010. AJCC Cancer Staging Manual and Handbook, 7th ed. Springer-Verlag, New York.
*Detected by imaging studies (excluding lymphoscintigraphy) or by clinical examination and having characteristics highly suspicious for
malignancy or a presumed pathologic macrometastasis based on fine-needle biopsy with cytologic examination.
TNM, Tumor/node/metastasis.

Breast Cancer and Breast Reconstruction
85
9
Table 9.2  TNM Stage and Survival
STAGE
TNM CATEGORY*
RECURRENCE FREE AT
10 YEARS (NO SYSTEMIC
ADJUVANT THERAPY)
0
TisN0M0
98%
I
T1N0M0
80% (all stage-I patients)
T <1 cm
90%
T >1-2 cm
80-90%
IIA
T0N1M0 or T2N0M0
60-80%
T1N1M0
50-60%
IIB
T2 N1M0
5-10% worse than IIA and based
on node status
T3N0M0
30-50%
IIIA
T0, T1, or T2N2M0;
T3N1; or N2M0
10-40%
IIIB
T4N0, N1, or N2M0
5-30%
IIIC
Any T and N3M0
15-20%
IV
Any T, any N, and
M1
<5%
*See Table 9.1 for TNM definitions.
TNM, Tumor/node/metastasis.
5. Breast cancer treatment
• Breast-conserving therapy
■ Lumpectomy and radiation
○ Equivalent to mastectomy in long-term survival
○ Requires adjunctive radiation to limit risk for local
recurrence
○ General indications
◆ Women who have small, easily accessible cancer
with relatively large breasts and desire to avoid
mastectomy
○ Contraindications
◆ Large cancer with small breasts, such that tumor
removal would result in significant distortion of
the remaining breast
○ Complications
◆ Contracture and scarring
◆ Radiation-related complications
◆ Unfavorable esthetic outcomes (estimated to be
20% to 35%)
○ Reconstructive options (see Figures 9.1 and 9.2)
◆ Oncoplastic reduction or mastopexy
➔ Balancing the resection with breast landmarks
and shape to preserve aesthetics
◆ Lat flap
Ptotic breast
Mastectomy
Small or medium
breast size
Large parenchymal
defect or significant
skin defect
Small parenchymal
defect
Favorable location
(lateral or superior)
Vertical reduction
mammaplasty
Latissimus dorsi
flap or TAP flap
Mastectomy
Latissimus dorsi
flap or TAP flap
Unfavorable location
(e.g., Inferior to nipple
-areolar complex)
Nonptotic breast
with significant
skin loss
Local tissue
rearrangement
or composite flap
Figure 9.1.  Proposed algorithm for partial
breast reconstruction in small- or medium-
breasted patients. TAP, thoracodorsal artery
perforator. (Reprinted from Beahm, E., 2013. In:
Neligan, P.C. [Ed.], Plastic Surgery, 3rd ed. Elsevier,
266.)

Breast Cancer and Breast Reconstruction
86
• Mastectomy
■ Removal of all breast parenchyma
■ Mastectomy types
○ Radical: Wide excision of all breast tissue, overlying
skin, pectoralis major muscle, and en bloc dissection
of level-I, -II, and -III nodes
○ Modified radical: All of the above, except pectoralis
muscle resection, with en bloc removal of the level-I
and -II axillary lymph nodes
○ Skin sparing: Resection of all breast tissue through a
circumareolar incision, including the nipple-areolar
complex (NAC), but preserving as much of the skin
envelope as possible to facilitate immediate
reconstruction
◆ Reported recurrence rate of 2% at 4 years
○ Nipple sparing: Excision of breast tissue with
preservation of the NAC
◆ Requires intraoperative retroareolar frozen section
◆ Indications: Isolated single-tumor focus <3 cm,
located >2 cm from the NAC; prophylactic
mastectomy patients
◆ Contraindications: Multifocal disease, tumor in
close proximity to NAC (<2 cm), tumor >3 cm,
clinical invasion of the NAC, positive retroareolar
frozen section, positive nodal disease
◆ Complications: NAC compromise
➔ Risk factors: Large periareolar scar, thin
mastectomy flaps
➔ Preferred incisions for nipple-sparing
mastectomy (NSM) include radial incisions
+/− periareolar extension and inframammary
fold incisions.
○ Prophylactic: Resection of a breast that does not have
a diagnosis of cancer
◆ Indications: Women with known genetic
predisposition and those with unilateral breast
cancer who desire contralateral mastectomy
Figure 9.2.  Proposed algorithm for partial breast reconstruction in obese or large-breasted patients. TAP, thoracodorsal artery perforator.
(Reprinted from Beahm, E., Lang, J.E., 2013. In: Neligan, P.C. [Ed.], Plastic Surgery, 3rd ed. Elsevier, 266.)
Large breast size
or obese patient
Small parenchymal
defect (<15%)
Breast-conserving
therapy
Medium parenchymal
defect (15-30%)
Reduction
mammaplasty
Reduction
mammaplasty
Latissimus dorsi
flap or TAP flap
Large parenchymal
defect (>30%)
Local tissue
rearrangement
or composite flap
Mastectomy
• Sentinel lymph node biopsy
■ Indicated for all oncologic breast interventions to sample
for possibility of lymphatic spread
■ Not indicated in prophylactic interventions
• Lymph node dissection
■ Indications: Positive sentinel lymph node biopsy or
clinically positive nodes found to be positive for cancer
preoperative or intraoperative
■ Complications
○ Lymphedema
○ Sensory disturbance of the upper, medial arm from
injury to the intercostobrachial n. and the medial
brachial cutaneous n.
• Neoadjuvant therapy
■ Indications: Use of chemotherapy or endocrine therapy
to reduce tumor burden such that a lumpectomy may be
feasible or to determine whether a patient responds to a
given therapy that is useful to determine prognosis
■ Currently, there is no survival advantage for neoadjuvant
therapy versus traditional or surgery + adjuvant
approaches unless the patient develops a pathologic
complete response that portends a favorable prognosis.
■ Complications: See below
• Chemotherapy
■ Indications: In general, patients with positive axillary
lymph nodes are candidates for chemotherapy.
○ Patients with estrogen-receptor- or progesterone-
receptor-positive invasive breast cancer should receive
adjuvant endocrine therapy (i.e., tamoxifen for
premenopausal women and aromatase inhibitors for
postmenopausal women).
■ Complications: Wound healing derangements, nausea/
vomiting, alopecia, immunosuppression

Breast Cancer and Breast Reconstruction
87
9
• Reconstruction types
■ Implant-based breast reconstruction
○ Tissue expanders, placed in the subpectoral space,
used to stretch the skin envelope, followed by
expander-implant exchange at a second stage
○ Preferred option in patients who do not need
adjuvant radiation therapy and desire a quick
recovery with minimal scarring
○ Advantages: Relatively short operative time, no
second donor site, good symmetry achieved in
bilateral reconstructions, patient participation in
choosing size of reconstruction
○ Disadvantages: High risk of wound healing
complications, infection, exposure in setting of
radiation therapy; symmetry with contralateral native
breast is difficult in unilateral reconstructions;
requires two operative stages and multiple office
visits; less natural in appearance and feel than
autologous reconstruction, implant-related
complications
○ Can include a lat flap or perforator flap to improve
appearance or as salvage of an exposed or infected
implant
○ Can be used with acellular dermal matrix
◆ Advantages: Increased initial fill of the expander,
potentially decreased capsular contracture
◆ Disadvantages: Increased seroma and infection
rate, cost
○ Newer expanders on the market use an osmotic
gradient to allow self-filling
◆ Advantages: Frequent postoperative office visits
not required for expansion; no external expander
access required, which reduces risk
◆ Disadvantages: No external control of expansion
process, expansion occurs at a set rate that cannot
be adjusted, fill malfunction
■ Autologous tissue reconstruction
○ Use of second donor site to reconstruct breast with
patient’s own tissue
○ Transverse rectus abdominis myocutaneous (TRAM)
flap (see Figure 9.3)
◆ Based off epigastric a./venae comitantes
➔ Can be pedicled (superior epigastric a.) or
“free” (inferior epigastric a.)
 Pedicled TRAM: Shorter operative time,
decreased risk of total flap loss, higher
incidence of fat necrosis and partial flap loss,
increased length of hospital stay
 Free TRAM: More flexibility in flap shaping
and insetting, decreased abdominal wall
morbidity, recommended for patients who
are diabetic, overweight, or cigarette smokers
• Radiation
■ Indications: Women undergoing breast-conservation
therapy, tumors >5 cm (T3), 4 or more positive lymph
nodes (N2); strongly recommended for 1 to 3 axillary
lymph node involvement
○ Radiation therapy is also considered for patients with
lymphovascular invasion or close surgical margins.
■ Complications: Skin damage, fibrosis of soft tissue, poor
wound healing, reduced cosmesis of reconstruction,
increased postreconstruction complications (especially
with implant-based reconstruction)
■ Radiation skin damage progression
○ Acute changes: Vessel thrombosis, erythema
○ Chronic changes: Impaired neutrophil activation and
fibroblast function, leading to poor wound healing
◆ Late radiation tissue injury (LRTI) occurs in
approximately 5% to 15% of long-term survivors
and can occur months to years after exposure.
➔ Characterized by progressive tissue deterioration
followed by fibrotic replacement
➔ Development of late or new ulceration within
radiation field is concerning for possible
malignancy and biopsy should be considered.
 Squamous cell carcinoma (Marjolin’s ulcer)
 Radiation-induced sarcoma
➔ Chronic radiation wound management requires
autologous tissue.
 Latissimus dorsi flap is preferred option
■ Safest option after immediate expander insertion with
unexpected need for postoperative radiation therapy is
explantation, followed by delayed autologous
reconstruction.
6. Reconstructive options
• Reconstruction timing
■ Immediate: At the time of the mastectomy
○ Advantages: Psychosocial benefits, take advantage of
available skin, supple soft tissues that are relatively
free of scar
○ Disadvantages: Formal pathologic evaluation not
completed, risk of mastectomy flap necrosis that
could compromise esthetic results
■ Delayed: Delayed for some time after the mastectomy
incisions have healed
○ Advantages: Full pathologic evaluation completed
along with any necessary adjunctive therapies
○ Disadvantages: Operating in a scarred field, greater
skin requirement than immediate reconstructions,
delayed psychosocial benefits of reconstruction
○ Delayed autologous reconstruction is the preferred
reconstructive choice in the setting of adjuvant
radiotherapy.