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CTA or MRA
Not routine but should be considered in the
preoperative work-up of patients with 22q11.2 deletion
syndrome as they often have aberrant anatomy of
internal carotid with medial displacement
TREATMENT
Nonsurgical
Speech therapy
Key component of treatment of VPI
Can be used to correct compensatory misarticulations
after surgery
Prosthetics
Obturator to fill area of tissue deficit to allow for VP
closure
Custom prosthetic appliance made by prosthodontist
Important for patients who are not surgical candidates
or as a temporary solution for those awaiting surgery
Speech Surgery
Type of surgery is based on formal perceptual speech
analysis, VP closure characteristics (VP gap size, closure
pattern, location), and surgeon preference.
Ideally speech surgery should be done around 5 years of
age.
Palatal Lengthening Techniques
Double opposing Z-palatoplasty
Indications: small VP gaps with sagittal closure pattern
and sagittally oriented LVP; either in unrepaired or in
previously repaired palate with minimal muscle
repositioning
Repositions LVP transversely, improves palatal motion,
lengthens palate (see Chapter 14: Cleft Palate)
Buccal myomucosal flap (Fig. 15-2)
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Figure 15-2 Buccal myomucosal
flap. A. Design of a buccal
myomucosal flap. B. Markings. C. Flap
elevation. D. Flap inset into a palatal
defect. E. Division of base of flap.
(From Pearson GD. Palatal fistula. In:
Chung KC, ed. Operative Techniques
in Plastic Surgery. Wolters Kluwer;
2020:2696-2705. Tech Figure 8.13.3.)
Indications: small to moderate central VP gaps
Buccinator myomucosal flaps are raised from the
bilateral cheeks
Buccal mucosa and buccinator m.
Transposed and advanced lengthens the soft
palate
Pharyngeal Augmentation Techniques
Posterior pharyngeal flap
*Indications: moderate to large VP gap but with
good lateral wall motion
Static, nonphysiologic technique
Myomucosal flap from posterior pharynx
Mucosa and superior pharyngeal constrictor m.
Superiorly based and sutured to posterior soft
palate
Creates a tissue “bridge” between palate and posterior
pharyngeal wall with two lateral ports for nasal airflow,
which are occluded by the lateral pharyngeal walls
during VP closure
Sphincter pharyngoplasty
*Indications: restricted or absent lateral pharyngeal
wall movement
Dynamic, physiologic technique
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Superiorly based myomucosal flaps from the posterior
tonsillar pillars
Mucosa and palatopharyngeus m.
Flaps are transposed and overlapped in midline of
posterior pharyngeal wall
Creates a single, central VP port
Posterior pharyngeal wall augmentation
Indications: small, central VP gaps or to augment other
techniques with small gap.
Can be used to augment the posterior pharyngeal wall.
Historically, many different materials used for
augmentation, but fat is most common.
Hand assisted liposuction on available donor site,
usually abdomen or flank.
Inject fat into submucosa of posterior pharyngeal wall
to narrow distance to velum.
COMPLICATIONS
Acute Airway Obstruction
Obstructive Sleep Apnea
Up to 35% of patients who have posterior pharyngeal flap
can develop OSA in the early postoperative period.
Estimated 9% of patients with posterior pharyngeal flap will
need revision for OSA.
Persistent Velopharyngeal Insufficiency: normal in the early
postoperative period, will need to continue with speech therapy
initially but should gradually improve in time
Hyponasality: can be caused by excessive narrowing of the VP
port, minimizing air movement
QUESTIONS YOU WILL BE ASKED
1. What defines the velopharyngeal port?
Velum, lateral pharyngeal walls, posterior pharyngeal wall.
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1.
2.
2. What must a patient have in order to be considered for a
posterior pharyngeal flap for VPI?
Good lateral wall movement.
3. What muscle is included in the sphincter pharyngoplasty?
Palatopharyngeus.
Recommended Readings
Gart MS, Gosain AK. Surgical management of velopharyngeal insufficiency.
Clin Plast Surg. 2014;41(2):253‐270.
Goudy SL, Tollefson TT. Complete cleft care: cleft and velopharyngeal
insufficiency treatment in children. In: Hiscock TY, Owen Zurhellen J, eds.
Speech/Resonance Evaluation. Thieme; 2015.
*
Denotes common in-service examination topics.
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16
Craniosynostosis and
Craniofacial Syndromes
Alexandra O. Luby
CRANIOFACIAL EMBRYOLOGY AND
DEVELOPMENT
Skeletal tissues of the head and face derive from mesenchyme
and cranial neural crest cells.
Bone (Fig. 16-1)
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Figure 16-1 Major bones, fontanelles, and
cranial sutures of the newborn skull as
seen from (A) superior and (B) lateral
views. (From Digestive System. In: Sadler
TW. Langman’s Medical Embryology. 15th
ed. Wolters Kluwer; 2024:232-258. Figure
10.5.)
Skull development starts at 23-26 days of gestation.
Neurocranium: develops into calvarium
Membranous neurocranium: precursor to the cranial
vault
Paired frontal, parietal, squamosal temporal, and
superior occipital bones
Bone formation through intramembranous
ossification (direct ossification of
mesenchyme)
Cartilaginous neurocranium: precursor to the skull base
Sphenoid, ethmoid, mastoid, petrous portion of
temporal bone, and inferior occipital bones.
*Bones develop through endochondral
ossification (ossification of cartilaginous
precursor).
Viscerocranium: precursor to the bones of the facial
skeleton.
Neural crest cells of the first pharyngeal arch
(Meckel cartilage) gives rise to the following:
Maxillary process (dorsal portion of first
pharyngeal arch) forms premaxilla, maxilla,
zygoma, and squamous temporal bone.
Mandibular process (ventral portion of first
pharyngeal arch) forms the mandible, malleus, and
incus.
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*Second pharyngeal arch (Reichert cartilage) gives
rise to stapes, styloid process of the temporal bone
and lesser horn and superior body of the hyoid
bone.
Bone formation through intramembranous ossification.
Cranial Sutures
Fibrous joints between calvarial bones
Metopic, sagittal, coronal, lambdoid, and squamosal
sutures (Fig. 16-1)
Adjacent osteogenic fronts, interposed mesenchymal
tissue, and underlying dura
Allow for head expansion during development and
deformational changes (ie, passage through birth
canal)
*Primary stimulus for skull growth is brain
growth.
Brain is 25% of adult size at birth, 50% at 6
months, and 75% at 1 year.
Full adult volume by ∼2.5 years.
Fontanelles (infantile “soft spots”) are the confluence of
two or more cranial sutures
Anterior fontanelle (bregma): Closes around 2 years of
age
Posterior fontanelle (lambda): Closes around 2 months
of age
Suture fusion sequence
Metopic: 3-9 months (only suture to obliterate during
childhood)
Sagittal: 20-22 years
Coronal: 23-24 years
Lambdoid: 26 years
Sinus Development
Maxillary and sphenoid: begins at 3 months gestation,
complete during childhood
Ethmoid: begins at 5 months gestation, complete during
childhood
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Frontal: begins at 5 years old, complete during
adolescence; the only one to begin development postnatally
CRANIOSYNOSTOSIS
OVERVIEW
Premature fusion of the cranial sutures
*Virchow Law
Growth restriction occurs perpendicular to the affected
suture.
Compensatory skull growth occurs parallel to the affected
suture.
Nonsyndromic (Primary) Craniosynostosis
Isolated suture fusion without associated abnormalities
Largely sporadic pattern of occurrence (incidence 0.6 in
1000 live births)
Syndromic Craniosynostosis
Heterogeneous group of disorders marked by premature
suture fusion
Associated dysmorphic features and congenital
abnormalities
Genetic heritability patterns (eg, autosomal dominant, a.
recessive, and X-linked)
Linked to specific gene mutations in some cases (see
below)
Secondary Craniosynostosis: premature suture fusion due to
other disease processes
Hyperthyroidism
Idiopathic hypercalcemia
Rickets
Microcephaly
Mucopolysaccharidoses
Hematologic disorders (thalassemia, polycythemia vera,
and sickle cell)
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