CME/MOC

MOC-PSSM CME Article: Nonsyndromic

Cleft Palate
John A. van Aalst, M.D., M.A.
Kamal Kumar Kolappa, B.S.
Michael Sadove, M.D.
Chapel Hill, N.C.; and Indianapolis,
Ind.
Learning Objectives: After reading this article, the participant should be able
to: 1. Understand the embryology of normal palate development, and the
genetic and environmental causes of clefting. 2. Delineate the anatomy of the
normal palate and the cleft palate. 3. Understand the Veau classification for
clefts of the palate and techniques used to repair various clefts of the palate. 4.
Understand the factors that contribute to complications following palate repair,
including fistula formation, velopharyngeal insufficiency, maxillary growth in-
hibition, and sleep apnea.
Summary: Cleft palate is generally an isolated congenital abnormality but can
be associated with multiple syndromes. Careful evaluation of an infant with cleft
palate by a multidisciplinary team is required to rule out other potential ab-
normalities. In children with isolated nonsyndromic cleft palate, palate repair
is generally performed before 1 year of age. The goals for cleft palate repair
include separating the nasal and oral cavities (avoidance of fistulas), establishing
normal velopharyngeal function, and preserving maxillofacial growth. This
module reviews the incidence, epidemiology, and anatomical classification of
cleft palates; and repair techniques, timing, and potential complications asso-
ciated with palate repair.
The Maintenance of Certification module series is designed to help the clinician structure
his or her study in specific areas appropriate to his or her clinical practice. This article is
prepared to accompany practice-based assessment of preoperative assessment, anesthesia,
surgical treatment plan, perioperative management, and outcomes. In this format, the
clinician is invited to compare his or her methods of patient assessment and treatment,
outcomes, and complications with authoritative, information-based references.
This information base is then used for self-assessment and benchmarking in parts II and
IV of the Maintenance of Certification process of the American Board of Plastic Surgery.
This article is not intended to be an exhaustive treatise on the subject. Rather, it is designed
to serve as a reference point for further in-depth study by review of the reference articles
presented. (Plast. Reconstr. Surg. 121: 1, 2008.)

A
cleft of the palate occurs in one in 2000 live patients.2 Although syndromic cleft palate patients
births regardless of race.1 Cleft lip (with or make up a small portion of the entire cleft palate
without cleft palate), however, varies in in- population, it is important for the clinician to be
cidence from a high of one in 450 live births
among Asian and Native American populations, to
a low of one in 2000 live births in African Amer- Disclosure: None of the authors has a financial
icans. Cleft palates associated with other anoma- interest in any of the products, devices, or drugs
lies or syndromes tend to be isolated, without the mentioned in this article.
presence of lip or alveolar clefting. A syndrome is
diagnosed in nearly half of isolated cleft palate

From the Division of Plastic Surgery, University of North

Carolina, Chapel Hill Medical School, and Division of Plas-
tic Surgery, Indiana University School of Medicine.
Received for publication November 22, 2006; accepted
March 2, 2007.
Copyright ©2007 by the American Society of Plastic Surgeons
DOI: 10.1097/01.prs.0000294706.05898.f3
The test for the MOC-PS–aligned CME arti-
cle “Nonsyndromic Cleft Palate” by van
Aalst, Kolappa, and Sadove is available at
http://www1.plasticsurgery.org/ebusiness4/
OnlineCourse/CourseInfo.aspx?Id⫽12796.

www.PRSJournal.com 1
 Plastic and Reconstructive Surgery • January 2008
suspicious of syndromes in the initial evaluation;
genetic evaluation of the patient and family is
therefore critical. This review focuses on nonsyn-
dromic cleft palate and surgical management of
this anomaly.
EMBRYOLOGY
Embryologically, the nose, lips, and palate are
divided into the primary and secondary palates.
The primary palate (which eventually forms the
lips and nose) begins to form during the fifth week
of gestation. The frontonasal process, a central
and anterior area of mesenchymal tissue anterior
to the brain, develops two thickened areas along
its lateral edges, referred to as the nasal placodes;
these placodes invaginate to form two nasal pits
(that eventually form the nostrils). The ridges of
tissue that form on either side of the nasal pits are
known as the medial and lateral nasal promi-
nences. Over the next 2 weeks of gestation, the two
maxillary prominences, which are inferior and lat-
eral to the nasal pits, migrate medially and fuse
with the medial nasal prominences to form the
primary palate.3 Normal fusion of the primary pal-
ate is complete by the sixth week of gestation. The
structures that develop from the primary palate
include the nose, lip, prolabium (central upper
lip), and premaxilla.4 These structures are ante-
rior to the incisive foramen (Fig. 1).
Development of the secondary palate begins
during the sixth week of gestation; at this time, the
maxillary prominences form two shelf-like out-
growths, the palatine shelves. These shelves ini-
tially grow downward on each side of the tongue;
during the seventh week of gestation, they ascend,
growing horizontally above the tongue, and even-
tually fuse to form the secondary palate.3 Fusion
begins at the incisive foramen and proceeds pos-
teriorly toward the uvula. Normally, the shelves
fuse in the midline to form the bony hard palate;
the hard palate fuses to the vomer of the nasal
septum at the ninth week of gestation. Palatal fu-
sion continues posteriorly, with full formation of
the secondary palate by the twelfth week of
gestation.4,5 The secondary palate (posterior to
the incisive foramen) includes both the hard pal-
ate and the soft palate (Fig. 2).
GENETIC AND ENVIRONMENTAL
CAUSES OF CLEFTING
The genes involved in clefting are becoming
increasingly understood. Genetic predisposition
for the development of palate defects along with
environmental hazards can disrupt normal em-
bryogenesis. Multiple chromosomal abnormali-
2
ties have been shown to cause clefting, including
chromosomes 1, 2, 4, 6, 11, 14, 17, and 19. The
specific genes involved include the methylenetet-
rahydrofolate reductase (MTHFR) gene on chro-
mosome 1,6 TGF-␣ on chromosome 2,7 MSX-1 on
chromosome 4,8 TGF-␤3 on chromosome 14,9,10
RAR-␣ on chromosome 17,11 and BCL3 and TGF-␤
on chromosome 10.12
Multiple environmental factors have also been
noted to cause clefting, including alcohol use, cig-
arette smoking (two-fold increase),13 folate acid de-
ficiency (and a host of potential other nutritional
factors),14 steroid use (three-fold increase),15 and the
use of anticonvulsants such as phenobarbital and
phenytoin (10-fold increase).3,16 Other environmen-
tal factors that predispose to cleft palate formation
include hypoxia17 and retinoids (vitamin A).18 The
process of anterior to posterior palatine fusion takes
approximately 1 week longer in female fetuses than
in male fetuses; this added time allows for longer
teratogenic exposure and may explain the increased
incidence of isolated cleft palates in girls.4
The interaction of genetic predisposition and
environmental factors enhances the environmen-
tal risk for palatal clefting. For example, in pa-
tients with a TGF-␣ genotype (chromosome 2 ab-
normality), cigarette use increases the risk of
clefting by six-fold, rather than the usual two-fold;
an MSX1 defect causes an increased susceptibility
to use of alcohol and to cigarette smoking. Moth-
ers with a methylenetetrahydrofolate reductase
enzyme deficiency are more susceptible to folic
acid deficiency.6,19
ANATOMY
The normal palate divides the oropharynx and
nasopharynx and is composed of the hard and soft
palates. The normal hard palate is covered with a
dense mucous membrane that adheres closely to
the underlying periosteum, creating a mucoperi-
osteal covering of the oral bony surface. The nasal
surface is also covered with a dense mucoperios-
teum; the vomer of the nasal septum is fused to the
midline. The greater palatine neurovascular bun-
dles emerge from the palatine canals; the artery is
located between mucoperiosteum and bone,
along the posterolateral edge of the hard palate
(Fig. 2).5
The hard palate maintains the width and an-
terior projection of the maxillofacial architecture,
whereas the soft palate works as an active muscular
valve, referred to as the velopharyngeal sphincter.
This sphincter raises the soft palate toward the
posterior pharyngeal wall, dynamically separating
the nose from the mouth.4 The soft palate’s in-
Volume 121, Number 1 • Nonsyndromic Cleft Palate

Fig. 1. Facial development in the embryo. The medial and lateral nasal prominences join to
form the nasal pit; the medial nasal prominence and the maxillary prominence fuse to form
the primary palate. The nasal tip, columella, and philtrum are derived from the medial nasal
prominence; the lateral upper lip forms from the maxillary prominence.

trinsic muscular function aids in proper breath-
ing, swallowing, blowing, and phonation.5 Five
pairs of muscles constitute the soft palate: the
levator veli palatini, tensor veli palatini, uvulas,
palatopharyngeus, and palatoglossus muscles.20
The tensor and levator veli palatini muscles, both
of which arise from the eustachian tube, are key
anatomical features in cleft palate repair. The ten-
sor veli palatini muscles arise from the medial
pterygoid plate, course inferiorly, becoming a ten-
don that wraps laterally around the pterygoid
hamulus before inserting medially into the soft
palatal aponeurosis near the junction of the soft
and hard palates. These muscles control the open-
ing of the eustachian tube, aerating the middle ear
and preventing recurrent otitis media. The levator
veli palatini muscles, which arise from the petrous
portion of the temporal bone, a part of the skull
base, and from the medial lamina of the cartilage
of the auditory tube, course inferiorly and medi-
ally, interdigitating at the midline, forming the
bulk of the anterior portion of the “levator sling,”
raising the palate to the pharynx and thus pro-
viding the anterior portion of the velopharyngeal

3
 Plastic and Reconstructive Surgery • January 2008

Fig. 2. The incisive foramen separates the structures of the primary palate (lip and
alveolar process) and secondary palate (hard and soft palate). Note the greater palatine
foramen at the posterolateral aspect of the hard palate. The greater palatine artery
emerges from this foramen.

sphincter.1 The superior pharyngeal constrictor CLEFT PALATE CLASSIFICATION

forms the posterior aspect of the sphincter; during
velopharyngeal closure, a central ridge of the su-
perior pharyngeal constrictor moves anteriorly
to touch the velum. This ridge is referred to as
Passavant’s ridge. The palatoglossus and palato-
pharyngeus muscles originate at the midline of the
soft palate and insert into the tongue and lateral
pharyngeal wall, respectively, also supporting this
sphincter function by constricting the oropharyn-
geal aperture.1
Clefts involving the soft palate disrupt both the
levator sling and the normal muscular insertions
in the palatal aponeurosis. Muscles that ordinarily
join at the midline insert along the posterior edge
of the hard palate.1 Sphincter function is there-
fore compromised, leading to velopharyngeal in-
sufficiency and problems with speech develop-
ment. Eustachian tube control is also lost, often
leading to chronic otitis media, with the risk of
permanent hearing loss. Clefts involving the hard
palate involve a central bony and mucosal gap of the
hard palate, in addition to the cleft of the soft palate.
Through the central gap, a variable amount of the
underlying vomer may be visualized.
Cleft palate classification is based on anatom-
ical disruption of the primary and secondary pal-
ates and includes the categories of complete and
incomplete, unilateral and bilateral, and submu-
cous clefting. Multiple classifications have been
used; of these, the Veau classification is the sim-
plest and most utilitarian. There are four Veau
classifications: Veau class I is an incomplete cleft,
involving only the soft palate (Fig. 3). Veau class
II is a cleft involving both the soft and hard palates
but limited to the secondary palate (Fig. 4). Veau
class I and II clefts, both of which are limited to the
secondary palate, are not designated as either uni-
lateral or bilateral. A Veau class III cleft is a com-
plete unilateral cleft including both the lip and
palate (the primary and secondary palates) (Figs.
5 and 6). Veau class IV is a complete bilateral cleft
(Figs. 7 and 8). The unilateral complete cleft de-
rives its name from the effect it has on the primary
palate; the effect on the hard palate is that only
one palatal shelf fuses to the nasal septum, and the
resulting cleft defect is to one side of the midline.
With a bilateral cleft, neither palatal shelf fuses

4
Volume 121, Number 1 • Nonsyndromic Cleft Palate
Fig. 3. Veau class I, an incomplete cleft of the soft palate.
Fig. 4. Veau class II, a complete cleft of the secondary palate,
including both the soft and the hard palates.
with the nasal septum, leaving a wider midline
defect and the vomer of the nasal septum exposed
and suspended superiorly.
The submucous cleft involves a separation of
the intrinsic soft palate musculature, whereas the
overlying soft palatal mucosa remains intact (Fig.
9).1 This type of cleft is often difficult to diagnose,
because the entire palate may appear grossly in-
Fig. 5. Veau class III, a complete unilateral cleft of the lip and
alveolus (primary palate) (see also Fig. 6).
Fig. 6. Veau class III, a complete unilateral cleft of the hard and
soft palates (secondary palate) (same patient as shown in
Fig. 5).
tact. Often, the only anatomical clues suggesting
a submucous cleft palate are a bifid uvula, a
notched posterior hard palate, and a translucent
area in the midline of the soft palate, known as the
zona pellucida, where the levator veli palatine
musculature has failed to fuse. Often, this cleft
type is not discovered until a child develops velo-
5
 Plastic and Reconstructive Surgery • January 2008
Fig. 7. Veau class IV, a complete bilateral cleft of the lip and al-
veolus (primary palate). This patient has markings for a Bardach
two-flap palatoplasty with vomer flap (see also Fig. 8).
pharyngeal incompetence, manifested as hyper-
nasal speech.21 Although this is the most difficult
type of cleft palate to diagnose, it is still the most
common type of posterior palatal cleft.22 The exact
Fig. 8. Veau class IV, a complete bilateral cleft of the hard and soft
palates (same patient as shown in Fig. 7).
6
Fig. 9. A submucous cleft of the soft palate; findings include a
bifid uvula, a midline thinning of the soft palate with absent le-
vator palati muscle interdigitation, and a notch at the posterior
hard palate.
incidence of submucous cleft palate is difficult to
determine, because it is usually discovered only if a
patient is referred for velopharyngeal incompe-
tence. Attempts to measure the incidence in the
general population by anatomical criteria have re-
vealed rates in the range of two to eight per 10,000.21
PREOPERATIVE ASSESSMENT
Preoperative assessment of a child with a cleft
palate following birth involves identification of
any associated syndromes and potential comor-
bidities; this process involves multidisciplinary
evaluation. In those children determined to have
isolated clefts of the palate, feeding issues are the
predominant concern early in life. Because a child
with cleft palate is unable to generate a closed seal
for sucking, the child is not able to breast-feed (the
exception being a very limited cleft of the poste-
rior soft palate); this inability necessitates special
feeding regimens that include easy-flow nipples,
which allow the child to use pressure from the
alveolar ridge to initiate milk flow. The regimen
may also require a more upright position during
feeding and for longer periods after feeding. In
Volume 121, Number 1 • Nonsyndromic Cleft Palate
children with persistent feeding problems despite
these maneuvers, a temporary nasal feeding tube
may be required as the child is learning to feed
from a bottle. In rare instances, the child may
require a surgically placed gastric feeding tube.
CLEFT TEAM EVALUATION
One of the most important aspects of preop-
erative preparation for a child with an isolated
cleft palate involves assessment by a team of health
care workers devoted to care of children with oro-
facial clefts. A typical craniofacial team includes
craniofacial surgeons, otolaryngologists, speech
pathologists, pediatric dentists, orthodontists, psy-
chologists, social workers, geneticists, and pedia-
tricians. The team helps prepare families for sur-
gical repair of the cleft palate and establish a
treatment course that will lead the child into child-
hood, adolescence, and adulthood. Follow-up
with the craniofacial team should be on a yearly
basis with full team evaluation as the child’s speech
develops and as dentition erupts.
OPERATIVE TECHNIQUES
The goals of palatoplasty are to achieve com-
plete and intact closure of the palate, and resto-
ration of the velopharyngeal sphincter. The goals
of palatoplasty include avoidance of palatal fistula,
restoration of velopharyngeal function, and opti-
mization of maxillary growth. To achieve these
goals, repair of the cleft palate must include clo-
sure in three layers, including a nasal layer, muscle
layer, and an oral mucosal layer. Compromising
closure of any of these layers increases the inci-
dence of postoperative complications, including
possible fistula and velopharyngeal insufficiency.
Complete nasal layer closure requires dissection
of this layer as a separate flap for closure at the
level of the soft palate, dissection and release of
the nasal layer from under the posteromedial as-
pect of the hard palate, and possibly vomer flaps
for anterior closure of this layer. Closure of the
muscle layer requires release of abnormal mus-
cular attachments to the posterior edge of the
hard palate, changing the muscle fiber orienta-
tion from a longitudinal orientation to a trans-
verse direction so that they may be approxi-
mated at the midline. Oral mucosal closure
needs to be tension free and may require lateral
releasing incisions and full release of the greater
palatine pedicles for easy medialization of the
oral mucosal layer. The following discussion fo-
cuses on techniques used for palate repair.
TECHNIQUES FOR REPAIR OF THE
SOFT PALATE
Intravelar Veloplasty
Intravelar veloplasty proposed by Kriens in
1969 was an improvement on previous soft
palatoplasties.23 Kriens’ innovation was to restore
the levator sling and palatal musculature at the
midline where they normally meet. This is accom-
plished by dissecting the anteriorly malpositioned
muscle bundles from the posterior edge of the
hard palate and repositioning them in the mid-
line. This technique is widely used today, though
there is much variability among surgeons in how
the musculature is dissected and repositioned.
Until recently, the results of this technique had
not been compared objectively with the older stan-
dard technique of side-to-side approximation of
the muscle advocated by Veau. In 1989, Marsh and
colleagues published results from a prospective
study that compared the effects of intravelar velo-
plasty and traditional side-to-side techniques on
velopharyngeal insufficiency. They found that
repositioning of the levator muscles during pri-
mary palatoplasty was no better at improving
velopharyngeal insufficiency than the side-to-
side veloplasty.24 However, this study was limited
by a small patient population (51 patients) at a
single institution. In 1995, Cutting questioned
whether the intravelar veloplasty technique ad-
equately dissected and repositioned the muscu-
lature.25 It remains a challenge to prove by prospec-
tive, well-controlled, multicenter studies whether the
intravelar veloplasty is a more effective technique
than its simpler predecessor.
Some practitioners have suggested that use
of an operating microscope to perform palate
repair, which allows for improved lighting, vi-
sualization of the muscle fibers results in im-
proved outcomes.26,27 Sommerlad reported on
442 palate repairs with at least 10 years of fol-
low-up and observed that velopharyngeal insuf-
ficiency rates have decreased from 10.2 percent
to 4.6 percent. He attributes this improvement
to radical dissection and repositioning of the
velar musculature. Whether this is the result of
the radical dissection or the use of the micro-
scope cannot be determined from the longitu-
dinal study.
Furlow Double-Opposing Z-Plasty
The Furlow double-opposing Z-plasty tech-
nique was unofficially introduced in 1978 and
then introduced in published form in 1986 (Fig.
10).28 Over the past decade, it has become the
7
 Plastic and Reconstructive Surgery • January 2008

Fig. 10. Furlow double-opposing Z-plasty. The technique involves opposing Z-plasties (above) that reorient
the soft palate musculature posteriorly into a normal, horizontal position (below).

veloplasty technique of choice among many sur-
geons. This technique uses two reversed Z-plasties
based on the cleft midline, both of which draw in
soft palate tissue from the sides to close the cleft
defect and restore the musculature to its anatom-
ical position. The inherent advantages of the Fur-
low repair are that it lengthens the palate and
restores normal muscular anatomy. A concern
shared by many surgeons, including Millard, is
that the Z-plasties in the soft palate tend to pull the
sides of the velum toward the midline to lengthen
disadvantage
the palate; this tightens the velum in the transverse
axis.29 Nonetheless, retrospective studies pub-
lished during the past decade have shown that
patients with Furlow repairs may have reduced
hypernasality and improved articulation and
speech.21,30 Prospective controlled trials are needed
to compare the Furlow palatoplasty to the intravelar
veloplasty and other procedures.21
TECHNIQUES FOR REPAIR OF THE vv
HARD PALATE B
Currently, there are three variations of repair
involving mucoperiosteal flaps, including the von
Langenbeck palatoplasty, the Veau-Wardill-Kilner
palatoplasty, and the two-flap palatoplasty that is
largely credited to Bardach. The first two are used
commonly to repair incomplete clefts involving
both hard and soft palates, and the third is used
in complete clefts of the lip and palate.
Von Langenbeck Palate Repair
The von Langenbeck palatoplasty involves re-
laxing incisions along the lateral edge of the hard
palate, starting anteriorly near the palatomaxillary
suture line, running posteriorly just medial to the
alveolar ridge, and ending lateral to the hamulus,
approximately 1 cm posterior to the greater tu-

8
Volume 121, Number 1 • Nonsyndromic Cleft Palate
Fig. 11. (Above) The von Langenbeck repair of the palate uses
lateral releasing incisions to allow medial movement of the pal-
atal mucosa; the technique preserves the greater palatine vessels
and the anterior incisive pedicle. (Center) The Veau-Wardill-Kilner
palate repair, referred to as the pushback technique, is similar in
initial markings to the von Langenbeck technique (above). How-
ever, the technique then divides the oral mucosa anteriorly, bas-
ing the mucoperiosteal flaps on the greater palatine pedicle
berosity of the alveolus (Fig. 11, above).1,2 The mu-
cosa along the edges of the cleft is also incised. The
entire mucoperiosteum is then raised from the
oral surface of the hard palate; care is taken to
preserve the two neurovascular pedicles, the
greater palatine pedicle posteriorly and the inci-
sive pedicle anteriorly. Thus, bipedicled muco-
periosteal flaps are created on both sides of the
cleft. The nasal side of the cleft is closed first, using
redundant mucoperiosteum from the incision
along the cleft edge. The muscle is then approx-
imated using an intravelar veloplasty. The bi-
pedicled oral mucosal flaps are approximated to
cover the oral surface of the cleft. The von Lan-
genbeck technique works well for incomplete
clefts of the secondary palate without the presence
of cleft lip or alveolus.1,23,24
Veau-Wardill-Kilner Palatoplasty
A variation of the von Langenbeck repair, the
Veau-Wardill-Kilner repair, or V-Y pushback, can
also be used for incomplete clefts involving the
hard palate (Fig. 11, center and below). The same
flap design as the von Langenbeck repair is used;
then, the superior pedicle is divided, leaving a flap
on either side of the cleft based solely on the
greater palatine pedicle posteriorly. The muco-
periosteal flaps can then be approximated either
directly or in a V-Y closure at the free anterior end
to actively lengthen the soft palate. This repair
technique allows more flap advancement than the
von Langenbeck repair; however, the gain in pal-
atal length (and possibly improved velopharyn-
geal function) is at the cost of denuding palatal
bone anteriorly on the oral surface. It has been a
concern that this denuded palate might adversely
affect midfacial growth in cleft palate patients.23 A
recently published retrospective study concludes
that satisfactory long-term midfacial growth can be
obtained with proper use of the Veau-Wardill-Kil-
ner repair.31 However, this study was limited to
analysis of a single surgeon’s patients; variability in
how the technique is performed by other surgeons
may not lead to similar favorable outcomes. In
fact, other studies have suggested that the Veau-
Wardill-Kilner repair has detrimental effects on
midfacial growth.23,32 Until the Veau-Wardill-Kil-
ner repair is exonerated of charges that it inhibits
facial growth, many surgeons opt for the more
alone (center). The tips of the two flaps are then sutured centrally
(thus, the term “pushback”) and leaves a denuded portion of hard
palate laterally (below).
9
 Plastic and Reconstructive Surgery • January 2008
conservative Von Langenbeck repair, in which the
relaxing incisions denude less palatal bone. The
von Langenbeck repair can be used in combina-
tion with the intravelar veloplasty or Furlow pal-
atoplasty to minimize the extent of mucoperios-
teal undermining.23 A recent retrospective study
compared the amount of denuded palate and out-
comes in three methods of hard palate repair.32
Comparisons were made between a Veau-Wardill-
Kilner repair (most denuded palate), the von Lan-
genbeck repair (less denuded palate), and a von
Langenbeck variation (least denuded palate) with
relaxing incisions moved from the lateral to me-
dial sides of the greater palatine bundle. The re-
sults suggest that both variations of the von Lan-
genbeck technique resulted in improved maxillary
growth, further confirming the belief that increases
in denuded hard palate result in decreased maxillary
growth.32 However, this study does not answer the
question as to whether growth restriction is related
primarily to denuded palate, which must heal by
secondary intention, or the extent of mucoperios-
teal undermining.
Two-Flap Palatoplasty (Bardach Variation)
The Bardach variation of the two-flap palato-
plasty is used to repair complete clefts of the pri-
mary and secondary palate (either unilateral or
bilateral). The anterior mucosal flaps involve the
entire oral mucosa of the hard palate; incisions are
made along the medial edge of the alveolar ridge
to the alveolar cleft and along the cleft margin at
the junction of oral and nasal mucosa (Fig. 12).33
Including the entire oral palatal mucosa allows
maximal tissue to close the cleft to the level of the
alveolar cleft anteriorly. Comparisons of growth
following the two-flap palatoplasty (with complete
undermining of the mucoperiosteum) and von
Langenbeck or Veau-Wardill-Kilner repair would
be worthwhile. The two-flap palatoplasty under-
mines the most, followed by the von Langenbeck
and then the Veau-Wardill-Kilner. The two-flap
palatoplasty leaves a lateral area of denuded bone,
as does the von Langenbeck, with a more anterior
area of denuded bone in the Veau-Wardill-Kilner
technique.
Vomer Flap
With a bilateral, complete cleft palate, further
technical considerations are required for closure
of the cleft. Because the vomer is not attached to
either free edge of the hard palate and the cleft
gap is often too wide for direct approximation of
nasal mucosal edges, a vomer flap (Fig. 13) can be
10
used for closure of the nasal mucosa. An incision
is made along the free margin of the vomer, which
is exposed in the cleft gap; two septal-mucosal
flaps are raised, creating the vomer flaps. These
flaps are then used to bridge the gap to the nasal
mucosa recruited from the underside of the me-
dial edge of the hard palate. The two-flap palato-
plasty combined with a vomer flap results in a
four-flap palatoplasty. The vomer flap has been
used particularly for wider bilateral clefts since the
1920s; more recently, its use has been advocated
as a standard repair for all bilateral clefts.23
CHOOSING APPROPRIATE SURGICAL
TECHNIQUES
Submucous Cleft Palate
Surgical repair of the submucous cleft pal-
ate is considered if velopharyngeal insufficiency
is present. In 1972, Weatherley-White et al.
showed that one in nine patients known to have
a submucous cleft palate exhibit velopharyngeal
insufficiency.34 More recent studies suggest this
fraction may be even greater.35 Classic repair of the
submucous cleft palate has been performed by
excising the entire region of the zona pellucida
and then using a posterior wall pharyngeal flap.29
This method does not restore the single, anatom-
ically normal velopharyngeal sphincter but creates
two sphincters on either side of the pharyngeal
flap. According to analysis conducted within the
past decade, a pharyngeal flap can be performed
as the primary repair of the submucous cleft pal-
ate, without need for other adjunct procedures.22
Alternatively, a Furlow repair can be used in
younger patients (younger than 20 years old) with
a small velopharyngeal gap (⬍5 mm). Given the
very different strategies used in these techniques,
prospective studies are needed to compare out-
comes after these alternative repairs.
Incomplete Cleft of the Soft Palate: Veau Class I
In this case, an infant presents with a cleft
involving only the soft palate (Fig. 3). The primary
goal of repair in this case is restoration of velo-
pharyngeal competence. This is achieved both by
lengthening the palate for proper apposition of
palate and posterior pharyngeal wall and reorga-
nization of the palatal musculature. The most
widely practiced methods of soft palatoplasty are
intravelar veloplasty or the Furlow repair.
Cleft of the Soft and Hard Palates: Veau Class II
This case involves a cleft of the entire second-
ary palate, both soft and hard palates, to the level
Volume 121, Number 1 • Nonsyndromic Cleft Palate

Fig. 13. The vomer flap allows closure of the nasal layer mucosa
in a bilateral cleft of the palate. The mucosa of the central vomer
is divided; two mucoperiosteal flaps are raised to either side
(above). These mucosal flaps are then sutured to mucosal flaps
raised from the undersides of the medial hard palate (below).

of the incisive foramen (Fig. 4). The goals of this

repair are realignment of the soft palate mucosa
and musculature to restore velopharyngeal com-
petence; closure of the bony gap between the
edges of the hard palate, which restores structural
integrity; and maintenance of growth of the oral
cavity and mid-face. Repair of a cleft of the entire
secondary palate could be performed with several
of the previously mentioned techniques, includ-
ing the von Langenbeck or Veau-Wardill-Kilner

Fig. 12. Markings for a Bardach two-flap palatoplasty (above). alone (center). The tips of the two flaps are then sutured centrally
Two anterior mucoperiosteal flaps are elevated from the hard (thus, the term “pushback”) and leaves a denuded portion of hard
palate. The aberrant muscle attachments to the posterior hard palate laterally (below).

11
 Plastic and Reconstructive Surgery • January 2008
repair. Both are popular methods and are chosen
based on surgeon preference. Some surgeons may
choose a two-flap palatoplasty to repair this cleft.
The soft palate may be repaired using either the
intravelar veloplasty or the Furlow double-oppos-
ing Z-plasty.
Unilateral Complete Cleft Palate (with Cleft
Lip): Veau Class III
A complete cleft of the lip and alveolus (primary
palate) and the hard and soft palates (secondary
palate) requires correction using the two-flap pala-
toplasty (Figs. 5 and 6). The mucoperiosteal anterior
flaps are closed to the level of the anterior cleft of the
alveolus. The soft palate may be corrected with an
intravelar veloplasty or with a Furlow double-oppos-
ing Z-plasty.
Bilateral Complete Cleft Palate (with Cleft Lip):
Veau Class IV
The bilateral complete cleft (involving the lip,
alveolus, and the entire hard and soft palates) also
requires closure using a two-flap palatoplasty tech-
nique (Figs. 7 and 8). There tends to be a paucity
of oral mucosa, requiring careful release of both
neurovascular bundles to medialize the oral mu-
cosal flaps. In addition, because of a greater width
across the hard palate cleft, the need for a vomer
flap arises, to provide a continuous closed nasal
mucosal layer. The portion of the cleft involving
the soft palate could be closed with either a Furlow
double-opposing Z-plasty or an intravelar velo-
plasty to appropriately recreate the muscle sling.
TIMING OF REPAIR
Appropriate timing for repair of the palate
continues to be debated. There is evidence that
earlier repair benefits speech development36 and
that delayed repair benefits maxillofacial growth,
because transverse facial growth is not complete
until 5 years of age.29 Historically, maxillofacial
growth has been emphasized as an outcome mea-
sure for determining appropriate timing for pal-
ate repair, resulting in delayed palate repair, with
some surgeons advocating delayed repair of the
hard palate until after the age of 837; more re-
cently, however, speech outcomes have been em-
phasized and earlier timing of primary palato-
plasty (before 2 years of age) has become the
norm.23 Some surgeons repair the palate within
the first few weeks of life, claiming that this further
optimizes speech results.38 The current debate fo-
cuses on how early the repair should be per-
formed. LaRossa has recommended repair of both
12
hard and soft palate defects by 18 months of age.23
A comprehensive review by Rohrich et al. recom-
mends a two-stage palate repair, with soft palate
repair at 3 to 6 months of age and hard palate
repair at 15 to 18 months of age.39 The majority of
practitioners, however, repair both hard and soft
palates simultaneously between 9 and 12 months
of age, finding a compromise between the benefits
of early repair for speech outcomes and delayed
repair for growth outcomes. Long-term outcome
studies in the United States are currently in the
process of comparing patients in whom palato-
plasty was performed between 9 and 12 months of
age to those in whom palatoplasty was performed
at an earlier age.40
Because more than half of children with cleft
palate deformities may have other anomalies, tim-
ing strategies for palatoplasty change with these
comorbidities. In children with Pierre Robin se-
quence, for instance, the timing of palatoplasty is
dependent on the child’s airway status; it is often
prudent to delay primary closure until after 12
months of age to minimize the risk of airway ob-
struction. Similar strategies are also required for
patients with other syndromes in which airway ob-
struction is an issue, such as Treacher-Collins, Ap-
ert, or Crouzon syndrome.41 Overall, however the
trend in timing for palatoplasty is moving toward
repair before 1 year of age.
OUTCOMES
Complications following palatoplasty include
fistula formation, velopharyngeal insufficiency,
midface growth retardation, and sleep apnea. Fis-
tula rates after primary palate repair have varied
widely in the literature from a high of 50 percent
to a low of 3.4 percent.42 Multiple factors influence
fistula rates, including surgeon,43 type of repair,44
cleft size,45 and timing of repair.46 Younger, more
inexperienced surgeons tend to have higher fis-
tula rates; Veau-Wardill-Kilner pushback repairs
reportedly result in higher fistula rates than von
Langenbeck repairs, which were in turn are re-
portedly higher than Furlow/intravelar veloplasty
repairs.44 Wider clefts or those clefts involving the
primary palate (in addition to the secondary pal-
ate) result in higher fistula rates.45 Fistulas are
more common in bilateral clefts than in unilateral
clefts following palatoplasty.46 The relationship of
timing of repair appears to lead to mixed results,
with some studies suggesting that early repair
leads to fewer fistulas.39 Of all palatal fistulas, 87
percent occur in the area of the hard palate clo-
sure, and over half of these occur immediately
posterior to the alveolus.44
Volume 121, Number 1 • Nonsyndromic Cleft Palate
Velopharyngeal insufficiency following palate
repair is characterized by a typical hypernasal
speech that may require secondary palatal surgery
for correction, and results from poor function of
the soft palate. Rates of velopharyngeal insuffi-
ciency vary in the reported literature and depend
significantly on an exact definition of velopharyn-
geal insufficiency. Completely normal speech may
be difficult to achieve for multifactorial reasons.47
Depending on the initial definition of velopha-
ryngeal insufficiency, rates of approximately 20
percent are generally reported, with the best re-
sults in the single digits.48
There is an inherent midface hypoplasia that
results from the presence of clefts.49 This growth
disturbance is more pronounced in patients with
clefts of both the primary and secondary palates
than with clefts of the secondary palate alone.
However, some studies of unrepaired clefts of
both the primary and secondary palates (lip and
palate) suggest that growth of the maxilla is
normal.50 It has been suggested that surgery itself
is the culprit in causing growth hypoplasia,51 pri-
marily in the lip repair52 and, to a lesser extent, in
the palate repair.53 Although all patients may be at
risk for the development of sleep apnea, the chil-
dren at highest risk would be those with syn-
dromes and children with Pierre Robin sequence.
CONCLUSIONS
Clefts of the secondary palate are the result of
a complex interplay of genetic and environmental
causes. Certain genetic backgrounds enhance the
risk for clefting caused by tobacco use, alcohol
consumption, and folic acid deficiency. After de-
livery of a child with a cleft of the palate, feeding
issues predominate. Close monitoring of weight
gain is critical for the child. Evaluation by a cranio-
facial team is essential to rule out other potential
anomalies and/or syndromes in these children.
Simultaneous repair of both the hard and soft
palate cleft is performed by most practitioners at
approximately 10 months of age, though some
practitioners advocate early palate repair and oth-
ers perform staged repairs of the soft and hard
palates. The choice of technique for repair is often
surgeon dependent. The goals of surgery, how-
ever, should be similar, and they include separa-
tion of the oral and nasal cavity, with restoration
of the velopharyngeal sphincter, allowing normal
speech. Careful interdisciplinary postoperative
follow-up is necessary to detect and potentially
correct fistula formation, velopharyngeal insuffi-
ciency, maxillary growth deficiencies, and sleep
apnea.
John A. van Aalst, M.D., M.A.
Division of Plastic Surgery
University of North Carolina, Chapel Hill
7033 Burnett-Womack Building, CB 7195
Chapel Hill, N.C., 27599
john_vanaalst@med.unc.edu
CPT Codes Commonly Used in Cleft
Palate Surgery
Code Procedure
42200 Palatoplasty, soft and/or hard palate only
42205 Palatoplasy, with closure of alveolus; soft tissue
only
42210 Palatoplasy, with closure of alveolus; with bone
graft (includes obtaining graft)
42215 Palatoplasty; major revision
42220 Palatoplasty; secondary lengthening procedure
42225 Palatoplasty; with attachment of pharyngeal flap
42226 Palatal lengthening, and pharyngeal flap
42227 Palatal lengthening, with island flap
42235 Repair of anterior palate, including vomer flap
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