Cleft Palate.pptx

Cleft Palate
Presented by:
Dr. Neha Umakant Chodankar
PG OMFS

Contents
• Introduction
• History
• Embryology
• Epidemiology
• Genetics and Etiology
• Associated Syndromes
• Anatomy
• Classification
• Clinical Features and Evaluation
• Treatment Planning and Timing
• Cleft palate surgery
• Complications
• Secondary deformities of cleft palate
• Conclusion
• References

Introduction
The comprehensive treatment of cleft lip and palate deformities requires
thoughtful consideration of the anatomic complexities of the deformity and
the delicate balance between intervention and growth.
Goals of surgical care:
• Normalized esthetic appearance of the lip and nose
• Intact primary and secondary palate
• Normal speech, language, and hearing
• Nasal airway patency
• Class I occlusion with normal masticatory function
• Good dental and periodontal health
• Normal psychosocial development

History
• 1st recorded operative treatment of only cleft lip -- Chin (Tsin) Dynasty (c390 AD)
• The first diagrammatic representation -- Ambrose Pare in the 14th century
• The first cleft palate repair --by a dentist, Le Monnier, in 1766 in Paris
• John Stephenson (1797–1842), a physician --wrote the earliest recorded
description of Palatoplasty performed by Philibert Roux (1780–1854 Paris)-- the
primary repair of velum at age of 22
• Roux later published his account of the procedure in 1825, --“staphyloraphie”
• Carl Ferdinand von Graefe (1787–1840), proclaimed that he, was the first surgeon
to perform velar closure in 1819. Von Graefe eventually reported a successful
repair in 1820.

• The first successful closure of the soft palate in America --John Collins
Warren in 1820 in Boston.
• Johann Friedrich Dieffenbach (1792–1847 Berlin) -expanded the technique
of soft palate repair to include closure of the hard palate.
• Bernhard von Langenbeck (1810–1887) --first to describe the
mucoperiosteal plane of dissection and to use its advantage in mobility to
cleft palate closure.
• In the mid 19th century, Hullihen, recognized as the father of American oral
and maxillofacial surgery, published a treatise on comprehensive care of
cleft lip and palate deformities.

• von Langenbeck (1859, 1861) extended these concepts, and
described a Bipedicled flap procedure
• Veau (1931) converted the bipedicled flaps of von Langenbeck to
single pedicled flaps based on greater palatine vessels, and
emphasized the need for palatal lengthening
• Wardill (1937) and Kilner (1937) modified Veau's procedure
• Dorrance and Barnsfield (1946) described the use of a skin graft in the
raw palatal surface after the procedure.

Embryology
• The failure of fusion of the
frontonasal and maxillary processes
at 6 weeks IUL, gives rise to the
cleft of the primary palate, which
includes the lip, alveolar process,
and the hard palate anterior to the
incisive foramen.

• The lateral palatal shelves fuse
later than the primary palate,
around 7–8 weeks gestation
• They rotate from vertical to
horizontal orientation.
• This fusion proceeds from anterior
to posterior, which helps to
understand the spectrum of clefts
of the secondary palate.

Epidemiology
• Clefts of the upper lip and palate are the most common major congenital
craniofacial abnormality ---1 in 700 live births
• Bilateral clefts of the lip are most often associated primary and secondary
cleft palates
• Cleft palate alone is seen in approximately 1 in 2,000 live births and this
incidence is similar in all racial groups
• In the majority of cases unilateral cleft lip and palate is an isolated
nonsyndromic birth defect that is not associated with any other major
anomalies

Genetics and Etiology
Cleft lip and palate is not considered a single gene disease, although
inheritance may play a role--- multifactorial
• These factors may include chemical exposures, radiation, maternal hypoxia,
teratogenic drugs, nutritional deficiencies, physical obstruction, or genetic
influences.
• Recently multiple genes have been implicated in the etiology of clefting---
MSX, LHX, goosecoid, and DLX genes
• Disturbances in growth factors or receptors—FGF, TGF, PDGF and EGF

Associated Syndromes
• Stickler’s syndrome
• Van der Woude’s syndrome
• DiGeorge syndromes
• Treacher Collins Syndrome
• 22q deletion Syndrome
• Pierre Robin Sequence

Classification
Based on morphology
I Davis & Ritchie's classification
II Veau's classification
Based on embryology
1. Fogh- Anderson classification
2. Kernahan's & Starks classification
3. American cleft palate association
Graphic methods of recording clefts
1. Pfiefer classification
2. Kernahan's striped Y classification
3. Millard's modification of striped Y classification

Davis & Ritchie's classification (1922)
Group I: Prealveolar process cleft
1. Unilateral (right/left: complete/incomplete)
2. Bilateral (right: complete/incomplete; left: complete/incomplete)
3. Median (complete/incomplete)
Group II: Postalveolar process cleft
1. Soft palate
2. Hard palate
Group III: Alveolar process cleft
1. Unilateral
2. Bilateral
3. Median

Veau' s classification (1931)
• Group 1- cleft of the soft palate only
• Group 2-cleft of the hard and soft palate to
the incisive foramen
• Group 3-complete unilateral cleft of the soft
hard palate & lip & alveolar ridge on one
side
• Group 4-complete bilateral cleft of the soft
hard palate & lip & alveolar ridge on both
sides

Fogh –Anderson Classification (1942)
1.Harelip (single or double)
2. Harelip with cleft palate
3. Isolated cleft palate
4. Rare atypical clefts, e.g., median cleft lip

Kernahan & Stark’s Classification (1958)
A) Clefts of primary palate
1. Unilateral complete/ incomplete
2. Median
complete (premaxilla absent)
incomplete (premaxilla rudimentary)
3. Bilateral complete/incomplete
B) Clefts of secondary palate only
Complete/ Incomplete/ Submucous
C) Clefts of primary and secondary palate
1. unilateral complete/incomplete
2. median complete/ incomplete
3. bilateral complete/ incomplete

American Cleft Palate Association Classification
1. Clefts of the prepalate (cleft of lip and embryologic primary palate)
a. Cleft lip (cheiloschisis)
b. Cleft alveolus (alveoloschisis)
c. Cleft lip, alveolus, and primary palate (cheiloalveoloschisis)
2. Clefts of the palate (cleft of the embryologic secondary palate)
a. Cleft of the hard palate (uranoschisis)
b. Cleft of the soft palate (staphyloschisis or veloschisis)
c. Cleft of the hard and soft palate (uranostaphyloschisis)
3. Clefts of the prepalate and palate (alveolocheilopalatoschisis)

4. Facial clefts other than prepalatal and palatal
a. Cleft of the mandibular process
b. Naso-ocular clefts
c. Oro-ocular clefts
d. Oroaural clefts

Spina classification (1974)
• Group I – Pre-incisive foramen clefts
• Unilateral
• Bilateral
• Median (CL with or without alveolar), total or partial
• Group II – Trans incisive foramen clefts
• Unilateral
• Bilateral
• Group III – Post incisive foramen clefts
• Total
• Partial
• Group IV – Rare facial clefts

Kernahan’s Stripped Y Classification 1971

Millard’s Modification Of Stripped Y 1976

Clinical Features
Cleft palate with cleft lip and alveolus
• Asymmetry
• Alveolar cleft between the maxillary lateral incisor and
canine tooth roots
• Malposition of the maxillary lateral incisor and cuspid in
both the deciduous and permanent dentition
• Unilateral complete cleft palate is characterized by direct
communication between the entire length of the nasal
passage and oropharynx

• The nasal septum is deviated and buckled toward the
cleft side
• The absence of a portion of the inferior piriform
aperture and the hypoplasia of the lateral nasal bony
platform at the maxillary wall contribute to the cleft
nasal deformity
• the nasal base is depressed, the ala is collapsed, and the
floor is wide

• In the bilateral complete cleft lip and palate, the pre-
maxillary segment containing the central and lateral
incisor teeth is discontinuous from the alveolar arch
• The lateral segments often collapse inward and
lingually, resulting in “locking out” of the premaxilla
• Speech problems and nasal regurgitation of fluid

Clefts of the secondary palate
• a cleft of the secondary palate may be variable, from an opening in
the posterior soft palate to a cleft extending up to the incisive
foramen
• There is almost always a separation of the bony shelves of the hard
palate
• Most commonly, dentition is normal and symmetric.

Ear Pathology
• Chronic obstruction of drainage
leads to serous otitis media, and
long-standing effusion can result in
hearing loss
• Untreated children with clefts and
severe effusions may have total
deafness

Speech
• The ability to partition the
oropharynx and
nasopharynx is crucial for
normal speech production
• The palate elevates during
production of any sounds
requiring positive pressure
in the oropharynx; the
levator palatini is primarily
responsible for this
movement.

• If palate function is not corrected, velopharyngeal insufficiency results
• When complete closure cannot be anatomically or functionally obtained,
compensatory mechanisms for sound production are learned
• Eliminating these learned compensatory articulations is difficult, even with
the best of speech and language therapy
• Compensatory articulations may persist even in the face of a functional
palate repair, especially in later repairs or secondary correction of
velopharyngeal insufficiency

Growth
• Cleft infants exhibit poor weight gain in early infancy
• Initial growth retardation by the time they undergo surgical lip repair
• When the same children reach the age for palatoplasty, they have
significantly lagged on the growth curve
• Causes: --feeding difficulties early in life before palate repair
- intrinsic growth disturbances
- increased frequency of ear and airway infections
- multiple operative procedures
- growth hormone levels may be diminished

Feeding and swallowing
• Most infants with clefts are unable to breast-feed
• Infants with clefting limited to the posterior velum can often use posterior
tongue position to generate a partial negative seal
• The exception to this is the child with Pierre Robin sequence and isolated
velar cleft, who can develop respiratory distress or ineffective suction from
glossoptosis

Feeding and swallowing
• Infants who are unable to breast-feed because of cleft palate have a number
of options for feeding:
-specialty nipples such as lamb’s nipples
-crosscutting of standard nipples
-long soft nipples that place the liquid at the posterior tongue
-Special flow bottles such as gravity flow and squeeze bottles allow the caregiver
to carefully control the flow rate
• Children with clefts generally do not have difficulty with swallowing and
aspiration unless intrinsic neuromuscular abnormality of the tongue or
pharynx is present.

• Aspiration with swallowing --diagnostic evaluation, including
-thin barium swallow studies
-bronchoscopy
-gastroscopy
• Children may cough or sputter with reflux of the ingested material into the
nose, particularly if volume or rate of feeding is excessive
• When the palate has an open cleft, food may reflux into the nasal passage
• Nasal reflux is irritating to the nasal mucosa and can predispose to sinusitis
and ulceration
• regurgitation of food through the nose

Submucous cleft palate
• Calnan’s classic triad of
-a midline clear zone (zona pellucida)
-a bifid uvula
-a palpable notch in the posterior hard palate
• With contraction of velar musculature, a
distinct midline muscle diastasis may be seen
• symptomatic with regard to speech, serous
otitis media, or hearing loss

• Patients with velopharyngeal insufficiency and submucous cleft palate on
examination require full evaluation, including speech evaluation and
endoscopy
• Even in the absence of obvious findings on clinical examination, anatomic
abnormalities are found (>90%) at the time of surgery----occult submucous
cleft palate
• Corrective surgical technique ---anatomic correction of the velar muscle
diastasis
• Primary means of treatment-- pharyngeal flaps and sphincter
pharyngoplasty
• The Furlow double opposing Z-plasty is an ideal procedure

2 schools of thought
1. Only soft palate closed 12 – 18 months
Hard palate 5 -- 10 years
2. Soft palate + hard palate -- 18 months
• Most severe deformity , when palate repaired between 8 – 12 years (rapid maxilla
growth)
• Maxillary underdevelopment
To allow maxillary growth
Because speech is critical
Management

Timing of palate repair
Speech
• The driving force for palatoplasty is the development of normal speech
• Two crucial aspects of palatoplasty are important in optimal speech
outcome: (1) surgical technique and (2) timing of palate repair
• Victor Veau first made the observation of a correlation between age at
repair and speech outcome in 1931
• Variables of technique, surgeon’s skill, lack of standardization of speech
evaluations, and therapies preclude exact determination of optimal age at
repair

Maxillary growth
• Transverse growth of the maxillary arch is narrowed---- resulting in typical
malocclusion traits of crowding, lateral cross-bite, and open bite
• due to surgical scarring or intrinsic maxillary underdevelopment
• There may be a sagittal growth deficiency
• It is more difficult to establish normal speech in older children after cleft
repair than to correct occlusion with a combination of orthodontic
treatment and orthognathic surgery

Procedure Timing
Cleft lip repair After 10 weeks
Cleft palate repair 9–18 months
Pharyngeal flap or pharyngoplasty 3–5 years or later based on speech development
Maxillary/alveolar reconstruction
with bone grafting
6–9 years based on dental development
Cleft orthognathic surgery 14–16 years in girls, 16–18 years in boys
Cleft rhinoplasty After age 5 years but preferably at skeletal maturity;
after orthognathic surgery when possible
Cleft lip revision Anytime once initial remodeling and scar maturation is
complete but best performed after age 5 years

The primary goals of cleft palate surgery are
• Construction of an air- and water-tight velopharyngeal valve
The three procedures used today for constructing a tight valve are
(i) Closure of palate with reconstruction of the levator muscle sling
(ii) V-Y retropositioning of the palate
(iii) Simultaneous closure of palate and primary pharyngeal flap
• preservation of hearing
• preservation of facial growth
• functional occlusion and aesthetic dentition

Surgical technique
• Perioperative considerations
-general health and the developmental status of the child
-Audiology evaluation
• The use of a RAE endotracheal tube
• placement of the Dingman gag without kinking the tube
• Constant assessment of the airway
• LA infiltrated into the palate 7–10 min before incision; (maximum of 1
mL/kg is used)

• The important aspect of surgical anatomy is the location of the greater
palatine neurovascular bundle
• Incisions on each side are best made with the surgeon’s contralateral hand
to bevel the incision away from the vascular pedicle
• Circumferential freeing of the palatal attachments around the pedicle and
gentle stretching of the pedicle out of the foramen are essential to obtain a
tension-free closure of the oral flap
• The goal is to obtain complete nasal and oral closure
• The most difficult area for closure, around the junction of the hard and soft
palate, is the most common location for fistulas

Objectives of Palatoplasty
• To produce anatomical closure of the defect
• To create an apparatus for development and production of normal
speech
• To minimize the maxillary growth disturbances and dentolveolar
deformities
Agrawal--Cleft palate repair variations S103 Indian J Plast Surg Supplement 1 2009 Vol 42

Principles of Palatoplasty
• 9-12 months of age
• 8-10 kgs weight
• Dissection under magnification
• Closure of the defect in 3 layers
• Correction of abnormal position of the muscles of the soft palate
• Reconstruction of the muscle sling
• Retro-positioning of the soft palate

Schweckendiek’s Primary veloplasty
Medial margin incision: the uvula Medial and lateral incisions.

Mucosal nasal surface
Sutures through mucosa
and muscle
Closure of soft palate(9 mths).
Suture tips of uvula together and clip suture onto head towels
Evert uvula.
Complete
sutures on
nasal surface
and return on
oral surface
including
muscle in both
layers
Closure of soft palate
Pack with
Lyostypt if
there is a
large deficit
Undermining of
mucosa at site of
previous“incisions
or incise and rele
Incision around margin of residual defect,
eversion of mucosa and closure
Bipedicled flaps raised and
advanced medially to close oral
surface
Closure of hard palate (14 mths)

von Langenbeck
Simple approximation of
the cleft margins with a
relaxing incision that
began posterior to the
maxillary tuberosity and
followed the posterior
portion of the alveolar
ridge

The essence of the
pushback repair is the
central V incision on the
hard palate that is then
closed in a straight line,
creating length on the oral
side of the closure
V-Y pushback (Veau–Wardill–Kilner)

Advantages
• provides increased length for the palate
• places the levator muscle in a more favorable position
Disadvantage:
• Large open areas are left anteriorly and on the nasal surface
• Heal by contraction and decrease in length
• Contraction of the oral mucosal defects results in loss of maxillary width
anteriorly
• The arch may also be flattened anteriorly
• The closure anteriorly in a complete cleft is a single layer of nasal mucosa
only, which gives rise to a higher fistula rate

Two-flap
Palatoplasty
A technique of freeing
mucoperiosteal flaps from
the cleft margins only

Vomer flaps
• one-layer (nasal) closure
Incisions- through nasal mucosa on underside of nasal
septum (vomer) and mucosa of cleft margins.
• Mucosa of nasal septum is dissected and inserted under
palatal mucosa at margins of cleft and sutured .
Undersurface of nasal mucosa will epithelialize

Intravelar veloplasty
• Victor Veau first advocated midline reapproximation of the levator palatini
muscle
• Braithwaite was the first to perform more extensive muscle dissection and
freeing of the muscle for posterior repositioning and tension-free
approximation
• Cutting has described a technique of veloplasty that includes division of the
tensor palatini tendon and repositioning of the muscle at the Hamulus
• This method, known as radical levator transposition, requires an extensive
dissection of the levator muscle, freeing it from both nasal and oral mucosa

Postoperative care
• In the immediate postoperative period, breathing is the critical concern--
use of a traction suture
• Monitoring with continuous pulse oximetry and minimizing narcotic use
• Adequate pain relief
• Observe for at least 48h for tongue edema
• Bleeding is not uncommon after palate repair (12–24 h)
• Light pressure on the hard palate repair at the end of the procedure
• Application of ice packs to the posterior neck
• Postoperative feeding is generally limited to liquids for 10 –14 days
• Arm splints

Complications
SURGICAL
COMPLICATIONS
ANESTHETIC
COMPLICATIONS
INTRAOPERATIVE
COMPLICATIONS
IMMEDIATE
POSTOPERATIVE
COMPLICATIONS
LATE
POSTOPERATIVE
COMPLICATIONS
COMPLICATIONS OF
PALATOPLASTY
• HEMORRHAGE
• RESPIRATORY
OBSTRUCTION
• HANGING
PALATE
• DEHISCENCE
• FISTULAE
• BIFID UVULA
• VPI
• MAXILLARY
HYPOPLASIA
• DENTAL
MALALIGNMENT
• OTTIS MEDIA
• HEMORRHAGE
• PEDICLE LOSS
• FLAP TEARING
• TUBE
DISCONNECTION
• DIFFICULT
INTUBATION
• HYPOTHERMIA

Management of Secondary Deformities
• Timing: --Symptomatic fistulas usually require surgical repair
--asymptomatic fistulas can be addressed during other procedures

Technique:
Nasal layer closure can be accomplished with
• Turnover flaps from the mucosa lining the fistula
• Mucoperiosteal vomer flaps, or from mucosa of the posterior pharyngeal
wall
Oral layer closure can be accomplished using
• local palatal mucoperiosteum
Flaps may be designed unilaterally or bilaterally, elevated in either unipedicle
or bipedicle fashion

• When closing the oral layer with local or adjacent tissue
Design of the flaps:
olarger than the defect
othere should be minimal tension on these flaps at the time of closure
oosteotomize the greater palatine foramen if needed
oislandization of hemipalatal flaps can be performed to release additional
tension
oavoid overlapping the nasal and oral layer suture lines

• Closure using biomaterial:
-Kirschner et al. used acellular dermis (Alloderm) to augment palatal fistula
repair by sandwiching a thin sheet between the recreated nasal and oral
mucosa layers
• There are still situations in which a tension-free repair is not possible with
palatal tissue-----regional axial pattern flaps

• 3 intraoral tissue options for palatal fistula
closure:
-buccal mucosa
-the tongue
-the posterior pharyngeal wall
• The buccal tissue can also be harvested based
on the facial artery
This axial flap can be based either superiorly (relying on retrograde flow) or
inferiorly (relying on antegrade flow)
The superiorly based flaps are primarily used to close defects involving the hard
palate and alveolus, while inferiorly based flaps are used to close defects in the
posterior hard palate, soft palate, and posterior portions of the alveolus

• Advantages:
- its design prevents damage to the
facial nerve and Stensen’s duct
- its robust blood supply
- the flap can be designed to be
long (length-to-width ratio of
5 : 1)
- Flap can be folded over on to itself
to form a two-layered structure

• For particularly recalcitrant defects--the tongue flap
-Initially, the flap was raised as a thick and bulky flap
-Assuncao ---thin (5 mm at base, and 3 mm distally) flaps
could be based anteriorly
Disadvantages—
othe tongue must be tethered to the palate for 2–3 weeks
othe texture and color are a poor match
ochanges in articulation postoperatively
oSecond surgery needed

• The temporoparietal flap
• When local and regional flaps have failed, microvascular tissue transfer
-the radial forearm flap is the flap of choice
-first dorsal metatarsal artery dorsalis pedis flaps
-the osseous angular scapular flap
- the lateral upper arm fasciocutaneous flap
• Prosthetic obturation
• dento-osseous transport distraction osteogenesis in persistent nasoalveolar
fistulas

Velopharyngeal incompetence
• The main characteristic of VPI is the hyper nasal quality of speech
• The procedures available for the correction of VPI are
o Palatal lengthening procedures
o Pharyngeal flaps
o Augmentation of the posterior pharyngeal wall
o Reconstruction of velopharyngeal sphincter

Conclusion
Overall, results of cleft palate repair have improved as far as speech
outcomes and is probably due to the growth of centers for cleft care as well
as to refinement of techniques.
The team approach has decreased the number of operations needed to
obtain better outcomes as the surgeon has gained knowledge from the other
specialists involved in cleft care.
The increased application of methods that incorporate reconstruction of the
levator palatini muscle has produced much more predictable speech results.

References
• Neligan Plastic Surgery vol 3
• Petersons principles Oral and Maxillofacial Surgery 3rd ed
• Text book of plastic surgery - Joseph McCarthy; VOL 4.
• Text book of oral and maxillofacial surgery - Peter Ward Booth, vol 2.
• Textbook of Plastic Surgery Mc MCarthy
• AOMSI clinicians manual
• Slideshare

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