2. INTRODUCTION
common congenital disorder
have numerous associated problems,
including
basic anatomic deformity,
deficient facial growth,
dental problems
speech problems
otologic problems
psychologic disorders, and
additional congenital anomalies.
3. History
400BC Hippocrates and 150AD Galen mentioned cleft lip
500 AD 1st Operation on palate due to inflammation of the uvula
1564 Pare described the use of obturators for palatal perforations
1556Cleft palate recognised as a congenital disorder by Franco.
1764 LeMonnier, a French dentist performed 1st successful
repair of a cleft velum.
1834Dieffennbach performed the 1st closure of the hard palate
1861Von Langenbeck described the use of mucoperiosteal flaps in
cleft palate closure
1930Kilner and Wardill independently developed the ‘pushback’
procedure.
1944 Schweckendiek began closing cleft defects in young patients.
4. Epidemiology and Genetics
The incidence of cleft palate only is half the incidence of
CL/P (more than 1 : 2000 live births).
There is usually little difference between racial groups.
The incidence is much higher (about 4 : 1) in females
than in males.
About 20% to 30% of human cleft palate only are
syndromic.
Pierre-Robin Sequence,
Treacher-Collins Malformation,
Trisomies 13 and 18,
Apert’s Syndrome,
Stickler’s Syndrome and
Waardenburg’s Syndrome.
5. Epidemiology and Genetics
Familial risk
One sibling with cleft, no parent with cleft 2%
One sibling and one parent- 10-17%
No sibling with cleft and are parent with cleft 7%
Environmental factors exerting their
teratogenic effects
Those with proven clefting potential in humans
include
phenytoin,
retinoic acid (vitamin A) derivatives,
folic acid antagonists.,
cigarette smoking creating fetal hypoximia
alcohol use in the first trimester of pregnancy
6. Anatomy
Primary palate or premaxilla is
a triangular area of the anterior hard palate extending from the
anterior to the incisive foramen and to a point just lateral to each
lateral incisor tooth. It includes the alveolar ridge containing the
four incisor teeth.
Secondary palate:-
Consist of all remaining hard palate and are the soft palate.
Hard palate-
Formed by palatine processes of maxilla and horizontal lamina of
palatine bones.
Blood supply internal maxillary art- greater palative Ar.
Soft Palate
A fibromuscular shelf made up of several muscles attached like a
sling to the posterior portion of the hard palate
Function- close off the nasopharynx
7. EMBRYOLOGY
The primary palate develops between 4 and 5
weeks gestation
secondary palate between 8 and 9 weeks
gestation.
The primary palate, lip and alveolus develop as
a mesodermal and ectodermal proliferation of
the frontonasal and maxillary processes.
A primary cleft is a failure of proliferation, not a
failure to meet in the midline.
The secondary palate develops as a medial
ingrowth of the lateral maxillae with fusion in the
midline.
9. CLASSIFICATION
no standard classification is universally
accepted.
Cleft palate
A. Location in reference to incisive foramen
1. Primary—anterior
2. Secondary—posterior
B. Unilateral or bilateral
C. Complete or incomplete
Submucous cleft palate
10. Classification (Iowa system)
Group I - cleft of lip only
Group II - Cleft of palate only
Group III - Clefts of lip alveolus
Group IV - Cleft of the lip and alveolus+
Palate
Group V - Miscellaneous
11. GENERAL MANAGEMENT
The multidisciplinary cleft team approach
The comprehensive multidisciplinary team
surgeon (plastic, pediatric surgery, oromaxillofacial surgery, or
otolaryngology)
otolaryngologist/otologist,
dentist (pedodontist, orthodontist, prosthodontist, oral surgeon),
speech language pathologist,
audiologist,
geneticist,
Social worker,
nurse,
nutritionist, and
psychiatrist/psychologist.
12. Management: Neonatal Period.
The pediatrician is ideally suited for counseling
in the immediate postpartum period.
Children with clefts of the secondary palate
usually have severe difficulties feeding.
A soft bottle with a large opening is usually required.
palatal prosthesis.
A nasogastric tube is rarely required.
palatal prosthetic plates.
plates mold the palate into a more ideal position, leading to
less difficulty feeding and an easier surgical repair.
improve facial growth and children require less intervention
throughout time
13. Management:
The timing of the repair is controversial
Palatal repair is performed anywhere from
6 months onward.
delay in palatal repair results in improved midfacial
growth
earlier repair results in better speech
14. Management: Toddler Years.
The most important process in the toddler
years is the development of adequate
speech
requires speech therapy
The child is trained to speak slowly and forcefully in order to
maximize palatal elevation and minimize hypernasality
up to 20% of patients still require
pharyngoplasty to reduce VPI
recurrent or chronic ear infections
growth hormone deficiency is 40 times more
common in this population
15. Management: School Years
orthodontic management
psychological growth
psychotherapist is essential to ensure
adequate social development
high rate of depression and poor self esteem
Child abuse is also more common
16. Management: Teenage Years.
The teenage growth spurt is marked by
midface retrusion, altering appearance.
Palatal repair is likely responsible
ideal timing for palatal repair so that midface retrusion is minimized is
currently an area of intense research, with many conflicting studies in
the literature
The treatment requires maxillary
advancement through a combination of
LeForte I, II and III osteotomies.
The treatment of midfacial retrusion requires maxillary
advancement through a combination of LeForte I, II and
III osteotomies.
usually performed in young adulthood, after growth is complete
Rhinoplasty, when required, is usually the last surgery
performed.
17. Surgical Techniques
The child with CLAP usually undergoes
numerous surgical procedures.
The first procedure is repair of the lip, which occurs around
10 weeks.
The palate is usually repaired between 6 and 18 months,
with newer studies advocating earlier repair
Pharyngeal flaps, if required, are performed around age 4.
Alveolar bone grafting occurs between ages 9 and 11,
definitive orthodontics at age 12-13.
Maxillary advancement and rhinoplasty are delayed until
the later teenage years.
18. Surgical Techniques
Palatoplasty
The basic surgical techniques of palate repair
include Schweckendiek’s procedure or primary
veloplasty,
Von Langenbeck’s palatoplasty,
V-Ypush-back
double reversing Z-plasty (Furlow’s palatoplasty),
and two-flap palatoplasty.
A combination of palatoplasty and pharyngeal flap
may be used for the repair of extremely large
clefts15 and occasionally for primary palate repair.
19. • Pre-Surgical
Orthopedics allowing
gingivoperiosteoplasty.
A: Wide unilateral cleft lip with separation of
the arch and collapse of the lesser segment.
B: Improved arch alignment and nasal shape
after presurgical orthopedic treatment.
C: Results after rotation-advancement lip
repair, nasal repair, and
gingivoperiosteoplasty, all performed at the
first operation, when the child is
approximately 3 months of age.
20. Palatoplasty Technique. A: Cleft palate closure after healing of
gingivoperiosteoplasty at 11–12 months of age. Bilateral, unipedicle
mucoperiosteal flaps based on the greater palatine arteries are elevated. B:
Anteriorly, the nasal floor is repaired by suturing the vomerine mucosa to the nasal
mucosa on the cleft side.
21. Palatoplasty Technique. The levator
muscles are dissected free from the oral and nasal mucosa and released from the
posterior edge of the hard palate. The levator muscles are approximated to each other
in the midline. D: The oral mucosa is reapproximated in the midline with interrupted
horizontal mattress sutures.
25. SUBMUCOUS CLEFT PALATE
The submucous cleft palate is traditionally defined by a triad of
deformities:
a bifid uvula,
a notched posterior hard palate, and
muscular diastasis of the velum.
A submucous cleft palate can vary considerably, however, and
muscular diastasis can occur in the absence of a bifid uvula.
The majority of patients with are asymptomatic, although
approximately 15% will develop velopharyngeal insufficiency.
Velopharyngeal incompetence (VPI) correlates with short palatal
length, limited mobility, and easy fatigability of the palate.
Since the majority of patients remain asymptomatic, a
nonoperative approach is recommended until speech can be
26. Otologic Disease
Children with cleft palate suffer from a greater
incidence of middle ear disease and hearing loss,
the primary pathology being eustachian tube dysfunction due to
abnormal insertion of the palatal musculature
Robinson et al performed a prospective study of 150
cleft palate children whose palates were repaired
between 2 and 18 months.
They found 92% of these children developed chronic otitis media
with effusion which required tympanostomy tubes
Muntz et al,
who found 96% of cleft palate children developed chronic middle
ear effusions
decreasing incidence of middle ear disease with age.
27. Otologic Disease
An aggressive approach is required in the
management of middle ear disease including
frequent myringotomy and
tympanostomy tube placement
the goal of the management of ear disease in
cleft palate patients is to
provide adequate hearing,
maintain ossicular continuity,
Maintain adequate middle ear space, and
prevent deterioration of the tympanic membrane until the
patient develops adequate eustachian tube function.
28. Otologic Disease
Indications for myringotomy and
insertion of ventilating tubes
include
persistent middle ear effusion with a
conductive hearing loss despite
adequate medical management,
recurrent acute otitis media failing
prophylaxis,
a combination of both, or
presence of a retraction pocket
29. Otologic Disease
Abnormal insertion of the levator and tensor veli palatini
muscles
into the posterior margin of the hard palate and the muscular
hypoplasia appears to be the primary cause of eustachain tube
dysfunction in cleft patients.
Recent evidence that the nature of middle ear effusions in
cleft patients is different from that in noncleft patients.
Hutton and others recently published a study on the characterization
of mucin from the effusions of cleft patients.
When compared with mucoid and serous effusions from
noncleft patients, the mucin in the middle ears of cleft
patients, contained larger glycopeptides with a larger
hydrodynamic size.
This suggests that infections in cleft patients may be
different from those in noncleft patients.