- Cleft palate is the result of epithelial breakdown with in growth failure of mesodermal tissue and lack of lateral palatal segment fusion.
- Most cleft cases are polygenic but the 5% of cleft cases associated with syndromes are said to be monogenic.
- Environmental factors like nutritional deficiencies, stress, infections, alcohol, drugs, toxins and ischemia may cause clefts.
Basic Functions of Palate
Sucking is effected by an intraoral negative pressure. Lips grasp the object tightly, soft palate moves upward, simultaneously contraction by the buccal muscles and closure of the glottis affects closure of the oral cavity from the nasopharynx.
Swallowing starts as a voluntary movement. Bolus of food is taken to the posterior part of the tongue, then the involuntary movement begins and this helps to take the food into the pharynx. Retroflux of the food into the nasal cavity is prevented by the contraction of palatopharyngeal muscles, which narrow the nasopharyngeal isthmus and the levator palatini muscles draw the soft palate upward and backward to press it against the posterior pharyngeal wall. At the same time tensor palatini muscles open the eustachian tubes to equalize the pressure. Hence the food is not allowed to go back into the oral cavity.
Speech is produced by the expired air, which is used to vibrate the vocal cords to produce a sound. The sound produced is thus modified by the voluntary changes in the size and shape of the oral and nasal passages. These passages act as a dynamic resonating chamber, e.g. soundbox. The outgoing air may be almost completely stopped in the oral cavity to produce the plosive sounds or may be allowed to go into the nose to produce nasal sounds.
In cleft palate deformity, oral and nasal cavities are not separated from each other, hence the main purpose of repair of the cleft palate is to improve these functions of sucking, swallowing and speech, which are greatly affected.
Veau classification of Cleft palate
- Class I: Cleft limited to soft palate
- Class II: Defects of both hard and soft palate. They extend till the incisive foramen
Cleft palate can either be complete or incomplete:
- Complete cleft includes cleft of soft and hard palate to the incisive foramen.
- Incomplete cleft involves the velum and a portion of the hard palate.
- Class III: These are complete unilateral clefts extending from the uvula to the incisive foramen in the midline and the alveolar process unilaterally.
- Class IV: Complete bilateral clefts involving the soft and hard palate and alveolar process on both sides of premaxilla leaving it free and often mobile.
- Cleft of soft palate including submucosal clefts are associated with eustachian tube dysfunction, recurrent otitis media and hearing deficits.
- Dental anomalies include congenitally missing lateral incisor, supernumerary teeth, delayed tooth formation, enamel hypoplasia, micro/macrodontia and fusion.
Syndromes associated with cleft palate
- Beckwith–Wiedemann syndrome
- Cleidocranial dysplasia
- Crouzon syndrome (craniofacial dysostosis)
- Ehlers–Danlos syndrome
- Fetal alcohol syndrome
- Gorlin syndrome (basal cell nevus syndrome)
- Marfan syndrome
- Pierre Robin syndrome
- Rubinstein–Taybi syndrome
- Treacher Collins syndrome (mandibulofacial dysostosis)
- Van der Woude syndrome
Repair of the Cleft Palate
According to Swedish school only soft palate is first closed at 6 to 12 months of age. Hard palate is not repaired till 6 to 8 years of age, lest it may interfere with the growth. Veau (1931) modified the Langenback’s operation of pushback. Wardill (1933-37) evolved four-flap method of repair.
- Proper preoperative evaluation is desired.
- Timing of surgery must be related to the assets and deficits of an individual case.
- The same surgical procedure can yield different results.
- The surgeon does not always have complete control of the rehabilitative outcome.
- Velopharyngeal capability is related to the pharyngeal architecture and to the size and activity of the velum, rather than to the cleft type.
The object of operation is to provide for a mechanism to close the pharyngeal isthmus during speaking and swallowing. Hence the objective of surgery is to obtain a long and mobile palate.
Anterior palate is usually closed along with the lip in first stage of the cleft lip repair surgery. A single layer closure of the anterior palate is well-accepted. However, a mucosal flap is raised from the cleft side buccal mucosa as described by Muir (1966) can provide buccal layer closure.
Cleft in the alveolar gap is usually closed by a single nasal layer. Buccal side is left with raw area which granulates. Skoog used a mucoperiosteal flap to cover this raw surface and later proved radiologically not only bony fusion of the alveolar cleft is seen, but also the growth of tooth in this segment is observed.
Having anaesthetized the patient, neck extension is given with the sandbags placed under the shoulders to visualize the palate. A mouth gag – Dott-Kilner or East Grinstead with cheek blades is used to retract the palate. Then saline adrenaline solution 1:1 lakh is used to infiltrate proposed lines of incision of the mucoperiosteum and the margins of the cleft. Mucoperiosteal flaps are then raised one from either side. These are island flaps based on greater palatine vessels.
The flaps are elevated to the posterior bony margin. The greater palatine vessels are teased from the foramen and off the palatal flaps for the distance. Next the elevator is passed laterally and posteriorly separating the soft tissues from the medial plate of the pterygoid bone. The palatal muscles are dissected from posterior edge of the hard palate. The free edge of the soft palate is slit open. The amount of posterior displacement of soft palate varies from 1 to 2 cm. Nasal mucosa is separated on the nasal side. Levator muscle aponeurosis and nasal mucosa are carefully separated from the posterior bony margin.
To achieve adequate pushback not only the oral layer, but the nasal layer is also lengthened. It is detached from its attachment to the posterior margin of the hard palate allowing it to move back posteriorly.
Soft palate is sutured using vertical mattress sutures. Suture knots of nasal layer are placed on the nasal side, while that of oral layer, on the oral side. Absorbable suture material (either chromic catgut or vicryl 4/0 in small children and 4/0 in older children and adults, on a Dennis brown needle) is used. A majority of surgeons still use two layer closure—nasal and oral. But as the functional importance of palate is being recognized more and more, dissection of palatine muscles under magnification and then their suturing in normal anatomical configuration is being preferred. Thus a three-layer closure—first nasal mucosa, second muscle and then the oral mucosa may hold some advantage. Fracture of the hamulus to release tensor palatini is debatable. Often in older children, when the soft palate musculature does not move centrally without tension, hamulus should be fractured and the palatine muscles brought medially and sutured to that from the other side. A cleft uvula must be dissected and muscle uvulae sutured together. Palatine shelves laterally (from where mucoperiosteal flaps are raised) can be left as such. Their surface granulates quite fast.
In very wide clefts with limited tissue, it may not be possible to achieve full closure. Under these conditions, pushback must never be sacrificed at the cost of complete closure of the cleft. If flaps do not reach till right anterior region, it is quite acceptable to leave a fistula anteriorly for which an obturator can be used.
Elbows are splinted in extension. Spoon feeding with only strained liquids (a food particles stick in the oral cavity and become a residue for bacterial growth) is done for 10 days. It is essential that suction with sterile catheters be kept by the bedside at least for first 24 hours. Child should be nursed on his side to avoid the danger of tongue falling back. It is preferable to keep the child following palate surgery in the hospital for 10 days or at least under observation.