Two-Flap Palatoplasty
David K. Chong
Kathryn V. Isaac
Kenneth E. Salyer
DEFINITION
Cleft palate is the failure of fusion of the palatal shelves during embryological development.
Cleft palate may occur in isolation or in combination with a cleft lip. It may occur as part of a syndrome or in the absence of associated anomalies.
A cleft of the palate may lead to feeding difficulties, speech impairment, chronic Eustachian tube dysfunction, hearing loss, and altered facial growth.
Varying surgical approaches for cleft palate repair are utilized depending on the type of cleft palate and beliefs regarding facial growth and speech repercussions.
ANATOMY
Embryologically, the cleft may affect the primary or/and secondary palate.
Anatomically, the cleft is defined according to the involvement of the hard and soft palate.
The hard palate is the bony palate, and surgical anatomy involves
Palatine process of maxilla
Horizontal plate of palatine bone
Hook of hamulus and pterygoid plates of sphenoid bone
Vomer/septum
Greater palatine foramina
Soft palate is the mobile part of the palate, and surgical anatomy involves
Levator veli palatini
Tensor veli palatini aponeurosis
Palatopharyngeus
Palatoglossus
The Veau classification provides a clinically useful description of the cleft type according to the involvement of the alveolus, the hard palate, and the soft palate. It guides selection of the surgical treatment.
The two-flap palatoplasty is most commonly performed for clefts of the hard and soft palate. It is not commonly used for isolated clefts of the soft palate and is not used for submucous clefts.
PATHOGENESIS
The etiology of cleft palate is multifactorial: environment, teratogen exposure (alcohol, anticonvulsants, steroids, diazepam), nutrition, maternal infections (rubella, toxoplasmosis), and genetics.
Cleft palate repair restores anatomical closure between the oral and nasal cavities.
An unrepaired cleft palate may result in impaired:
Breathing
Feeding
Speech
Hearing
NATURAL HISTORY
Orofacial clefting is the most common craniofacial birth defect, occurring in 1:750 live births.
The incidence of cleft palate alone is 1:2000, with a female-to-male ratio of 2:1.
The incidence of cleft palate in combination with cleft lip is greater, estimated at 1:1000 with a reverse gender ratio.
In the population of children with cleft lip and/or cleft palate (CL+/-P), approximately 50% will have CLP, 30% to 35% CP, and 15% to 20% CL.
Approximately 40% of CP patients will have a syndrome, and 15% of CLP will have a syndrome.
PATIENT HISTORY AND PHYSICAL FINDINGS
The diagnosis of a cleft palate is made by prenatal ultrasonography or by physical examination at birth and in early infancy. A detailed assessment is made of the child’s breathing, feeding, growth, and development.
Airway assessment must exclude presence of sleep apnea and micro-/retrognathia.
Assessment of growth and weight is key to identify and monitor feeding difficulty, gastroesophageal reflux, and use of feeding aids (Haberman/Pigeon teat).
Hearing and middle ear function must be assessed and treated early by an otolaryngologist.
The plastic surgeon should define the cleft palate type according to the anatomic structures involved, the laterality, width of the palate, and presence/absence of a cleft lip.
Also, the child should be assessed for associated anomalies suggestive of a syndrome: craniofacial dysmorphism, airway compromise, cardiac defects, ocular and auricular abnormalities, and musculoskeletal anomalies. A genetics referral is suggested if suspicious of syndromic cleft palate.1
NONOPERATIVE MANAGEMENT
It is very uncommon not to repair a cleft palate.
If the child is unable to undergo surgical treatment secondary to airway concerns or medical fitness, a palatal obturator may be considered.
SURGICAL MANAGEMENT
Cleft palate repair is ideally performed between 9 and 12 months of age,2 with the infant weighing greater than 8 kg.
Airway and middle ear disease assessment is performed and treated prior to or simultaneously with cleft palate repair.
Risks of the procedure are hemorrhage/hematoma, airway compromise, wound dehiscence, infection, oronasal fistula, flap necrosis, velopharyngeal insufficiency, and reduced midfacial growth.
The main objectives of the cleft palate repair are as follows:
To separate the oral and nasal cavities
To reposition to the velar musculature for restoration of the velopharyngeal sphincter, in particular the reconstruction of the levator muscular sling
To improve Eustachian tube function
To minimize detrimental effects on subsequent maxillary growth
The main steps of the procedure are (a) marking and elevation of mucoperiosteal flaps off the hard palate; (b) isolation and lengthening of pedicles (greater palatine artery) for mobilization of the oral mucoperiosteal flaps; (c) dissection and separation of the nasal mucosa, velar musculature, and oral mucosa; (d) tension-free closure of nasal mucosal layer; (e) reconstruction of the velopharyngeal sphincter with repositioning of the levator sling; (f) recreation of the uvula; and (g) closure of the oral mucosal layer.
Preoperative Planning
Active or passive dentofacial orthopedics is utilized for aligning the cleft maxillary arches by many teams today and is applied in the first few weeks of infancy. The orthopedic device is discontinued once the maxillary arches have been satisfactorily repositioned.
With the patient anesthetized, the width of the cleft is measured at the junction of the soft palate and hard palate. The width of the cleft is important to predict difficulty of the cleft palate repair and anticipated amount of dissection required for closure. A cleft gap of:
Less than 11 mm closes with ease
12 to 16 mm will require more extensive dissection to mobilize the greater palatine vessel and achieve nasal lining mobilization
Greater than 17 mm will require special maneuvers detailed below to achieve tension-free closure (greater palatine foramina osteotomy)
Positioning
The patient is positioned supine with shoulder roll to allow neck extension. A south-facing oral RAE tube is carefully taped centrally with a mesentery. Corneas are protected with eye tapping.
Access and visualization of the entire palate is very important and cannot be understated. It is especially important to ensure visualization from the uvuli to the anterior extent of the palate.
It is essential for the surgeon to ensure that positioning is correct prior to scrubbing. This will facilitate the procedure.
The surgeon should have a headlight or lighted instruments for optimizing visualization in the confined space and a skilled attentive assistant. It is also advantageous to have a bed that allows for Trendelenburg positioning. Some surgeons stand to perform palate surgery from below but having the baby’s head supported with the surgeon seated operating upside down provides the best exposure and is the preferred position by many surgeons.
Approach
The aim of cleft palate surgery is tension-free closure of the palate oral and nasal mucosal layers and restoration of the velopharyngeal muscular sphincter.
Difficulties anticipated include the following:
Access
Lighting
Unforgiving tissue
Bleeding obscuring visualization
Surgical approaches differ with regard to the amount of dissection performed to achieve tension-free closure and muscle repositioning.
Importance lies in adequate exposure and dissection of tissues to allow comfort for the operating surgeon to achieve tension-free closure.
Oral layer mobilization is largely dependent on careful mobilization of the greater palatine artery from its periosteal sleeve.
Nasal layer mobilization is largely dependent on careful mobilization of the mucosa as a sheet from its dense bony attachments.
TECHNIQUES
▪ Two-Flap Palatoplasty for a Unilateral Complete Cleft Palate
Markings
Carefully insert an intraoral gag and a throat pack (it is the surgeon’s responsibility to insert and remove).
Mark the incision lines:
Along the medial edges of the cleft from the uvuli to the anterior junction of the hard palate and alveolus
Laterally at the junction of the hard palate and maxillary alveolus, extending from the posterior maxillary tubercle to the anterior medial marking (TECH FIG 1)
Inject local anesthetic with adrenaline into the hard palate and soft palate (average of 8 mL). The vasoconstrictive properties reduce blood loss and obstruction of the visual field. Local anesthetic also allows for hydrodissection of the mucoperiosteal flaps off of the hard palate and tissue expansion for ease of layer dissection in the soft palate.Related posts:
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