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Cleft palate: introduction
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History and evolution of palatoplasty
Cleft palate surgery has been refined over hundreds of years. Early cleft care simply focused on physically separating the oral cavity from the nasal cavity. In the thirteenth century, Jehan Yupperman, a Flemish surgeon, found that he could correct hypernasal speech of untreated cleft patients by plugging the palatal defects with cotton, or plates of silver or lead. Others continued this practice using various materials such as plates of gold and silver to occlude palatal clefts, but it was Ambroise Paré in 1564 who first used the term “obturateur”. Two hundred years later, in 1764, the first reported cleft palate repair was performed by Le Monnier, a French dentist. He described a three-step operation in which he introduced sutures, cauterized the cleft edges, and then realigned the freshened edges. Hard palate closure proved to be more challenging to surgeons at the time due to the less distensible mucosa of the hard palate. In 1826, Johann Diffenbach introduced relaxing incisions and mobilized tissues to close the hard palate, but the poorly perfused mucosa-only flaps were unreliable. In 1861, Bernhard von Langenbeck’s contribution was to realize the importance of elevating the periosteum with the mucosa, the “mucoperiosteal flap”. Over time, knowledge of velopharyngeal physiology grew more sophisticated and the importance of palatal length for normal speech was recognized. During the 1930s, Victor Veau, Thomas Kilner, and William Wardill in 1937 described modifications of von Langenbeck’s technique to increase palatal length. The Veau–Wardill–Kilner V–Y “pushback” palatoplasty was designed with bilateral posteriorly based unipedicled mucoperiosteal flaps that are closed in a V–Y fashion allowing posterior advancement and lengthening of the soft palate. While this technique would seem to successfully lengthen the velum, these authors question the outcome of this procedure. In their experience, the V–Y maneuver of the hard palate mucoperiosteal flaps have little impact at the uvula, largely because of the tethering effect that the greater palatine neurovascular bundle imposes at the junction of the hard and soft palates.
The 1960s marked the beginning of the next important phase of palatoplasty with focus turned towards dynamic functional muscle restoration of the palate. In August of 1969, Hoopes and Dellon reported on the importance of the levator veli palatini (LVP) in velopharyngeal competence and Edgerton and Dellon followed that report in 1971 with a description of the surgical repair of the LVP and its impact on speech. In January of 1969, Otto Kriens coined the term “intravelar veloplasty” (IVVP) in which he released the abnormal attachments of the levator from the posterior edge of the hard palate and reapproximated the musculature at the midline. Taking this concept further, Brian Sommerlad in one report and Grant in another advocated for radical dissection and retropositioning of the levator muscles. The levator muscles – tethered anteriorly by the tensor – were freed with tensor tenotomy, allowing for the muscle sling to be reconstructed in an optimized anatomic position.
The next evolutionary phase in the quest for dynamic muscle reconstruction continued in the late 1980s when Leonard Furlow designed the double opposing Z-plasty palatoplasty. This ingenious procedure elegantly reconfigures the levator muscle sling while simultaneously lengthening the palate. Despite its significant advantages, wide clefts frequently require lateral relaxing incisions.
The deficiency of palatal tissues historically has been an inherent element of cleft palate pathology that has largely been ignored. Long-term outcomes studies suggest that relaxing incisions increase surgical scar burden, which may induce maxillary growth restriction and palate contracture. The most recent evolutionary phase in palatoplasty has seen the addition of tissue to augment the repair and to replace the inherent deficiency of tissue. Kirschner and Losee have reported the use of acellular dermal matrix (ADM) to surgically treat as well as prevent fistulas. Performing a radical IVVP, and repositioning the LVP muscles results in a large area of “dead space” at the posterior edge of the hard palate. This dead space is feared to result in significant scarring and contraction that results in a relapse in LVP malposition and the loss of velopharyngeal competence over time. Buchman has described filling this dead space with vascularized pedicled buccal fat pads. Robert Mann has reported addressing the inherent tissue deficiency with his “anatomic cleft restoration philosophy” by adding bilateral buccal myomucosal flaps to augment the Furlow double opposing Z-plasty. Secondary palatal lengthening, for the treatment of velopharyngeal insufficiency, with the interposition of bilateral buccal myomucosal flaps at the junction of the hard and soft palate, one for nasal lining and one for oral lining, has largely replaced pharyngoplasty operations (posterior pharyngeal flaps and sphincter pharyngoplasties) for many cleft surgeons. Long-term outcomes demonstrate low recurrence rates of velopharyngeal insufficiency.
Anatomy
The palate is divided functionally into the hard palate, which provides structural support and is a growth center for the maxilla, and the soft palate or velum, which is dynamic and provides velopharyngeal competence. The soft palate can be further divided into three sections from a functional standpoint: the anterior 25%, the middle 50%, and the posterior 25%. The anterior 25% of the soft palate is relatively static containing the tensor veli palatini, whereas the middle 50% contains the dynamic LVP muscle sling, which is the principal motor of the velum. The right and left levator muscles emerge from the eustachian tube and cranial base and run downward, forward, and medially forming a continuous muscle sling as they meet in the midline of the velum. LVP contraction produces an upward, backward, and lateral pull on the soft palate during velopharyngeal closure.
The palatoglossus and palatopharyngeus muscles take origin within the middle 50% of the soft palate but extend to the posterior 25% along with the muscularis uvulae. The LVP is bounded by the two heads of the palatopharyngeus muscle; the inferior head originates on the oral surface of the levator, and the superior head on the nasal surface, before it travels inferiorly as the posterior tonsillar pillar. The primary actions of the palatopharyngeus muscle are to tense the soft palate and draw the pharynx anteriorly during breathing. The palatoglossus muscle originates from the dorsolateral transverse fibers of the tongue and then runs cephalad as the anterior tonsillar pillar before fanning out to insert as the most superficial muscle of the velum. Its primary action is with swallowing by pulling the soft palate towards the tongue. The tensor veli palatini (TVP) originates from the medial pterygoid plate of the sphenoid bone and Eustachian tube and then vertically descends sharply hooking around the anterior aspect of the hamulus before it fans out to form the relatively elastic aponeurosis in the anterior third of the velum. As its name suggests, the TVP tenses the soft palate.
In the setting of a cleft palate, the LVP muscles no longer form a continuous sling that transversely courses through the middle 50% of the velum. The muscles are abnormally positioned sagittally along the cleft margin, running posterior to anterior where they insert onto the posterior edge of the hard palate. With this abnormal configuration, the levator muscles cannot effectively power the velar mechanism to close the palate against the posterior pharyngeal wall during velopharyngeal closure. Consequently, air escapes through the nose during speech. In addition to its abnormal course, the clefted LVP has three abnormal attachments: (1) the posterior medial edge of the clefted hard palate; (2) the aponeurosis of the tensor veli palatini; and (3) lateral adhesions to the superior constrictor. These abnormal attachments must be released during the primary palatoplasty to allow the LVP to be reconfigured in a more anatomic and retropositioned orientation – an IVVP. In addition to speech problems, the levator’s abnormal tethering to the tensor tendon impairs the function of the TVP muscle in assisting Eustachian tube function.
Victor Veau developed a practical classification system that characterizes the spectrum of cleft palate. The Veau I cleft involves the soft palate only. The Veau II cleft is a complete cleft of the secondary palate involving the soft and hard palate extending to the incisive foramen. The Veau III cleft is a unilateral complete cleft of the primary and secondary palate, where the vomer is attached to the maxilla on the non-cleft side. Finally, the Veau IV cleft is a complete bilateral cleft of the primary and secondary palate. These patients have a protruding premaxilla, and the vomer is in the midline.
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