eMedicine Specialties > Plastic Surgery > Craniofacial
Craniofacial, Pharyngoplasty and Pharyngeal Flaps
Updated: Feb 23, 2009
Introduction
A competent and dynamically functional velopharyngeal sphincter is essential for normal eating, normal breathing, and intelligible speech. The sphincter is positioned between the oral and nasal cavities and coordinates appropriate airflow through each chamber to allow a voice that has quality, richness, and carrying power. Closure of the velopharyngeal port prevents nasal regurgitation during eating and allows pronunciation of consonants, while opening of the port allows for normal respirations and specific nasal articulations. Velopharyngeal dysfunction (VPD), velopharyngeal incompetence, velopharyngeal insufficiency (VPI), and velopharyngeal inadequacy are frequently used terms to denote an improperly functioning velopharynx. Several interventions are available for management of VPD, depending on differential diagnosis and etiology of pathology.
History of the Procedure
Surgery directed to correct velopharyngeal incompetence is not a novel topic. A documented awareness of the connection between cleft palate and poor speech may date back to Pierre Franco in 1561.1 During the 19th century, surgical procedures were developed that are still being used in modified forms today. In 1865, after a detailed study of velopharyngeal physiology, Passavant was the first to tether the uvula to the pharynx in an attempt to restore a competent valvular mechanism during speech.2 Since that time, in addition to the use of removable devices designed to obturate the velopharyngeal (VP) space, numerous surgical procedures have been devised to restore the physiologic closure of this sphincter-like mechanism. In 1875, Schoenborn, using the earlier concepts of Trendelenburg, devised an inferiorly-based pharyngeal flap,3 and Roselli later reported on the superiorly-based flap.4
More recently, Jackson and Silverton, Orticochea, and Moss et al have emphasized an anatomic reconstruction using adynamic sphincter pharyngoplasty.5 Over the years, numerous VP augmentation techniques have been suggested in lieu of pharyngeal flaps or pharyngoplasties. These procedures bring autogenous, allogeneic, or synthetic materials into the retropharynx but have fallen out of favor.
Problem
VPD includes any structural and/or neuromuscular disorder of the velum and/or pharyngeal walls at the level of the nasopharynx that results in interference of the normal sphincteric closure. VPD may result from anatomic, myoneural, behavioral, or a combination of disorders. Because this article details pharyngoplasty and pharyngeal flaps, the term velopharyngeal dysfunction specifically refers to speech and resonance symptoms related to a known structural deficit that has been determined by perceptual and instrumental differential diagnosis. VPD is diagnosed clinically by a constellation of symptoms that includes pathologically-incurred nasal resonance (hypernasality), compensatory misarticulations, escape of air through the nose (nasal emissions), and aberrant facial movements (grimacing).
Frequency
Approximately 20-38% of children who undergo cleft palate repair develop velopharyngeal insufficiency that requires active intervention, which comprises speech therapy, surgery, or both.
Etiology
The etiology of VPD can be divided into 2 categories: (1) structural deficiency of the palate or its related musculature (eg, cleft palate) and (2) neurologic deficiency (eg, myasthenia gravis, cerebrovascular accident, upper or lower motor neuron lesions, head trauma). Peterson-Falzone discusses noncleft causes of VPD, such as neuromuscular disorders, palatopharyngeal disproportion, and the effects of tonsils and adenoids.6 The degree to which each component contributes to VPD is difficult to determine.
Pathophysiology
VPD also may be anatomically classified as one of the following:
- Poor mobility of the soft palate secondary to various factors, including short palate, scarred/tightened palate, or dysfunction/malposition of the levator palatini muscle
- Poor mobility of the posterior and lateral pharyngeal walls due to poor muscular mobility
The latter is more commonly caused by a neurologic deficit.
Presentation
VPD manifests with hypernasality (hyperresonant) and often, but not always, misarticulated speech. Hypernasality is a quality perceived by the listener due to inappropriate nasal coupling, which refers to the balance of air traveling through the oral and nasal airways during speech. Errors in articulation of vowels and consonants occur from an inability to produce appropriate high intraoral pressure consonants, specifically, the stops, fricatives, and affricates. Tests such as the modified Müller maneuver cannot help distinguish patients with hypernasality.
Stop plosives (ie, "p, b, t, d, k, g" as in "go") are brief, purposeful interruptions of the airstream resulting in intraoral pressure buildup, with explosive release of that pressure buildup. Fricatives refer to sounds ("s, z, sh, zh, f, v," both voiced and voiceless "th") produced by constricting the airstream through a narrow channel between the 2 speech articulators. Affricates ("ch" and "g" as in "George") are high intraoral pressure consonants that begin as stops, but are released as fricatives.
Indications
Patients with symptoms of velopharyngeal (VP) dysfunction (ie, hypernasality, nasal emission, facial grimacing, compensatory misarticulations) are referred to a multidisciplinary VP diagnostic center for video-recorded standard perceptual, nasoendoscopic, and fluoroscopic speech evaluations. The videos provide direct visualization of VP closure for review by the interdisciplinary VP dysfunction team, and a consensus is reached for recommended management. Candidates for surgery fulfill the criterion of VP dysfunction resulting from an anatomic, myoneural, or combined deficiency of the VP sphincter that is not expected to be managed by speech therapy alone.
Relevant Anatomy
The 3 muscles (levator veli palatini, tensor veli palatini, uvularis) of the palate work in concert with the palatopharyngeus, the palatoglossus, and the pharyngeal constrictor muscles to produce VP closure. The tensor veli palatini muscles arise from the membranous wall of the eustachian tube. Their tendons pass around the hamular processes of the medial pterygoid plate of the sphenoid and insert into the palatine aponeurosis. The levator veli palatini muscles also have their origin along the eustachian tube orifice. They meet in the midline in a sling-like fashion above and behind the aponeurosis. The uvularis is a small midline muscle sitting above and behind the levator sling.
An unimpaired velum moves posteriorly and superiorly, the posterior pharyngeal wall can move ventrally diffusely or as a well-defined shelf (known as the Passavant ridge), and the lateral pharyngeal walls move toward the midsagittal midline. The uvularis also contracts during speech, adding bulk to the area of convexity on the upper surface of the soft palate. The adenoids, residing in the posterior pharyngeal wall, and the pharyngeal tonsils, on the lateral pharyngeal walls, may augment or interfere with the function of those walls in velopharyngeal closure.7
As a person prepares to speak, the velum is partially raised and held at the ready position before speech begins; it then moves to the closed position as phonation starts. For nasal sounds (eg, "m, n"), the sphincter remains open. The ability of the sphincter to close is essential for compression of air behind the point of constriction so that consonants, especially plosives (eg, "f, s, th") can release with sufficient strength.
Contraindications
Patients with known obstructive sleep apnea or other upper airway compromise must be approached with caution with regard to performing posterior pharynx surgery. Because of the possibility of triggering apneic episodes, pharyngeal flaps can be dangerous if performed in these patients. Patients requiring surgical velopharyngeal (VP) management who have risk factors for upper airway obstruction are preferentially recommended for sphincter pharyngoplasty based on reports of its minimal effect on the airway.
To stimulate collapse of the pharyngeal walls in patients with obstructive sleep apnea, have the patient perform a modified Müller maneuver. Instruct the patient to breathe rapidly with the mouth closed and the nose partially closed. Surgery to decrease the velopharyngeal port is contraindicated in these patients.
In addition, syndromic patients (ie, those with velocardiofacial syndrome) may have anomalous carotid artery anatomy, which places these structures within the operative field of posterior pharynx surgery.
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References
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Further Reading
Keywords
velopharyngeal dysfunction, VPD, velopharyngeal insufficiency, velopharyngeal inadequacy, velopharyngeal incompetence, VPI, VP inadequacy, VP incompetence, VP insufficiency, VP augmentation, velopharyngeal augmentation, cranio-facial surgery, cranio-facial pharyngoplasty, craniofacial pharyngoplasty, pharyngeal flap, speech disorder, resonance disorder, hypernasality, misarticulation, escape of air through the nose, nasal emissions, aberrant facial movements, grimacing, cleft palate repair, cleft palate, structural palate deficiency, myasthenia gravis, cerebrovascular accident, upper motor neuron lesion, lower motor neuron lesion, head trauma, short palate, scarred palate, tightened palate, levator palatini dysfunction, levator palatini malposition, poor pharyngeal wall mobility, misarticulated speech, palatal prosthesis, velar lift, VP obturator, velopharyngeal obturator
Overview: Craniofacial, Pharyngoplasty and Pharyngeal Flaps