Velopharyngeal Dysfunction 

Updated: Mar 26, 2018
Author: Luke J Schloegel, MD; Chief Editor: Ravindhra G Elluru, MD, PhD 



The activities of swallowing and speaking depend upon the ability to obtain adequate closure of the velopharyngeal port. Both are complex motor skills that involve the coordination of a diverse group of muscles along the upper aerodigestive tract. Velopharyngeal movements during phonation are quite distinct from those involved in swallowing, as is clinically evident in patients who are able to obtain good closure during swallowing yet are unable to obtain adequate closure when speaking.

Velopharyngeal closure (VPC) is an important part of speech. All phonemes in the English language, with the exception of the three nasal phonemes (/m/, /n/, /ng/), are produced with oral airflow, meaning that the velopharynx should be closed. The nasal phonemes are produced with nasal resonance, meaning that the velopharynx must open during their production. With so many phonemes in English requiring oral airflow, oral resonance is important to production of intelligible speech.

Phonation involves the generation of a column of air pressure passing from the subglottis into the upper airway. If VPC is inadequate, air is allowed to escape through the nose during the generation of consonants requiring high oral pressure, leading to inappropriate nasal resonance during speech production. The consequence of impaired VPC is velopharyngeal dysfunction (VPD), the constellation of speech production disorders that includes velopharyngeal insufficiency (VPI), velopharyngeal incompetence, and velopharyngeal incorrect learning. (See Pathophysiology.)

Causes of hypernasality and VPD are many and range from structural causes (eg, cleft palate) to neuromuscular problems (eg, those observed in velocardiofacial [VCF] syndrome). Functional etiologies also exist, including splinting of the palate after tonsillectomy, imitation of cultural or familial role models, and phoneme-specific problems. (See Etiology.)

Patients with VPD may present with hypernasality, nasal emission, or facial grimacing. In their attempt to be understood, affected patients often develop compensatory maladaptive articulations that are very difficult to reverse if left untreated. (See Clinical Presentation.)

Patients with VPD should be treated within in the context of multidisciplinary team care. (See Treatment.) In 1988, an international working group convened to standardize definitions and assessment methodologies.[1] The working group strongly recommended implementing a multidisciplinary team approach and using multimodal instruments to evaluate preoperative and postoperative speech outcomes.

The group also asserted that comprehensive analysis of specific causes of speech production disorders, through perceptual and instrumental measures of velopharyngeal function, allows for customized treatment algorithms for specific patients.

Definitions of key terms

In describing the problem of hypernasal speech, differentiation between velopharyngeal incorrect learning, velopharyngeal incompetence, and VPI is important.[2] Ideally, care providers representing the various disciplines of the cleft team should use the same nomenclature so that they can effectively organize and communicate their knowledge.[3, 4] Trost-Cardamone developed a useful taxonomy to classify possible causative factors of VPD.[5]

Velopharyngeal incorrect learning is best described as incorrect closure of the velopharyngeal port in the nasopharynx as a result of articulation difficulties; inconsistent hypernasality or phoneme-specific hypernasality is typical of this condition. It may be the result of phoneme-specific nasal emission and deafness or hearing impairment.

Velopharyngeal incompetence is inadequate VPC occurring as a result of neurogenic causes, such as a functional problem with the oral motor mechanism, as may be seen in paresis, apraxia, and dysarthria.

In VPI, there is insufficient tissue to accomplish closure of the velopharyngeal sphincter. The typical cause is a structural problem with the velum (eg, submucous cleft palate, shorted velum relative to the depth of the posterior pharyngeal wall, or overt cleft palate). VPI can also be due to mechanical interferences with closure (eg, excessively large tonsils, webbing of the posterior tonsillar pillars, or both).[6]

As a rule, velopharyngeal incorrect learning, VPI, and velopharyngeal incompetence have approximately the same effect on the patient’s speech. For this reason, these terms are typically used interchangeably or are subsumed under the general heading of VPD.

It is also important to be familiar with the terms used to describe key manifestations of VPD.[7, 8]

Nasalance is an acoustic correlate of nasal resonance. It is calculated as the ratio of nasal to nasal-plus-oral energy.

Nasal airflow (nasal emission) is different from the nasal acoustic energy associated with hypernasality. It involves a nasal, rather than an oral, increase in airflow. Nasal air emission results from an attempt to build up intraoral air pressure for the production of consonants in the presence of a leak in the system, fistula, or incompetent velopharyngeal valve. Some of the airflow is released through the nose, causing a disruption in the aerodynamic process of speech.

Nasal air emission is noted on pressure-sensitive phonemes, plosive fricatives, and affricates (though not on vowels), and it can occur with normal resonance. Whether it is audible depends on the size of the opening: the bigger the opening, the less the resistance to flow. However, a small velopharyngeal gap may often release a paradoxically high stream of airflow pressure, making an audible noise and generating a misleadingly high nasalance score.

Nasal rustle or turbulence is a distracting sound that accompanies consonant production. Generally, small constrictions in the nasopharynx produce a distinctive fricative sound on the voiced pressure consonants b, d, and g.

Hypernasality is produced by nasally escaping air reverberating in a confined postnasal space. Specifically, it is abnormal nasal resonance during the production of nonnasal oral sounds. Hypernasality is a resonance disorder that is usually related to VPD as a result of the lack of a barrier between the oral and nasal cavities, which leads to abnormal coupling (sharing of acoustic energy) of these cavities during speech. Whereas hypernasality usually refers to velopharyngeal sphincteric function, it may be secondary to a fistula or an unrepaired cleft palate.

Grimacing is an aberrant facial muscle movement. It represents a subconscious attempt by the patient to inhibit abnormal nasal airflow by constricting the nares.

Hyponasality is a blocked-up tone that may occur with nasal obstruction from enlarged adenoids, a deviated septum, an inadequate nasal airway, or chronic catarrh.

Go to Surgical Treatment of Velopharyngeal Dysfunction for complete information on this topic.


The velopharyngeal sphincter comprises the following six muscles:

  • Tensor veli palatini
  • Levator veli palatini
  • Uvular muscle (musculus uvulae)
  • Palatoglossus
  • Palatopharyngeus
  • Superior constrictor

The tensor veli palatini arises from the scaphoid fossa, spine of the sphenoid, and the cartilaginous portion of the eustachian tube. It inserts into a tendon winding around the hamular process. Innervated by the mandibular branch of cranial nerve V, it tenses the soft palate and opens the eustachian tube during swallowing.

The levator veli palatini arises from the petrous apex and the cartilaginous portion of the eustachian tube. Its fibers fan out in the soft palate and blend with the contralateral levator. Innervated by the pharyngeal plexus from cranial nerves IX and X, it pulls the velum in a posterosuperior direction and serves as the major elevator for the velum.

The uvular muscle arises from the palatal aponeurosis posterior to the hard palate and inserts into the uvula mucosa. Innervated by the pharyngeal plexus, it functions to add bulk to the dorsal aspect of the uvula.

The palatoglossus arises from the anterior surface of the soft palate and inserts into the lateral aspect of the tongue base. Innervated by the pharyngeal plexus, it simultaneously lowers the velum and elevates the tongue upwards and backwards. It depresses the palate for nasal speech.

The palatopharyngeus arises from the soft palate and inserts into the posterior border of the thyroid cartilage. Innervated by the pharyngeal plexus, it positions the velum and narrows the velopharyngeal orifice by adducting the posterior pillars and constricting the pharyngeal isthmus. This muscle also raises the larynx and lowers the pharynx.

The superior constrictor arises from the lower portion of the pterygoid plate and the hamular process and inserts into the median raphe. Innervated by the pharyngeal plexus, it produces medial movement of the pharyngeal walls and assists in drawing the velum posteriorly. The inferior portion of this muscle forms the Passavant ridge. Early descriptions of speech described contact of the soft palate with this fold of the posterolateral pharyngeal wall. However, newer observations suggest that the soft palate contacts the posterior nasopharyngeal wall above the level of this ridge.

On endoscopy, the velopharynx (nasopharynx) has several topical anatomic features that are important to note.

  • Pharyngeal ostium of the eustachian (auditory) tube
  • Pharyngeal tonsil (ie, adenoid)
  • Posterior pharyngeal wall
  • Pharyngeal surface of the soft palate

The pharyngeal ostium of the eustachian (auditory) tube and its associated structures make up the lateral wall of the nasopharynx. The ostium is bordered anteriorly by the salpingopalatine fold and posteriorly by the cartilaginous torus tubarius. Posterior to the torus tubarius is the pharyngeal recess. Extending inferiorly from the torus tubarius is the salpingopharyngeal fold, which overlies the salpingopharyngeal muscle. Inferior to the ostium and torus, the pterygopharyngeal portion of the superior pharyngeal constrictor muscle makes up the lateral wall of the nasopharynx.

The adenoid, a closely aggregated collection of lymphoid nodules, is directly posterior in the nasopharynx and overlies the basilar portions of the sphenoid and occipital bones. It lies directly between the tori tubarii on either side and may extend laterally into the pharyngeal recess, where it is commonly known as the eustachian or Gerlach tonsil. Superiorly, it may extend up into the nasal choanae; inferiorly, it ends at or near the level of the anterior arch of the atlas. The prevertebral fascia and the atlanto-occipital membrane lie deep to the pharyngeal tonsil.

The posterior pharyngeal wall, which is immediately inferior to the pharyngeal tonsil, comprises mainly the superior pharyngeal constrictor muscle.

The pharyngeal surface of the soft palate is formed by the aponeuroses of several muscles, including the levator veli palatini muscle, the tensor veli palatini, the palatopharyngeus, and the uvular muscle (see above). The insertion and innervation of these muscles is described above.


Oral resonance (as contrasted to nasal resonance) is obtained by means of VPC, which creates a seal between the nasopharynx and the oral cavity. Typically, VPC is accomplished by elevation of the velum and approximation of the lateral walls to close off the nasopharynx. In a small group of patients, formation of a Passavant ridge on the posterior pharyngeal wall may contribute to closure.

Four basic types of closure patterns are used to describe velar closure: coronal, sagittal, circular, and circular with the Passavant ridge (see the image below). Defining the type of closure pattern is important when surgical intervention for correction of VPD is under consideration.

Pharyngeal closure patterns: (A) coronal, (B) sagi Pharyngeal closure patterns: (A) coronal, (B) sagittal, (C) circular, and (D) circular with Passavant ridge.

Coronal closure, the most common closure pattern, is present in 55% of patients with normal velar function. The major contribution to closure is from the soft palate as it contacts a broad area of the posterior pharyngeal wall. Little medial motion of the lateral pharyngeal walls occurs. A coronal closure pattern is often present with an enlarged adenoid pad.

Sagittal closure, the least common pattern, is present in 10-15% of people. Here, palatal elevation is minimal. The main contribution is from medial motion of the lateral pharyngeal walls. This is the pattern seen most commonly in patients with persistent VPD after repair of a cleft palate.

Circular closure, which is present in approximately 20% of individuals with normal closure, involves contributions from both the soft palate and the lateral pharyngeal walls. This results in a closure that resembles a circle getting smaller.

Circular closure with the Passavant ridge, which occurs in 15-20% of the population, is a circular pattern that involves anterior motion of the posterior pharyngeal wall (known as Passavant’s ridge).

VPD is what happens when VPC is impaired. The effects of VPD on a patient’s speech include hypernasality, decreased speech intelligibility, and nasal emissions (ie, air escape out of the nose during speech). Several factors determine how severely a patient’s speech is affected, including the amount of gap with a closed velum, the patient’s articulation and oral motor ability, and compensatory strategies the patient may have developed to decrease nasal emission or hypernasality.

Common compensatory strategies include speaking with soft intensity (ie, volume) to decrease airflow through the nasal cavity, speaking with loud intensity or pushing to try to project the voice, and substituting phonemes that require less airflow. Straining to increase oral airflow often results in vocal nodules, and hoarseness is a common finding with VPD.


The etiology of VPD includes structural abnormalities of the palate, dynamic impairment of a structurally normal palate, and functional abnormalities that are unassociated with anatomic or dynamic palatal defects. The following is an overview of the most common causes.

Palatal and other physical causes

Overt cleft palate, either before or after repair, is by far the most common cause of VPD, occurring in approximately 1 of every 2000 live births. VPD has been reported in as many as 30-50% of patients after palate repair. Studies have shown that children born with a complete cleft palate are more likely to require VPI surgery than children with incomplete clefts.

A submucous cleft palate is defined by the presence of a bifid or double uvula, muscular diastasis of the soft palate, and notching of the posterior border of the hard palate. This is usually evident on examination of the oral cavity, especially with elevation of the palate when the patient pronounces the phoneme /ah/.

By contrast, an occult submucous cleft palate is an absence or deficiency of the musculus uvulae with a diastasis of the levator veli palatini but without the presence of a bifid uvula or grooving of the oral surface of the soft palate. An occult submucous cleft is best visualized endoscopically as the absence of the bulge and the presence of a central groove on the nasal surface of the soft palate during speech.

Most patients with either overt or occult submucous cleft palate can produce normal speech. However, because of their abnormal musculature, these patients may be predisposed to VPD by any changes to the velopharyngeal anatomy, such as those occurring as a result of adenoidectomy or velocardiofacial syndrome.

VPD may be caused by tonsil hypertrophy that prevents the palate from adequately moving superiorly during attempted velopharyngeal closure. Tonsillectomy may be appropriate in these patients.

Syndromic causes

Patients with trisomy 21 (ie, Down syndrome) are predisposed to VPD. The combination of oromotor and developmental delays, generalized hypotonia, and intellectual delays constitutes a significant risk factor for VPD, especially after adenoidectomy.

VCF syndrome is an autosomal dominant disorder linked to microdeletions in the long arm of chromosome 22. Major findings include cleft palate (overt, submucous, or occult submucous), conotruncal heart anomalies, frequent infections (as part of DiGeorge syndrome), and a characteristic facial appearance with asymmetry of the lower lip (see the image below).

Child with velocardiofacial syndrome. Characterist Child with velocardiofacial syndrome. Characteristic clinical findings included unilateral lower lip palsy, small bulbous nose, wide palpebral fissures, and small external ear canals. Patient's speech has hypernasal resonance.

VPD is common in patients with VCF syndrome, not only because of the presence of a cleft palate, but also because of pharyngeal hypotonia.[9, 10, 11, 12] VPI has been reported to be present in approximately 75% of patients with 22q11 deletions, with only 10% of those patients showing actual submucous clefts, providing credence to the theory that VPI occurs in patients with either anatomic or syndromic (ie, functional) causes.

VPD is also a common feature in Kabuki syndrome (KS). Many findings of Kabuki syndrome are similar to those of VCF syndrome, including cleft palate, cardiac abnormalities (typically coarctation of the aorta), muscular hypotonia, and characteristic facial features. As in patients with VCF syndrome, poor muscular tone of the velopharynx is a major cause of VPD in patients with KS.

Velopharyngeal incompetence or VPI may also be a feature of other syndromes, such as neurofibromatosis, myotonic dystrophy, or any syndrome in which low muscle tone is a feature. The importance of syndrome recognition in patients with VPI is critical, as this population may be at particular risk for postoperative airway obstruction, respond less reliably to surgical correction, and require more aggressive adjunctive speech therapy.

Postoperative causes

Transient VPD with hypernasal resonance after adenoidectomy, with or without tonsillectomy, is not uncommon. This condition may persist for several days to weeks and usually resolves spontaneously. Some nasal regurgitation of liquids may be present during this period. Incidence of persistent velopharyngeal dysfunction after adenoidectomy has been reported to range from 1 per 1500 to 1 per 10,000 patients.

Although the adenoid pad is not necessary for normal VPC, it may assist in closure in children with structural or functional abnormalities of the soft palate. Children at risk of developing persistent VPD after adenoidectomy can often be preoperatively identified by presence of repaired cleft palate, submucous cleft palate, 22q11 deletion, palatopharyngeal disproportion (ie, abnormally deep pharynx), or palatal hypotonia.

Other acquired causes

VPD may develop in children with a stroke or head injury, especially if damage occurs to the motor centers that control the cranial nerves responsible for pharyngeal muscle control or to higher centers controlling complex motor tasks.

Neurologic diseases, such as muscular dystrophy, multiple sclerosis, or brain herniation due to Arnold-Chiari malformation, may result in VPD. Traction on the lower cranial nerves results in paresis of the pharyngeal musculature.

Although primarily seen in adults, amyotrophic lateral sclerosis (ALS) and Parkinson disease may lead to VPD in the more advanced stages of disease.

Children or adults with apraxia or dysarthria may experience VPD and nasal emissions.


Because VPD is multifactorial, the frequency is unknown. For functional causes, determining the frequency is impossible, because some etiologies are acquired and some are congenital. Structural causes of VPD due to cleft palate occur in 1 in 2000 live births. Almost half of all cleft palates have a syndromic cause; the most common syndrome is VCF syndrome (del 22q11.2).[13] VPD occurs in approximately 20% of children who undergo palatoplasty.[14]


Several studies have been published in support of each of the available options for management of VPD; however, most of the data have not been validated by large numbers of patients, nor have these results been subjected to critical analysis. Most of these studies lack a multidisciplinary evaluation, standardized evaluation and treatment criteria, and methods for assessing surgical outcome.

For example, there are several different types of sphincter pharyngoplasties, though they are often grouped together as if they were the same. These procedures differ in terms of transposition of the flaps, use of muscle tissues, levels of insertion, and whether a synchronous pharyngeal flap is used. Other uncontrolled variables include the status of the tonsils and whether a full-thickness transverse cut is made in the posterior pharyngeal wall mucosa. This heterogeneity of sphincter pharyngoplasties explains some of the difficulty in describing postoperative outcomes.

Cleft palate populations, migratory patterns of treating physicians, and dogmatism among surgeons regarding the best technique are all inherently unstable. Additionally, the study designs often do not include rigorous documentation of the preintervention, peri-intervention, and postintervention states or the methodology for evaluation of the intervention.

Achieving a high compliance rate from a patient population stratified for age, sex, socioeconomic factors, and number of surgical interventions is an arduous task. The outcome assessment instrument must be designed to allow analysis of intrarater and interrater reliabilities of all the extramural raters and, at the same time, not be so cumbersome and burdensome as to reduce compliance.

In the future, outcome reporting based on clinical evidence will probably set the standards for cleft surgery. Surgeons who help manage VPD will be judged by the evidence that their interventions are—or are not—doing the most good for the most people at a price that patients and/or insurance agencies are willing to pay.

Evidence-based practice is the integration of the best research evidence with clinical expertise and patient values. The best evidence comes from randomized clinical trials, which are expensive, time-consuming, and not always possible. Sometimes we must settle for good evidence, which may be the best that is available. Nevertheless, the future demands good evidence, and as cleft surgeons and researchers, we need to supply that evidence.




When a patient is referred for surgical treatment of velopharyngeal dysfunction (VPD), the first steps should be to try to elicit specific information germane to speech problems, cleft palate, or both. A multidisciplinary approach consisting of an initial assessment conducted by an otolaryngologist and a speech pathologist is most effective for the diagnosis and management of VPD.

Historical factors in VPD are primarily related to problems with speech intelligibility. The voice is described as having a nasal resonance; nasal emissions (ie, air escape through the nasal passage with speech) may also be present. Compensatory articulation errors are often present, worsening speech intelligibility. Hoarseness is commonly present in children with VPD.

Nasal regurgitation, especially in infants, may also be a clue to the presence of velopharyngeal dysfunction. Parents may describe food and liquids coming through the nose with feeding and spitting up. Older patients may describe reflux of thin liquids into the nasal cavity, as with drinking water from a fountain.

In older children and adults, recurrent and chronic sinus infections may be a sign of nasopharyngeal reflux resultant from repeated contamination of the nasal cavity. Persistent otorrhea with ear grommets in place may also be due to nasopharyngeal reflux, extending up the eustachian tube and through the middle ear. This problem is particularly common in children with a cleft palate or other structural defect. A history of snoring or middle ear effusions may also be signs of palatal dysfunction.

It is important to look for other factors that may lead to diagnosis of a congenital syndrome. Cleft palate, frequent infections, low muscle tone, heart murmur, and lower lip weakness may suggest velocardiofacial (VCF) syndrome.[14] Poor feeding and hypotonia in infancy may suggest the presence of a neuromuscular disorder. Congenital heart defects in association with VPD are common features of both VCF syndrome and Kabuki syndrome (KS). A family history may reveal other affected individuals, also pointing to a genetic etiology.

Exploring the social impact of the child’s speech intelligibility can affect management strategies. Children with significant social integration issues may warrant more aggressive treatment.

Physical Examination

Aside from abnormal resonance of the voice and articulation problems, the physical examination may be normal. Important physical findings would include the presence of a cleft palate, either overt or submucous. Evidence of previous surgery or traumatic injuries should be noted.

A thorough oropharyngeal examination should be done, looking for palatal fistulae, enlarged tonsils, visibly aberrant carotid pulsations along the posterior pharyngeal wall, a prominent adenoid pad, palatal zona pellucida (trough), a palpable notch at the junction of the hard and soft palate, or a bifid uvula. An assessment of palatal function by asking the patient to phonate /ah/ is also important.

Otoscopy should be performed to look for evidence of eustachian tube dysfunction, such as middle ear atelectasis or middle ear effusion. Nasal examination should assess for signs of sinus infection or other evidence of nasal reflux. Other physical findings may point to an association with a genetic syndrome. Lower lip asymmetry, orbital hypertelorism, small external ear canals, bulbous nasal tip, or heart murmur may signify velocardiofacial syndrome.



Diagnostic Considerations

If a patient is presenting with speech delay, articulation problems, hypernasality, or nasal regurgitation, it is important to differentiate between a primary articulation problem and one related to either functional or anatomic velpharyngeal dysfunction (VPD). Patients with primary articulation disorders are treated with speech therapy alone.

In patients found to have VPD, a careful approach should be used to localize the cause, as discussed above, of the dysfunction. This helps to tailor the appropriate intervention. For example, if velopharyngeal closure is hindered by enlarged tonsils, tonsillectomy may actually improve the voice. If the problem is a velopharyngeal gap, then a surgical intervention can be selected to address the specific defect.



Approach Considerations

Acquisition of objective, quantitative, preoperative, and postoperative evaluation data allows for a rational informed decision regarding surgical and nonsurgical intervention.[15, 16, 17, 18] Determining the precise etiology of the velopharyngeal dysfunction (VPD) is paramount before embarking on treatment modalities.

Simple bedside maneuvers can help define the speech problem. A handheld pocketsize mirror can be placed beneath the patient’s nares to allow observation of nasal airflow (audible air nasal emission). A straw may be placed at the corner of the patient’s mouth while he or she recites a speech task. The listener at the other end of the straw can perceive amplified air sound, unmasked hypernasality, or both.

Listen to both spontaneous speech and structured provocative samples of speech. Try to ascertain overall intelligibility in running, spontaneous, connected speech. Patients with suspected VPD are incapable of achieving velopharyngeal closure (VPC) on maximum effort when producing properly articulated phonemes that require closure.

Provocative samples of speech are designed to elicit phonemes that require VPC. A representative sequence might include the following words or phrases: “ma, ma, ma,” “puppy,” “puffy,” “muffin,” “pamper,” “sissy,” “go get a big egg,” “bye-bye Bobby,” “Katy likes cookies,” “Sally sees the sky.” Production of voiceless consonants such as p, t, k, s, f, and sh requires maximal pulmonary pressures and thus can be used as a brief screening for the integrity of plosive sounds.

It must be emphasized that for the surgeon, errors in these sequences of sounds should serve only as a red flag; interpretation of the significance of these errors should be left to a qualified speech and language pathologist (SLP). Most physicians are unfamiliar with the behavioral variables that can affect velopharyngeal function, such as oronasal discrimination proficiency, the presence of maladaptive articulations, the effects of coarticulation, the range of articulatory motion, and the contribution of speaking effort.

The speech evaluation should include attention to error types and the “stimulability” of performance during visualization of dynamic speech activity. Arguably, the SLP is the care provider who best understands and interprets the movements and the articulatory and vocal structures. (See Voice and Resonance Evaluation.)

Several diagnostic modalities can be used to assess speech production in patients who demonstrate symptoms of VPD; detailed descriptions are found in published articles.[19] These modalities include video-recorded standard perceptual speech screenings (ie, acoustic evaluation of sounds or listener judgments), nasoendoscopy, nasometry, aerodynamics, and fluoroscopic speech evaluations.[20] (See Fiberoptic Nasoendoscopy and Videofluoroscopy.)

These studies have the advantage of being readily archived on digital media for review, for study, and for strobe analysis, among other tasks. Usually, test results are reviewed by the interdisciplinary velopharyngeal staff of specialists, including an SLP, an otolaryngologist, a prosthodontist, and a plastic surgeon.

If cephalometric evaluations are available, they can facilitate diagnosis.[21] Tracings can quantitatively assess the ratio of velar length to velopharyngeal depth, which is often a good predictor of patients who require physical management of the velopharynx.

Exciting new technologies are on the horizon, such as dynamic magnetic resonance imaging (MRI) of the velopharynx, which may soon be available for clinical use.

MRI data can be reformatted to simulate endoscopy. Planar images may be converted to three-dimensional (3D) volumes. Although this technology is still in its infancy, someday it may allow clinicians to feel as if they can actually go inside the anatomic structures they have scanned with “fly-throughs,” focusing on specific pathologies. Such an approach has the potential of evolving into noninvasive endoscopy, provided that it can meet or exceed the criteria standards currently available.[22]

Voice and Resonance Evaluation

The SLP can offer informative data to help determine the appropriate course of treatment for VPD by completing a voice and resonance evaluation. A thorough voice and resonance evaluation for VPD includes articulation assessment, oral motor assessment, and measurement of nasal airflow.

Articulation assessment

Objective measures of articulation ability, such as the Arizona Articulation Proficiency Scale, are administered at the single-word level to determine articulation errors. The patient’s speech intelligibility is then rated on the basis of this scale, and the dysfunction is characterized as mild, moderate, or severe.

The SLP also describes the types of articulation errors, including nasal emissions, glottal stops, and nasal fricatives. The patient’s responses to corrections of articulation errors, distortions, nasal emissions, and hypernasality are then assessed to determine prognosis for improvement with speech therapy.

Oral motor assessment

A subjective oral motor assessment is completed by observing the range of motion and speed of the lips and tongue, as well as elevation of the soft palate and velum with pronunciation of the phoneme /ah/. Overall facial symmetry and muscle tone are also noted.

Measurement of nasal airflow

The MacKay-Kummer sensory nerve action potential (SNAP) test is administered to children aged 3-9 years with the Kay Elemetrics Nasometer to assess the ratio of oral airflow to nasal airflow. For children aged 9 years and older and for adults, the Zoo Passage, Rainbow Passage, and Nasal Sentences are substituted as standard reading passages.

Nasometer results are compared with normative data. A score that is three standard deviations above the mean indicates hypernasal resonance (ie, speaking with too much airflow and resonance in the nasal cavity). A score that is three standard deviations below the mean indicates hyponasality, which is defined as insufficient nasal resonance for the nasal phonemes (ie, /m/, /n/, /ng/).

Visualization of the velopharyngeal mechanism can be achieved by means of either fiberoptic nasoendoscopy (FN) or multiplanar videofluoroscopy (VF).

Fiberoptic Nasoendoscopy

After voice and resonance evaluation, a determination of the need for FN is made on the basis of the test results. Indications for FN include hypernasality (either consistent or inconsistent), poor oral airflow with nasal escape, and structural abnormalities of the soft palate.[23] If none of these conditions exist and the patient presents with sufficient oral airflow for most phonemes, speech therapy typically is recommended with periodic reevaluation before completion of FN.

Sedation is not typically used for this procedure. In certain patients, however, such as children younger than 5 and older children who are uncooperative, sedation may be helpful. If sedation is to be used, oral midazolam is administered at a dose of 0.5 mg/kg (up to 10 mg) and given 15-20 minutes before FN. This dose provides adequate amnesia and sedation while allowing the child to perform the necessary tasks for the examination. Higher doses of midazolam may make the examination difficult because the child is sedated too heavily.

Before placement of the fiberscope, the nasal cavity is examined for any obstructions that may inhibit passage of the scope into the nasopharynx. The nose then is decongested and anesthetized with a mixture of 4% lidocaine and 0.05% oxymetazoline hydrochloride, which is sprayed into the nose with an atomizing device.

The fiberscope is passed through the nostril, superior to the inferior turbinate, to the posterior nasal choana (see the image below). Passage along the floor of the nose does not position the fiberscope high enough to allow for visualization of the entire velopharyngeal sphincter.

Preoperative nasoendoscopic view of velopharynx, s Preoperative nasoendoscopic view of velopharynx, showing nasal septum (1), lateral nasoparyngeal wall (2, 4), and velum (3).

With the fiberscope in place, the patient is asked to repeat a series of words and sentences loaded with phonemes that require increased oral airflow (eg, plosives, fricatives) so that the velar closure pattern can be observed. The examination is videotaped for later review. Patients who are unable to vocalize these phonemes may be grossly assessed by this technique by looking at overall VPC and identifying any deficiency in each of the specific planes of closure.

FN is superior to VF for assessing VPD in that it allows direct visualization of the velopharyngeal sphincter. This is especially important in the postsurgical patient when the velopharyngeal anatomy is altered, as occurs with placement of a pharyngeal flap. Compared with VF, FN is slightly more invasive and requires a moderate degree of cooperation from the child to obtain an adequate examination.


VF is performed by the SLP in conjunction with a radiologist. Unlike FN, VF can be used to see through tissues so that movement can be discerned at all vertical and horizontal positions within the pharynx. A 3D perspective can be gained by using frontal, lateral, and base or Towne projections.

VF is usually performed without sedation. Barium is instilled through the nose with a nose dropper to contrast soft tissues against the surrounding skeletal structures. Fluoroscopic views are then obtained in the lateral, anteroposterior (frontal), and base projections while the patient articulates phonemes that require increased oral airflow. The lateral view helps the examiner visualize the velum, posterior pharyngeal wall, and tongue. The frontal view enables assessment of the lateral pharyngeal walls along the entire vertical extent of the pharynx.

The advantage of VF is that it allows more precise localization of the level of VPC by measuring the level against the spine. Observation of the tongue is also important because the tongue may contribute to closure in a compensatory fashion by lifting the palate, as is seen in swallowing. This information could be missed with FN alone. VF has the obvious disadvantage of radiation exposure. In addition, when normal anatomy is altered (eg, after surgery), interpretation of the images may be difficult.

Preoperative Planning

Assessment of velopharyngeal closure pattern

Four main patterns of VPC have been described on the basis of FN and VF: coronal, sagittal, circular, and circular with the Passavant ridge. (See Pathophysiology.) The type of closure pattern is determined by the relative contribution of the palate and lateral pharyngeal walls to closure of the velopharyngeal sphincter.

Determination of a patient’s closure pattern is clinically significant, as is the determination of the vertical level of closure. The type of closure pattern determines the type of surgical intervention, because surgical intervention is most effective when it targets the point of maximal pharyngeal motion.[24]

Preoperative tonsillectomy and adenoidectomy

An important preoperative consideration is the need for adenoidectomy, tonsillectomy, or both.[25] In most instances, preoperative adenoidectomy is necessary for either sphincter pharyngoplasty or a pharyngeal flap procedure. Indications for preoperative tonsillectomy vary.

In the case of sphincter pharyngoplasty, adenoidectomy makes room for placement of the lateral pharyngeal wall flaps. Failure to remove the adenoids makes attachment of the flaps to the posterior pharyngeal wall difficult.

The need for tonsillectomy before pharyngoplasty is determined by the degree of obstruction. This determination is somewhat subjective and is based on the size of the tonsils and whether they interfere with the raising of the lateral pharyngeal wall flaps. Leaving the tonsils in place often helps preserve the posterior tonsillar pillars, which are used to create the pharyngoplasty flaps.

Before a pharyngeal flap procedure, removal of both the tonsils and the adenoids often is necessary. Placement of a pharyngeal flap makes subsequent adenoidectomy difficult if not impossible, and residual adenoid tissue may obstruct the lateral pharyngeal ports. Similarly, the tonsils may obstruct the pharyngeal ports from below, so their removal typically is recommended.

Other considerations

One factor to consider in preoperative planning is whether breathing is obstructed preoperatively. Placement of a pharyngeal flap increases the degree of nasal airway obstruction and may worsen any preexisting obstructive sleep apnea. This is especially true in patients with Pierre Robin syndrome, in which retrognathia may result in upper airway obstruction. In such instances, consideration should be given to pharyngoplasty instead of a pharyngeal flap because the risk of worsening airway obstruction postoperatively is lower with pharyngoplasty. Children with both obstructive sleep apnea and VPD should have treatment of the sleep apnea prior to surgical management of the VPD.

The location of the internal carotid arteries (ICAs) as they traverse the lateral pharynx is also an important consideration, especially in patients with velocardiofacial syndrome (VCF).[26] In patients with VCF syndrome, the ICA can take a more medial position and thus is theoretically at risk for injury with pharyngeal surgery. Preoperative evaluation with contrast-enhanced computed tomography (CT) or magnetic resonance angiography (MRA) can elucidate the course of the ICA.[27]

In practice, the ICA will lateralize when the head is extended for surgery and will not be in the operative field during pharyngoplasty or pharyngeal flap surgery, and the presence of a medially displaced ICA is not necessarily a surgical contraindication.

The presence of a primary bleeding disorder (ie, hemophilia or von Willebrand disease) may complicate surgical management. Likewise, anticoagulation for reasons such as a prosthetic heart valve may be a contraindication to surgery.



Approach Considerations

Perceptual speech evaluation by a qualified speech and language pathologist (SLP) with experience and expertise in cleft pathology is the mainstay of evaluation and ongoing treatment, in that the goal of therapy is the ability to communicate successfully using speech.

In patients with cleft palate, residual articulation abnormalities associated with hypernasality should be corrected after palate closure but before secondary surgery for velopharyngeal dysfunction (VPD). Learned compensatory misarticulations must be addressed and corrected through focused intervention with a trained SLP. Early speech therapy results in increased speech accuracy and can help improve long-term outcomes. Parents can be trained to effectively deliver speech therapy to young children with cleft palate.

Van Demark and Hardin discussed the effectiveness of exclusive articulation therapy in children with cleft palate and noted less improvement and slower improvement than expected.[28] Ruscello reviewed nonsurgical palatal training procedures, such as articulation therapy, sucking and blowing exercises, electrical and tactile stimulation, speech appliances, and biofeedback techniques.[29] These techniques have never been demonstrated to be of any value, and all clinicians should make sure that their patients are not receiving ineffective speech therapy.

The prosthetic speech bulb is most useful in patients with little or no velopharyngeal motion. Velopharyngeal movement is essential to surgical success with a pharyngeal flap procedure or sphincter pharyngoplasty. Patients with little velopharyngeal movement are good candidates for prosthetic management. A velopharyngeal speech prosthesis can elevate the velum (lift), fill the residual velopharyngeal gap (obturator), or both (lift-orator). The nasal valve is another prosthetic option.

The primary indications for surgical intervention include structural defects of the velum and functional problems that result in poor or inconsistent velar closure.

One study that compared speech outcomes from prosthetic management with those from surgical management showed no difference for patients who complied with the prosthesis.[30] However, because nearly 30% of patients referred for prostheses did not comply, surgery was more efficacious overall.

Speech Therapy

Speech therapy improves velopharyngeal function in patients whose VPD is minimal or due to articulation errors and in postoperative patients. Compensatory articulation techniques secondary to VPD also can be corrected with speech therapy. However, in patients with a specific anatomic deficiency that precludes adequate closure of the velopharynx, speech therapy cannot replace surgery. Surgical management may also be necessary in cases where closure is possible but nasal speech persists with connected speech.

Upon completion of speech and language testing, the SLP determines if VPD and hypernasality are related to articulation errors or if the condition is phoneme-specific. If either is the case, the VPD usually is not related to structural abnormalities, and correction with speech therapy most likely is possible.

VPD also can be a result of decreased muscle tone in the oral musculature and soft palate. Decreased muscle tone can be observed on fiberoptic nasoendoscopy (FN) when the soft palate closes inconsistently or when closure appears slow in connected speech. A period of speech and language therapy focusing on improving overall oral motor skills and improving strength and elevation of the velum may be able to correct VPD in such cases. Speaking slowly and deliberately is another strategy to improve speech intelligibility.

Visual Feedback

In some children, especially those with hearing impairments, visual feedback can assist in therapy to improve VPD. Several devices are available to assist with this method. Simple tools (eg, a cold mirror or a paper paddle) can serve to show the patient when nasal escape occurs. Other devices are commercially available, such as the See-Scape, which is placed at the nose and causes a ball to rise when airflow is nasal rather than oral.

A more sophisticated method is the use of a nasometer, which graphically displays a ratio of oral sound energy to nasal sound energy. The visual readout can help the therapist and patient develop compensatory techniques to reduce nasalance. In older children, video-recorded nasopharyngoscopy has been used to achieve the same goals. The latter method has been shown to be effective in patients with VPD and cleft palate.

Nasal Continuous Positive Airway Pressure Therapy

Continuous positive airway pressure (CPAP) therapy is a palate-strengthening program completed 6 days a week for 8 weeks in the patient’s home. It is beneficial for patients whose VPD seems to be related to oral motor issues or velar weakness rather than to structural problems of the velum.

The CPAP equipment includes a nasal mask, which is attached to the patient. With the mask in place, the patient repeats a series of consonant-vowel combinations and sentences designed to cause the velum to open and close against air pressure from the nasal mask. CPAP pressures are increased on a regimented schedule, producing exercises similar to a weightlifting program for the soft palate.

The disadvantages of CPAP therapy are the high degree of regimentation and the need for cooperation and participation for up to 24 minutes, 6 days per week, which is difficult to achieve with young children. Wearing the nasal mask and speaking with nasal air pressure also can be frightening for some young children.

Studies of the efficacy of CPAP for hypernasality have demonstrated variable results; however, significant reductions in hypernasality are seen in some patients undergoing therapy.[31, 32] Further research is required to establish its effectiveness.

Prosthetic Management

In a small number of cases, prosthetic management may be the best solution for VPD.[33] Prostheses may be used as a temporary reversible trial; they can provide diagnostic information in cases of variable VPD where it is unclear whether surgery alone will significantly improve speech quality. They may be useful in some patients with a short, scarred velum or in other patients with a long, supple, paretic velum. Some authors have hypothesized that prostheses may stimulate neuromuscular activity,[34] though definitive proof for this hypothesis is lacking.[35]

The main types of prostheses include the following:

  • Palatal lift
  • Speech bulb/obturator
  • Nasal valve

Devices that include features of both lifts and obturators (so-called lift-orators) also exist.

Palatal lifts (see the images below) are used when adequate palatal length exists but dynamic motion of the palate is poor as a consequence of neuromuscular etiologies. Palatal lifts reduce the distance the palate must traverse to produce adequate closure.

Palatal lift. Hard and soft palatal components are Palatal lift. Hard and soft palatal components are shown.
Palatal lift in situ. Palatal lift in situ.

An obturator is usually necessary when the velum is short and scarred, and the ratio of velar length to nasopharyngeal depth is excessive, such as seen in some patients with repaired cleft palate. Obturators can substitute for tissue deficiency and are attached to the palate or teeth. In certain cases, the obturator can be downsized gradually so that the native tissue, if adequate in bulk, can strengthen over time and compensate for the decreasing obturator size.

A combined prosthesis (lift-orator) is useful when elevation of the velum alone is not sufficient to achieve closure. Such speech prostheses are fitted under endoscopic control by an interdisciplinary team that includes a prosthodontist, an SLP, and an endoscopist.

The nasal valve is an appliance fitted to each nostril.[36] A one-way valve on either side allows the patient to breathe in through the nose, but stops nasal airflow with exhalation or speech.

Surgical Therapy

As noted previously, the primary indications for surgical intervention include structural defects of the velum and functional problems that result in poor or inconsistent velar closure. Maximum benefit can be achieved when the surgical technique takes advantage of whatever native velopharyngeal function exists in the patient. 

Information obtained during the objective evaluation via physical examination, FN, and multiview videofluoroscopy (VF) can greatly aid in determining the best way to make use of remaining velopharyngeal function. Some claim that successful outcomes in fact depend on matching the functional capability of the patient with the surgical procedure. Others have disputed this claim, reporting that there is no difference in outcomes regardless of surgical technique or preoperative sphincter characteristics.

Four patterns of velopharyngeal closure (VPC) have been described on the basis of FN and VF: coronal, sagittal, circular, and circular with the Passavant ridge. (See Pathophysiology.) The type of closure pattern is determined by the relative contribution of the palate and lateral pharyngeal walls to closure of the velopharyngeal sphincter. Determination of a patient’s predominant VPC pattern (see the videos below) directs the surgeon to the most appropriate treatment for the patient.

Coronal closure.
Sagittal closure.
Circular closure.
Circular closure with Passavant's ridge.
Velar closure noted as patient pronounces /s/. Circular closure pattern is noted with central defect and air escape. Palate closure is noted with swallow in middle portion of frame.
Palate closure noted against adenoid pad as the patient speaks /p/. Phoneme-specific velopharyngeal dysfunction is diagnosed, and speech therapy is recommended to improve articulation. Adenoidectomy in this patient would most likely result in structural velopharyngeal insufficiency.

The four main surgical approaches to velopharyngeal corrective surgery are as follows[37, 38] :

  • Palatoplasty
  • Pharyngeal flap
  • Sphincter pharyngoplasty
  • Posterior pharyngeal wall augmentation

Go to Surgical Treatment of Velopharyngeal Dysfunction for complete information on this topic.


Palatal procedures most often include the Furlow palatoplasty, which involves a double Z-plasty lengthening of the palate. This technique appears to work best when the orientation of the palatal levator musculature is sagittal or when a small preoperative velopharyngeal gap size is noted.

Pharyngeal flap

The pharyngeal flap is the preferred surgical approach in patients with good lateral pharyngeal wall motion who have a persistent central gap resulting from poor palatal motion, as is common following repair of a cleft palate. The procedure aims to develop a central flap of tissue to obturate the midline of the pharyngeal port and decrease the degree of air escape into the nasal cavity.[39, 40, 41, 42, 43]

Schoenborn first reported this procedure in 1876 when he described an inferiorly based posterior wall flap sutured to the nasal surface of the soft palate.[44] He later modified this procedure by using a superiorly based flap when he found that an inferiorly based flap tended to contract and tether the palate downward over time, worsening the patient’s velopharyngeal insufficiency (VPI).

The flap is raised down to the level of the prevertebral fascia, creating a tissue flap of superior constrictor muscle with its overlying mucosa. This flap is raised superiorly so that its base is at the level of the arch of C1. Typically, splitting the soft palate in the midline is necessary to provide better access to the nasopharynx during creation of the flap. The flap then is sutured to the nasal surface of the palate by incorporating it into the split repair.

Alternatively, the flap can be inset into the palate by performing a fish-mouth incision on its nasal surface. Raising a longer flap than necessary is advantageous to accommodate any future flap contracture. Red rubber nasal trumpets (4 French) are placed through the resulting lateral ports to alleviate any immediate postoperative obstructive breathing patterns.

One large series of 500 patients reported normalization or resolution of hypernasality in 90% of patients. Failure to improve is related to inadequate flap width either by design or due to contracture. Conversely, a flap that is too wide narrows the lateral ports and produces hyponasal speech. Postoperative airway obstruction is most likely to occur within the first 24 hours and in one series resolved within 2 days in more than 90% of patients.

The drawback to this surgery is the potential for prolonged postoperative obstructive sleep apnea development in up to 50% of patients. Care must be taken in the pediatric population to ensure adequacy of nasal respiration following paryngeal flap surgery. In many cases, this includes hypervigilance for obstructive sleep apnea both before and after surgery. Surgeons should definitely contemplate removal of large tonsils and adenoids prior to pharyngeal flap surgery.

Sphincter pharyngoplasty

Sphincter pharyngoplasty is advantageous when coronal or circular closure is present and lateral pharyngeal wall motion is deficient. The goal is to develop a more functional sphincter by improving the dynamics and bulk of the velopharyngeal tissues and by tightening and reducing the size of the velopharyngeal opening.[45, 46, 47, 48, 49]

Hynes was the first to describe pharyngoplasty in 1950 as the elevation of two superiorly based flaps comprising the right and left salpingopharyngeus muscles and overlying mucosa.[50] The flaps were rotated 90° and sutured to the mucosal edges of a transverse incision made across the nasopharynx just below the level of the tori tubarii.

In 1968, Orticochea described a modification of the pharyngoplasty procedure using two superiorly based flaps comprising the posterior tonsillar pillars with the underlying palatopharyngeus muscles.[51, 52] A small inferiorly based posterior pharyngeal wall flap then was elevated, and the two lateral flaps were rotated 90° and inserted onto the posterior flap.

Jackson further modified this method by sewing the lateral flaps onto a superiorly based posterior pharyngeal wall flap, allowing higher placement of the lateral wall flaps.

Theoretically, the sphincter becomes dynamic. However, one study featured selective electromyographic evaluation of the muscular pharyngeal sphincter during speech and revealed no intrinsic muscular activity. It is important to place these flaps high in the sphincter to reduce the need for revision surgery.[53] The sphincter pharyngoplasty has also been recommended for use in cases of stress-induced VPI, such as in wind-instrument players.

As noted, the need for adenoidectomy and possible tonsillectomy is determined preoperatively. (See Workup.) Adenoidectomy is performed several weeks (minimum, 6 weeks) preoperatively to allow the velopharyngeal sphincter to heal. If the tonsils are enlarged to a degree that may make raising the palatopharyngeal flaps difficult, they must be removed. Velar closure is then reassessed after adenoidectomy (and tonsillectomy) because the muscular dynamics may have changed.

Several studies have reported a success rate (ie, correction or significant reduction in hypernasality) from 78-100% with pharyngoplasty. The incidence of postoperative hyponasality is estimated to be 12-17%.

Posterior-wall augmentation

Posterior-wall augmentation is appropriate in the presence of a persistent gap in the central velopharyngeal port measuring at most 1-3 mm. It also is indicated when the patient can achieve touch closure that is not tight enough to prevent air escape with high oral pressure. Persistent postadenoidectomy VPI is also an appropriate indication for this procedure. Both autogenous tissue[54] and foreign implants have been used for this approach.

A superiorly based pharyngeal flap incorporating the superior constrictor is raised down to the prevertebral fascia. The superior extent of elevation is defined just above the point of maximal closure. It then is buckled onto itself and sutured in place. Initially good results can become less favorable as the flap can atrophy with time, and this procedure is recommended only for small gaps.

A wide variety of implantable materials have been used to augment the posterior wall. Problems with extrusion, migration, resorption, and infection have been reported. The US Food and Drug Administration (FDA) has banned silicone because of a high extrusion rate. Teflon is not approved for use in the pharynx because of concerns over the risk of injection into large blood vessels. Autologous tissues such as fat or rolled dermis have been less problematic, but they tend to resorb with time.

Subsequent reports described the use of calcium hydroxyapatite injected into the posterior pharyngeal wall.[55] This technique has been demonstrated to have a reasonably high success rate with no migration or extrusion of the injected material. Polyethylene implants imbedded into the posterior pharynx have also demonstrated success in some adult patients.[56]

Although these procedures appear to be safe and relatively easy to perform, critical evaluation of procedures for posterior wall augmentation have not demonstrated significant improvements in speech following surgery. Autologous fat injections may be of some benefit in further augmentation after either sphincter pharyngoplasty or a pharyngeal flap procedure. The use of injectable collagen materials for pharyngeal augmentation has not been reported.

Predictors of postoperative outcome

Perceptual speech assessment is a key subjective tool used to diagnose VPI in children, determine disease severity, and measure improvement after treatment. Speech intelligibility is very important to patients with VPI and can have a large impact on quality of life. It is also important to develop standardized methods for use in research and improve overall management of patients with VPI.

One study validated a new disease-specific instrument, the Velopharyngeal Insufficiency Quality of Life (VPIQL) survey. This study identified that children with VPI and their parents perceive a reduced quality of life when compared with age-matched controls.[57] Another prospective cohort study implemented the Pediatric Voice Outcome Survey, an instrument used to assess general voice-related quality of life, and showed that parents perceived at least short-term improvements in fuctional outcomes and quality of life following surgery for VPI in their children.[58]

The greatest predictor for postoperative final speech outcomes from VPI surgery is the patient's preoperative condition. Children with syndromes such as VCF are more likely to have suboptimal outcomes after surgery than children anatomic, nonsyndromic causes of VPI. The type of surgical procedure used does not seem to be as important as the experience of the surgeon. A large, prospective, randomized study from Mexico found no difference in outcomes between sphincteroplasty and pharyngeal flaps, regardless of preoperative velopharyngeal sphincter characteristics.[59]

In summary, outcomes after VPI surgery are probably dependent on a multitude of factors, including severity of preoperative VPI, gap size, presence or absence of comorbidities or syndromes, and surgeon comfort.

There seems to be no long-term effect on growth after VPC over time. The ratio of cephalometric measurements of velar length to pharyngeal depth was similar in patients with repaired clefts and their normal control subjects. This ratio remained stable with growth from age 4 years through puberty.[60]

Postoperative Care

Immediate postoperative concerns deal mainly with upper-airway obstruction. Placement of nasal trumpets overnight, while the patient is still under the effects of anesthesia, is helpful. A 2-0 suture placed through the tongue tip and used to protrude the tongue can be helpful in temporary airway management in the postanesthesia recovery area.

Patients are admitted overnight primarily for airway management and intravenous (IV) hydration. Discharge home is on the first postoperative day as long as oral diet is tolerated and pain control by mouth is adequate.

Postoperative pain management is typically limited to narcotics, such as acetaminophen with either codeine or hydrocodone. Stronger narcotics, such as morphine or meperidine, may cause increased sedation, thereby worsening airway obstruction.

Once oral fluids are tolerated and any postoperative nausea has cleared, the patient resumes a diet of thick liquids and soft foods. With pharyngoplasty, a diet similar to that for tonsillectomy patients is used and may include most foods as tolerated. Patients undergoing a pharyngeal flap procedure follow dietary restrictions similar to those for patients undergoing palatoplasty. Typically, these patients are restricted to thick liquids or soft foods (eg, mashed potatoes) until the palatal incision has healed (usually 10-14 days).


Complications after VPI surgery include persistent VPI, flap dehiscence, and obstructive sleep apnea (OSA).

Concerns about long-term OSA development after pharyngeal flap surgery led some centers to abandon this procedure all together. A study of 222 consecutive pharyngeal flap operations reported a relatively low postoperative OSA incidence and concluded that when appropriately performed, pharyngeal flap surgery was well tolerated and effective for the treatment of VPI and that there was no reason to avoid applying it to children for fears of postoperative OSA.[61]  In the case of severe persistent OSA after a superiorly based pharyngeal flap, division of the flap generally results in improvement in symptoms and some persistent speech benefit.

In a sphincter pharyngoplasty, more superiorly raised palatopharyngeal flaps lead to a greater degree of velopharyngeal obturation. If this is excessive, an obstructive pattern of breathing can develop.[62, 63]  However, even if the obturation is not excessive, some patients still develop some mild temporary obstructive sleep patterns in the immediate postoperative period. For this reason, most surgeons place a nasal trumpet through the sphincter intraoperatively and remove it the next morning.

Long-term considerations include shrinkage of the flaps and nasopharyngeal scarring. Over time, the flaps may shrink, reducing the bulk of the repair and altering speech results. Patients with return of velopharyngeal escape over time may be a candidate for flap augmentation with fat injection. Nasopharyngeal stenosis may also result, especially if the dissection is carried up onto the soft palate. Resultant upper airway and nasal obstruction may require revision pharyngoplasty with tissue grafts.

After a pharyngeal flap procedure, failure to improve is related to inadequate flap width, whether through faulty design or as a result of contracture.[64, 61]  Conversely, a flap that is too wide narrows the lateral ports and produces hyponasal speech. Postoperative airway obstruction is most likely to occur within the first 24 hours[65] ; in one series, it resolved within 2 days in more than 90% of patients.

After posterior-wall augmentation, problems with extrusion, migration, resorption, and infection have been reported.


A team approach is important to success in the treatment of VPD. Close communication between the SLP and the surgeon is critical to determine the appropriate treatment modalities used. As speech motor patterns are set between age 8-12 years, timely consultation is crucial to good speech outcomes.

Role of speech and language pathologist

The surgeon, the SLP, and other health care providers work closely together to achieve the goal of optimal treatment for the patient. These practitioners collaborate in their reviews of the in-depth diagnostic assessment results and the individual patient’s medical history.

Consensus evaluation usually provides an appropriate course of management for affected individuals and may yield a differential diagnosis that leads to differential management.[66] Ideally, this means that care providers attempt to match the gap size, shape, and VPC pattern to the most appropriate intervention.

Surgeons, as well as lay people, are usually capable of recognizing speech “differences.” Perception of a speech difference does not require a sophisticated understanding of speech physiology, but determination of the causes, severity, and magnitude of that difference and formulation of a suitable treatment plan do require such an understanding.

SLPs are particularly adept at sorting out the components of a communication disorder and their respective weights, a process that frequently dictates whether a particular component receives surgical attention, not whether it receives attention at all. This sorting ability is a skill and a talent that surgeons and lay people rarely possess.

Relationship between speech and language pathologist and surgeon

Making the distinction between velopharyngeal valve dysfunction (structural defect) and speech dysfunction is critical. For example, consider the following analogy: If a newly licensed 16-year-old driver is involved in a motor vehicle accident, differentiating between a mechanical failure of the car and a failure of the just-learning driver to maintain control of the vehicle is important.

The investigator might logically ask: Was the driver taking mind-altering drugs? Was the accident the result of a mechanical problem with the car, or was it the fault of an inexperienced or misbehaving driver? The answers to these questions are basic to the investigational algorithm. They tell the investigator where to look next, while reminding him or her that more than one party might be at fault.

The same logic holds true for the evaluation and management of VPD. Is the velopharyngeal valve (the car) at fault, or is the speech disorder (the driver) at fault? The answer to this question tells the investigator what to do next and who should do it.

Examining the velopharyngeal valve should be quite straightforward. A simple mirror test at the bedside, with a definitive yes-or-no answer, can help determine if the patient can eliminate nasal escape. Treatment may involve fixing the velopharyngeal valve (which calls for a surgeon’s expertise) or teaching the patient (which calls for the expertise of an SLP).

The presence of hypernasality is much more difficult to evaluate. Using vocal, nonverbal testing can obviate such problems as phoneme-specific VPI. An astute SLP should be able to make the determination despite the confounding glottal stops, fistulae, and other factors.

The surgeon must emphasize to parents, patients, and other providers that surgical success can be anticipated with respect to nasal escape and hypernasality. The SLP must then assume the responsibility of helping patients achieve speech and language success, including articulation and other facets of verbal communication.

Long-Term Monitoring

The initial follow-up appointment is at 7-10 days, at which time the wound is examined for proper healing. A determination regarding resuming a regular diet also is made at this time. Snoring and upper airway obstruction, if present at this point, usually resolve over the next several weeks as edema decreases and flap shrinkage occurs.

At 6 weeks, healing is usually complete, and a speech and resonance reassessment is performed. Surgical correction of structural defects in the velopharyngeal port does not necessarily change function, and articulation problems may persist after surgery. On the basis of the postoperative speech and resonance evaluation findings, speech therapy may be resumed at this point as necessary.