Abstract
Obstructive sleep apnea (OSA) is a state-dependent phenomenon in which the pharyngolarynx undergoes repetitive collapse. Retropalatal obstruction is often the primary site of sleep-disordered breathing. Traditional uvulopalatopharyngoplasty (UPPP) as described by Fujita has important potential limitations including non-physiologic modification, residual proximal palatal obstruction, and risk of nasopharyngeal stenosis and velopharyngeal insufficiency. The two techniques discussed in this chapter, expansion sphincter pharyngoplasty and transpalatal advancement, represent advanced palatal surgery modifications that employ more reconstructive (rather than excisional) methods to improve effectiveness and reduce morbidity over traditional UPPP. Expansion sphincter pharyngoplasty (ESP) is the reverse of sphincter pharyngoplasty, which is used to address velopharyngeal incompetence. In ESP, the palatopharyngeus (posterior pillar) is transected inferiorly and the muscle pedicle is rotated anteriorly, superior, and laterally to enlarge the lateral velopharyngeal dimension. While it bears similarity to UPPP in its effect on the distal palate, it avoids potential untoward consequences of UPPP such as nasopharyngeal stenosis and globus sensation (at least in part by maximal mucosal and uvular preservation). Transpalatal advancement (TPA) is designed to address proximal palatal obstruction, especially for those patients with a vertically oriented soft palate and maxillary deficiency. TPA removes a segment of hard palate and advances the soft palate anteriorly to increase the distance between the posterior nasal spine and posterior pharyngeal wall.
Keywords
expansion pharyngoplasty, obstructive sleep apnea (OSA), palatal surgery, transpalatal advancement pharyngoplasty, uvulopalatopharyngoplasty
Introduction
Obstructive sleep apnea (OSA) is a state-dependent phenomenon in which the pharyngolarynx undergoes repetitive collapse. Retropalatal obstruction is often the primary site of sleep-disordered breathing. Traditional uvulopalatopharyngoplasty (UPPP) as described by Fujita has important potential limitations, including nonphysiologic modification, residual proximal palatal obstruction, and risk of nasopharyngeal stenosis and velopharyngeal insufficiency. The two techniques discussed in this chapter, expansion sphincter pharyngoplasty (ESP) and transpalatal advancement (TPA), represent advanced palatal surgery modifications that use more reconstructive (rather than excisional) methods to improve effectiveness and reduce morbidity over traditional UPPP.
ESP is the reverse of sphincter pharyngoplasty, which is used to address velopharyngeal incompetence. In ESP, the palatopharyngeus (posterior pillar) is transected inferiorly and the muscle pedicle is rotated anteriorly, superior, and laterally to enlarge the lateral velopharyngeal dimension. Although it bears similarity to UPPP in its effect on the distal palate, it avoids potential untoward consequences of UPPP, such as nasopharyngeal stenosis and globus sensation (at least in part by maximal mucosal and uvular preservation).
TPA is designed to address proximal palatal obstruction, especially for those patients with a vertically oriented soft palate and maxillary deficiency ( Fig. 54.1 ). TPA removes a segment of hard palate and advances the soft palate anteriorly to increase the distance between the posterior nasal spine and posterior pharyngeal wall.
Key Operative Learning Points
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Anatomic phenotyping with drug-induced sedation endoscopy (DISE) or other imaging or endoscopic techniques is essential for proper patient and procedure selection.
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ESP is ideally suited for a more obliquely or horizontally oriented soft palate with a large lateral oropharyngeal wall component and a circumferential pattern of collapse at the velum.
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TPA is ideally suited for a more vertically oriented soft palate with maxillary retrusion and anterior-posterior pattern of soft palate collapse at the genu and velum.
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Maximal mucosal preservation is key to preserving the largest potential velopharyngeal airway, as well as to maintaining the physiologic function of the palate and reducing morbidity.
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To minimize flap dehiscence in ESP, ensure that the suspension suture passed through the muscle belly contains fascia and that the anchor suture passed near the hamulus contains aponeurosis of the tensor tendon and/or buccopharyngeal raphe.
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To minimize risk of oronasal fistula in TPA, include hearty palatal aponeurosis in the suture around the bony keel segment.
Preoperative Period
A comprehensive sleep medicine history is the critical first step before considering surgical therapy for any OSA patient. Approximately one-third of OSA patients have been reported to have another primary sleep disorder or sleep-modulating medical comorbidities, such as psychophysiologic insomnia, chronic pain, shift work sleep disorder, restless legs syndrome, or narcolepsy. Medications that negatively affect control of breathing (e.g., opiates or benzodiazepines), or alter sleep architecture or continuity directly (e.g., antidepressants), must also be taken in account in evaluating a patient’s candidacy.
Because surgery is most commonly a second-line or alternative treatment strategy, it is also important to thoroughly evaluate and exhaust first-line medical therapy options. For patients who are unable to tolerate or achieve benefit with positive airway pressure (PAP) therapy, a detailed analysis of the PAP data download software and troubleshooting of specific PAP side effects remain important strategies prior to surgery. Many of the common mask-related, pressure-related, and psychosocial side effects of PAP can be overcome with therapy or equipment adjustments, behavioral modifications, positional therapy, or other conservative interventions. Furthermore, in patients with symptomatic nasal obstruction or chronic sinonasal disease, medical or surgical therapy of the nose can provide a pathway to improved adherence and results with PAP therapy (see Chapter 95 ; Chapter 97 ).
For patients who have exhausted PAP, oral appliance, positional therapy, and/or weight loss and require an effective option for disease reduction and symptomatic improvement, successful surgical therapy requires effective phenotyping of the patient’s anatomy and sleep-disordered breathing pathophysiology. A standardized anatomic and physiologic staging system does not exist; however, physical examination, upper airway endoscopy, and imaging techniques are available to describe the upper airway anatomy and tailor a surgical treatment plan appropriately.
History
- 1.
History of present illness
- a.
Sleep-related symptoms and impact on quality of life, including snoring, witnessed apnea, gasping, choking, nocturnal awakenings, nocturia, morning headaches, daytime sleepiness, and cognitive dysfunction.
- b.
Timing, duration, and onset of symptoms. Severe OSA that has already been present and untreated for many years may have implications on cardiovascular comorbidities. OSA symptom onset that coincides with specific events, such as a nasal injury, jaw surgery, weight gain, cerebrovascular event, or change in sleep position due to musculoskeletal problem, may have therapeutic implications.
- c.
Presence of other sleep disorders, such as insomnia and restless legs syndrome, that may confound the assessment of OSA outcome measures. Successful management of the patient will often require treatment of both the OSA and other sleep pathology. A comprehensive sleep medicine history is essential.
- d.
Prior OSA treatment history, both medical and surgical, including detailed information on side effects, treatment response, and adherence with PAP and other medical devices. Excellent PAP adherence in the setting of persistent daytime sleepiness, for example, is suggestive of other non-OSA etiology of sleepiness, and surgery may not be indicated.
- a.
- 2.
Sleep laboratory testing
- a.
Type of study: home sleep apnea test (HST) versus in-lab polysomnography (PSG)
- b.
Sleep efficiency: Poor sleep efficiency may raise concern for unreliable sleep study results or the possibility of comorbid insomnia.
- c.
Sleep architecture: Abnormal sleep architecture may be caused by OSA, as well as by medications (e.g., antidepressants, steroids) or other sleep pathology.
- d.
Sleep continuity: An elevated arousal index or abnormal sleep continuity can also be caused by OSA or by chronic pain, medications, or other sleep or medical pathology.
- e.
Respiratory analysis: snoring, apnea-hypopnea index (AHI), respiratory disturbance index (RDI), and oxygen saturations should be assessed to determine the severity of OSA. The presence of central sleep apnea, Cheyne-Stokes respiration, or other sleep-related hypoventilation or hypoxemia conditions (e.g., due to cardiopulmonary disease) should be ruled out because surgery may be contraindicated in many such conditions.
- f.
Signs of other sleep pathology: PSG should evaluate for periodic limb movement disorder (PLMD), nocturnal seizure activity, rapid-eye movement (REM)-behavior disorder (RBD), or other nonrespiratory sleep disorders.
- a.
- 3.
Past medical history
- a.
Comorbidities associated with OSA (hypertension, diabetes, myocardial infarction, atrial fibrillation, cerebrovascular event, depression, gastroesophageal reflux disease, erectile dysfunction)
- b.
Chronic back or neck pain, fibromyalgia, or other pain syndromes that may negatively impact sleep
- c.
Cardiopulmonary disease (e.g., chronic obstructive pulmonary disease, valvular heart disease, or congestive heart failure) that may complicate control of breathing at night and introduce additional respiratory pathology beyond OSA
- d.
History of dysphagia
- e.
History of neuromuscular disease
- a.
- 4.
Past surgical history
- a.
Prior sinonasal surgery
- b.
Prior pharyngeal or skeletal OSA surgery
- c.
Prior bariatric surgery
- a.
- 5.
Medications
- a.
Anticoagulants
- b.
Opiate pain medication, benzodiazepines, or other medications that can alter nocturnal control of breathing
- c.
Selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), lithium, or other neuropsychiatric medication that can independently alter sleep architecture and continuity
- d.
Stimulant therapy (e.g., modafinil or methamphetamines), which may confound the assessment of daytime sleepiness
- a.
- 6.
Family history
- a.
Strong family history of OSA may provide insight in the anatomic/structural vulnerability.
- a.
- 7.
Social history
- a.
Occupation
- 1)
OSA in truck drivers, airline pilots, railroad engineers, and other occupations involving public safety risk has additional implications on treatment and report of outcomes.
- 2)
Shift workers may have residual sleep-related symptoms due to their circadian rhythm disturbance even after otherwise successful OSA treatment.
- 1)
- b.
Alcohol: Evening alcohol use has been correlated with increased obstructive respiratory events.
- c.
Tobacco: Smoking has been shown to independently increase the risk of moderate-to-severe OSA, as well as increase sinonasal and pulmonary disease.
- d.
Total sleep duration: Behaviorally induced insufficient sleep is one of the most common causes of daytime sleepiness and may confound the assessment of OSA treatment outcomes. Sleep deprivation has also been shown to exacerbate OSA.
- a.
Physical Examination
- 1.
Anterior rhinoscopy
- a.
Acquired nasal deformity, septal deviation, turbinate hypertrophy, rhinitis, nasal polyps, and nasal valve pathology may increase upper airway resistance and directly contribute to sleep-disordered breathing.
- b.
Increased nasal resistance may also increase negative intraluminal pressure in the pharynx and increase the fraction of maladaptive mouth breathing, further contributing to OSA pathophysiology.
- c.
Nasal surgery to lower nasal resistance should be considered either in conjunction with or prior to pharyngeal surgery in most cases.
- a.
- 2.
Facial skeleton
- a.
Significant maxillary or mandibular hypoplasia may require orthodontic or orthognathic surgical correction prior to consideration of pharyngeal surgery.
- b.
Occlusion
- 1)
Angle classification
- 2)
Degree of overjet and overbite
- 1)
- a.
- 3.
Oral cavity
- a.
Tongue ridging or scalloping suggests relative macroglossia for the available mandibular size.
- b.
Quality and quantity of dentition have implications on the availability of adjunctive custom mandibular repositioning device (oral appliance) in the treatment plan.
- c.
Height and width of the hard palate. A narrow high-arched soft palate may increase the difficulty of soft tissue work on the soft palate and may negatively affect treatment outcomes.
- d.
The presence of large palatal tori may reduce operative exposure and make palatal surgery more technically challenging.
- a.
- 4.
Oropharynx
- a.
Sagittal configuration of the soft palate (see Fig. 54.1 )
- 1)
ESP is ideally suited for a more obliquely oriented soft palate with an open maxilla and open genu.
- 2)
TPA is ideally suited for a more vertically oriented soft palate with anteroposterior collapse pattern and maxillary retrusion.
- 1)
- b.
Soft palate length
- c.
Modified Mallampati (MM) or Friedman Tongue Position (FTP). Low (stage I or II) MM or FTP scores have been associated with more favorable outcomes with isolated palate surgery.
- d.
Tonsil size. Larger (3+ or 4+) tonsil sizes have been correlated with improved surgical outcomes.
- e.
Lateral oropharyngeal wall component. The size and position of the posterior tonsillar pillars (palatopharyngeus muscles) have treatment implications. ESP specifically targets and repositions the lateral oropharyngeal wall collapse.
- f.
Uvula size and configuration
- a.
- 5.
Neck
- a.
Neck circumference
- b.
Hyoid bone position: A low or inferiorly positioned hyoid bone suggests a longer pharyngeal airway and greater risk of hypopharyngeal collapse that will likely require additional treatment beyond palatal or oropharyngeal surgery alone.
- a.
- 6.
General health
- a.
Blood pressure
- b.
Cardiovascular
- c.
Respiratory
- d.
Mental
- a.
- 7.
Drug-induced sleep endoscopy (DISE)
- a.
The length, width, and depth of the soft palate space are documented. Specifically, endoscopy assesses the position of the hard palate, the levator muscle sling (genu), the velum, and the lateral velopharyngeal walls.
- b.
ESP is more conducive to the complete concentric pattern of collapse with an oblique soft palate and obstruction more distally at the velum due to large lateral velopharyngeal wall components ( Fig. 54.2 ).
- a.
