by Jeffrey R. Prinsell, DMD, MD
Surgery for obstructive sleep apnea (OSA) is indicated when applicable conservative therapies are unsuccessful or intolerable and for patients with an underlying specific surgically correctable abnormality that is causing the OSA.1,2 It can provide definitive treatment and, thus, eliminate issues of patient compliance with other therapies, but only if performed competently, both in terms of technical skill and on the correctly identified area(s) of upper airway (UA) obstruction. Disproportionate UA anatomy may include specific single or multiple structures or areas (e.g. unilevel or multilevel) that can be diffusely complex, which varies between different patients.
OSA surgical procedures can be classified anatomically as intrapharyngeal or extrapharyngeal.3 Intrapharyngeal procedures are performed on soft tissues that compose or lie within the velo-orohypopharyngeal airway wall or lumen, whereas extrapharyngeal surgery involves skeletal structures that lie outside the UA. Common intrapharyngeal sites include an elongated or retropositioned soft palate in the velopharynx, and hypertrophied tonsils and macroglossia or a retropositioned tongue base in the oro-hypopharynx. Hypoplastic or retropositioned extrapharyngeal lower facial skeletal structures, including the maxilla, mandible, and hyoid, may also be causative of OSA because they support or stabilize these velo-orohypopharyngeal soft tissues. In contrast to extrapharyngeal surgery, intrapharyngeal procedures can produce life-threatening UA edema in the immediate post-operative period and are often subtherapeutic because they address isolated sites or limited areas and can result in cicatricial scarring and dysfunctional distortion of the UA.
The soft palate is a tissue organ whose known primary function is to prevent reflux of air and liquids into the nasopharynx during speech and swallowing, respectively. Also, its role in snoring may be a self-protection warning “bell” (to the bedpartner), of partial or impending UA obstruction. Retropalatal narrowing and collapse, often induced by swallowing (eg., during nasopharyngolaryngoscopy), should be understood as normal velopharyngeal closure, rather than perhaps misinterpreted as a site of obstruction dictating surgery. A dysmorphic or abnormal-looking soft palate may be an anatomic variant of normal that ensures compensatory functioning and, therefore, may not always be a cause of OSA. Surgical ablation or distortion may produce dysfunction such as velopharyngeal insufficiency; stenosis; voice changes; dysphagia; and, in cases of “social” snoring amelioration, may produce “silent” apnea — either of immediate or delayed (with advancing age and/or weight gain) onset.4 In addition, pain, hemorrhage, and UA obstruction in the immediate postoperative period may occur due to velopharyngeal edema which, particularly if compounded with coexisting untreated hypopharyngeal narrowing, can result in death.5
Telegnathic maxillomandibular advancement (MMA) is a highly therapeutic multilevel treatment of OSA that utilizes LeFort I (LF) and bilateral saggital split ramus osteotomies (BSSRO) to “pull forward” the anterior pharyngeal tissues (eg., soft palate and tongue) attached to the maxilla, mandible, and hyoid in order to structurally enlarge the entire velo-orohypopharyngeal airway (Figure 1); and enhance the neuromuscular tone of the pharyngeal dilator musculature (eg., tensor veli palatini and genioglossus) – via an extrapharyngeal operation with minimal risks of postoperative edema-induced UA embarrassment or pharyngeal dysfunction.4 Telegnathic MMA preserves the functional integrity of the pharyngeal tissues and postoperative edema from the labial vestibular MMA incisions and tissue dissection is anatomically shielded from the UA by the underlying bony structures and, thus, is confined to the facial soft tissues.6 The entire velo-orohypopharyngeal airway is more patent at the moment of skeletal advancement, like the immediate UA opening produced by a CPR “jaw-thrust” maneuver.
While orthognathic surgery includes maxillary and mandibular osteotomies to treat malocclusion to improve mastication, speech, and esthetics, telegnathic surgery includes skeletal (i.e., maxillary, mandibular and hyoid) advancement to anatomically enlarge and physiologically stabilize the velo-orohypopharyngeal airway to treat OSA. Ideally, MMA may harmoniously satisfy the goals of both telegnathic and orthognathic surgery.3 However, this may not always be feasible and, accordingly, should not be viewed as failure, but rather, accepted as known limitations of telegnathic surgery. For example, telegnathic MMA may be therapeutic for OSA but yet maintains an existing, albeit “untreated,” malocclusion in a patient who does not pursue orthodontic therapy. In cases of hypopharyngeal narrowing in the absence of skeletal hypoplasia (a normal profile), MMA might create an unesthetic bimaxillary-protrusive face.
Counterclockwise rotational advancement of the maxillomandibular complex with anterior maxillary impaction allows for mandibular advancement greater than maxillary to increase orohypopharyngeal enlargement to treat OSA with an esthetically-acceptable facial appearance.7 The amount of mandibular advancement is typically the main determinant of MMA’s therapeutic efficacy because the hypopharynx is usually the most critical site of UA obstruction. However, the limiting factor for the amount of MMA advancement is typically the degree of maxillary protrusion, which causes thinning of the upper lip, excessive maxillary incisor show, alar base flaring, and nasal tip upward rotation. Esthetic enhancements of counterclockwise rotation include correction of excessive maxillary incisal show or gummy smile and lip incompetence in dolichocephalic faces, increased horizontal and vertical dimension of the lower face, accentuation of the lower jawline and hyoid elevation that raises the chin-neck angle in mandibular retrognathism cases, and tightening or rejuvenation of neck skin laxity in relatively older patients (Figure 2).
The primary anatomical criterion for MMA is hypopharyngeal narrowing that can be measured by the lateral cephalometric end-tidal volume posterior airway space (PAS) < 9 mm.8 Specific measurements for other imaging modalities as inclusion criteria for MMA have not been published. In the setting of hypopharyngeal narrowing, coexistent velopharyngeal narrowing, as well as other extrapharyngeal sites, may also be treated with MMA.
OSA cases due to diffusely complex or multiple sites of disproportionate anatomy, create difficult dilemmas in terms of the staging and combinations of surgical procedures. There exists variability in the use of MMA as a primary versus secondary (second stage) operation and what concomitant adjunctive procedures can be performed safely to enhance therapeutic efficacy. Although highly therapeutic as a secondary operation,9 MMA may be also performed initially for selected cases of multiple or diffusely complex sites of velo-orohypopharyngeal obstruction, including coexistent soft palatal dysmorphism and mild-to-moderate tonsillar hypertrophy.4 This is done to enlarge and stabilize the entire velo-orohypopharyngeal UA to either: definitively treat the OSA and obviate the need for invasive segmental intrapharyngeal procedures; or to decrease the risk of postoperative edema-induced airway embarrassment after intrapharyngeal surgery that may be necessary later for clinically significant residual OSA, perhaps with advancing age and/or weight gain.10
In general, MMA therapeutic efficacy may be enhanced with concomitant adjunctive extrapharyngeal procedures such septoplasty with turbinate reduction, anterior mandibular lingual tori removal4 to increase tongue space in the floor of the mouth, cervicofacial lipectomy to reduce excessive adipose tissue (“weight”) against the underlying anterior pharyngeal tissue particularly during supine sleep, and an anterior inferior mandibular osteotomy (AIMO) for additional advancement of the tongue-related and suprahyoid musculature (an indirect hyoid suspension without invasive hyoid surgery). An inferiorly-based trapezoid-shaped AIMO includes all these muscle insertions and preserves the esthetic contour of the chin4 (Figures 1-2).
On the other hand, intrapharyngeal procedures should probably not be performed concomitantly with MMA for several reasons. First, intrapharyngeal postoperative edema may cause UA embarrassment that may be difficult to manage, particularly in the setting of maxillomandibular fixation (jaws wired shut). Second, intrapharyngeal pain, particularly when compounded with that of MMA, may require excessive use of centrally-acting opiate and opioids that may precipitate narcotic-induced respiratory depression. Third, intrapharyngeal pain may impede swallowing of liquids and pureed nutrition, which is already difficult for patients following MMA. Fourth, intrapharyngeal procedures may compromise the therapeutic efficacy of MMA. For example, uvulopalatopharyngoplasty (UPPP) with concurrent maxillary advancement may create excessive tension on the soft palatal wound that may exacerbate velopharyngeal cicatricial scarring and stenosis.3
Telegnathic MMA is the most successful acceptable (excluding tracheostomy) surgical treatment for OSA, with a therapeutic efficacy comparable to Nasal CPAP.1,3 As a comprehensive, safe, nondysfunctional, extrapharyngeal operation that structurally enlarges and physiologically stabilizes the entire velo-orohypopharyngeal UA, MMA may eliminate the need for (and thus circumvent the staging dilemmas associated with) multiple, segmental, subtherapeutic and invasive intrapharyngeal procedures. MMA should not be limited to cases of severe OSA or dentocraniofacial skeletal deformities or when other surgery have failed, but rather is also indicated as the initial surgical treatment of choice for (velo-oro) hypopharyngeal narrowing, even in the setting of relatively mild OSA and in the absence of retrognathism.7
MMA as a potentially definitive primary single-stage surgical treatment of OSA, particularly when performed in a relatively young adult population, may result in a significant improvement in quality of life and a reduction in OSA-related health risks (eg., hypertension, cardiovascular dysrhythmias, stroke and myocardial infarction, depression, and cognitive dysfunction, as well as hypersomnolence-induced injuries such as those caused by motor vehicle accidents) that, when projected over an average normal lifetime, should result in considerable financial savings for the health care system.11
Nevertheless, MMA should not be used indiscriminately, as it is technically difficult to perform and laden with potential morbidity such as bleeding and neurosensory deficits. Although skeletal osteotomies when healed to a bony union are stable with no significant relapse, and the relatively long-term results of MMA are promising, the effect of soft tissue laxity that occurs with natural aging (with or without weight gain) in terms of possible progressive velo-orohypopharyngeal narrowing and worsening of residual OSA, is unknown. “How far” to advance the maxillomandibular complex may be a combination of OSA severity and the degree of hypopharyngeal narrowing, limited by physiologic and esthetic constraints of the overlying facial soft tissue envelope.3 Titration of mandibular advancement via oral appliances or distraction osteogenesis may help predict optimal therapeutic efficacy of telegnathic MMA. Additional studies are warranted, with larger numbers of cases and longer follow-up periods.
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