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P. Yalamanchi and P. T. Hoff
. Fig. 18.10 Tongue base suspension procedure
Tongue base suspension
Hyoid suspension
18
Thyrohyoidpexy
. Fig. 18.11 Hyoid suspension procedures
advancement and/or with palatal repositioning proce­dures for obstructive sleep apnea, . Fig.18.11. The thy­rohyoidpexy procedure advances the hyoid bone over the thyroid lamina which is then secured with perma­nent sutures placed through the superior portion of the thyroid cartilage. Anterior repositioning of the hyoid bone by attaching it to the thyroid cartilage expands the airway. While there is variable success with hyoid advancement, the procedure is generally well tolerated with surgical risks limited to infection, seroma forma­tion, and dysphagia.
The hyoid can also be suspended to the posterior sur­face of the mandible, which pulls the tongue base in an anterior-superior direction. The hyoid bone is xed to the mandible with anchor sutures placed through a sub-
Hyoidmandibulopexy
mental incision. This is a minimally invasive technique and works well for patients with a large muscular tongue base without lymphoid hypertrophy.
Suspension procedures have been shown to be mod­estly effective when performed in isolation; the best results are obtained when performed in conjunction with palatal surgery.
18.8.6 Maxillomandibular Advancement
(MMA)
Maxillomandibular advancement increases the retropala­tal and retrolingual airway by advancing the maxilla and mandible through Le Fort I maxillary and sagittal- split
Hypophar yngeal Surgery forOSA Patients
279
a
18
b
. Fig. 18.12 Inspire hypoglossal nerve stimulator: a Inspire pulse generator, sensing lead, and stimulating lead, b Inspire layout, c intra-
operative image of hypoglossal nerve dissection with red vessel loop around inclusion branches of the nerve
mandibular osteotomies. Typically, this procedure is per-

18.9 Future Directions

formed when other surgical interventions have been unsuccessful. Potential complications include malocclu­sion, nonunion, or malunion temporomandibular joint problems and nerve paresthesia. Despite the risks and relative morbidity of the procedure, the success rate of this procedure has been reported to be between 80% and 90%.
Increasingly, neurostimulation treatment strategies are viewed as a preferred alternative to bony or soft tissue surgical interventions for treatment of OSA in CPAP­intolerant patients. These procedures have a lower risk prole and are associated with signicantly reduced postoperative pain and recovery time. While strict inclu­sion criteria and cost are currently the primary barriers
18.8.7 Hypoglossal Nerve Stimulators
for increasing adoption of hypoglossal nerve stimulation, novel stimulation strategies are being designed and
HNS therapy has been shown to signicantly reduce AHI in moderate-to-severe OSA patients with strict inclusion criteria including BMI <32, an AHI between 15 and 65, and favorable pattern of upper airway obstruction during DISE. The hypoglossal nerve stimulator system involves three main components: the implantable pulse generator (IPG), the sensing lead, and the stimulator lead,
.
Fig. 18.12. The IPG is surgically implanted into an
infraclavicular subcutaneous pocket supercial to the pec­toralis major and produces electrical impulses. The sensing and stimulation leads are tunneled subcutaneously from the IPG, respectively, to the lower ribs and hypoglossal nerve. Closed-loop stimulating systems produce impulses with inhalation through the IPG to the hypoglossal nerve via a tripolar electrode that wraps around the nerve result­ing in opening of the retroglossal airway as well as the ret­ropalatal airway due to mechanical coupling of the palatoglossal and genioglossus musculature, . Fig.18.13.
invigorating the eld of sleep medicine. Additional clin­ical trials are underway assessing the efcacy of external HNS stimulation devices.
Patient selection is an area of active research. It is now widely recognized that surgeons must address both the anatomic and nonanatomical parameters such as loop gain (a measure of ventilatory stability) and arousal threshold using a physiology-based model to better pre­dict outcomes after upper airway surgery for obstructive sleep apnea.
Additionally, recent research has indicated that effer­ent motor pathways may be stimulated through recruit­ment of reex afferent input to respiratory and upper airway motor control centers. Compared with direct unilateral hypoglossal nerve stimulation, recent studies in animal models has suggested esophageal distention, electrical auricular stimulation, sciatic nerve stimula­tion, and pulsed nasal insufation of heated, humidied
c
280
P. Yalamanchi and P. T. Hoff
18
. Fig. 18.13 Effects of
hypoglossal nerve stimulation. (Courtesy of Inspire Medical Systems)
Inspire hypoglossal nerve stimulation eects
No stimulation Mild stimulation
Base of tontgue Base of tontguePalate Palate
air may activate respiratory brainstem motor nuclei to initiate a more coordinated brainstem response involv­ing several cranial nerves and upper airway muscles to improve airway patency during sleep. The eld of neuro­stimulation for treatment of OSA is exciting and nascent as promising new approaches for activating efferent and afferent motor pathways are currently in early stage development.

References

1. Stuck BA, Leitzbach S, Maurer JT. Effects of continuous positive airway pressure on apnea-hypopnea index in obstruc­tive sleep apnea based on long-term compliance. Sleep Breath. 2012;16(2):467–71.
2. Fujita S. Obstructive sleep apnea syndrome: pathophysiol­ogy, upper airway evaluation and surgical treatment. Ear Nose Throat J. 1993;72(1):67–72. 5–6
3. Riley RW, Powell NB, Guilleminault C.Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg. 1993;108(2):117–25.
4. Weaver TE, Laizner AM, Evans LK, Maislin G, Chugh DK, Lyon K, Smith PL, Schwartz AR, Redline S, Pack AI, Dinges DF.An instrument to measure functional status outcomes for disorders of excessive sleepiness. Sleep. 1997;20(10):835–43.
5. Thaler ER, Rassekh CH, Lee JM, Weinstein GS, O’Malley BW Jr. Outcomes for multilevel surgery for sleep apnea: obstructive sleep apnea, transoral robotic surgery, and uvulopalatopharyn­goplasty. Laryngoscope. 2015;126:266.
6. Vicini C, Dallan I, Canzi P, Frassineti S, Nacci A, Seccia V, etal. Transoral robotic surgery of the tongue base in obstructive sleep
Apnea-Hypopnea syndrome: anatomic considerations and clini­cal experience. Head Neck. 2012;34(1):15–22.
7. Kezirian EJ.Nonresponders to pharyngeal surgery for obstruc­tive sleep apnea: insights from drug-induced sleep endoscopy. Laryngoscope. 2011;121(6):1320–6.
8. Vicini C, Dallan I, Canzi P, Frassineti S, La Pietra MG, Monte­vecchi F.Transoral robotic tongue base resection in obstructive sleep apnoea-hypopnoea syndrome: a preliminary report. ORL J Otorhinolaryngol Relat Spec. 2010;72(1):22–7.
9. Blumen MB, Coquille F, Rocchicioli C, Mellot F, Chabolle F. Radiofrequency tongue reduction through a cervical approach: a pilot study. Laryngoscope. 2006;116:1887–93.
10. Steward DL, Weaver EM, Woodson BT.Multilevel temperature­controlled radiofrequency for obstructive sleep apnea: extended follow-up. Otolaryngol Head Neck Surg. 2005;132:630–5.
11. Woodson BT, Steward DL, Weaver EM, Javaheri S.A random­ized trial of temperature controlled radiofrequency, continuous positive airway pressure, and placebo for obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg. 2003;128:848–61.
12. Lin HS, Rowley JA, Badr MS, Folbe AJ, Yoo GH, Victor L, et al. Transoral robotic surgery for treatment of obstructive sleep apnea-hypopnea syndrome. Laryngoscope. 2013;123(7): 1811–6.
13. Vicini C, Montevecchi F, Campanini A, Dallan I, Hoff PT, Spector ME, et al. Clinical outcomes and complications associated with TORS for OSAHS: a benchmark for evalu­ating an emerging surgical technology in a targeted applica­tion for benign disease. ORL J Otorhinolaryngol Relat Spec. 2014;76(2):63–9.
Suggested Reading
Friedman M, Hamilton C, Samuelson CG, Kelley K, Taylor D,
Pearson-Chauhan K, et al. Transoral robotic glossectomy for the treatment of obstructive sleep apnea-hypopnea syndrome. Otolaryngol Head Neck Surg. 2012;146(5):854–62.
Management ofObstructive Sleep Apnea (OSA) inCraniofacial Patients
MikhailDaya andJasonE.Portnof
Contents
19.1 Diagnosis andManagement of Childhood Obstructive Sleep Apnea Syndrome – 282
19.1.1 Imaging – 282
19.2 Role ofSleep Upper Airway Endoscopy intheDiagnosis ofOSA – 282
19.2.1 Mandibular Deciency – 282
19.2.2 Mid-Face Deciency – 283
19.2.3 Both Mid-Face andMandibular Deciency – 284
281
19
19.3 Surgical Correction – 284
Bibliography – 290
© Springer Nature Switzerland AG 2021 K. B. Kim et al. (eds.), Management of Obstructive Sleep Apnea, https://doi.org/10.1007/978-3-030-54146-0_19
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19.1 Diagnosis andManagement of
Childhood Obstructive Sleep Apnea Syndrome
Many screening tools and questionnaires have been described for the evaluation of pediatric patients with suspicion of obstructive sleep apnea (OSA). These screening tools could not be relied upon in patients with craniofacial syndromes since they commonly present with other manifestations such as cognitive and hearing decits and ocular decits, among others.
Advanced imaging has shown to be powerful in the assessment of structural abnormalities and in helping to locate the anatomical location of the obstruction along the upper airway. Many software tools incorporate measuring tools to assess the airway, providing three­dimensional measurements.
Polysomnography has proven to be the gold standard for diagnosis of OSA in pediatric population. However, other alternatives have been proposed in the past for screening and diagnosis of this condition.
19.1.1 Imaging
Plain lm radiographs including lateral cephalometric radiographs, AP/PA cephalometric radiographs, and panorex radiographs have been used in the past as an efcient and inexpensive diagnostic tool in the assess­ment of dentofacial deformities since they are readily available at orthodontists and oral surgeons’ ofces. These X-rays are used to diagnose bony anatomy, posi­tion of the maxilla and mandible, length of the soft palate, and position of the hyoid bone. The major disad­vantage of pain lms is the inability to study soft tissues.
Computer tomography (CT) and cone-beam CT (CBCT) signicantly improve the soft tissue contrast and detail. In addition, 3D studies aid in examining the airway in all pains as compared to plain lms allow­ing for precise measurement of minimal cross sectional area and volumetric assessment of the airway. CT scans also provide with detailed anatomical information of the obstruction site, this is relevant in planning upper airway surgery when necessary. However, controversy still exists in the usefulness of 3D imaging in awake non­supine patients, since the true anatomy of asleep patient cannot be assessed accurately.
Comparison of CBCT before and after surgery determines the difference in airway volume. However, no guidelines have been established regarding minimal cross sectional area and airway volume to diagnose OSA based on these ndings.
Magnetic resonance imaging with compared to CBCT and CT scans offers various advantages includ­ing lack of ionized radiation and better analysis of the
soft tissue structures. The lack of ionized radiation makes MRI the imaging technique in children with OSA syndrome.
The application of these imagine technique in cra­niofacial patients can be challenging to the lack of coop­eration by the patient. Sedation may be required for the patient to tolerate these studies without moving while acquiring the imaging. On the other hand, obtaining the images with the patient sedated in a supine position may replicate the airway size and position during sleep, but this is still controversial and no advantages have been proved.
19.2 Role ofSleep Upper Airway Endoscopy
intheDiagnosis ofOSA
Sleep endoscopy has been used since 1991 to examine upper airway during pharmacologically induced sleep. Even though the goal standard up to date remains poly­somnographic studies, other studies such as sleep endos­copy aid in identifying the level and degree of upper airway collapse. This diagnostic tool can aid in the devel­opment of a treatment plan guided toward obstruction.
Multiple grading systems have been developed to grade the severity of OSA. Berchard etal. described a system that focuses on ve anatomical sites including nose and nasopharynx (N), palatine plane, uvula or ton­sils (P), tongue (T), larynx (L), and hypopharynx (H). Furthermore, the obstruction was categorized as partial (1) or complete (2) for each one of the above. So, if the patient has partial obstruction at the nose and tonsils and complete obstruction at the tongue, this would be labeled as N1P1T2 and would be assigned a value of 4 (1+ 1 +2). A score range of 0–2 was associated with mild OSA, 3–4 with moderate, and more than 4 with severe.
19.2.1 Mandibular Deciency
19.2.1.1 Pierre Robin Sequence
Pierre Robin Sequence (PRS) is a congenital malfor­mation occurring in 1in 30,000 live births. This condi­tion is characterized by the triad of severe mandibular hypoplasia, glossoptosis, and cleft palate. Many of these patients present with airway obstruction.
Sher et al. described four types of airway obstruc­tion in patients with PRS based on exible beroptic nasopharyngoscopy ndings. The most common form, TypeI, is dened by obstruction due to posterior move­ment of the tongue against the posterior pharyngeal wall. Type II obstruction is due to posterior and superior displacement of the tongue, causing obstruction from the tongue, the velum, and the pharyngeal wall in the
Management ofObstructive Sleep Apnea (OSA) inCraniofacial Patients
283
19
superior oropharynx. Type III obstruction is caused by prolapse of the medial pharyngeal wall. Type IV obstruc­tion is due to constriction of the pharynx circumferen­tially by lateral pharyngeal walls and the tongue.
Syndromes presenting along with this condition include Stickler syndrome, Nager syndrome, Treacher Collins, and velocardiofacial syndrome. Al-Samakri etal. showed up to 60% of Pierre Robin sequence cases present in combination with other syndromes; 80 to 90% of these patients also present with cleft lip and palate.
The prevalence of OSA in this population ranges from 46% to 100% across the literature. This is due to upper airway obstruction related to micrognathia, pos­terior position of the tongue, and cleft palate.
Management of OSA in patients with Pierre Robin sequence involves treating the upper airway by treating cleft palate, stabilizing the pharyngeal wall, and widen­ing the hypopharynx. Emergent tracheostomy is neces­sary in cases where airway is severely affected. Other necessary treatments include mandibular distraction and application of oral devices to widen the palate and the upper airway.
19.2.1.2 Craniofacial Microsomia
Craniofacial microsomia is condition characterized by structures derived from the rst and second branchial arches, including maxillomandibular complex, facial nerves, ears, and soft tissue. The incidence of craniofa­cial microsomia ranges from 1in 3500 to 1in 20,000 live births in the literature and it is the second most com­mon congenital facial defect, after cleft lip and palate. Craniofacial microsomia can be unilateral, known as hemifacial microsomia, or bilateral.
The mandible is commonly affected in craniofacial microsomia. Mandibular and maxillary hypoplasia, along with adenotonsillar hypertrophy and glossoptosis are important contributing factors for obstructive sleep disorders in this patient population.
The orbits, mandible, ears, nerve, soft tissue (O.M.E.N.S) classication has been widely used to describe the different anatomical variations and severity of this condition. Later, the word Plus was added to the classication to describe any alterations outside of the craniomaxillofacial complex. The OMENS-Plus score is calculated grading each anatomical abnormality from 0 to 3. Where 0 is normal, 1 is abnormal size, 2 is abnormal position, and 3 for the combination of both. Pruzansky graded the mandible, and this classication was later modied by Kaban. Mandibular grading assesses the mandibular ramus and condyle [0=normal; 1=small mandible, short ramus; 2 = abnormally shaped ramus and condyle] with (a) glenoid fossa anatomically accept­able compared to the contralateral side, (b) temporo­mandibular joint (TMJ) displaced anteriorly, medially, or inferiorly with hypoplastic condyle; and 3=complete absence of ramus and fossa.
The prevalence of OSA in patient with craniofacial microsomia varies signicantly in the literature from 7% to 67% taking into consideration the severity of the ana­tomical defects as well as the denition of OSA in the different studies.
19.2.2 Mid-Face Deciency
19.2.2.1 Crouzon’s Syndrome
Crouzon’s syndrome is an autosomal dominant con­dition. It is considered a syndromic craniosynostosis with birth prevalence of 1 in 60,000. This condition can present as an isolated entity or in combination with other malformations. Important clinical characteristics of this condition include bilateral coronal craniosyn­ostosis, exorbitism with hypertelorism, and maxillary hypoplasia, among other variations. The combination of skull and maxillary growth disturbance often results in increased intracranial pressure and obstructive sleep apnea; 40 to 85% of these patients are diagnosed with obstructive sleep apnea at some point and the severity is usually determined by the anatomy of the airway and the degree of mid-face deciency.
Treatment of obstructive sleep apnea for these patients is different from treatment of adults with just OSA.Children with Crouzon’s syndrome often present severe mid-face deciency, increased scleral show, and other craniofacial deformities. These deformities and skeletal deciencies causing obstructive sleep apnea must be address simultaneously. Many surgical options have been proposed for treatment of OSA in children with Crouzon’s syndrome depending on the severity of the case. Severe emergent cases may require tracheos­tomy for immediate airway protection. Other treatment modalities include LeFort III osteotomies for severe mid­face deciency, LeFort I osteotomies, distraction osteo­genesis (DO), and orthodontic/orthognathic surgery. Conservative methods such as CPAP application have been recommended for less severe cases.
19.2.2.2 Apert Syndrome
Apert syndrome is a rare condition that affects 1in every 65,000 births. It is an autosomal dominant transmitted disorder that results in the abnormal development of the skull and face due to the premature closure of sutures, primarily the coronal sutures resulting in brachycephaly and turricephaly (Omar Breik).
This syndrome is characterized by craniosynostosis, mid-facial hypoplasia, syndactyly of the hands and feet, and other malformations of the limbs (Omar Breik). In this syndrome, the maxilla is also involved in the synos­tosis. Therefore, up to 75% of these patients present with cleft palate or bid uvula.
The causes of OSA in patients with Apert syndrome are similar to those mentioned in Crouzon syndrome. OSA
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is often multi-level problem in these children. However, since mid-face deciency is the primary cause for airway constriction, monoblock or LeFort III advancement with distraction is usually the treatment of choice (Doerga).
19.2.3 Both Mid-Face andMandibular
Deciency
19.2.3.1 Treacher Collins Syndrome
Treacher Collins syndrome is an autosomal dominant condition that affects 1in 25,000 to 1in 50,000 births. This craniofacial syndrome is characterized by cranio­maxillofacial soft tissue and skeletal hypoplasia of the rst and second branchial arches. The major features include mandibular micrognathia, conductive hearing loss, malar deciency, and down-slanting eyes and in 33% of the cases with cleft palate.
The treatment of this patient population is carried through the different growth phases. First, to support the airway when the child is born, then during early childhood to support feeding and speech, and deni­tive treatment is performed when growth has been com­pleted to address the facial defects.
19.2.3.2 Goldenhar Syndrome
Goldenhar syndrome is a congenital disorder that affects the rst and second branchial arches and it affects 1 of 5600 live births. Unlike microal microso­mia, Goldenhar syndrome also affects ears, eyes, and vertebrae. Cardiac and neurologic conditions are associ­ated with this disorder; however, they are not necessary for the nal diagnosis.
Obstructive sleep apnea affects 11.6% of patients with Goldenhar syndrome. The etiology of the obstruc­tions is multifactorial, including anatomical and neu­rological alterations. Unlike patients with hemifacial microsomia, patients with this syndrome show increase in CO2. This additional nding may correlate with dys­function of the regulation of respiration during sleep caused by neurological impairment.
Treatment of OSA in patients with Goldenhar syn­drome like in other syndromes varies depending on the severity of OSA as well as the anatomical area in the obstruction. Severe cases require more aggressive inter­ventions such as tracheostomy to protect the airway and improve oxygenation levels while denitive treatment is performed.

19.3 Surgical Correction

In the newborn emergency setting, tongue–lip adhesion and/or tracheostomy may be required to secure and main­tain the airway in craniofacial syndromes with profound airway obstruction and respiratory distress. Tracheostomy
is a bypass procedure that can be used as a temporary measure to maintain the airway while other procedures to improve the airway are planned and performed.
These immediate procedures, performed shortly after birth to address the airway, are then revised. Once facial growth is adequate and life-threatening obstruc­tion is treated, release of the tongue–lip adhesion and a reversal of tracheostomy are performed.
Tonsillectomy/adenoidectomy and palatal procedures such as uvulopalatopharyngoplasty (UPPP) address obstructions of the oropharynx. Adenotonsillectomy is the procedure of choice for surgical management of OSA in children.
Procedures such as hyoid suspension, partial glossec­tomy, and radiofrequency ablation of the tongue base are soft tissue procedures that will address obstruction of the hypopharynx.
Timing of surgery can be during active phases of growth or after growth cessation.
It is possible that surgery performed during active phases of growth is susceptible to relapse and there is need for additional surgical procedures including repeat of the surgical procedure to obtain the desired functional result.
Ilizarov described his concept of distraction osteogen­esis (DO) for limb reconstruction in 1952 and McCarthy described the application of DO to the human cranio­maxillofacial skeleton in 1989. As described, the principle includes a surgical osteotomy after subperiosteal dissec­tion, a latency period of 4–5 days, a distraction period of a rate of sometimes greater than 1.0mm per day, and then a consolidation period. Commonly used distraction protocols are based on a clinical goal of 20% overcorrec­tion. The overall treatment time for distraction of the cra­niofacial skeleton can be less than 3months. Successful maxillary, mid-face, zygomatic, orbital, mandibular, and cranial bone distraction have all been described.
Distraction osteogenesis is a viable treatment option for obstructive sleep apnea in craniofacial syndromic patients. Depending on the anatomic location of the obstruction, the patient may be a candidate for mandib­ular or mid-face distraction (see .
Fig. 19.1). Virtual
surgical planning based on medical grade computed tomography scans or cone-beam CT scans (CBCT) can be helpful to predict the surgical design.
Mid-face distraction osteogenesis can be performed intraorally or extraorally with a rigid external distrac­tion (RED) device. With proper patient selection, RED can be utilized from age 5 through adulthood (see
Fig. 19.2). Similarly, mandibular distraction can be
.
performed with an internal or external device.
Unilateral or bilateral costochondral graft (CCG) reconstruction of the mandible can be an option for craniofacial patients with severe mandibular deciency involving the ramus and condyle unit (see . Fig.19.3). It is recommended that patients who receive mandibu­lar reconstruction with either distraction osteogenesis
Management ofObstructive Sleep Apnea (OSA) inCraniofacial Patients
. Fig. 19.1 Graphic description of extra-oral mandibular distractor (left) and rigid external distractor (RED) device (right)
285
19
. Fig. 19.2 Mid-face deciency in teenager patient with history of cleft lip and palate treated with distraction osteogenesis with rigid exter-
nal distractor (RED) device (left). Postoperative lateral cephalogram with RED device (right)
286
M. Daya and J. E. Portnof
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. Fig. 19.3 Patient with Pierre Robin Sequence and severe mandibular hypoplasia treated with bilateral condylectomies and costochondral
graft. Top picture shows virtual surgical planning and bottom pictures postoperative panoramic X-ray
Management ofObstructive Sleep Apnea (OSA) inCraniofacial Patients
287
19
or costochondral graft follow a similar protocol as has been described by Kaban etal. for the management of TMJ ankylosis in children, which includes the following:
1. Lining of joint with temporalis fascia
2. Rigid xation
3. Early mobilization of jaw (a) if DO is used to reconstruct, mobilize day of
surgery
(b) if CCG is used, early mobilization with minimal
maxillomandibular xation (not to exceed 10days)
4. Aggressive physiotherapy
Among the many therapies offered for OSA, maxillo­mandibular advancement (MMA) is recognized as a powerful technique for relieving upper airway obstruc­tion. This orthognathic surgical procedure generally involves LeFort I maxillary and sagittal split mandibu­lar osteotomies (see .
Fig.19.4). It is possible that in
the craniofacial patient, a sagittal split osteotomy would be insufcient to allow for the large mandibular discrep­ancy that can oftentimes be greater than 1cm. In these patients, extra-oral inverted L osteotomies with bone graft augmentation may be necessary (see . Fig.19.5).
MMA surgery will simultaneously enlarge the pha-
ryngeal airway dimension at the nasopharynx, orophar­ynx, and hypopharynx. The facial skeletal framework is
expanded, with benecial airway effects based on improved positioning of the pharyngeal soft tissues and the tongue. In addition to maxillomandibular advancement, an advancement genioplasty can be performed with a sim­ple anterior mandibular horizontal osteotomy (AMHO) and this technique will allow to advance the genioglossus attachment further opening the airway (see .
Fig.19.6).
However, genioglossus advancement may compro­mise facial aesthetics by over-projecting the chin promi­nence. A modication of the AMHO genioplasty was described by Heggie etal. with a design involving a rota­tional repositioning that allows for advancement of the genioglossus attachments while avoiding excessive pro­jection of pogonion.
In the genial tubercle advancement, a rectangular bone window of the anterior mandible that incorpo­rates the genial tubercle is osteotomized. The bone fragment is advanced, rotated 90 degrees, and stabi­lized. The bony advancement stretches the genioglos­sus muscle and addresses hypopharyngeal soft tissue obstruction. During this operation, the chin point is not changed, and it can be used in patients with an orthognathic prole without a negative impact on facial aesthetics.
Surgical treatment planning for correction of OSA in patients with craniofacial syndromes will often be a component of a multimodality approach.