Overview of phase I surgery for obstructive sleep apnea syndrome.

Introduction

Although the exact etiologic factors of obstructive sleep apnea syndrome (OSAS) have not been clearly elicited, it is well recognized that disproportionate anatomy of the upper airway exists in OSAS, leading to obstruction during sleep. [1-3] The three major regions of obstruction are the nose, palate (pharynx), and base of tongue (hypopharynx). An anatomic obstruction at one or all of these levels can create increased airway resistance and contribute to nocturnal obstruction.

Surgical therapy using tracheotomy was the first treatment to manage OSAS in "Pickwickian" patients. Since the first tracheotomy was performed by Kuhlo, [4] various procedures have been developed to alleviate anatomic obstruction in patients with OSAS. Current surgical therapy is directed to specific anatomic regions (table 1). Therefore, accurate presurgical evaluations are essential for the appreciation of the anatomic abnormality present. This allows for the utilization of a surgical protocol that results in improved clinical outcomes.

At our center, a thorough clinical head and neck evaluation in combination with fiberoptic pharyngolaryngoscopy are performed to isolate and direct treatment at the region or regions of obstruction. A lateral cephalo metric radiograph is also used to assist in treatment planning. Although cephalometric radiography is only a static two-dimensional method of evaluating a dynamic three-dimensional area, it does provide useful information on the posterior airway space. The posterior airway space measurement on lateral cephalometric radiography has been shown to correlate with the volume of the hypopharyngeal airway on three-dimensional computed tomography. [5] In addition, it is a valuable study to assess the relationship of the maxillofacial skeleton and the hyoid bone to the airway (figure 1).

General indications for treatment

The consequences of OSAS include excessive daytime sleepiness, secondary to sleep fragmentation, and cardiovascular derangements that are manifested as hypoxemia, increased negative intrathoracic pressure, and autonomic nervous system alterations. These physiologic effects are associated with morbidity and mortality in OSAS. [6-8]

The general indications for surgery are well established (table 2). A respiratory disturbance index (RDI) greater than or equal to 20 is used at our center as one of these parameters. It has been demonstrated that there is an increased risk of mortality at this level. In addition, most patients have excessive daytime sleepiness at this RDI level. It must be emphasized, however, that patients with an RDI of less than 20 and patients with upper airway resistance syndrome can experience significant sleep fragmentation and excessive daytime sleepiness; therefore, treatment should be considered.

Surgical treatment philosophy

Continuous positive airway pressure (CPAP) is considered the gold standard treatment modality. At our institution, we have established a surgical goal to define cure (table 3). Adherence to this strict criteria enables us to compare our surgical results with CPAP results. A two-phase surgical protocol was established that combines the evaluation, the indications for treatment, and the treatment philosophies to meet and better attain this goal (figure 2). A treatment plan is formulated by identifying the region or regions of obstruction and applying the specific surgical procedure to alleviate the obstruction(s). This two-phase approach was established to minimize surgical interventions and avoid unnecessary surgery while achieving a cure. After the completion of phase I surgery, patients are given 4 to 6 months to heal before a postoperative polysomnogram is obtained to evaluate their outcome. Patients whose sleep apnea persists are offered phase II surgery (maxillomandibular advancement).

It is important to review all possible treatment options and explain the rationale for this staged approach for upper airway reconstruction. In our opinion, combining phase I and phase II surgery is contraindicated because of the potential that phase II surgery might not be necessary and because of the increase in surgical morbidity and postoperative airway compromise. Our concern for postoperative airway compromise has prompted us to further establish a CPAP surgical protocol. [9] Patients whose RDI is greater than or equal to 40 and whose oxygen desaturation is 80% or less are placed on CPAP therapy 2 weeks prior to surgery. These patients are maintained on CPAP postoperatively until 2 weeks before the followup polysomnogram (i.e., 4-6 mo postoperatively). A temporary tracheotomy is considered for patients with severe sleep apnea (RDI: [greater than]60, [SaO.sub.2]: [less than]60) who are intolerant of nasal CPAP.

Phase I surgery

Phase I surgical protocol includes nasal reconstruction, uvulopalatopharyngoplasty (UPPP), mandibular osteotomy with genioglossus advancement, and hyoid myotomy and suspension. Nasal reconstruction and UPPP are designed to treat obstructions at the nasal and pharyngeal levels. The operative indications and techniques are well known, so they will not be reviewed again here. However, our preferred technique of pharyngeal reconstruction using the uvulopalatal flap has several advantages over conventional UPPP, and it will be described here. [10]

Hypopharyngeal obstruction involves airway blockage at the tongue base and supraglottic regions. Because the mechanism of obstruction is complex, multiple procedures have evolved for the reconstruction of this region. They include mandibular osteotomy with genioglossus advancement and hyoid myotomy and suspension. The mandible, tongue, and hyoid complex plays a major role in OSAS at the hypopharyngeal level. [1,2,11] The rationale for surgical intervention at the tongue base is to minimize its collapse and posterior displacement during sleep. Anterior repositioning of the genioglossus muscle is achieved by a conservative mandibular osteotomy that advances the genial tubercle without moving the teeth or mandible. It improves the tension of the genioglossus muscle and decreases its collapsibility during sleep, thus alleviating obstruction. The rationale for altering the hyoid position in the treatment of tongue base obstruction is the fact that anatomically, the hyoid complex is an integral part of the hypopha rynx. Anterior movement of the hyoid complex improves the posterior airway space, and numerous reports have supported the concept that surgical intervention at the hyoid level improves the hypopharyngeal airway. [12-15]

In 1984, we first described the inferior mandibular osteotomy with hyoid myotomy and suspension for hypopharyngeal reconstruction. [16] Our technique has evolved and been refined over the years in order to improve outcomes and minimize morbidity. The current technique of mandibular osteotomy with genioglossus advancement involves a limited osteotomy intraorally to isolate and advance the genial tubercle. It is a minimally invasive procedure that is routinely completed within 30 minutes.

Although hyoid myotomy with suspension also improves hypopharyngeal obstruction and is included in the phase I surgical protocol, it is not always performed simultaneously with genioglossus advancement. This is because most patients with OSAS have diffuse airway obstruction, and genioglossus advancement is generally combined with UPPP. The added insult to the infrahyoid region that is inflicted by combining the genioglossus advancement and the hyoid myotomy and suspension results in increased edema, and this is thought to be inappropriate in some patients. We have also found that in some patients, the hypopharyngeal airway obstruction can be treated with genioglossus advancement only, so a hyoid procedure is not always necessary. Furthermore, in some elderly patients ([greater than]60 yr), airway edema following simultaneous genioglossus advancement and hyoid myotomy and suspension can result in prolonged dysphagia that can require several days to resolve. For these reasons, we perform hyoid myotomy and suspension only in some patients and only as a separate surgical step.

Surgical procedures

Uvulopalatal flap. The uvulopalatal flap procedure is a modification of UPPP (figure 3). This technique reduces the risk of nasopharyngeal incompetence and nasal stenosis and decreases postoperative pain. The procedure involves retracting the uvula toward the junction of the hard and soft palate. The opening to the nasal pharynx is examined, the overlapping mucosa is excised as diagrammed, and the tip of the uvula is removed. The lateral pharyngeal wall redundancy is improved by carrying the mucosal excision laterally. The flap is repositioned and closed with 3-0 Vicryl sutures.

Mandibular osteotomy with genioglossus advancement. This procedure is designed to advance the tongue at the genial tubercle attachment (figure 4). The surgery is limited in that the jaw and teeth do not move; only the genial tubercle is repositioned anteriorly. The limiting factor in this forward movement is the thickness of the mandibular symphysis. It must be emphasized that no additional room is anatomically created for the tongue in this procedure. The advancement of the genial tubercle increases the tension on the tongue musculature, thus limiting its posterior displacement during sleep. Preoperative radiographic analysis, including a lateral cephalometric radiograph and a panoramic dental x-ray, are necessary to assist the surgeon in surgical planning. The cephalometric radiograph will document skeletal deformities and soft tissue airway narrowing. It will further assist in the evaluation of anatomic and airway changes following surgery. The panoramic radiograph will demonstrate the course of the infer ior alveolar nerve canal, the mental foramen, and the anatomy of the mandibular teeth. It will also detect any pathologic processes, such as periodontal disease and odontogenic cysts.

The surgical procedure is performed completely intraorally. The mucosal incision is made just below the mucogingival junction, and a subperiosteal flap is reflected to expose the anterior mandible and mental nerves. The genial tubercle and genioglossus muscle can be identified by finger palpation in the floor of the mouth and with the aid of the lateral cephalometric radiograph. It is recommended that the superior horizontal bone cut be at least 5 mm below the root apices to minimize paresthesia of the teeth. A minimum of 10 mm of the inferior border of the mandible should be preserved by proper placement of the inferior horizontal bone cut to reduce the risk of a pathologic mandibular fracture. The lateral and vertical bone cuts are completed without extending beyond the canine teeth. Before the osteotomy is completed, a titanium screw is placed in the outer cortex to control and manipulate the genial tubercle fragment. Bleeding is controlled with electrocautery and a hemostatic agent, such as Gelfoam. The fragment is advanced and partially rotated to prevent retraction back into the floor of the mouth. The outer cortex and marrow are removed, and the inner cortex is rigidly fixed with a 2.0 mm titanium screw.

Hyoid myotomy and suspension. Our current technique involves suspending the hyoid to the superior thyroid cartilage (figure 5). [17] The surgical approach is through a horizontal skin incision above the hyoid bone. The dissection is carried along the suprahyoid musculature to the body of the hyoid. The infrahyoid and suprahyoid muscles are partially dissected off to enable the advancement of the hyoid complex. Occasionally, the stylohyoid ligament must be amputated from the lesser cornu to improve the mobilization of the hyoid bone. It is important not to extend beyond the lesser cornu because of the risk to the superior laryngeal nerve. The hyoid is suspended anteriorly to the superior thyroid cartilage with four permanent sutures. It is recommended that a surgical drain be placed for 1 or 2 days to prevent seroma or hematoma formation.

Perioperative management

Diligence and compulsion must be practiced in the perioperative management of patients with OSAS because of the coexisting medical conditions that can complicate therapy. [18] As stated earlier, nasal CPAP should be attempted at least 2 weeks before surgery to reverse sleep debt and prevent rapid eye movement rebound during the postoperative period. Anesthesia induction and intubation are performed with the surgeons present. A fiberoptic intubation or tracheotomy while the patient is awake should be considered in difficult airway situations, especially in obese patients with a large neck circumference ([greater than]46 cm) and associated skeletal deformities (mandibular deficiency and low hyoid bone). All patients are extubated while they are awake in the operating room immediately following surgery. All patients who undergo multiple procedures (UPPP combined with geniog lossus advancement and/or hyoid myotomy and suspension) and all those who have significant coexisting medical conditions (hypertension, coro nary artery disease) are monitored in the intensive care unit (ICU) on the first postoperative day. Nasal CPAP or humidified oxygen (35%) via a face tent are administered to all patients, and oximetry monitoring is performed throughout the hospitalization. Blood pressure is monitored closely, and hypertension is treated aggressively with intravenous antihypertensive medications to minimize postoperative bleeding and edema.

Although some authors have cautioned against the use of narcotics in OSAS patients who undergo surgery, [19,20] we have not encountered any problems associated with the judicious use of narcotics for pain control. Our protocol includes intravenous morphine or meperidine administered by a nurse in graduated doses (e.g., 1-5 mg of morphine ql-3h as necessary) in the ICU, while the nurse monitors the respiratory rate. All nurses who care for OSAS patients must be educated about sleep apnea and the use of narcotics. Patients are transferred to the ward on the second postoperative day, and intramuscular meperidine and oxycodone elixir are administered. Oral hydrocodone is prescribed a discharge medication. Discharge criteria include a stable airway, adequate oral in-take of fluids, and satisfactory pain control. Patients are urged to use nasal CPAP following discharge; patients with severe OSAS who cannot tolerate nasal CPAP are prescribed humidified oxygen for 2 weeks.

Surgical protocol clinical outcomes

Our surgical results were reported in 1992 (table 4). [21] Two hundred and thirty-nine patients underwent phase I surgery; most of them required intervention at the pharyngeal and hypopharyngeal levels. The overall cure rate was 61% (145/239 patients), based on the 6-month postoperative polysomnogram. The surgical results were comparable to nasal CPAP results. The mean preoperative RDI was 48.3, and the mean postoperative RDI was 9.5 (nasal CPAP RDI: 7.2; p=NS [not statistically significant]). The lowest oxygenation saturation (LSAT) improved from 75 to 86.6% (nasal CPAP LSAT: 86.4%, p=NS). Most of the patients who failed phase I therapy had severe OSAS (mean RDI: 61.9) and morbid obesity (mean body mass index: 32.3 kg/[m.sup.2]). Patients who underwent phase I surgery were further evaluated by comparing surgical success with the severity of OSAS (table 5). As would be expected, there was a higher cure rate in patients with mild to moderate disease (70%) than in those with severe disease (42%).

Postoperative morbidity associated with all the surgical procedures was low. The mean hospital stay after phase I surgery was 2.1 days. Complications associated with UPPP included postoperative bleeding ([less than]1%), infection (2%), minor lateral pharyngeal stenosis ([less than]1%), and transient nasal reflux ([less than]12%) that resolved within several weeks. No alteration of speech was observed. The complications associated with genioglossus advancement and hyoid suspension were infection ([less than]2%), injury to tooth roots requiring root canal therapy ([less than]1%), permanent paresthesia and anesthesia of the mandibular incisors ([less than]6%), and seroma ([less than]2%). Major complications such as mandibular fracture, alteration of speech, alteration of swallow, and aspiration were not encountered.

From the Center for Excellence in Sleep Disorders Medicine, Stanford (Calif.) University School of Medicine.

Reprint requests: Kasey K. Li, DDS, MD, 750 Welch Rd., Suite 317, Palo Alto, CA 94304. Phone: [phone]; fax: [phone]; e-mail: [e-mail]

Abstract

It is well established that obstructive sleep apnea syndrome is associated with increased morbidity and mortality. Surgical therapy has been demonstrated to be a viable treatment option for cure. Thorough presurgical evaluation with the identification of the type of airway abnormality is mandatory to allow for the utilization of a surgical protocol that results in improved clinical outcomes. Phase I surgical protocol is designed to apply specific surgical procedures to alleviate the obstruction(s) present. Following a logical, stepwise surgical approach in airway reconstruction will minimize surgical interventions and avoid unnecessary operations. The incorporation of a risk-management protocol will minimize treatment complications while achieving cure.

References

(1.) Rojewski TE, Schuller DE, Clark RW, et al. Videoendoscopic determination of the mechanism of obstruction in obstructive sleep apnea. Otolaryngol Head Neck Surg 1984;92:127-3l.

(2.) Rivlin J, Hoffstein V, Kalbfleisch J, et al. Upper airway morphology in patients with idiopathic obstructive sleep apnea. Am Rev Respir Dis 1984; 129:355-60.

(3.) Remmers JE, deGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978;44:931-8.

(4.) Kuhlo W, Doll E, Franck MD. Erfolgreiche Behandlung eines Pickwick-Syndroms durch eine Dauertrachealkanule. Dtsch Med Wochenschr 1969;94:1286-90.

(5.) Riley RW, Powell NB. Maxillofacial surgery and obstructive sleep apnea syndrome. Otolaryngol Clin North Am 1990;23:809-26.

(6.) Koskenvuo M, Kaprio J, Partinen M, et al. Snoring as a risk factor for hypertension and angina pectoris. Lancet 1985;l:893-6.

(7.) He J, Kryger MH, Zorick FJ, et al. Mortality and apnea index in obstructive sleep apnea: Experience in 385 male patients. Chest 1988;94:9-14.

(8.) Partinen M, Jamieson A, Guilleminault C. Long-term outcome for obstructive sleep apnea syndrome patients: Mortality. Chest 1988;94:1200-4.

(9.) Powell NB, Riley RW, Guilleminault C, Murcia GN. Obstructive sleep apnea, continuous positive airway pressure, and surgery. Otolaryngol Head Neck Surg 1988;99:362-9.

(10.) Powell N, Riley R, Guilleminault C, Troell R. A reversible uvulopalatal flap for snoring and sleep apnea syndrome. Sleep 1996;19:593-9.

(11.) Lowe AA, Gionhaku N, Takeuchi K, Fleetham JA. Three-dimensional CT reconstructions of tongue and airway in adult subjects with obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1986:90:364-74.

(12.) Kaya N. Sectioning the hyoid bone as a therapeutic approach for obstructive sleep apnea. Sleep 1984;7:77-8.

(13.) Van de Graaff WB, Gottfried SB, Mitra J, et al. Respiratory function of hyoid muscles and hyoid arch. J Appl Physiol 1984:57:197-204.

(14.) Patton TJ, Thawley SE, Waters RC, et al. Expansion hyoidplasty: A potential surgical procedure designed for selected patients with obstructive sleep apnea syndrome: Experimental canine results. Laryngoscope 1983:93:1387-96.

(15.) Patton TJ, Ogura JH, Thawley SE. Expansion hyoidplasty. 1983 First-Place Resident Research Award: Clinical category. Otolaryngol Head Neck Surg 1984:92:509-19.

(16.) Riley R, Guilleminault C, Powell N, Derman S. Mandibular osteotomy and hyoid bone advancement for obstructive sleep apnea: A case report. Sleep 1984;7:79-82.

(17.) Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea and the hyoid: A revised surgical procedure. Otolaryngol Head Neck Surg 1994;111:717-21.

(18.) Riley RW, Powell NB, Guilleminault C, et al. Obstructive sleep apuea surgery: Risk management and complications. Otolaryngol Head Neck Surg 1997;117:648-52.

(19.) Esclamado RM, Glenn MG, MeCulloch TM, Cummings CW. Perioperative complications and risk factors in the surgical treatment of obstructive sleep apnea syndrome. Laryngoscope 1989;99:1125-9.

(20.) Gabrielezyk MR. Acute airway obstruction after uvulopalatopharyngoplasty for obstructive sleep apnea syndrome. Anesthesiology 1988;69:941-3.

(21.) Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: A review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993;108:117-25.

                         Surgical protocol results
   Phase I          Successful Total no. Success
surgery groups       outcomes  patients   rate
GAHM [*] + UPPP [+]    133        223      60%
GAHM alone              4          6       67%
UPPP alone              8         10       80%
Total                  145        239      61%
(*.)Genioglossus advancement and hyoid myotomy with suspension.
(+.)Uvulopalatopharyngoplasty.
                         Phase I surgical protocol
                                                        Successful Total no.
OSAS severity                                            outcomes  patients
Mild (RDI [*] [less than]20; LSAT [+] [greater than]85)     20        26
Moderate                                                    45        58
 (RDI 20-40; LSAT[greater than]80)
Moderate-severe                                             36        51
 (RDI 40-60; LSAT [greater than]70)
Severe (RDI [greater than]20; LSAT [less than]70)           44       104
                                                        Success
OSAS severity                                            rate
Mild (RDI [*] [less than]20; LSAT [+] [greater than]85)   77%
Moderate                                                  78%
 (RDI 20-40; LSAT[greater than]80)
Moderate-severe                                           71%
 (RDI 40-60; LSAT [greater than]70)
Severe (RDI [greater than]20; LSAT [less than]70)         42%
(*.)Respiratory disturbance index.
(+.)Lowest oxygenation saturation.

Surgical procedures for treatment at designated levels

Nasal reconstruction

Uvulopalatopharyngoplasty

Mandibular osteotomy with genioglossus advancement

Hyoid myotomy with suspension

Maxillomandibular advancement

Tongue base resection

Tracheotomy (bypass all upper airway obstructions)

General indications for the treatment of OSAS

Altered daytime performance (excessive daytime somnolence)

Respiratory disturbance index [greater than or equal to]20

Oxygen desaturation [less than]90%

Arrhythmias and hemodynamic changes associated with obstruction

Negative esophageal pressure ([less than]-10 cm [H.sub.2]O) with sleep fragmentation

Criteria for cure

Postsurgical RDI [*] score and LSAT [+] level equal to CPAP [++] results

For patients without CPAP results:

* Postsurgical reduction [greater than or equal to]50% in RDI and an RDI score [less than or equal to]20

* Postsurgical LSAT level normal or with only a few brief falls below 90%

Normalization of sleep architecture

Neutralization of subjective complaints of excessive daytime sleepiness

(*.) Respiratory disturbance index.

(+.) Lowest oxygenation saturation.

(++.) Continuous positive airway pressure.3