Overview of phase II surgery for obstructive sleep apnea syndrome.
Obstructive sleep apnea syndrome (OSAS) can result in daytime fatigue and sleepiness that significantly affects, and even threatens, the life of the patient. Tracheotomy was the first treatment for OSAS. It bypasses all forms of obstruction in the upper airway, thus eliminating the disease. However, the morbidity associated with tracheotomy prevents its use in most patients.
Sullivan et al first reported the application of nasal continuous positive airway pressure (CPAP) to maintain upper airway patency for OSAS.  Because of its effectiveness, nasal CPAP is currently the first-line treatment for OSAS. However, patient compliance remains a major problem, and the long-term use of CPAP is likely to be an unrealistic expectation in many cases. [2-4]
In 1979, Fujita et al reported the initial results of uvulopalatopharyngoplasty in the treatment of OSAS.  Although the procedure has proved to be an excellent method of alleviating palatal (pharyngeal) airway obstruction, the untreated base-of-tongue (hypopharyngeal) obstruction resulted in only approximately 40% of patients responding to treatment. 
Recognizing that multiple levels of upper airway obstruction exist in OSAS, we developed several procedures to target the specific anatomic regions involved. Our two-phase surgical protocol was designed to alleviate the anatomic obstruction(s) while minimizing surgical interventions and avoiding unnecessary surgery. The phase I surgical protocol addresses obstructions at the nasal, palatal, and base-of-tongue levels. Phase I procedures include nasal reconstruction, uvulopalatopharyngoplasty, mandibular osteotomy with genioglossus advancement, and hyoid myotomy and suspension. In 1992, we reported a cure rate of 61% following phase I surgery.  Depending on the severity of OSAS, the success rate of phase I surgery ranges from 42 to 78%.  Clearly, many patients continue to experience persistent disease following phase I surgery, and most of them become candidates for phase II surgery. Phase II surgery consists of maxillomandibular advancement, a procedure that was first described for the treatment of craniomaxillofacial deformity.
Rationale for maxillomandibular advancement
The contributing causes that lead to OSAS are multifactorial, and they can have a negative influence on the delicate balance necessary for airway patency during sleep. In addition to obesity, male gender, age, and ethnicity, [8-10] craniomaxillofacial abnormality is a well-recognized predictor of OSAS. [11-13] Many of these patients have a maxillomandibular deficiency that results in a diminished airway dimension and leads to nocturnal obstruction. In 1983, we reported that maxillofacial surgery via mandibular advancement can play a role in the treatment of OSAS.  Mandibular movement forward will help in alleviating a hypopharyngeal obstruction. This finding has also been recognized by others. [15-17] In fact, it was reported that mandibular setback for the correction of mandibular prognathism has produced OSAS.  We subsequently investigated the effect of maxillomandibular advancement on the airway and have included this procedure as the second phase of our surgical protocol. 
Maxillomandibular advancement enlarges the pharyngeal and hypopharyngeal airway dimensions by physically expanding the skeletal framework. In addition, the forward movement of the maxillomandibular complex improves the tension and collapsibility of the suprahyoid and velopharyngeal musculature. The indications for maxillomandibular advancement are outlined in table 1.
Most patients who undergo phase II surgery have failed to fully respond to the phase I protocol. These patients have already undergone reconstruction of the airways at the nasal, pharyngeal, and hypopharyngeal levels. Phase I surgical failure almost always involves persistent obstruction at the hypopharyngeal level (occasionally combined with pharyngeal-level obstruction). Maxillomandibular advancement creates more tension and physical room in the upper airway, relieving residual obstructions. In order to maximize airway expansion, a major advancement of the maxillomandibular complex is required. However, in doing so, it is important to maintain a stable denial occlusion and a balanced aesthetic appearance. Many patients who enter the phase II protocol have craniomaxillofacial abnormalities, such as maxillary and/ or mandibular deficiencies, that invariably are improved following surgery. We have often found that even patients whose cephalometric measurements are normal also experience an improvement in their facial appearance following maxillomandibular advancement. This is because many of our patients are middle-aged adults who are already showing signs of facial aging as a result of soft tissue sagging. The skeletal expansion of the maxilla and mandible enhances their appearance by improving soft tissue support. This positive influence on aesthetics has been reported by others. [20-22]
Maxillomandibular advancement has been performed for many years to correct malocclusion in children and young adults, and it is well described in the maxillofacial surgery literature. However, it must be emphasized that the procedure for the treatment of OSAS is quite different from the conventional orthognathic procedure.
The procedure begins with an outer-table cranial bone harvest. Bone grafts are placed at the osteotomy sites to facilitate bony union. To maintain dental occlusion, either arch bars or orthodontic bands are required prior to osteotomy. A Le Fort I maxillary osteotomy (figure) is performed above the apices of the teeth. The maxilla is down-fractured after pterygomaxillary separation. The descending palatine arteries are identified and preserved. The mobilized maxilla is manipulated and advanced approximately 10 mm. Alignment of the maxilla in relation to the mandible, dentition, and the face is crucial to ensure acceptable occlusion and aesthetics. The maxilla is stabilized by rigid fixation with four plates, and the cranial bone grafts are used in the osteotomy sites.
Mandibular osteotomy is performed via the sagittal split technique. The medial and lateral cortex of the mandible are separated at the ramus region, while the inferior alveolar nerve is preserved. The dentated mandibular segment is advanced the same distance as the maxilla, and occlusion is restored. After the mandible is stabilized by intermaxillary fixation, rigid fixation is achieved with the placement of four positional screws (plates are also occasionally used to ensure rigidity).
We routinely use a prefabricated methylmethacrylate splint to ensure dental alignment. Skeletal fixation with suspension wires is sometimes used to enhance the stabilization of the maxillomandibular complex.
As always, anesthesia induction and intubation are especially critical for OSAS patients, and the surgeons should be present at all times. A fiberoptic intubation or tracheotomy while the patient is awake should be considered in difficult airway situations, especially in obese patients who have a large neck circumference ([greater than]46 cm) and associated skeletal deformities (e.g., mandibular deficiency and a low hyoid bone). Although blood transfusion is often unnecessary, we prefer to have two units of autologous blood available.
All patients are extubated while they are awake, and intermaxillary fixation is in place in the operating room immediately following surgery. Wire cutters are kept near these patients at all times. All patients are monitored via an arterial line in the intensive care unit during the first postoperative day. Either humidified oxygen (35%) through a face tent or nasal CPAP is administered throughout hospitalization. Patients who receive CPAP require nasal trumpets to prevent subcutaneous emphysema. Patients are transferred to the ward the following day. Discharge criteria include a stable airway, adequate oral intake of fluids, and satisfactory pain control. Intermaxillary fixation is left in place for several days.
Surgical protocol clinical outcomes
Of the 175 patients who underwent phase II reconstruction at our institution between 1988 and 1995, 166 (95%) had a successful outcome (table 2). Their mean respiratory disturbance index (RDI) was 72.3 before surgery and 7.2 afterward. Postsurgical RDI values were comparable with those for nasal CPAP (nasal CPAP RDI: 8.2; p=NS [not statistically significant]). The mean lowest oxygenation saturation (LSAT) level improved from 64 to 86.7% (nasal CPAP LSAT: 87.5%; p=NS). Eighty-six of these patients had failed our phase I surgical protocol, and 83 of them (97%) were cured with phase II surgery. Most of the patients who failed the phase I protocol and declined phase II surgery were older (mean age: 51.8 yr). The mean age of patients who underwent phase II treatment was 43.5 years.
The mean length of hospital stay after phase II surgery was 2.4 days. Surgical morbidity included transient anesthesia of the lower lip, chin, and cheek in all patients; 87% of these cases resolved in 6 to 12 months. There was no postoperative bleeding or infection. Mild malocclusions were seen in some patients, and they were treated adequately with occlusal adjustment. No major skeletal relapse has been reported.
To date, we have performed long-term followup on more than 50 patients who underwent phase II surgery. Thirty-three of these patients have undergone followup polysomnography (table 3). Eighteen patients who fused polysomnography are monitored through interviews that concern the subjective symptoms of OSAS. Four patients have been lost to followup.
Of the 33 patients who underwent followup polysomnography, 30 have experienced long-term surgical success; the other three patients had initial success, only to relapse to OSAS. Overall, the mean RDI in this group fell from 69.6 preoperatively to 8.9 at 6 months postoperatively and to 7.7 at long-term followup. Similar improvement over baseline was seen in 6-month and long-term LSAT values. Followup ranged from 12 to 110 months (mean: 39).
Of the 18 patients who were subjectively reviewed by the lead author, 16 continued to experience good subjective correction. They had no progressive snoring, no apnea and no excessive daytime sleepiness. Of the two patients who did not improve, one experienced a subjective failure (recurrence of snoring and daytime fatigue) and the other had both a subjective and objective failure (his primary care physician had referred him for a polysomnogram, which showed a recurrence of OSAS).
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: (650) 328-0511; fax: (650) 328-3419; e-mail: email@example.com
Maxillomandibular advancement is an extremely effective surgical procedure for the treatment of obstructive sleep apnea syndrome. When properly executed, it is associated with minimal morbidity and is well accepted by patients. It is a treatment option that achieves long-term cure.
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Phase II surgical outcomes Successful Total no. Success Surgery groups outcomes patients rate Failed phase I 83 86 97% Skeletal deformity 10 11 91% (without UPPP [*]) Failed UPPP [+] 73 78 94% Total 166 175 95% (*.)Uvulopalatopharyngoplasty. (+.)Outside referral for severe obstructive sleep apnea syndrome. Long-term polysomnographic followup Surgery groups RDI [*] LSAT [+] Pre-op 69.6 [plus or minus] 27.9 68.5 [plus or minus] 14.3 Post-op 8.9 [plus or minus] 5.5 85.4 [plus or minus] 4.6 Long-term 7.7 [plus or minus] 5.3 86.4 [plus or minus] 3.7 followup Surgery groups Months Pre-op -- Post-op 6 Long-term 39 [plus or minus] 24 [++] followup (*.)Respiratory disturbance index. (+.)Lowest oxygenation saturation. (++.)Range: 12 to 110 months.
Criteria for maxillomandibular advancement
Severe obstructive sleep apnea syndrome
Morbid obesity (body mass index: [greater than]33 kg/[m.sup.2])
Satisfactory desire and health to undergo and recover from surgery
Failure of other forms of treatment, both medical and surgical3
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|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Statistical Data Included|
|Date:||Nov 1, 1999|
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