No abstract

Obstructive sleep apnea is the most common sleep-related breathing disorder, with a surprisingly high prevalence. The treatment of choice is nasal continuous positive airway pressure (CPAP) ventilation during sleep, which has to be applied throughout the patient's whole life. Because of various underlying pathomechanisms in patients with certain craniofacial disorders--narrow posterior airway space and maxillary-mandibular deficiency--surgical therapy by craniofacial osteotomies seems possible. A series of 38 consecutive patients were treated by 10-mm maxillomandibular advancement by retromolar sagittal split osteotomy and Le Fort I osteotomy, respectively. Obstructive sleep apnea syndrome was improved considerably in all patients; there was no significant difference compared to the results under nasal CPAP. In 37 of 38 patients, the postoperative apnea-hypopnea index was reduced clearly to under 10 per hour, oxygen saturation rose, and sleep quality improved. This was achieved by maxillomandibular advancement of 10 mm without secondary refinements in all but 2 patients. In one patient, the apnea-hypopnea index could only be reduced to 20 per hour, probably because of insufficient maxillary advancement. These results indicate that successful surgical treatment is possible in a high percentage of selected patients with certain craniofacial characteristics. In addition to cardiorespiratory polysomnography, there should be routine cephalometric evaluation of all patients. Maxillomandibular advancement should be offered as an alternative therapy to all patients with maxillary and/or mandibular deficiency or dolichofacial type in combination with narrow posterior airway space.

This study demonstrates that maxillomandibular advancement is successful in a high percentage of patients carefully selected by cephalometric and polysomnographic investigation. Postoperative success has proved to be stable over a period of 2 yrs. Further preoperative evaluation seems necessary in patients with predominantly mixed or central apnoeas.

Obstructive sleep apnoea (OSA) is due to craniofacial changes and acromegaly. The question addressed by this study was whether growth hormone (GH) induced craniofacial changes might explain persisting OSA despite endocrine inactivity in acromegaly. Nineteen patients treated for acromegaly were examined cephalometrically for craniofacial changes and polysomnographically for OSA. Twelve patients proved to have OSA with an apnoea/hypopnoea index >15; seven patients showed no evidence of OSA at all. With respect to the endocrinological parameters, there were no differences between the two groups that would explain the presence or absence of OSA. Neither group differed with respect to sex, age, or body mass index. Craniofacial changes were predominantly found in the mandible. The group with OSA proved to have increased vertical, dolichofacial growth compared to those without OSA. Consecutively, in the OSA group the posterior airway space was narrowed, and the hyoid was displaced more caudally. Thus, it seems that craniofacial structures of patients with acromegaly and persisting obstructive sleep apnoea are different from those without obstructive sleep apnoea. Surgical corrections of pertaining acromegaly‐induced craniofacial changes should be performed with an awareness of the individual craniofacial condition so as not to enhance obstructive sleep apnoea. Eur Respir J 1999; 14: 196–202.

SUMMARY Impaired vigilance is a frequent daytime complaint of patients with obstructive sleep apnoea (OSA). To date, continuous positive airway pressure (CPAP) is a well established therapy for OSA. Nevertheless, in patients with certain craniofacial characteristics, maxillomandibular advancement osteotomy (MMO) is a promising surgical treatment. Twenty-four male patients with OSA (pretreatment respiratory disturbance index (RDI) 59.3 SD±24.1 events/h) participated in this investigation. The mean age was 42.7±10.7 years and the mean body mass index was 26.7±2.9 kg/ m 2 . According to cephalometric evaluation, all patients had a narrow posterior airway space, more or less due to severe maxillary and mandibular retrognathia. All patients except two were treated first with CPAP for at least 3 months and afterwards by MMO. Two patients only tolerated a CPAP trial for 2 nights. Polysomnographic investigation and daytime vigilance were assessed before therapy, with CPAP therapy and 3 months after surgical treatment. Patients' reports of impaired daytime performance were confirmed by a pretreatment vigilance test using a 90-min, fourchoice reaction-time test. The test was repeated with effective CPAP therapy and postoperatively. Daytime vigilance was increased with CPAP and after surgical treatment in a similar manner. Respiratory and polysomnographic patterns clearly improved, both with CPAP and after surgery, and showed significant changes compared to the pretreatment investigation. The RDI decreased significantly, both with CPAP (5.3±6.0) and postoperatively (5.6±9.6 events/h). The percentages of non-rapid eye movement Stage 1 (NREM 1) sleep showed a marked decrease (with CPAP 8.2±3.6% and after MMO 8.2±4.4% vs. 13.3±7.4% before treatment), whereas percentages of slow wave sleep increased significantly from 8.0±6.1% before therapy to 18.2±12.8 with CPAP and 14.4±7.3% after MMO. The number of awakenings per hour time in bed (TIB) was significantly reduced after surgery (2.8±1.3), compared to both preoperative investigation (baseline 4.2±2.0 and CPAP 3.4±1.5). Brief arousals per hour TIB were reduced to half with CPAP (19.3±20.0) and after MMO (19.7±13.6), compared to baseline (54.3±20.0). We conclude that the treatment of OSA by MMO in carefully selected cases has positive effects on sleep, respiration and daytime vigilance, which are comparable to CPAP therapy. maxillomandibular advancement, sleep apnoea, surgical treatment, daytime vigilance