【原创】Obstructive Sleep Apnea 英文翻译

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【原创】Obstructive Sleep Apnea 英文翻译

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TITLE: Obstructive Sleep Apnea
"This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion."
Upper Airway Obstruction
The primary sleep disorders that are brought to the attention of the otolaryngologist are those referable to upper airway obstruction. In a child this most often is related to adenotonsillar hypertrophy. In adults patients may present for a variety of reasons, or they may be incidentally picked up while being seen for other reasons. Diagnosis and management will be discussed below.The pathophysiology involves obstruction of the upper airway during sleep. This is often associated with snoring, though snoring may or may not be associated with airway obstruction. As the airway obstructs the patient becomes hypercapnic and hypoxemic. This leads to an sub-wakeful arousal which opens the airway. Thus, the obstruction is relieved but at the expense of sleep fragmentation. The patient therefore has non-restorative sleep.
Definitions
To understand the specific disorders one must understand some of the
definitions. An apnea is defined as cessation of airflow for ten seconds which results in an arousal. If the chest wall continues to mechanically move during this time, then it is an obstructive apnea. If the chest wall does not attempt to ventilate, then it is presumably due to a neurologic etiology and is termed a central apnea. Sometimes there are characteristics of both an obstructive and a central apnea, and this is termed a mixed apnea. The number of apneas per hour is termed the apnea index. A hypopnea is a less well-defined entity, but usually is considered a diminution in airflow which results in hypoxemia and results in an arousal. The number of hypopneas per hour is termed the hypopnea index.
Functionally, there is little difference between apneas and hypopneas, and the sum of these vents per hour is termed the apnea-hypopnea index (AHI). This is also referred to as the respiratory disturbance index (RDI). Occasionally a lab will also report the arousal index, which is the number of arousal per hour. This may be different than the RDI due to limb movement or other causes of arousal. Generally the obstructive sleep apnea syndrome (OSAS) is considered to be an RDI > 5. Also described is the obstructive sleep hypopnea syndrome (OSHS) which is a hypopnea index of greater than 15, but as mentioned there is little clinical utility in differentiating this from OSAS. Severity of OSAS is also stratified by the RDI, with mild being considered 5-20, moderate 20-40, moderate-severe 40-60, and severe > 60. As the field of sleep medicine progressed there arose an awareness of certain patients who report excessive daytime sleepiness but do not have OSAS (e.g. RDI < 5). By esophageal manometry some of these patients have been shown to have increased negative thoracic pressure during inspiration. Thus, their increased work of breathing is thought to be responsible for their symptoms. This syndrome has been termed the upper airway resistance syndrome (UARS). Together with OSAS these are jointly referred to as sleep-disordered breathing (SD Black Eye

. Those patients who snore but have an RDI < 5 and who do not have increased intrathoracic pressure upon inspiration simply have primary snoring. One hypothesis is that these disorders represent a spectrum of disease with primary snoring being the mildest, followed by UARS, and finally OSAS as the full manifestation of the disease.
Pathophysiology
Although incompletely understood, the pathophysiology of OSAS relates to airway collapse. This may occur at various levels, including the palate, the base of tongue, and the hypopharynx. Nasal obstruction appears to facilitate or exacerbate the syndrome although it does not appear to be primarily responsible. Unfavorable anatomy appears to be the most important cause. This can be due to a narrow palate, an elongated uvula, redundant tissue at the base of tongue, micro/retrognathia, a retrodisplaced hyoid, and so on. Adenotonsillar hypertrophy may be a cause as well, particularly in the pediatric population.
Experimental evidence shows that in the pharynx the collapse occurs predominantly from the lateral walls, not merely from anteroposterior collapse as might seem likely in patients with elongated palates. This also may explain the way in which obesity increases the prevalence of OSAS, as the lateral pharyngeal fat pads may narrow the airway in the lateral dimension.
Although unfavorable anatomy is important etiologically, there also appears to be a physiologic defect in the pharyngeal dilators. There is also experimental evidence that longitudinal tension appears to be inversely related to airway collapse. Additionally, extrinsic factors such as sedating medications may exacerbate the physiologic defects.
Rationale for treating OSAS?
Untreated, OSAS has a rather impressive list of deleterious consequences. For example, the incidence of systemic hypertension and its attendant sequelae is much higher in these patients. It is thought that this is due to systemic catecholamine release. Better understood is the link to pulmonary hypertension and cor pulmonale. The lung shunts blood away from hypoxic areas, presumably as a evolutionary efficiency mechanism during times of regional hypoxia (i.e. mucus plugging). However, during chronic episodic total lung hypoxemia the entire pulmonary vasculature constricts, and ultimately right-heart failure ensues.
Other abnormalities associated with OSAS include myocardial arrhythmias, coronary artery and cerbrovascular disease and polycythemia. Whether due to previously mentioned problems or due to an independent cause, patients with OSAS have been shown to have an increase in mortality. Lastly, the neurocognitive compromise associated with inadequate sleep has been linked to poor performance and increased rates of industrial and traffic accidents.
Evaluation History
Frequently a patient's bed partner may give more important information than the patient. Loud snoring and observed apneas are key historical points. Epidemiologically OSAS occurs more commonly in obese people, in men, and with increasing age. However, absence of these factors clearly does not exclude the possibility of sleep apnea. One should try to get a feel for the amount of fatigue a person experiences, as well as questions about sleep hygiene, such as amount of nighttime alcohol and caffeine. Persons with insomnia should be questioned about reading in bed or watching TV in bed, as these are thought to contribute to insomnia. Morning headaches and impotence may be a tip-off for OSAS. Lastly,the examiner should always be vigilant to the possibility of malignancy and investigate questions related to recent changes in symptoms, weight loss, and symptoms such as otalgia, dysphagia, dyspnea, and hoarseness. A questionnaire is also frequently administered to the patient in order to ascertain the patient's subjective level of fatigue. One such tool commonly used is the Epworth Sleepiness Scale. In this scale a patient rates the chance of dozing off in eight different settings and a numerical score is tabulated. This may help identify patients in whom the subjective level of fatigue is discordant with the RDI, such as those patients with UARS.
Physical
Frequently the OSAS patient is obese. Neck size over seventeen inches has been shown to be a risk factor for OSAS. In someone with a neck over seventeen inches who snores the incidence of OSAS has been quoted at 30%. As part of the vital signs it is a good idea to calculate the body-mass index (BMI), which is obtained by dividing the weight in kilograms by the square of the height in meters. Additionally, one should check the blood pressure, as the prevalence of hypertension is very high in this population. The rest of the physical exam should focus on sites of potential obstruction in the head and neck. In particular, one should look at the tonsils, the length and width of the soft palate, size of the tongue, and position of the jaw and hyoid. Nasal obstruction should be looked for, as well as dynamic nasal collapse. As always, a complete head and neck exam should be performed and the possibility of tumor excluded.
Muller's maneuver is designed to look for the site of collapse. With the flexible scope in position, the patient tries to inspire against a closed mouth and pinched nostrils. The inspiratory forces then serve to collapse the airway. By doing this one can get an idea of the relative collapsibility of the palate as compared to the base of tongue or the hypopharynx. Although not terribly sensitive or specific, it still can be a helpful diagnostic and decision-making aid and adds little effort to the physical exam.
Testing
The gold standard for assessing OSAS is the polysomnogram, or sleep study. Although not completely standardized, the typical polysomnogram (PSG) will have measurements including an electroencephalogram (EEG), electro-oculogram, submental and tibial electromyogram (EMG), nasal or oral airflow, respiratory movement or effort, oximetry, electrocardiogram (EKG), and sleeping position. Some may also include measurements of multilevel esophageal manometry. Some controversy exists about a split-night PSG. For economic and convenience reasons, frequently in the first half of the night a standard PSG is performed followed by PSG with CPAP titration during the second half. Due to changes in the sleep architecture during the night it is possible that OSAS might not be picked up during the first half of the night. Thus, a negative first half of the study does not exclude OSAS and a complete study should be done without CPAP titration. However, a positive first half study has been shown to be reliable for diagnosis of OSAS, and in studies looking at CPAP titration, no advantage was found in using the whole night's data over the first half of the night. Thus a positive study in the first half of the night may go on to CPAP titration in the second. Although efforts are underway to investigate limited polysomnograms or versions that patients can perform at home, the gold standard at this time is still the full PSG at a sleep lab. Cephalometric studies have been used to study potential OSAS patients. Using plain films of the head, measurements of various parameters are done and compared to normative data in an effort to predict the likelihood of OSAS in a particular patient. Although potentially useful as a screening tool, these studies are not routinely done at our institution.The multiple sleep latency test (MSLT) is another tool to study sleep disorders. During a person's normal waking hours he or she takes four or five monitored naps separated by a few hours. The time to fall asleep, or sleep latency, is measured (abnormal being too quickly). This may reveal dysfunction in patients with otherwise normal PSGs. For example, this may reveal narcolepsy. Also, patients with UARS who have been treated with CPAP have been shown to have an improvement in their MSLT testing. Lastly, any patient who is being considered for PSG should undergo thyroid testing, as thyroid dysfunction may cause similar symptoms and should be corrected prior to PSG testing. Also, many of the patients with OSAS will have cardiopulmonary dysfunction, and appropriate preoperative testing should be performed prior to any surgical intervention.
Treatment
Non-surgical
In obese patients one should consider weight loss. It is felt that there is a threshold level of weight for most individuals above which they experience symptoms and below which they do not. Also investigational tools such as computed tomography have demonstrated the increase in the airway with weight loss. Additionally, obese patients have many other medical benefits to gain from weight loss. Sleep hygiene should be reviewed. Alcohol and sedating medicines may exacerbate OSAS. Patients with insomnia should be counseled to avoid nighttime caffeine and avoid activities such as reading or watching television in bed. Lastly, since OSAS is usually worse when supine, some patients may benefits from relatively simple measures such as sewing a tennis ball into the back of a T-shirt to promote sleeping on the side.
Continuous positive airway pressure (CPAP) remains a mainstay of treatment. Via facemask or nasal mask, positive airway pressure is delivered. This prevents pharyngeal collapse and has been shown to alleviate PSG abnormalities and symptoms in many patients. If delivered at two different pressure levels (for inspiration and expiration) it is referred to as BiPAP. CPAP titration can be done, as mentioned previously, during the second half of a split-night sleep study. This is done to find the lowest level of pressure that alleviates the apneas. Despite its effectiveness, compliance is often an issue, as many cannot tolerate the mask or the high pressures necessary for certain individuals. Intolerance of CPAP is a common indication for surgery, and often the patient still requires CPAP after surgery but can tolerate it due to relief of nasal obstruction or the improved airway that requires lower pressures to achieve relief of OSAS. Oral appliances are also effective in relieving OSAS. These work by mechanically moving the jaw or tongue forward and opening the airway. They have been shown to be effective, more so for mild or moderate OSAS. Although some find them difficult to use, in general compliance is superior to CPAP. At around 62% compliance though, overall efficacy is lower than for surgical procedures. No single appliance has been shown to be superior to another.
Surgical
When a patient opts for surgical therapy the otolaryngologist has a variety of considerations. Most would agree that prior to surgical intervention a PSG should be obtained. Some argue that medical therapy should be tried first with surgery reserved for medical failures. Many times, though, a combination of medical and surgical therapy is necessary for optimum results. Anesthesia considerations are important in these patients. As many of them have cardiopulmonary issues, the appropriate pre-anesthesia testing is necessary. Also, many of these patients have the combination of a short, thick neck and some degree of retrognathia. This is a setup for an airway problem. Vigilant attention to intubation and extubation is necessary. Many anesthesiologists perform awake fiberoptic intubations and are very judicious in their use of medications which might compromise the airway. On the other end, it is recommended that extubation be done when relatively light. Of course, proper equipment for airway emergencies should be available. In this event, adjunctive measures such as the laryngeal mask anesthesia or trans-tracheal jet ventilation may buy the surgeon precious moments. As always, proper communication between the surgeon and anesthetist is important. Post-operative considerations include the possibility for post-obstructive pulmonary edema and the likelihood of post-operative hypertension. Depending on the individual patient, intensive care unit monitoring may be best for the first post-operative night. Surgery to relieve nasal obstruction should be performed in adjunct to other sleep apnea surgery. Nasal surgery alone has a very low rate of efficacy for obstructive sleep apnea. Adenoidectomy can be performed when adenoid hypertrophy exists, but as with nasal surgery, tonsillectomy and adenoidectomy alone have a very low rate of efficacy in adults with sleep apnea. If the obstruction appears to be at the palatal level，some palatal intervention is in order.The uvulopalatopharyngoplasty (UPPP) remains a mainstay of treatment. Described by Ikematsu in the 1950s for snoring, Fujita recognized in the 1980s that this was effective for the treatment of OSAS. In the procedure a portion of the soft palate, the uvula, and the tonsils are removed. The posterior pillars are sewn anterolaterally. Complications can include voice changes and oronasal regurgitation of food or liquids. Rarely, the devastating complication of nasopharyngeal stenosis can occur. Also described for the palate is the laser-assisted uvulopalatoplasty (LAUP). While this can be done in the office, it often requires multiple sessions. It may also be more appropriate for primary snoring. Radiofequency ablation can be used to create thermal lesions that have a similar effect to palatal surgery. These procedures must be done with the patient asleep because of associated pain. For hypopharyngeal and base of tongue obstruction, first-line therapy at this institution is genioglossal advancement and hyoid myotomy and suspension (GAHM). In this procedure, a portion of the central mandible is advanced, and the inner table secured at the level of the outer table. This mechanically advances the tongue relative to the posterior pharynx. A lingual suspension procedure using a suture that anchors the base of tongue forward to the mandible may achieve similar results (though the long term results are not yet known). Usually along with the genioglossal advancement, a hyoid myotomy and suspension is performed. The neck is opened, and the hyoid bone is freed of its muscular attachments. It is then secured anteriorly by four sutures to the thyroid cartilage, moving the base of tongue forward. Also described for tongue base obstruction are procedures such as the lingual tonsillectomy, uvulopalatopharyngoglossoplasty, laser midline glossectomy, lingualplasty, and radiofrequency volumetric tissue reduction. Lastly, the definitive surgery for OSAS is tracheotomy, which results in upper airway bypass. This is usually reserved for morbidly obese patients. Tracheotomy in this patient population is technically difficult and is not free of complications.
Conclusion
Sleep medicine is an exciting, relatively new field that has emerged. The otolaryngologist has become a key figure in the diagnosis and management of sleep disorders due to his or her familiarity with the airway and the ability to intervene surgically. An understanding of the medical and surgical issues involved is necessary for the otolaryngologist to deal with this field which is rapidly evolving.

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题目：阻塞性睡眠呼吸暂停
这个材料是耳鼻咽喉头颈外科的UTMB部门应住院医师继续教育的需要为研究生训练计划而制定的。然而它的目前的形式不是为了临床应用。它的目的是用来激发会议环境之中的小组讨论的。无论从直接的或含蓄的说都不能保证这个材料的正确性、完整性和适宜性。这个材料并不必然的反映UTMB院的成员现在或过去的意见，也不能在没有原始的会诊资料和专业意见的情况下做出诊断和治疗。
上气道阻塞引起耳鼻喉科医生注意的是与上气道阻塞有关的睡眠障碍，这是引起睡眠障碍的主要原因。儿童最常见的原因是腺样体肥大。在成年病人可由于许多原因引起，或者也许是其他疾病的伴随症状。下面将讨论上呼吸道阻塞的诊断和治疗。病理生理学表现为睡眠时上呼吸道阻塞，这一症状经常合并打鼾。尽管打鼾不一定伴随呼吸道阻塞。当呼吸道阻塞时病人的血氧不足同时伴有高碳酸血症，从而导致病人被刺激醒来才能解除呼吸道阻塞。这样尽管解除了呼吸阻塞但是患者损失是睡眠的连续性。病人因此得不到健康的睡眠。
界定
有一点必须了解才能理解这个特殊的疾病。呼吸暂停被定义为呼吸气流停止十秒以上而引起一次觉醒。如果在这期间胸壁继续机械运动，则称为阻塞性呼吸暂停。如果胸壁在这期间没有呼吸运动，则有可能是神经性因素造成的呼吸暂停，称为中枢性窒息。有时同时具有阻塞性呼吸暂停和中枢性窒息两者的特征就称为混合性呼吸暂停。每小时呼吸暂停的次数被称为呼吸暂停指数。呼吸不足是一种没有定义明确的表现，但是一般考虑为一种通气减少导致的低血氧症引发觉醒的结果。每小时呼吸不足的次数被称为呼吸不足指数（AHI）.这也指的是呼吸障碍指数（RDI）。偶尔一个实验室也报告觉醒指数即每小时觉醒的次数。觉醒指数也许不同于RDI因为有由于四肢移动或其他原因所引起的觉醒。一般如果呼吸障碍指数（RDI）??5则考虑为阻塞性睡眠呼吸暂停综合征（OSAS）。并且把呼吸不足指数大于15称为阻塞性睡眠呼吸不足综合征（OSHS），但是临床应用提到OSHS时是和SOAS有一点区别的。OSAS的严重程度也是用RDI来区分的：轻度的OSAS时RDI为2－20；中等的OSAS时RDI为20－40；中重度的OSAS时RDI为40－60；重度的OSAS时RDI为??60。随着睡眠医学领域的发展，出现了一类确定的病人，他们没有患OSAS（例如RDI??5）然而有报道他们白天睡眠过多。这类病人中的一些经食管测压术显示吸气时胸膜腔负压增高，这样他们的呼吸做功增加被认为是他们症状的原因。这一综合症状被称为上呼吸道阻力综合征（UARS）。UARS和OSAS共同称为睡眠障碍性呼吸（SDB）。那些RDI??5的打鼾病人在吸气时胸膜腔负压没有增高只是有初级的打鼾症状。一个假说认为这些初级的打鼾症状表示疾病处于初期，接下来是UARS,最后阶段是OSAS，这表现出疾病的全过程。  病理生理学
  尽管不是完全的了解，但是和OSAS的病理生理学相关的是呼吸道的塌陷。呼吸道的塌陷可以发生在不同的水平面，包括上腭、舌根和下咽部。虽然鼻塞不是主要的病因，但是鼻塞能促进和加重症状。解剖方面的不利因素是引起OSAS的最主要原因。这些因素包括：狭窄的上腭、悬雍垂松弛、舌底组织增生、颌后缩和舌骨后移位等等。增值体肥大也可能是一种原因，特别是在儿科病人中。
  实验结果显示软腭过长的病人咽部的狭窄主要是由于咽侧壁的塌陷而不是只因为看起来好象是前后位的咽部塌陷的原因，这也许能够解释为何肥胖者的OSAS患病率有所增高的现象。正是由于咽侧壁的脂肪垫增厚使得咽部通气道横向尺寸狭窄。虽然不利的解剖学因素是重要的病因，但是咽肌的生理缺陷也显示为一种因素。也有实验证明咽肌的纵向收缩导致了呼吸道的塌陷。另外象镇静药物等外来因素也可能加重这种生理缺陷。
  论述OSAS的原理
  OSAS不经治疗可以引起一系列的不良后果。例如，这些OSAS患者的系统性高血压的并发症的发病率要高的多。这被认为归因于系统儿茶酚胺的释放。具体的说就是引起肺动脉高压和肺源性心脏病。肺脏从低氧区域分流血液，类似一个高效的机械装置用在低氧区域（就是指粘液泵）。然而经过长期的肺部局部或全肺的血氧不足使得全部的肺部血管系统收缩，最终导致接踵而来的右心衰的发生。其他的OSAS的并发症包括心率失常、冠心病和红细胞增多症。不论是先前提到的那些原因所致的还是一个独立的原因所致，患有OSAS的病人的病死率显示增高。最终由于不充分的睡眠使机体效率低下，从而导致生产事故和交通事故的发生率增高。
  病史评价
  病人的伴侣可能常常会比病人自己提供更多的重要信息。高声的打鼾和观察到的呼吸暂停使病史上的重点。OSAS的流行学特点是通常发生在年长的肥胖男性身上。但是没有这些明显因素的人也不能排除患睡眠呼吸暂停的可能性。人们要设法减少会引起疲劳的个人习惯，同时注意健康睡眠。例如减少夜间的烟酒摄入量。不要躺着看书和看电视，这样会引起失眠。晨起头痛和性功能减退可能暗示着患有OSAS。最后检查者应该始终警惕恶性肿瘤的可能性，注意询问最近有无体重减轻的变化，和一些例如耳痛、吞咽困难、呼吸困难和声音嘶哑的症状的出现。一种调查问卷也经常要提供给病人来确定病人的主观疲劳水平。这个调查问卷通过在八个不同环境时患者的打瞌睡几率所得的分数来标度病人的疲劳水平。着个调查有助于鉴别那种RDI正常但是主观感觉疲劳水平不协调的患者，例如那些患有上呼吸道阻力综合征（UARS）的病人。
  身体检查
  OSAS患者通常是肥胖者。颈围超过17英寸被看作患OSAS的危险系数，证据表明颈围超过17英寸并有打鼾的人OSAS的患病率是30??。计算体重系数是一个较好的检查体征，体重系数即公斤体重与每米身高的平方的比值。另外一个应该检查的项目是血压，因为OSAS患者的高血压患病率非常高。其他的体格检查的重点应该放在头颈部的容易造成阻塞的部位。特别是应该检查扁桃体、软腭的长度和宽度、舌的大小以及下颌和舌骨的位置。除了鼻道狭窄以外还要检查是否有鼻塞。总的来说要进行全面的头颈部检查，而且要排除肿瘤的可能性。苗勒氏法（呼气后声门关闭再用力吸气的方法）是为了寻找呼吸道狭窄的位置而设计的一种方法。通过捏紧鼻孔和闭口使病人的呼吸阻力增加找到呼吸道易变形的位置。苗勒氏法可以对比软腭、舌根和下咽的呼吸道情况。尽管这种检查不具有特别的敏感性和特征性但是它对体格检查对ASOS的诊断可以提供一定的帮助。
  检查
  评定OSAS的金标准是多睡眠图或者是睡眠监测系统。尽管这个检查还没有完全标准化，但是典型的多睡眠图包括以下检查：脑电图、眼电图、肌电图、鼻或口呼吸、呼吸运动、血氧测量、心电图和睡眠姿势。另外可能还包括多导食道测压术的测量结果。关于分解多睡眠图还有一些争论，由于经济上的原因和方便的目的，一般在前半夜完成一个标准的多睡眠图而在后半夜做气道压力测定。由于夜间睡眠结构的变化有可能在前半夜OSAS没有被发现，这样一个阴性的前半夜检查结果并不能够排除OSAS，同时需要做一个完整的多睡眠图检查。然而一个阳性的多睡眠图检查结果就能明确的诊断OSAS，用一整夜的时间检查并不比前半夜的检查优势多。这样就适合前半夜做多睡眠图检查而后半夜做呼吸道压力测试。尽管多睡眠图检查可以让病人在家中进行，但是诊断的金标准还是要求病人在实验室做全面的多睡眠图检查。头影测量研究可以被用来研究患OSAS的可能性，通过测量头部平片的几个部位的结果和正常的数据的比较可以预测一个特殊病人患OSAS的可能性。尽管这种研究可能作为一种筛选检查，但是我院并没有把它当作一个常规检查来做。多重睡眠潜伏期试验是另外一种研究睡眠障碍的检测方法。在被检者正常的觉醒时段检测四到五个分段睡眠监护，测量入睡时间或者入睡前等待时间（太快了是不正常的）。某些在多睡眠图上表现正常的病人有可能在此项检测中显示不不正常。例如多重睡眠潜伏期试验可以显示嗜睡发作。另外那些经过持续肺泡正压给氧治疗的患上呼吸道阻力综合征的病人可以用多重睡眠潜伏期试验来检测病情改善情况。最后还要考虑做甲状腺功能检查来完善多睡眠图的检测，因为甲状腺功能减退可能引起类似的症状。另外一些患OSAS的病人患有心肺疾病，在外科手术治疗之前完善相关检查是必要的。
  治疗
  非手术治疗：
  肥胖的病人应该考虑减轻体重，大多数人都会感觉到有一个体重的阈水平，体重在该水平之上的感到有症状而体重低于该水平则无症状。象CT这类检查工具也显示通过减轻体重能够增大呼吸道。另外减轻体重也对病人的内科疾病有好处。睡眠卫生要注意，酒精和镇静药品可能加重OSAS。可以劝告那些失眠的病人避免夜间喝咖啡和在床上看书或看电视。最后考虑到仰卧睡眠加重OSAS，一些病人可以用一种简单的方法例如缝制一个网球在T恤背面来促使自己侧卧睡眠。连续气道正压通气(CPAP)是一种主要的治疗方法，通过面罩或鼻罩进行正压通气。CPAP减轻了咽部狭窄并且减少PSG检测中的异常现象和大多数病人的症状。如果应用两个压力水平进行正压通气（因为吸气期和呼气期压力不同）则要用双水平式呼吸道正压呼吸。象先前提到的CPAP滴定也可以做，象先前提到的夜间分离睡眠监测中的后半夜那样，这种低水平的正压通气方法可以减少呼吸暂停的次数。尽管CPAP是有效的治疗，但是应用起来还是有问题的，许多病人不能耐受面罩和必要的正压通气。不耐受CPAP的病人通常需要外科治疗。而术后的病人也往往需要CPAP治疗，能够坚持治疗有利于减轻鼻阻改善通气而且低水平的正压给氧可减轻OSAS。口腔矫正器也是对减轻OSAS的工具，它通过机械的把下颌和舌向前牵拉来改善通气道。对于轻中度的OSAS患者口腔矫正器显示是有效果的。尽管它使用起来有些困难，但是还是比CPAP容易接受。应用矫正器的患者有62??的效果不如外科手术治疗的效果。没有那种矫正器显示效果优于其它的类型。
  手术治疗
  当病人选择外科治疗，耳鼻咽喉科医生就要有多方面的考虑。大多数医生都同意在手术之前做多睡眠图监测。关于外科治疗前是否要进行药物治疗还有争论。尽管许多时候把内科治疗和外科治疗结合起来是最适宜的方法。麻醉方式的选择是非常重要的。因为许多这类病人合并有心肺疾患，所以进行适当的麻醉前检查是必要的。并且许多这类病人的脖子又短又粗还合并颌后缩，这是一个气道结构问题。重视插管和拔管中的问题。许多麻醉师应用清醒纤维光学插管法，而且在应用有可能损害呼吸道的药物是特别谨慎。另一方面，建议在相对明亮的条件下拔管。当然要提供紧急气道抢救的器械。在手术中的一些附属处置如喉罩麻醉和经气道喷射通气会为手术医生争取宝贵的时间。在手术医生和麻醉师之间的完全交流始终是重要的。术后要考虑的包括术后肺水肿和术后高血压。根据病人个体情况，术后当天晚上最好在重症监护室监护。单独的缓解鼻阻的手术对解决睡眠呼吸暂停作用较小，所以这类手术应作为其他睡眠呼吸暂停手术的辅助手术。腺样体肥大的病人应该做腺样体切除术，但是作为解除鼻阻的手术对患有睡眠呼吸暂停的成年人效率不高。如果阻塞出现在软腭水平则应该做调整软腭的手术。悬雍垂-腭-咽成形术（UPPP）是主要的术式。UPPP在1950年由Ikematsu首先应用于鼾症病人。Fujita在1980年验证它是处理OSAS有效的方法。在手术步骤中部分软腭、悬雍垂和扁桃体被依次切除，咽腭弓被缝到前外侧。手术并发症包括声音改变和饮水和进食时反流至鼻腔。很少有合并鼻咽狭窄的情况存在。也有激光辅助的悬雍垂-腭-咽成形术（LAUP）。尽管UPPP可以在门诊进行，但是需要复杂的讨论。UPPP也可能时比较适合初期的鼾症患者。微波的热效应也可以用在软腭手术中产生同样的效果。由于手术痛苦，这些操作必须在全麻下进行。对于下咽和舌根的阻塞，主要的处理方法时颏舌徙前术和舌骨切开悬挂术。此手术的步骤包括部分的中部的下颌骨前移，内板固定在外板水平。这个手术把舌前移使舌和后咽的距离增宽。把舌根向前缝合固定在下颌骨上也可以达到类似的目的但是远期效果还不是很明确。通常颏舌前移的同时做舌骨切开悬挂术。从颈部进路，分离舌骨和舌肌然后缝合固定在甲状软骨四个骨缝上，使舌底前移。另外舌扁桃体切除术、悬雍垂-腭-咽成形术、激光舌切除术和射频消融术等手术也可以用来缓解舌根阻塞。治疗OSAS最终的手术方法是气管切开术，这种手术可以使呼吸绕过上呼吸道。气管切开术常用于病态肥胖的患者。这类患者施行气管切开术有一定的技术难度，而且不可避免的合并手术并发症。
  结论
  内科治疗睡眠阻塞疾病是个令人兴奋的新领域。耳鼻喉科医生对OSAS的诊断和治疗的关键在于其对呼吸道的熟悉情况和外科手术的技能。OSAS的内科治疗和外科治疗是耳鼻喉科医生必须了解的，同时也要认识到OSAS的治疗方法是快速发展着的。

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