Both the pauses and his very loud snoring have increased over the past year since he put on an extra 30 lbs. An easy clinical diagnosis.
Or is it? A large number of individuals snore, and a lot of overweight patients have hypopneas and not overt obstructive apneas. And what about central apneas? Not all patients who snore and appear to stop breathing have obstructive sleep apnea. How do we know whether Mr. Smith has obstructive sleep apnea? The standard to confirm our suspicion is to ask the patient to have a nocturnal polysomnogram, the most common of sleep study.
However, the diagnosis of sleep apnea is not made by polysomnography alone; clinical evaluation also is required. Before proceeding with our discussion, we should look at some of the terminology that might be confusing for some and often for us. Many of these terms might be found by the primary care physician in a sleep study report or a sleep consultation letter. Sleep apnea is what we would expect from the term: a cessation of breathing during sleep. When the term is used in conversations both inside and outside of the medical profession, people are usually talking about obstructive sleep apnea.
Central apnea is indeed a cession of breathing, but in a different context. A corollary would be the use of the term "diabetes," which would generally refer to diabetes mellitus and usually not to diabetes insipidus. An obstructive sleep apnea is defined as cession of airflow for at least 10 seconds and due to obstruction of the upper airway. Respiratory-Effort Related Arousal RERA refers to a respiratory event during sleep that does not meet criteria for either an apnea or a hypopnea but that results in a disturbance in sleep or oxygenation.
The American Academy of Sleep Medicine Manual for the Scoring of Sleep and Associated Events defines an RERA as a sequence of breaths lasting at least 10 seconds characterized by increasing respiratory effort or flattening of the nasal pressure waveform leading to an arousal from sleep. Obstructive Sleep Apnea-Hypopnea Syndrome OSAHS refers to a cluster of clinical features caused by repetitive episodes of obstructive apneas and hypopneas what we are usually talking about when we say a patient "has sleep apnea".
These clinical features result from sleep fragmentation or hypoxemia, or both, and can include consequences such as sleepiness and hypertension. Sleep Disordered Breathing. The term probably would not be seen on an official sleep study interpretation but often is used in the consultation letter from a sleep specialist. Its primary use is to distinguish respiratory-related sleep problems from other sleep disorders such as narcolepsy or leg movement disorders. The sum of the obstructive apneas and hypopneas divided by the hours of sleep.
Upper Airways Resistance Syndrome UARS is a term that has started to fall into disuse recently and is not recognized by many insurance companies as a diagnostic entity. It has been used to describe sleep-disordered breathing that consists mostly of RERAs. It basically refers to some degree of inspiratory obstruction that is not enough to qualify as hypopnea and with no apnea. The term has been used primarily to describe loud snorers who do not have apnea but who have sleep fragmentation. If we look at the oral cavity of a patient with suspected sleep apnea, we would expect to see some sort of narrowing of the opening into the back of the throat.
If we shine a light into the mouth and ask the patient to say the traditional "aah," a wide open airway with good visualization of the entire back of the throat and a small uvula hanging down would make significant OSA much less likely although not impossible. A classification by Mallampati has been helpful in describing the physical features of upper airways narrowing.
See Figure 1. With a class 1 configuration, the entire uvula can be seen, along with any tonsillar tissue. A class 2 configuration demonstrates only part of the uvula, and class 3 shows only the base. With a Mallampati class 4 configuration to the posterior pharynx, none of the uvula is visualized and about all that can be seen is the tongue and the hard palate. Retropalatal and Retroglossal Regions behind the hard palate and behind the tongue. These locations are where the obstruction generally takes place.
Nasal congestion can cause an increase in the negative intraluminal pressure of the upper airways and can aggravate snoring, but the main problem in OSA generally is found behind the tongue. Alleviating nasal congestion with medication, polyp removal, or septal surgery can sometimes help snoring but usually will do very little for apnea. When a bed partner complains that a patient stops breathing at night, the nose is not the best place to look for a cause.
Redundancy of the tissue of the lateral pharyngeal walls also can be seen as an anatomic characteristic, as well as the presence of enlarged tonsils. A backward displacement of the mandible retrognathia also is described as an aggravating factor. However, in practical terms, this is not a common finding. Differentiating between an elevated tongue base and true macroglossia can be difficult, although both can contribute to symptoms of sleep apnea.
The pharyngeal airway is maintained open due to neuromuscular influences that can be suppressed and subsequently cause apnea. Substances that decrease the size of the upper airway include alcohol, sedatives, and opiates. It would not be unusual for a wife to elect to sleep in another bedroom on a football night when she knows that her husband is going to be drinking a generous amount of beer, with the snoring that follows.
The same laxity of the soft tissues that causes the snoring also can contribute to OSA. Another major contributing factor in OSA is weight gain. It is not uncommon for a patient's bed partner to describe an increase in the snoring and pauses in breathing with observed weight gain. Once a critical weight has been achieved, as little as a pound gain can trigger the onset of snoring and pauses both of which can disappear with a similar weight loss. This is more of a problem in men, since more fat is deposited in the upper body and trunk in men, whereas women have more in the lower body and extremities.
Obesity in older patients is especially problematic. Neck circumference greater than 18 inches is also a good predictor for OSA. It is important to realize how simple a process OSA can be to understand. One of the main activities of the upper airway muscles is to dilate and stiffen the airway. This counters the negative intraluminal pressure that develops when we inhale. This adds to the pharyngeal narrowing caused by the normal sleep-related reduction in the upper airway dilating muscle activity. The sleep state itself is associated with a decrease in motor output to the pharyngeal muscles and can add to the upper airway anatomic abnormalities often seen in sleep apnea.
The pharyngeal airway and not the nose is the site of upper airway closure during sleep. Sleep fragmentation and nocturnal oxygen desaturation are the ways by which OSA impacts daytime functioning. People normally awaken periodically during the night. This is usually not a problem because most people are able to promptly fall back asleep and have no recollection of these few, brief awakenings. A problem arises, however, when patients arouse from sleep frequently, as occurs with sleep apnea.
NREM sleep has three stages that occur in cycles.
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One can imagine that if an individual goes from awake to stage one, then back to awake, then back to stage one, then back to awake frequently during the night, the quality of that night's sleep will be diminished. Such repeated awakenings are the hallmark of sleep fragmentation. Fragmentation Triggers. The list of potential disturbances that can disrupt sleep is long and can include noise, a restless bed partner, an uncomfortable mattress, or respiratory distress because of apneas, hypopneas, or RERAs.
As far as sleep apnea is concerned, there are several mechanisms involved in the arousal process. The most obvious to an observer is the simple struggling to breathe that occurs as the patient tries to breathe against a closed upper airway. The obstruction and therefore the term "obstructive" sleep apnea is an inspiratory problem. Another major cause of arousals is hypoxia, which is why arousals are more common at the termination of apneic events. Arousals which generally are considered to be at least 3 seconds or greater often are not remembered by the patient.
Short periods of arousal frequently are associated with amnesia for the event, and patients can have arousals numbering in the hundreds and without being aware that their sleep has been fragmented. As the number of arousals increases, daytime sleepiness increases. Of special interest is the fact that excess daytime sleepiness occurs even when the total sleep time during the night is unchanged. It is the sleep fragmentation itself that is considered to be the cause of the excessive daytime sleepiness. A patient who goes in and out of sleep frequently during the night is also less likely to progress into the deeper stage-three sleep that generally is felt to be more restorative.
Data about African Americans also suggests that African ancestry may be a risk factor, but the evidence is not as strong as it is for Asians. Patients often ask whether sleep apnea can be inherited. The short answer is yes, but not in the strict Mendelian sense of the word as one sees in the trisomy 21 associated with Down's syndrome.
A positive family history increases the risk by two to four times. All of us inherit physical characteristics from our parents. If both of our parents have large Corinthian noses, there is a higher likelihood that we or one of our siblings will have a similar proboscis. OSA has strong anatomical characteristics, and family members often have shared craniofacial uniqueness both soft tissue and bony structures.
The contributing factors for OSA, however, are usually multifactorial. Obesity has a marked effect on apnea, and obesity is strongly heritable obesity increases risk for OSA fold. In summary, a positive family history of OSA is definitely a risk factor. Obstructive sleep apnea typically is diagnosed with a nocturnal polysomnogram. The patient arrives at the sleep center a little before bedtime, and a technician attaches electrodes and sensing devices to record oxygen saturation, electroencephalogram EEG , electrocardiogram ECG , electromyogram EMG , eye movements, snoring, and occasionally other physiologic signals.
Data then are retrieved from the computer readouts, and an analysis is made and coordinated with the sleep history and physical examination done previously. The study can detect exactly when the patient goes to sleep, the stages of sleep, what the breathing pattern is like, oxygen saturation, abnormal ECG and electroencephalographic patterns alpha delta sleep , leg movement disorders, as well as many other sleep abnormalities.
The diagnosis needs to be suspected first, however, by the primary care physician before a polysomnogram can be considered. Nocturnal Symptoms. Snoring is the most common complaint, although spousal concern about pauses in the patient's breathing is often the case. Snoring generally is more prevalent in the supine position, and the patient often complains of being awakened at night and told to roll over.
The snoring is seldom a problem for the patient, although patients sometimes complain of waking themselves. Of more concern are nocturnal awakenings due to snorts or gasps that follow pauses in the breathing pattern. Although snoring and sleepiness are the stereotypical symptoms, it is becoming increasingly clear that women who have sleep apnea present differently from men.
Women are much less likely to have been told that they snore or stop breathing during sleep and much more likely to present with insomnia, rather than sleepiness, than men. Daytime Consequences. Here is where it gets more difficult. The most frequent daytime complaint is often feeling "tired. This complaint has almost become part of the American way of life, with people finding creative methods of wearing themselves out through work and other activities while often sleeping less.
The combination of ambulatory monitoring and oximetry a. Although in-lab polysomnography has historically been the prime diagnostic tool to confirm the presence of obstructive sleep apnea, home testing has been evaluated as an alternative diagnostic approach. However, thinner, younger patients without lung disease can have significant breathing and sleep disturbance without remarkable oxygen desaturation. In other words, oximetry and portable testing can be used to help rule sleep apnea in, but they fall short in ruling it out.
This form of testing may be especially helpful in areas not served by facility-based sleep diagnostic centers such as in rural settings. Clinical Prediction Formulas. Several investigators have developed prediction formulas based on findings in the history or physical examination. Among the most useful of such findings are history of witnessed apneas, male gender, BMI, and neck circumference.
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In general, these formulas are sensitive but not as specific as those for PSG. One of the most reliable screening tools for sleep apnea is the Berlin Questionnaire. The information from such studies, however, needs to be correlated with other aspects of the clinical history and physical findings. Once the sleep study is done, the first decision to be considered is whether there is enough pathology to justify therapeutic intervention. As with many treatment options in today's managed care environment, the physician often does not make all of the decisions in this regard.
Studies have suggested that apnea with a frequency greater than 5 episodes per hour apnea plus hypopnea index can have significant detrimental effects. Many insurance companies and Medicare used to pay for treatment only if the index was over 15 per hour. After dialogues with sleep organizations such as the American Academy of Sleep Medicine, a compromise was reached, and most insurance carriers now allow treatment if the episodes are 5 or greater and if the OSA is accompanied by a history of excessive daytime sleepiness, ischemic heart disease, stroke, hypertension, insomnia, mood disorders, or impaired cognition.
From a practical standpoint, it is usually not difficult to find one of these symptoms in the typical OSA patient. This remains a somewhat murky area, however, in that the question often remains, how much hypertension, insomnia, etc. Other factors, such as whether nocturnal oxygen desaturation is present on the polysomnogram, usually can help in the decision making.
This number also is helpful in deciding if specific intervention for sleep apnea is justified. Would the patient with mild sleep apnea accompanied by oxygen desaturation do just as well with supplemental oxygen via nasal cannula as with CPAP? If we take an overweight, hypertensive patient with nocturnal oxygen desaturation and an apnea plus hypopnea index of only 5 episodes per minute, insurance carriers would most likely agree to reimburse for treatment.
However, if the patient is opposed to using either CPAP, surgery, or a dental device, it may be appropriate to simply use nasal cannula oxygen while the patient works on weight loss. Supplemental oxygen by itself, however, should not be used as a primary treatment for OSA. Correcting any hypoxia increases the length of apneas and thus CO 2 increases but does not correct the cardiovascular side effects of the apneas and hypopneas.
More importantly, it does not improve sleepiness, 18 so the patient remains at risk for the important complication of motor vehicle accidents. Clearly, behavioral change has a major role both in causing and treating this condition. Weight loss can be curative. Weight, appetite, and sleep are complex, interrelated factors that are probably mediated in part by leptin, cortisol, insulin, and metabolic rate. Patients newly diagnosed with obstructive sleep apnea have a greater increase in weight in the year prior to diagnosis than their weight-matched controls. All obese patients with SDB should be counseled about weight loss.
Cigarette smoking is an independent risk factor for snoring and for sleep apnea. In addition, nicotine disrupts sleep, and smokers generally have more sleep disturbances than nonsmokers. Smoking cessation advice should be routine in treating all patients who smoke. Muscle relaxants, including alcohol and sleeping pills, can make apneas longer by reducing airway tone and by increasing the arousal threshold.
Moderate drinking clearly has been shown to exacerbate OSA and should be discouraged. Before the first CPAP device became available in , the only viable treatment option was to perform a tracheostomy. Multiple improvements have been made to the technology, especially in the past decade. The treatment basically consists of a mask that either fits over the nose or both the nose and mouth full face mask.
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The mask is connected by a tube to a pressure generator that introduces ambient air under pressure into the upper airways and acts as an internal splint to keep the airway open and thus eliminate the obstructive events as well as the snoring. If this sounds uncomfortable, it usually is. I often tell patients not to use the CPAP the first night they have it, but simply put on the mask without hooking it up to the machine.
They can watch television, help with the dishes, etc. After a day or two, they can connect the air-generating machine and get used to breathing against the flow of air while they are awake. Once they feel comfortable using the CPAP, they can then take it to bed and usually tolerate it better than if they had started it the first night.
Determining how much a patient needs to use the CPAP for it to be effective has been a topic of contention for a number of years. Recent studies suggest that at least four hours of nightly use are needed to have an adequate therapeutic effect. Six hours are considered adequate presently, but these numbers may change as more research is done.
Current wisdom suggests that the more hours the CPAP is used during the sleep period, the better. Nevertheless, CPAP appears to be extraordinarily effective in intention-to-treat studies. If a primary care physician is notified by a medical supply company that memory chip information indicates suboptimal use of the CPAP, simply discussing this with the patient often is enough to improve compliance.
The emerging field of behavioral sleep medicine also has been helpful in improving compliance. The surgical approach to OSA was developed at about the same time CPAP was developed; however, this form of treatment never gained the popularity that the positive pressure therapy ultimately achieved.
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One reason for this was the poor response rate. Indeed, the Cochrane database has concluded that initial surgical treatment of sleep apnea cannot be justified on the basis of currently available data. I have never had a patient describe the aftermath in kind words, and some female patients have even suggested that they would have preferred childbirth to this type of surgery.
The most common surgery is uvulopalatopharyngoplasty UPPP. Basically, the posterior part of the soft palate is trimmed off, along with the uvula and with removal of any redundant tissue from the lateral pharyngeal walls. Long-term side effects can include voice changes especially with some foreign languages and liquids exiting through the nose if swallowed too quickly.
Some of the less invasive surgical techniques, such as laser surgery, can be considered in less severe cases, but, again, the failure rate is substantial. Surgical procedures that involve moving the lower jaw forward and placing bone grafts, such as in cases of retrognathia, are seldom needed and are generally limited to special referral centers. Dental Devices.
In contrast to the low surgical success rates, oral appliances are proving to be an effective treatment in select cases of mild to moderate sleep apnea and snoring. There is now a board examination for Dental Sleep Medicine with a promising increase in new data coming out showing favorable results in treating OSA. Nasal Dilators. The extent of something from side to side: broadness , wideness , width. Mentioned in? References in classic literature? They were from fifty to one hundred yards long, and they gradually tapered from a nine-log breadth at their sterns, to a three-log breadth at their bow-ends.
View in context. Space, my Lord, is height and breadth indefinitely prolonged. William Gilpin, who is so admirable in all that relates to landscapes, and usually so correct, standing at the head of Loch Fyne, in Scotland, which he describes as "a bay of salt water, sixty or seventy fathoms deep, four miles in breadth ," and about fifty miles long, surrounded by mountains, observes, "If we could have seen it immediately after the diluvian crash, or whatever convulsion of nature occasioned it, before the waters gushed in, what a horrid chasm must it have appeared!
Borne backward to the earth, he saw above him the dead and drawn face within a hand's breadth of his own, and then all was black. The whole extent of this prince's dominions reaches about six thousand miles in length, and from three to five in breadth : whence I cannot but conclude, that our geographers of Europe are in a great error, by supposing nothing but sea between Japan and California; for it was ever my opinion, that there must be a balance of earth to counterpoise the great continent of Tartary; and therefore they ought to correct their maps and charts, by joining this vast tract of land to the north-west parts of America, wherein I shall be ready to lend them my assistance.
Soon after we discovered the isle of Babelmandel, which gives name to the strait so called, and parts the sea that surrounds it into two channels; that on the side of Arabia is not above a quarter of a league in breadth , and through this pass almost all the vessels that trade to or from the Red Sea.
This distinguished scientist has expounded his views in a book entitled "Verschwinden und Seine Theorie," which has attracted some attention, "particularly," says one writer, "among the followers of Hegel, and mathematicians who hold to the actual existence of a so- called non-Euclidean space--that is to say, of space which has more dimensions than length, breadth , and thickness--space in which it would be possible to tie a knot in an endless cord and to turn a rubber ball inside out without 'a solution of its continuity,' or in other words, without breaking or cracking it.