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How to Evaluate a Diagnostic Sleep Study

Report

Lee Shangold, MD

KEYWORDS

� Diagnostic sleep study report � Obstructive sleep apnea � Sleep disorder

KEY POINTS

� All in-laboratory sleep study reports should include sleep architecture, respiratory sum- mary, periodic limb movements, sleep fragmentation and electrocardiography.

� Knowing what information to look for in all of these categories allows clinicians to treat pa- tients with obstructive sleep apnea in a thoughtful and comprehensive way.

� Home sleep testing does not give as much information as an in-laboratory sleep study, but there are still some patients in whom a home sleep test may be more appropriate.

Otolaryngologists are frequently called upon to treat patients with obstructive sleep apnea (OSA). One of the most important tools we have to help us decide what treat- ment options, if any, are in the best interest of our patients is the sleep study. A sleep study is a test that measures certain parameters to determine, among other

things, a patient’s degree of OSA. It can be used diagnostically or it can be used to measure a response to treatment, such as after surgery or with an oral appliance in place. A sleep study can be performed in a sleep lab or at home. It is usually performed at night. However, it is sometimes done during the day in patients, such as shift workers, who generally work at night and sleep during the day. A sleep study can also be used as a therapeutic procedure in an attempt to treat a

patient with OSA. This study can take the form of a continuous positive airway pres- sure (CPAP), bilevel positive airway pressure (BPAP), or adaptive servoventilation (ASV) titration. CPAP and BPAP titrations are performed to treat OSA, whereas an ASV titration is used in patients with central or complex sleep apnea.1,2 In general, whichever modality is used, low pressure is used at the beginning of the study. The pressure is then slowly advanced, in response to respiratory events and snoring, until the optimal pressure setting is identified. A therapeutic oral appliance titration can also be performed in the laboratory. During

this study, the mandible is protruded by advancing the oral appliance in response to

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events, similar to a positive airway pressure (PAP) titration, within parameters set by the titrating physician/dentist prior to the study.3

There are other studies that are performed in a sleep lab. These studies include a multiple sleep latency test (MSLT) and a maintenance of wakefulness test (MWT).4

The MSLT is used to assess someone’s ability to fall asleep in an attempt to quantify hypersomnolence as well as to identify patients with narcolepsy. It entails 4 to 5 nap periods on the day following a full night diagnostic sleep study. An MWT is used to measure a patient’s ability to maintain wakefulness. This test takes place during the day and consists of four 40-minute trials during which the patient sits up in bed with instructions to sit still and remain awake for as long as possible. It is frequently used for patients whose work, and ability to stay awake, may affect public safety. The gold standard diagnostic sleep study is an in-laboratory polysomnography. Un-

derstanding the information that can be gleaned from an in-laboratory sleep study not only allows clinicians to treat patients with OSA but also allows home sleep apnea tests (HSATs) to be put in perspective. When reviewing a sleep study with a patient in the office, it is easy to look at the apnea-

hypopnea index (AHI) and/or respiratory disturbance index (RDI) and decide on treat- ment options. However, there is more information on a sleep study report than just the AHI/RDI. If clinicians know what information to look for on a sleep study report, it al- lows a more comprehensive and effective treatment plan for our patients with OSA. How a sleep study report looks is predicated on what software was used to create it.

Thus, sleep studies from 2 different sleep labs may look very different. However, if cli- nicians understand what categories to look for in a sleep study report, and what infor- mation is important within each category, it becomes easy to get the most information out of any given report. If most of the sleep studies assessed by a physician come from 1 laboratory, it is simple, within a short period of time, to be able to quickly peruse a study for what information is important and relevant. Before looking at what general categories make up a sleep study report, it is helpful

to look at what information is collected during a sleep study and how this information is presented. After patients check in at the sleep lab, they are brought to a private room. The sleep

lab technician then hooks up the patient by attaching all of the appropriate leads. The patient is then instructed to go to sleep. During the course of the night, data are collected from all of the leads. If a lead falls off, the technician sees this on a computer monitor in a separate monitoring room and goes back into the patient’s room to reat- tach the lead. After the patient leaves the laboratory, the collected data are then scored by a sleep technologist. The sleep technologist puts in the stages of sleep and marks the events. Subsequently, this scored study is then interpreted by a sleep physician who looks at all of the scored data and restages sleep/wakefulness and overscores events as deemed necessary. It is beyond the scope of this article to teach readers how to score and interpret the

raw data on a sleep study, but it will be easier for readers to look at a sleep study report if they have a visual of what is recorded during the course of a study night. The leads used during an in-laboratory diagnostic sleep study are standardized.5

Each lead contributes to the overall picture that develops during the course of a study. The leads that are represented on the top half of sleep study raw data help clinicians to determine whether someone is awake or asleep. The leads represented on the bottom half of the page/screen generally provide information about events, including respira- tory events, limb movements, and cardiac events (Fig. 1). The top half of a sleep study screen includes 2 electrooculography (EOG), or eye,

leads; 6 electroencephalography (EEG) leads; and a chin electromyography (EMG)

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Fig. 1. Full screen of a sleep study. The top half is viewed in a 30-second window and the bottom half in a 2-minute window. The leads from top to bottom include 2 eye movement leads, 6 electroencephalography (EEG) leads, a chin electromyography (EMG) lead, electrocardiography (ECG), 2 leg leads, snore microphone, nasal pressure, airflow, the sum of the effort belts, thoracic and abdominal effort belts, pulse oximetry, pulse, and body position.

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lead. As stated earlier, taken together, these leads have definable findings that help clinicians determine not only whether the patient is awake or asleep but, if asleep, what stage of sleep the patient is in. In a sleep study, sleep is artificially broken down into 30-second epochs. Whatever

stage of sleep, or wakefulness, constitutes most of a 30-second epoch is the stage the epoch gets scored as. If a patient’s total recorded time on a sleep study is, for example, 5 hours, there will be 600 epochs that need to be staged. Five hours is 300 minutes. Each minute has 2 epochs of 30 seconds and, therefore, 300 minutes � 2 epochs/min 5 600 epochs. Findings that help to define stages of sleep include alpha waves encompassing

greater than 50% of an epoch in stage W (wakefulness) (Fig. 2); low-amplitude, mixed-frequency EEG activity and alpha waves of less than 50% of an epoch in stage N1 (Fig. 3); sleep spindles andK complexes in stage N2 (Fig. 4); and delta waves in stage N3 (Fig. 5). Clearly, when asleep, the EOG, or eye, leads, help to determine whether the patient is in stage rapid eye movement (REM) sleep (Fig. 6). The figures in this article show typical findings in drowsiness before sleep onset and each stage of sleep. They are presented here, and visualized best on a sleep study, in a 30-second window. The chin EMG also helps to stage sleep. There is a steady decrease in tone repre-

sented on the EMG from wakefulness to stages N1, N2, N3, and then into stage REM. This progression is evident on the lowest line (green) on Figs. 2–6. Keep in mind that the EEG montage, or configuration, that is used for sleep studies

is not as comprehensive as the montage used for EEGs that are used specifically to assess seizure activity. The bottom half of the page generally includes nasal pressure and airflow readings,

chest and abdominal effort belt leads, a microphone to record snoring, body position sensor, electrocardiography (ECG), and 2 leg EMG leads. All of these leads are gener- ally best viewed in a 2-minute screen, other than the ECG lead, which is easier to analyze in a 30-second window (see Fig. 1). In general, there are 5 categories to look for in a sleep study: sleep architecture, res-

piratory summary, periodic limb movements, arousal analysis or sleep fragmentation, and cardiac analysis (ECG).

SLEEP ARCHITECTURE

In life, there are 3 states of being: wakefulness, non-REM sleep, and REM sleep. When everything is working well, these 3 states of being are separate and distinct. People flow smoothly from one state to another in a fairly standard pattern during a typical 24-hour period. Sleep architecture is the basic structural organization and pattern of sleep. It is what

happens with respect to the order and pattern of staging of sleep during the course of the night. One component of the sleep architecture is what percentage of the night people spend in each sleep stage. As stated earlier, sleep is separated into non-REM sleep and REM sleep. In adults,

non-REM sleep is usually w75% to 80% of the night, whereas stage REM is usually w20% to 25% of the night.6 Until recently, non-REM sleep was separated into stages 1, 2, 3, and 4. In 2008, the American Academy of Sleep Medicine (AASM) discontinued the use of stage 4 sleep. Now, non-REM sleep is separated into stages N1, N2, and N3. Stage N3 encompasses what used to be stages 3 and 4.5

Normal sleep architecture changes with age. Not only do newborns spend much more time sleeping during a 24-hour period than adults, but they spend w50% of their sleep in stage REM or active sleep. Stage N3 sleep slowly decreases with age.

Fig. 2. Drowsy (before sleep onset) alpha waves, seen in EEG leads (red rectangle), occupy greater than 50% of the 30-second epoch.

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Fig. 3. Stage N1, sleep onset. Alpha waves (red rectangle) are less than 50% of the 30-second epoch.

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Fig. 4. Stage N2: K complexes (red rectangles) and sleep spindles (green rectangles).

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Fig. 5. Stage N3 or slow-wave sleep: numerous delta waves.

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Fig. 6. Stage REM. Note REMs on the top 2 lines and low tone on chin EMG on the bottom line.

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Stage N1 sleep is light or drowsy sleep with a very low arousal threshold. It is frequently the interface between wakefulness and the deeper stages of sleep. It is nonrestorative. When falling asleep at night, people generally go from wakefulness, briefly into stage N1, and then into stage N2. After awakenings at night, people some- times again transition through stage N1 to the deeper stages of sleep. Some patients with very severe OSA, or significantly disrupted sleep for any reason, have frequent arousals and then transition through stage N1. They therefore have a much higher per- centage of stage N1 than is normal or desired. Adults generally spend more time in stage N2 than any other stage of sleep. There is

a higher arousal threshold in stage N2 than in stage N1 sleep. Stage N3, or slow-wave sleep, is generally considered to be the deepest stage of

sleep and the most restorative. Physiologically, it is a very stable stage to be in. During this stage, the heart rate is generally at its lowest, as is the blood pressure. Sleep ap- nea events are less frequent during this stage of sleep than in any other sleep stage because of its stability. Stage REM sleep is generally the stage in which people dream. Physiologically,

several things happen during stage REM. First, the brain is very active. The brain uses as much glucose during stage REM as it does when awake.7

Second, people are in effect paralyzed during stage REM. People lose muscle tone in all of the muscles of the body except the eyes, the heart, and the diaphragm. If peo- ple had muscle tone during stage REM, they could get out of bed and act out their dreams. It is, therefore, protective to be paralyzed in stage REM. The inability to lose muscle tone during stage REM is seen in an entity called REM

Behavior Disorder. This entity can be dangerous to the patient, and to those around the patient. Patients act out their dreams without an awareness of the consequences. This condition is seen most commonly in patients with Parkinson’s disease. In contrast, the downside of losing muscle tone in stage REM is that many patients

with OSA tend to have a higher AHI or RDI in stage REM than in non-REM sleep. Less muscle tone leads to more airway collapse, and therefore, more respiratory events. Adults with normal sleep go from wakefulness to drowsiness to non-REM sleep. Af-

ter w80 to 110 minutes, the first REM period occurs. People generally go through 4 to 6 non-REM to REM cycles during the night before awakening in the morning. This sequence can be seen most easily on a sleep study report by looking at the hypno- gram. The hypnogram is an overall view or gestalt of what transpired in the course of a night with respect to sleep staging. The hypnogram in Fig. 7 shows essentially normal sleep architecture. It shows a pa-

tient going from wakefulness into non-REM sleep. The patient then transitions through stage N2 and then into stage N3, and then stage REM. This patient has 6 non-REM/ REM cycles. Slow-wave sleep, stage N3, predominates in the first third of the night, whereas stage REM is more prevalent in the last third of the night.

Fig. 7. Hypnogram of essentially normal sleep architecture (gray line is wakefulness, yellow is stage N1, green is stage N2, blue is stage N3 and red is stage REM).

Diagnostic Sleep Study Reports 1317

The hypnogram in Fig. 8 is representative of a patient with very severe OSA. Note how he cannot stay in the deeper stages of sleep and has frequent arousals with reentry to sleep through Stage N1 (yellow). After the hypnogram, the author looks at a table that shows what percentage of the night was spent in each stage of sleep and compares this with normal values. The total sleep time (TST) is the amount of time during the night that the patient was

asleep, as verified by EEG. Sleep efficiency is the percentage of the night, from the time the sleep technician says

“Lights out, go to sleep” until the lights are turned on in the morning, that the patient was actually sleeping. Normal sleep efficiency is greater than 85%. Keep in mind that the pa- tient is sleeping in a strange place and is attached to many wires, which may decrease the patient’s sleep efficiency artificially. This is especially true during the patient’s first sleep study secondary to what is called “first-night effect” in the sleep lab.8

The sleep latency shows how long it took for the patient to get into the first epoch of sleep from the time the technician says, “Lights out, go to sleep.” Normal sleep latency is less than 30 minutes. Again, keep in mind that a decreased sleep efficiency and an increased sleep latency may be secondary to the environment in which the patient is sleeping in. In contrast, a high sleep efficiency (eg, 98%) with a low sleep latency (eg, 2 minutes),

in this kind of environment, may be secondary to significant hypersomnolence; the pa- tient is so tired that they can fall asleep anywhere, anytime, under any circumstances. The author frequently sees patients who are dragged into the office by their bed

partners for snoring, and possible sleep apnea. The patient may deny that they have any sleep issues because they can fall asleep anywhere as soon as their head hits the pillow. Here is an opportunity to explain to them that this is not normal. A normal sleep latency is 5 to 30 minutes, not 30 seconds. Another latency that is very important is the REM latency. This is how long it takes a

person to progress from the first epoch of sleep to the first epoch of stage REM sleep. Normal REM latency is 80 to 110 minutes. A very short REM latency, such as 5 minutes, can be pathologic. It suggests, but is not pathognomonic for, the possibility of narcolepsy. Narcolepsy is the intermingling of wakefulness and stage REM sleep. The symptom

of cataplexy is pathognomonic for narcolepsy but is only seen in w50% of patients with narcolepsy. Cataplexy is a sudden attack of muscle weakness that is usually trig- gered by strong emotion (laughing more commonly than crying). As can be seen above, there is a lot of useful information that can be obtained from

understanding sleep architecture, both normal and abnormal, before even considering the respiratory summary.

RESPIRATORY SUMMARY

The respiratory summary is the main section of a sleep study when the purpose is to establish whether the patient has sleep apnea and, if so, to what degree.

Fig. 8. Hypnogram of a patient with severe OSA (yellow is Stage N1, green is Stage N2, blue is Stage N3 and red is Stage REM).

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To understand the respiratory summary, clinicians must first know the definitions of the terms that make up the all-important indices.5 An apnea is defined as a decrease in the airflow by greater than 90% for at least 10 seconds (Fig. 9). There are 2 definitions for a hypopnea, which is the most common respiratory event

seen in the sleep lab. The definition that the AASM recommends is a decrease in nasal pressure by greater than 30% for at least 10 seconds with either a decrease in oxygen saturation by at least 3% or an arousal as determined by EEG (Figs. 10 and 11). The alternative definition that the Centers for Medicare and Medicaid Services require is a decrease in nasal pressure reading by greater than 30% for at least 10 seconds with a concomitant decrease in oxygen saturation by at least 4%. The relevance of these 2 definitions is that a patient with Medicare or Medicaid may have a lower AHI or RDI than a patient with commercial insurance despite having identical recordings. There- fore, it is important to know which criteria were used in the scoring of the study before treating the patient based on the study results. The final respiratory event that can be included in degree of OSA is a respiratory

effort–related arousal (RERA). This event does not meet the criteria for an apnea or hypopnea but nonetheless shows increased effort of breathing with a disruption in sleep. To be certain that there is an increase in respiratory effort before an arousal, patients need to have an esophageal probe in place, but very few patients would come to a sleep lab if this were the case. However, a RERA can be extrapolated from the typical data collected. There are signs of increased respiratory effort on the parameters that are measured, such as flattening of the nasal pressure curve.9

The 2 main indices that are used to measure degree of OSA are the AHI and the RDI:

AHI 5 (# of apneas 1 # of hypopneas)/TST

RDI 5 AHI 1 (# of RERAs/TST)

Some sleep labs report the AHI, some report the RDI, and some report both. The degree of OSA based on the AHI/RDI is as follows (Table 1). Apneas can be divided into obstructive and central. An obstructive apnea, which is

the more common type seen in the laboratory, is secondary to airway collapse with subsequent blockage of the upper airway during sleep. Central apneas are secondary to lack of signal from the brain to breathe. Central apneas are commonly seen in pa- tients with congestive heart failure, people who are at high altitudes before accli- mating, patients on narcotics, and patients with primary central sleep apnea (CSA). Patients in the sleep lab have belts around the chest and abdomen. These are effort

belts. During an obstructive event, there is a signal coming from the belts that, despite the patient not breathing, the patient is trying to breathe. During a central event there is no signal coming from the belts, so there is no inspiratory effort. This distinction is important because OSA and CSA may be treated differently.1

In addition to the overall AHI/RDI, the AHI/RDI is also reported by position and REM versus non-REM sleep, which may have a significant impact on the recommendations of treatment. OSA is usually worse in the supine position than in a non-supine position. Therefore,

it is important to assess the total AHI/RDI as well as the supine and non-supine AHI/ RDI. This information reveals whether positioning therapy is a potential treatment op- tion for the patient. Positioning therapy can be performed using appropriate T-shirts, wedges, and pillows that are designed for this purpose. As stated previously, OSA is usually worse in stage REM than in non-REM sleep.

Thus, it is important to assess the percentage of stage REM that the patient had during

Fig. 9. Two obstructive apneas with a greater than 90% decrease in airflow (red rectangles) lasting longer than 10 seconds.

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Fig. 10. Three hypopneas with greater than 30% decrease in nasal pressure (light blue rectangles within the long green rectangle) with greater than or equal to 3% decrease in oxygen saturation (thin mauve rectangles near the bottom of the page).

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Fig. 11. Hypopnea with greater than 30% decrease in nasal pressure (green rectangle) that ends with an arousal (red rectangle) without at least a 3% decrease in oxygen saturation (long black rectangle).

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Table 1 Degree of OSA based on AHI/RDI in adults

AHI/RDI (/h) Degree of OSA

<5 Essentially normal

5–15 Mild

15–30 Moderate

>30 Severe

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the night (normal is 20%–25%). If it is low, such as 0% or 5%, this study may have underestimated the true degree of OSA if the patient has more stage REM at home. Pediatric sleep apnea is recorded, scored, and graded differently than in adults

(Table 2). End-tidal CO2 is evaluated in pediatric studies, but not adult studies. It is used to evaluate for hypoventilation.10

The difference, for the most part, in scoring is the length of time needed to score an event and the number of events per hour that is considered significant. As opposed to the 10 seconds required for apneas, hypopneas, and RERAs in adults, with children an event is scored, if it meets the other criteria, if it lasts longer than 2 breaths. In addition, the grading is much stricter in children. For example, an adult with an

AHI of 14/h is considered to have mild OSA, whereas a child with this same AHI is considered to have severe OSA. The last part of the respiratory summary to assess is what happens to the oxygen

saturation during the course of the study. There are several ways to approach this. The most commonly listed number is the oxygen saturation nadir, which is the lowest oxygen saturation seen during the night in response to a respiratory event. In general terms, normal is greater than or equal to 90%, mild is 85% to 89%, moderate is 80% to 84%, and severe is less than or equal to 79%. Another way the oxygen saturation may be presented is as a percentage of the TST

from 90% to 100%, 80% to 89%, 70% to 79%, and less than 70%. Clearly, a fleeting nadir of 79% does not have the same implications as a patient who spent 10% of the night with an oxygen saturation less than 80%. In addition, it may be presented as an oxygen desaturation index, which is either the

number of desaturations of 3% or greater per TST or the number of desaturations of 4% or greater per TST.

PERIODIC LIMB MOVEMENTS

The next broad category is periodic limb movements of sleep (PLMS). PLMS is a re- petitive movement of the legs, and less commonly the arms, during sleep. It is measured by EMG leads on the lower extremities. There are clear criteria that need to be met for a periodic limb movement (PLM) to be scored.5 A PLM index (PLMI) of greater than 15/h is considered abnormal in adults, whereas a PLMI of greater than 5/h is abnormal in children.11

Table 2 Degree of OSA based on AHI/RDI in children less than 18 years of age

AHI/RDI (/h) Degree of OSA (<18 y of Age)

<1 Essentially normal

1–5 Mild

5–10 Moderate

>10 Severe

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PLMs may or may not be associated with an EEG arousal (Fig. 12). They can disrupt sleep and contribute to excessive daytime sleepiness (EDS); for example, a patient who snores and has significant EDS. A sleep study is obtained that reveals an RDI of w2/h and a PLMI of greater than 50/h. It may be the PLMs that are contributing to the EDS. Patients are considered to have PLM disorder (PLMD) if they have an increased

PLMI and some daytime consequence, such as EDS, that is not secondary to some other cause. Patients who have an increased PLMI but no sequelae secondary to this are not considered to have PLMD. PLMS is thought to be related to restless legs syndrome (RLS). RLS is a diagnosis

made solely by history. The diagnosis of PLM is made by a sleep study. RLS is a sen- sory disorder; that is, it can be felt. PLMD is a motor disorder. Bed partners of patients with PLMS may say that they kick their legs during sleep. More than 80% of patients with RLS have an increased PLMI on a sleep study. In contrast, less than 30% of pa- tients with PLMS have RLS.12

RLS and PLMs share the same pathophysiology and often respond to the same medi- cation. The cause remains unclear but is most likely related to dopaminergic systems and brain iron metabolism. There are some potentially controllable exacerbating fac- tors, including sleep deprivation, caffeine, selective serotonin reuptake inhibitors, alcohol, nicotine, and iron deficiency. They are seen more commonly in patients who are pregnant or have renal failure, myelopathy, diabetes, or Parkinson disease. If the pa- tient has an increased PLMI, blood work for possible contributing factors should be considered, including serum ferritin, complete blood count , blood urea nitrogen/creat- inine levels, thyroid function tests (TFTs), folate level, and vitamin B12 level.

SLEEP FRAGMENTATION

The fourth major category to be assessed on a sleep study report is sleep fragmenta- tion. Frequently, the driving force behind a sleep evaluation is the symptom of EDS. This category may help to determine the underlying cause for this particular symptom. As stated previously, in-laboratory sleep studies use an EEG montage to show when

a patient is awake versus asleep and, if asleep, what stage of sleep the patient is in. In addition, the EEG identifies arousals from sleep. Every arousal gets marked and assigned a cause, if known. Clinicians want to know the cause of the arousals so that they can evaluate what is disrupting the patient’s sleep. Some arousals occur at the end of an apnea, hypopnea, or RERA (obviously, there

cannot be a respiratory effort–related arousal without an arousal). These arousals are all clearly respiratory related secondary to sleep disordered breathing (SDB). Some arousals occur after a limb movement, and these are called limb movement arousals. If the cause of an arousal is not clear, it is categorized as a spontaneous arousal. Spontaneous arousals have several different possible causes, which are not usually

obvious from the sleep study. Spontaneous arousals may be secondary to hypervig- ilance from sleeping in a strange place, and being attached to multiple leads with a camera watching the person sleeping. Spontaneous arousals frequently are second- ary to any form of pain, such as fibromyalgia or chronic back pain. In a sleep study report, there is a section for arousals. It may be called Sleep

Arousals or Sleep Fragmentation. There is a respiratory arousal index, a PLM arousal index, a spontaneous arousal index, and a total arousal index, and these are important in evaluating patients who have EDS that is not explained by OSA. Also, keep in mind that there are causes of EDS other than SDB. Probably the most

common cause for EDS is insufficient sleep. Average adults need w7.5 hours of sleep to function optimally. Teenagers need w9 hours of sleep. Causes for EDS other than

Fig. 12. Periodic limb movements (green ovals), one of which has an associated arousal (red rectangle), with normal nasal pressure, airflow, and pulse oximetry readings.

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Diagnostic Sleep Study Reports 1325

insufficient sleep, SDB, and PLM include, but are not limited to, medication side effect, mood disorder (especially depression), RLS, circadian rhythm disorders, insomnia, narcolepsy, and idiopathic hypersomnia. Tools to help clinicians make the correct diagnosis for EDS include comprehensive sleep history, sleep study, 2-week sleep log, Beck Depression Inventory, and MSLT.

CARDIAC ANALYSIS

An additional category on an in-laboratory sleep study is the cardiac analysis, which is usually just a sentence or two about the ECG reading during the course of the night. Having the ECG in a sleep study is akin to having a Holter monitor. Untreated moderate and severe OSA are independent risk factors for, among other

things, hypertension and myocardial infarction. In some patients with significant OSA, the first sign of resultant cardiac disorder is ECG abnormalities seen during a sleep study (Fig. 13). Such things as multifocal premature ventricular contractions or heart block (other than Wenckebach) can be signs of significant cardiac disease that needs to be addressed in a timely fashion, in addition to the OSA.

HOME SLEEP APNEA TESTING

To this point, this article has been about in-laboratory sleep study reports. HSATs have become prevalent over the last several years, partially because some patients tolerate an HSAT better, but mostly because it is dictated by some insurance companies in an attempt to save money. In the long run, this may not be true.13

Table 3 shows the parameters that are measured in all in-laboratory studies compared with what is measured with HSATs. This process can be taken a step further. Table 4 shows which of the 5 main cate-

gories discussed in this article can be seen in HSATs. As stated previously, the respi- ratory summary is the basis of sleep testing and is what is ultimately used to assess someone’s degree of OSA. Also keep in mind that on in-laboratory sleep study reports, the all-important indices,

AHI, RDI, and PLMI, use TST as the denominator in their equations. For example:

AHI 5 ðtotal # of apneasÞ1ðtotal # of hypopneasÞ

ðtotal sleep timeÞ HSAT devices either use total recorded time or some surrogate measure for sleep,

such as actigraphy, for the denominator. If the patient has a low sleep efficiency, to- tal recorded time, as the denominator, gives a falsely low index. In contrast, actig- raphy is a reasonable measure of sleep in that it records movement; for example, of the wrist. The wrist movement is generally different whether a person is awake or asleep. There are advantages and disadvantages of both in-laboratory tests and HSATs.

The advantages of in-laboratory studies include that there are consistent, easily reviewable data; that clinicians can diagnose and treat OSA in a single split-night sleep study in which the first half of the night is a diagnostic portion and the second half is a therapeutic PAP titration; and that disorders other than OSA can be identified. Such disorders include seizures, PLMs, and malignant arrhythmias. The advantages of home sleep studies include potential cost savings; the comfort

and convenience of patients sleeping in their own homes; and fewer leads attached and, therefore, possibly a more typical night sleep than might be seen in the laboratory.

Fig. 13. Thirty-three–beat nonsustained wide complex tachycardia that may be ventricular tachycardia or supraventricular tachycardia with aberrancy. Cardiology evaluation for structural heart disease should be pursued.

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Table 3 In-laboratory versus HST parameters measured

In-laboratory Parameters Measured HST Parameters Measured

Airflow: nasal/oral Airflow: nasal/oral or arterial tonea

Pulse oximetry Pulse oximetrya

Effort: thoracic/abdominal Effortb

Body position Body positionb

ECG ECG (almost all include pulse)c

Leg movements Leg movementsc

Eye movements Eye movementsc

EEG EEGc

EMG: chin EMG: chinc

a HSAT parameters that are always measured. b HSAT parameters that are usually measured. c HSAT parameters that are infrequently measured.

Diagnostic Sleep Study Reports 1327

SUMMARY

When seeing a patient in the office to review the results of a sleep study, I first spend a minute looking at the study before walking into the examination room. I want to know what transpired during the night the patient spent in the sleep lab. In addition, I want to formulate what options to present to the patient to manage any sleep-related issues that the patient may have. It is easy to look at the AHI/RDI, walk into the examination room, and explain that the

patient has a certain degree of OSA and what the treatment options are. Clinicians may be confronted with a patient who has slept in the sleep lab for as little as 35 mi- nutes all night. The patient may ask how a treatment plan can be formulated if the pa- tient did not sleep. If the clinician had checked the TST (35 minutes) and sleep efficiency (10%), the clinician would have started the conversation with a phrase such as, “I see you had a poor night’s sleep in the lab. Please tell me this is not a typical night’s sleep for you.” Instead of losing the patient’s confidence, the clinician now has the patient’s attention. First-night effect in the sleep lab can be explained to the patient and other options presented, including an HSAT. Another example of using all of the information on a sleep study to treat the patient in

a thoughtful fashion is as follows. A 62-year-old man presented to the laboratory with a

Table 4 Comparison of what is included in an in-laboratory versus HST reports

In-laboratory Study Reports HST Reports

Respiratory summary Respiratory summarya

Sleep architecture Sleep architectureb

ECG ECG (almost all include pulse)c

Periodic limb movements Periodic limb movementsc

Sleep fragmentation Sleep fragmentationc

a HSAT reports include category always. b HSAT reports include category sometimes. c HSAT reports include categories infrequently.

Table 5 RDI totals in a patient with very positional OSA

By Sleep Stage By Position

TotalNREM REM Supine Non-supine

Sleep Time (min) 198.5 39.5 176.5 61.5 238.0

Apnea

Obstructive 11 21 32 0 32

Mixed 4 1 5 0 5

Central 47 2 48 1 49

Total Apnea 62 24 85 1 86

Apnea Index 18.7 36.5 28.9 1.0 21.7

Hypopnea 144 7 149 2 151

Total Apneas and Hypopneas 206 31 234 3 237

AHI 62.3 47.1 79.5 2.9 59.7

Flow Limitation Events (RERA)

2 0 1 1 2

RDI 62.9 47.1 79.8 3.9 60.3

Abbreviation: NREM, non–REM sleep.

Shangold1328

Down

history of snoring, witnessed apnea, EDS, and coronary artery disease (CAD). His sleep study revealed severe OSA with an overall RDI of 60.3/h (Table 5). After a titra- tion, he was put on CPAP. He did not tolerate it. On reevaluating the patient’s original sleep study, he clearly had overall severe OSA,

but it was exceedingly positional. He had a supine RDI of 79.8/h and a non-supine RDI of 3.9/h. Further history revealed that the patient rarely slept on his back at home. He felt obligated to sleep mostly supine while in the sleep lab secondary to all of the wires

Table 6 Summary of how to evaluate sleep study report

What to Look at in Sleep Study Report Significance

1 AHI/RDI Gives degree of OSA

2 TST/sleep efficiency/ hypnogram

Gives a sense of how well the patient slept

3 REM latency Normal is 80–110 min; if exceedingly low (ie, <20 min), consider evaluation for narcolepsy

4 AHI/RDI in supine and non-supine positions

Consider positioning therapy if very positional

5 Percentage of stage REM If none or low, total AHI/RDI may underestimate degree of OSA

6 Periodic limb movement index

If high, may be contributing to EDS, especially in patient with no, or well-treated, OSA

7 Total arousal index and breakdown of arousals

May help determine cause for EDS (ie, respiratory, limb movements, or spontaneous)

8 Oxygen saturation nadir and percentage <90%

Contributes to cardiovascular risk

9 EKG Summary Identifies potentially unknown arrhythmias

Diagnostic Sleep Study Reports 1329

and the instructions of the sleep technician. He was intolerant of CPAP because it was set to his optimal pressure when he was in the supine position. When he slept non-su- pine at home, the pressure was not only too high, but possibly not even necessary. To achieve a comfort level for the patient sleeping non-supine at home, with a low RDI, an HSAT could be done and the patient instructed to sleep how he normally sleeps. This case provides another example of treating the patient based on all of the information that can be gleaned from a sleep study report. Table 6 lists what I look at on a sleep study report, and its significance, before dis-

cussing the study with the patient. In conclusion, this article presents a pathway to comprehensively assess all of the

information on a sleep study report in a way that allows clinicians to most effectively treat patients who have OSA, and other sleep disorders.

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How to Evaluate a Diagnostic Sleep Study Report

Key points
Sleep architecture
Respiratory summary
Periodic limb movements
Sleep fragmentation
Cardiac analysis
Home sleep apnea testing
Summary
References