TITLE: =
Polysomnography (Sleep Studie=
s)=
SOURCE: Grand Rounds Presentation, The University of Texas Medical Branch, =
Dept=
. of
Otolaryngology
DATE: January 31, .2011
RESIDENT PHYSICIAN:<=
span
style=3D'font-size:12.0pt;mso-bidi-font-size:11.0pt;font-family:"Times New =
Roman","serif"'>
Angelia Smith, MD
FACULTY PHYSICIAN: Harold Pine, MD
DISCUSSANT: Harold Pine, MD
SERIES EDITOR: Francis B. Quinn, Jr., MD
ARCHIVIST: Melinda Stoner Quinn, MSICS
=
"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."
Polysomnography
This grand rounds covers the following topics:
•stages
of sleep
•indications
for polysomnography
•what
happens to the patient
•what
is measured
•how
it is interpreted
•what
it all means
•treatment
options
The emphasis will be on the sleep study itself = as the surgical options for threatment of sleep apnea were covered in a lecture by= our chairman that same day.
Sleeping and arousal are governed by a complex interaction of central nervous system components. Arousal mechanisms are governed by the reticular formation in the brainstem, referred to as the reticular activating system (RAS). It communicates with the cerebral cortex through the thalamus: senso= ry input from the cerebral cortex can activate the RAS and cause arousal. During sleep, fewer stimuli arise = from the cortex because of a feedback loop to the cortex from the RAS. However, = the cortex can be stimulated, but the stimulus intensity must be much higher th= an needed to cause a cortical reponse during consciousness.
Any talk about polysomnography must include the stages of sleep. By definitio= n, awake is one necessary stage of sleep. Awake is characterized by alpha waves on EEG and reactivity to exter= nal stimuli is maintained. The ot= her stages of sleep are broken into Non-Rapid Eye Movement (NREM) and Rapid Eye Movement (REM). NREM has three stages and REM is its own stage.
Sta= ge 1 NREM sleep is characterized by drowsiness. EEG rhythms slow to mixed delta and theta waves. There is reduced muscle activity, decreased minute ventilation and increased PaCO2. Heart rate and cardiac output decr= ease from increase in parasympathetic tone.
Sta= ge 2 NREM sleep is the next stage, a deeper sleep than stage 1. It comprises 45-55% of total sleep= time. The EEG shows sigma waves and K complexes. This stage of slee= p requires a higher intensity stimulus for arousal.&n= bsp; Reduced muscle activity, decreased minute ventilation and increased PaCO2 continue. Heart rate and cardiac output decreased more than Stage 1 NREM sleep from continued increa= se in parasympathetic tone.
Sta= ge 3-4 NREM sleep was recently combined into one stage. It comprises 13-23% of total sleep= time in adults. It has an EEG with characteristic slow delta waves, and this phase requires highest intensity stimulus for arousal. The res= piratory rate is most regular in this phase, and this is the phase most associated w= ith restful, restorative sleep.
The REM stage of sleep is characterized by rapi= d eye movements and dreaming. EEG shows mixed frequencies with alpha waves, simil= ar in character to the awake EEG. However, skeletal muscle tone is decreased, = most importantly the upper airway tone is decreased so that the airway has the l= east amount of protection at this stage of sleep. During REM sleep, surges in autono= mic activity, suspected to be related to dreaming, can destabilize heart rate a= nd cause fatal arrhythmias. Resp= iratory rate can increase because of these same surges, but actual airflow is decre= ased because of muscular atony. Al= so, hypoxic ventilatory response is depressed as well.=
Now that we have covered the basics of sleep, w= e turn to the basics of the sleep study, formally known as polysomnography. The indications for ordering a sle= ep study include:
L1
How does one go about diagnosing sleep related disorders? Sleep history is key to diagnosis. Sleep disordered breathing symptoms include snoring, witnessed apneas, nocturnal choking or gasping, restlessne= ss, and excessive daytime sleepiness are key symptoms that point towards a diagnosis of sleep disordered breathing.&n= bsp; Epworth Sleepiness Scale can be helpful in distinguishing the severi= ty. Evaluation of daytime sleepi= ness should include evidence of sleep deprivation, use of alarm clock, shift wor= k, snoring, recent weight gain, family history, morning headache, or a sore th= roat or dry mouth. One should also= ask about alchol consumption, nasal congestion, hypothyroidism, and menopause as these factors can affect the restfulness and restorative function of sleep.= A sleep log can be helpful to diagnose daytime sleepiness as being from lack = of sleep time vs. pathologic sleep patterns.
Children are not just small adults. Their symptoms and treatments can = differ greatly. Behavioral problems, learning problems, lack of attentiveness, and hyperactivity can characterize sleep disordered breathing in children more than classic signs of fatigue t= hat adults suffer.
The next step towards diagnosing a sleep disord= er is doing a physical exam. Findin= gs that support diagnosis of sleep disordered breathing in adults are obesity, hypertension, and cardiopulmonary disease.= In children, adenotonsillar hypertrophy and obesity point towards sl= eep disordered breathing.
When you send a patient to a sleep lab, what ac= tually happens? In our sleep lab at = UTMB, the patients arrive around 9 p.m. to be set up. In the pediatric population, famil= ies are allowed to sleep in the same room (but not in the bed with the patient = as this can confound the readings). I decided to follow one of our patients through his setup in the sleep lab. Introducing “Tony” an adolescent patient of Dr. Harold Pine, he= re for follow up sleep study after his tonsillectomy and adenoidectomy perform= ed for obstructive sleep apnea/hypopnea syndrome (OSAHS). Please refer to the “Polysomnography Demystified” powerpoint presentation for pictu= res and graphics.
When “Tony” is set up in our sleep = lab, one of the two techs on duty that evening place the electrodes:
L1
The room is then darkened and the tech goes thr=
ough a
series of tests of the sensors to make sure they are recording properly.
Before venturing over to our sleep lab, I searc= hed the internet for sleep study patient pictures to use in this presentation, = and came across the fascinating case of Haven.= I was given permission to use her pictures by her mother if I would = take a moment to talk about her syndrome.
Haven is a 6 year old girl with a rare syndrome= that has been termed ROHHAD: Rapid-Onset Obesity With Hypothalamic Dysfunction, Hypoventilation, and Autonomic Dysregulation. This syndrome is characterized most often by rapid onset obesity occuring around the age of 3. Other frequent hypothalamic dysfun= ction symptoms are hyperphagia, polydipsia, polyuria, and hypernatremia.
Autonomic dysregulation often follows around th= e age of 4, most frequently manifested in ophthalmic problems (e.g. strabismus), = GI dysmotility, altered sweating, thermal dysregulation, and tumors of neural crest origin. Haven has ganglioneuroblastoma that= was diagnosed in 2007 at the same time as her ROHHAD syndrome. Present in all patients is alveolar hypoventilation that begins to manifest at the average age of 6. Obstructive sleep apnea is common, and death can occur suddenly from cardiorespiratory arrest from central apneas. Seizures are also seen with this syndrome.
Haven sleeps with a pulse oximeter at night that alarms so her mom can go in and arouse her if her oxygen saturations dip too low. Haven undergoes sleep st= udies every 6 months to try and catch central apnea before it is symptomatic. She has confirmed obstructive sleep apnea and her mother and doctors are planning to have her tonsils and adeno= ids removed in the near future. H= er arterial CO2 used to run about 50 but she has undergone chemothe= rapy with cyclophosphamide, rituximab, IVIG, and prednisone that has her weight steady and her arterial CO2 down to 45.
Back to the topic of polysomnography. Many things are measured during a = sleep study. The EEG measures the brain’s neuronal activity. Brain waves have characteristic frequencies, amplitudes, and morphologies and each stage of sleep has characteristic brain waves. Drawings of the waves are available on the powerpoint presentation.<= /p>
Alpha waves are the first brain waves discovere= d. They are predominant in relaxed wakefulness and have a characteristic frequency of 8-13 Hz. Theta waves are predominant in Sta= ge 1 NREM sleep and have a characteristic frequency of 12-14 Hz. Spindles and K complexes are chara= cteristic of Stage 2 NREM sleep and they occur in setting of variable low frequency w= aves. Delta waves are predominant in Sta= ge 3-4 NREM sleep and have a frequency between 0.5 and 2 Hz. The EEG of REM sleep looks very si= milar to Stage 1 NREM but it is characterized by rapid oscillating eye movement a= nd skeletal muscle atony.
The EEG tracings, the muscle electrodes, and th=
e eye
movement sensors are used to break the tracings down into the stages of
sleep. The
|
Stage=
|
EEC |
EOG |
EMG |
|
Wakefulness |
Eyes closed; alpha
prominent in the occipital region. Alpha attenuates with concentration |
Voluntary control; =
blinks,
REMs, SEMs if drowsy |
Tonic activity, rel=
atively
high, voluntary movement |
|
NREM Stage I |
Low voltage mixed
frequency, theta activity, vertex sharp waves |
SEMs |
Tonic activity, sli=
ght
decrease from wakefulness |
|
Stage II |
Relatively low volt=
age
mixed frequency background. Sleep spindles and/or K complexes |
Occasionally SEMs n=
ear
sleep onset; otherwise, reflects EEG activity |
Tonic activity |
|
Stage III-IV |
>20% delta waves,
0.5–2 Hz; greater than 75 uV in amplitude |
Reflects EEG activi=
ty |
Tonic activity |
|
REM |
Relatively low volt=
age
mixed frequency, possible sawtooth waves, theta activity |
Phasic REMs |
Tonic suppression, =
phasic
twitches |
|
Movement time |
Obscured |
Obscured |
Very high activity<= o:p> |
Please refer to the Powerpoint presentation for
typical examples of tracings.
The other leads (chin movement, leg movement, c= hest wall movement, abdominal movement, air flow, both nasal and oral, and pulse oximetry) are used to characterize breathing patterns during the phases of sleep. Apnea is the cessation= or near cessation of airflow for a minimum of 10 seconds. It is usually associated with desaturation and an EEG arousal at terminus. Hypopnea is a 50% decrease in airflow for at least 10 seconds followed by an arousal and/or 4% oxygen desaturation. Respiratory Eve= nt Related Arousals (RERA) are periods of increased breathing effort during increased airway resistance, with subsequent arousals, but in the absence of hypopneas, apneas, or O2 desaturations.
After the polysomnogram, the study is then scor= ed according to AASM guidelines and a report is generated. Measurements include total recordi= ng time, total sleep time, sleep latency (amount of time from lights out to sl= eep stage 1), number of REM periods, number of stage shifts, number of arousals, number of apneas and type, number of hypopneas, pulse oximetry, and leg movements.
The key equation that summarizes all the data a= nd provides guidelines for treatment is the Apnea Hypopnea Index (AHI).
An AHI greater than 5 is diagnostic for Obstruc= tive Sleep Apnea/Hypopnea Syndrome (OSAHS) in adults. An AHI greater than 1 is OSAHS in children. An AHI of 5-30 is m= ild, 30-60 is moderate, and greater than 60 is severe OSAHS.
Another important equation is the Respiratory Disturbance index.
Upper = Airway Resistance Syndrome (UARS) is defined as daytime sleepiness associated = with a sleep breathing disorder with RERAs but not enough apneas/hypopneas to diagnose OSAHS. No consistent= RDI number has been defined to make a diagnosis.
Now that we can diagnose OSAHS, what can we do = about it? Treatment options include= , nothing, weight loss, oral appliances, positive pressure ventilation, and a variety = of surgeries. Since they are not= just little adults, children’s options are a bit different.
It has been noted that some patients with OSA o= nly have it in the prone position. The obstruction disappears when the patient is lying on their side, so sleep positioning can offer a cure. These are usually mild cases with AHI <30.
The Sleep AHEAD study showed that changes in we= ight, waist circumference, and neck circumference were strongly associated with reduction in AHI. The best improvement in AHI was found in the group that lost more than 10 kg.
Oral appliances are designed to advance the man= dible. They require a personalized dental appliance, and they’re only effective in mild cases of OSAHS.
Positive pressure ventilation is a well known treatment for OSAHS. It creat= es a “pneumatic splint” in the upper airway to prevent collapse, and there are several variants: nasal CPAP, autotitrating CPAP, BiPAP. This treatment is only as effectiv= e as the compliance to it, reported as 46-89%.&= nbsp; Interestingly, the least compliant patients are the ones who present= for evaluation only at the urging of their spouses and not because of their own symptoms.
Surgical options abound, but have mixed efficacy. Tracheostomy is the= only surgical procedure consistently effective in the treatment of OSAHS, but it= is indicated only for life threatening disease such as cor pulmonale, arrhythmias, or se= vere hypoxemia. The surgery most frequently performed on adults for OSAHS is uvulopalatopharyngoplasty (UPPP). This is generally considered only 50% effective. Some research stat= es that this is more effective in patients with lower body mass index and lower AHI.
Another technique available surgical correction= of OSAHS is maxillomandibular advance= ment (MMA). The maxilla and the mandible are both advanced, with the mandible advanced slightly more than t= he maxilla. In combination= with UPPP or other procedures, the success rates are reported between 66.7% and 97.8% as long as the advancement is 10 mm or more relative to the original = bony position.
In children, the treatment of choice for OSAHS = is adenotonsillectomy. Complicat= ions after the procedure occurs more often in children younger than 3, those with severe OSA, and those with other medical problems. In children with obesity, this may= not completely resolve OSAHS, so in those cases, CPAP and weight loss can help = if adenotonsillectomy gives an incomplete cure.
Please refer to the Powerpoint presentation for diagrams and pictur=
es.
Discussant:&nbs=
p;
Harold Pine, MD
That was very good, Dr. Smith,=
and
I’m sorry I wasn’t able to join you at the sleep lab at nine
o’clock but I have done that in the past and I think you can now
appreciate what a hurdle it is for us to get one of these started. It’s not the simplest thing =
in the
world and yet it’s really amazing to me that the overwhelming majorit=
y of
kids are able to get hooked up, fall asleep and give us some really useful
data. My hat goes off to the
terrific sleep techs we have here at UTMB.=
I have the occasional child where they just do not tolerate being ho=
oked
up to all this stuff and they have to call it a wash.
A couple of comments about thi=
ngs
you said or didn’t say: I
wanted to put in a plug for the twenty two question sleep questionnaire tha=
t I
use routinely in my clinic. D=
r. Chervin
and his team developed this and while not meant for clinical use I find it =
very
helpful in pointing out to parents some of the relevant issues involved.
Pediat=
ric
sleep questionnaire (PSQ): validity and reliability of scales for
sleep-disordered breathing, snoring, sleepiness, and behavioral problems.
Chervin RD, Hedger K, Dillon JE, Pituch KJ.
Department of Neurology, University of Michigan, Ann,
Arbor, USA
A positive sleep questionnaire=
along
with a good history helps raise your suspicions and have a meaningful
discussion with parents and pediatricians alike. This is a validated questionnaire =
with a
sensitivity around 80% and a specificity around 87% so it’s certainly
something easy to do and it can help you discuss with the family the likeli=
hood
of there being sleep disordered breathing.=
We are all sent children for
potential sleep disordered breathing and it is a very reasonable question to
ask the parents, “Well, what do you see when the kid sleeps?”
For the sleep studies themselv=
es, a
couple of interesting comments: For
people who do this in the pediatric realm completely, they suggest that
it’s also very, very important to have a CO2 monitor because lots of =
kids
while not having frank obstructive sleep apnea have hypoventilation and
hypercarbia and that’s not something we routinely measure. Could we be missing some chi=
ldren
with obstructive hypoventilation? Also, which I find interesting, depending=
on
where you send your patients for a sleep lab will depend on whether you get=
an
AHI or an RDI. Now for our
purposes, we’re looking for the appropriate indication to do surgery.=
For
me, it’s better to get the RDI, because what might otherwise have bee=
n a
negative study, the RERAs can push the final score over that magical number=
of
RDI >1 and gives you a good indication for surgery. At Harborview, which is part of our
system and at American Sleep Labs which is not part of our system, they
routinely report just the AHI. When
reviewing these studies done in children, if the RDI is greater than ten, m=
ost
people consider that significant or severe OSA. The other thing to recognize and p=
oint
out to our anesthesia colleagues is if the O2 saturation has dropped below
eighty percent on the sleep study. That puts the child at higher risk of ha=
ving
respiratory compromise after surgery.
So, I routinely point that out to our pediatric anesthesiologists.
And then one final comment. In=
some
of the papers I have read they suggest that when trying to make a diagnosis=
of
obstructive sleep apnea in children, they should pull central apneas out of=
the
equation, because, as you know, central apneas are more common in children =
than
in adults. * So if a kid has a few central apneas, that may push their over=
all
RDI past the limit, while if you took those out, they still may be negative=
for
a total RDI. As far as I can tell it all gets thrown into the pot together =
when
calculating the RDI here.
Sleep studies are a valuable t=
ool in
helping to sort out a host of sleep issues and not just OSA. They are expensive and certainly n=
ot
every child needs a sleep study but they are becoming easier to obtain and =
can
provide very useful information.
Does anyone know if there are any pure pediatric sleep labs out
there? I bet it would be a lu=
crative
venture.
*Anesth Analg. 2009 Jul;109(1):60-75=
.
Schwengel
DA, Sterni
LM, Tunkel
DE, Heitmiller
ES
Dr. Underbrink’s remarks:
It was very informative and I =
would
like to encourage all of you that all of those tracings are on there and th=
ey
make you mix and match which ones are sleep arousals and which ones are
RERA’s and it’s quite involved so maybe we should all review the
nuts and bolts of sleep studies because those are required for our main
certification as though it would seem, though I think you could avoid it if=
you
wanted to.
Secondly, I don’t know i=
f you
know the answer to this but do you use the RDI as though it were and AHI
because when I get some sleep studies that only report an RDI I don’t
know if there’s any literature to prove that we can or can’t.
Dr. Pine:
I use them interchangeably and I’ve only h=
ad a
couple kids so for the most part the kids I’m seeing don’t have
that …it was no apneas =
but
there were a hundred RERA’s.
References:
=
•Fundamentals
of Sleep Technology,
1st Edition Butkov, Nic; Lee-Chiong, Teofilo Copyright ©2007 Lippincott
Williams & Wilkins
=
•Clinical
Sleep Disorders
by Carney, Paul R. Berry, Richard B and Geyer, James D. Copyright 2005 by
Lippincott, Williams, and Wilkins
=
•Iber,
C; Ancoli-Israel, S; Chesson, A; Quan, SF for the
=
•Practice
Parameters for the Indications for Polysomnography and Related Procedures: =
An
Update for 2005 Kushida, et al, SLEEP 2005;28(4):499-521.
=
•Rapid-Onset
Obesity With Hypothalamic Dysfunction, Hypoventilation, and Autonomic
Dysregulation Presenting in Childhood, Ize-Ludlow, D, et al Pediatrics <=
/i>2007;120;e179-e188
=
•Butkov
N: Atlas of Clinical Polysomnography (vol 1).
=
•A
randomized study on the effect of weight loss on obstructive sleep apnea am=
ong
obese patients with type 2 diabetes, Foster, GD et al., Arch Intern Med.
2009;169(17):1619-1626
..
Polysomnography
Demystified