Главная » Библиотека сна

Practice Parameters for the Respiratory Indications for Polysomnography in Children

Practice Parameters for the Respiratory Indications for Polysomnography in Children

R. Nisha Aurora, MD1; Rochelle S. Zak, MD2; Anoop Karippot, MD3; Carin I. Lamm, MD4; Timothy I. Morgenthaler, MD5; Sanford H. Auerbach, MD6;

Sabin R. Bista, MD7; Kenneth R. Casey, MD8; Susmita Chowdhuri, MD9; David A. Kristo, MD10; Kannan Ramar, MD5

Background: There has been marked expansion in the literature and

practice of pediatric sleep medicine; however, no recent evidencebased

practice parameters have been reported. These practice parameters

are the first of 2 papers that assess indications for polysomnography

in children. This paper addresses indications for polysomnography

in children with suspected sleep related breathing disorders. These

recommendations were reviewed and approved by the Board of Directors

of the American Academy of Sleep Medicine.

Methods: A systematic review of the literature was performed, and the

American Academy of Neurology grading system was used to assess

the quality of evidence.

1. Polysomnography in children should be performed and interpreted

in accordance with the recommendations of the AASM Manual

for the Scoring of Sleep and Associated Events. (Standard)

2. Polysomnography is indicated when the clinical assessment suggests

the diagnosis of obstructive sleep apnea syndrome (OSAS)

in children. (Standard)

3. Children with mild OSAS preoperatively should have clinical evaluation

following adenotonsillectomy to assess for residual symptoms.

If there are residual symptoms of OSAS, polysomnography

should be performed. (Standard)

4. Polysomnography is indicated following adenotonsillectomy to

assess for residual OSAS in children with preoperative evidence

for moderate to severe OSAS, obesity, craniofacial anomalies

that obstruct the upper airway, and neurologic disorders (e.g.,

Down syndrome, Prader-Willi syndrome, and myelomeningocele).

(Standard)

5. Polysomnography is indicated for positive airway pressure (PAP) titration

in children with obstructive sleep apnea syndrome. (Standard)

6. Polysomnography is indicated when the clinical assessment suggests

the diagnosis of congenital central alveolar hypoventilation

syndrome or sleep related hypoventilation due to neuromuscular

disorders or chest wall deformities. It is indicated in selected

cases of primary sleep apnea of infancy. (Guideline)

7. Polysomnography is indicated when there is clinical evidence of a

sleep related breathing disorder in infants who have experienced

an apparent life-threatening event (ALTE). (Guideline)

8. Polysomnography is indicated in children being considered for

adenotonsillectomy to treat obstructive sleep apnea syndrome.

(Guideline)

9. Follow-up PSG in children on chronic PAP support is indicated

to determine whether pressure requirements have changed as a

result of the child’s growth and development, if symptoms recur

while on PAP, or if additional or alternate treatment is instituted.

(Guideline)

10. Polysomnography is indicated after treatment of children for

OSAS with rapid maxillary expansion to assess for the level of

residual disease and to determine whether additional treatment

is necessary. (Option)

11. Children with OSAS treated with an oral appliance should have

clinical follow-up and polysomnography to assess response to

treatment. (Option)

12. Polysomnography is indicated for noninvasive positive pressure

ventilation (NIPPV) titration in children with other sleep related

breathing disorders. (Option)

13. Children treated with mechanical ventilation may benefit from

periodic evaluation with polysomnography to adjust ventilator settings.

(Option)

14. Children treated with tracheostomy for sleep related breathing

disorders benefit from polysomnography as part of the evaluation

prior to decannulation. These children should be followed clinically

after decannulation to assess for recurrence of symptoms of

sleep related breathing disorders. (Option)

15. Polysomnography is indicated in the following respiratory disorders

only if there is a clinical suspicion for an accompanying

sleep related breathing disorder: chronic asthma, cystic fibrosis,

pulmonary hypertension, bronchopulmonary dysplasia, or chest

wall abnormality such as kyphoscoliosis. (Option)

16. Nap (abbreviated) polysomnography is not recommended for

the evaluation of obstructive sleep apnea syndrome in children.

(Option)

17. Children considered for treatment with supplemental oxygen do

not routinely require polysomnography for management of oxygen

therapy. (Option)

Conclusions: Current evidence in the field of pediatric sleep medicine

indicates that PSG has clinical utility in the diagnosis and management

of sleep related breathing disorders. The accurate diagnosis of SRBD

in the pediatric population is best accomplished by integration of polysomnographic

findings with clinical evaluation.

Keywords: Polysomnography, pediatric, indications, clinical utility,

sleep related breathing disorders, obstructive sleep apnea syndrome

Citation: Aurora RN; Zak RS; Karippot A; Lamm CI; Morgenthaler TI;

Auerbach SH; Bista SR; Casey KR; Chowdhuri S; Kristo DA; Ramar K.

Practice parameters for the respiratory indications for polysomnography

in children. SLEEP 2011;34(3):379-388.

Practice Parameters for the Respiratory Indications for Polysomnography in Children

R. Nisha Aurora, MD1; Rochelle S. Zak, MD2; Anoop Karippot, MD3; Carin I. Lamm, MD4; Timothy I. Morgenthaler, MD5; Sanford H. Auerbach, MD6;

Sabin R. Bista, MD7; Kenneth R. Casey, MD8; Susmita Chowdhuri, MD9; David A. Kristo, MD10; Kannan Ramar, MD5

Address correspondence to: Sharon L. Tracy, PhD, American Academy of

Sleep Medicine, 2510 North Frontage Road, Darien, IL 60561-1511; Tel:

(630) 737-9700; Fax: (630) 737-9790; E-mail: stracy@aasmnet.org

SLEEP, Vol. 34, No. 3, 2011 380 Practice Parameters—Aurora et al

In particular, it involves development of a list of specific indications

derived from the scientific evidence. Completion of rating

sheets that evaluated the appropriateness of these indications

was conducted in 2 rounds by members from both the SPC and

task force. Based on these ratings, indications were classified as

appropriate, uncertain, or inappropriate. Indications that were

classified as appropriate were used to develop these recommendations;

indications that were uncertain or inappropriate were

rejected.

The Board of Directors of the AASM approved these recommendations.

All members of the AASM Standards of Practice

Committee and Board of Directors completed detailed conflictof-

interest statements and were found to have no conflicts of

interest with regard to this subject.

These practice parameters define principles of practice that

should meet the needs of most patients in most situations. These

guidelines should not, however, be considered inclusive of all

proper methods of care or exclusive of other methods of care

reasonably directed to obtaining the same results. The ultimate

judgment regarding propriety of any specific care must be

made by the physician, in light of the individual circumstances

presented by the patient, available diagnostic tools, accessible

treatment options, and resources.

The AASM expects these guidelines to have an impact on

professional behavior, patient outcomes, and, possibly, health

care costs. These practice parameters reflect the state of knowledge

at the time of publication and will be reviewed, updated,

and revised as new information becomes available. This parameter

paper is referenced, where appropriate, using squarebracketed

numbers to the relevant sections and tables in the

accompanying review paper, or with additional references at the

end of this paper. For this paper, the Standards of Practice Committee

decided to use an evidence grading system developed by

the American Academy of Neurology (AAN) for assessment of

diagnostic tests. The system involves 4 tiers of evidence, with

Level 1 studies judged to have a low risk of bias and Level 4

studies judged to have a very high risk of bias. Table 1 describes

the essential features of the evidence grading system used by

the task force. Definitions of levels of recommendations used

by the AASM appear in Table 2.

A detailed evidence-based and consensus-based review of

PSG was conducted during development of the AASM Manual

for the Scoring of Sleep and Associated Events under the aegis

of the AASM Scoring Manual Steering Committee.7 This document

specifies the optimal equipment for PSG and standardizes

the scoring of events. The SPC considers this the standard of

practice, and therefore did not conduct a separate, independent

review for this practice parameter.

In the opinion of the task force, PSG is best tolerated by

the child and parent under the following conditions: (a) when

PSG is performed with the caretaker present; (b) when the

Assessment for sleep disorders in children has long relied

on a comprehensive history and physical exam. In certain

conditions, most commonly sleep related breathing disorders

(SRBD), polysomnography (PSG) was performed as an adjunctive

tool to aid in the diagnosis. PSG also has been used to evaluate

abnormal sleep related movements and behaviors as well

as part of the diagnostic assessment for narcolepsy. Because

PSG is relatively expensive, time consuming, and not consistently

applied by pediatric physicians, it is important to understand

its strengths, limitations, and clinical utility in children.

Over the past 30 years, pediatric sleep medicine has exponentially

advanced in terms of improved awareness of pediatric

sleep disorders and the development of many important technical

tools. The early data supporting the clinical utility of PSG

were limited because of inconsistency in polysomnographic

criteria for SRBDs. Clinical guidelines regarding indications

for pediatric PSG based on these early data were published by

professional organizations,1,2 but these older publications were

largely consensus-based due to a paucity of evidence-based data.

In 2007 the AASM commissioned a task force to review

the literature published on the indications for PSG in children.

Because the task force identified such a large number of publications,

it divided the project into 3 separate review papers:

(1) the respiratory indications for PSG; (2) the non-respiratory

indications for PSG; and (3) the indications for PSG in children

with attention deficit hyperactivity disorder (ADHD) or autistic

spectrum disorder (ASD). It should be noted that in 2009 the

SPC changed its grading system to the GRADE methodology,

redefining criteria for Standards, Guidelines, and Options to be

consistent with GRADE specifications.3 Because this project

began in 2007, the older grading process in use at that time was

used to grade the evidence.

This parameter paper focuses on the respiratory indications

for PSG. It is based on a comprehensive review of the literature

to evaluate the validity and reliability of PSG and to determine

its clinical utility for assessment and management of various

respiratory disorders. It highlights pediatric respiratory disorders

with a high prevalence of polysomnographic abnormalities

and addresses various treatment modalities such as surgery and

positive airway pressure.

The Standards of Practice Committee of the AASM, in conjunction

with specialists and other interested parties, developed

these practice parameters based on the accompanying review

paper.4 A task force of content experts was appointed by the

AASM in 2007 to review and grade evidence in the scientific

literature regarding the validity, reliability, and clinical utility

of PSG in pediatric sleep disorders. In most cases recommendations

are based on evidence from studies published in

the peer reviewed literature or on generally accepted patient

care strategies. When scientific data were absent, insufficient

or inconclusive, the Rand/UCLA Appropriateness Method was

used to develop consensus recommendations by identifying the

collective opinion of the SPC and task force. The Rand/UCLA

Appropriateness Method combines the best available scientific

evidence with the collective judgment of experts to yield statements

regarding the appropriateness of performing procedures.

SLEEP, Vol. 34, No. 3, 2011 381 Practice Parameters—Aurora et al

symptoms rather than for any individual parameter.13,24 Audio or

video recordings correlated with PSG respiratory parameters,

but 2 Level 211,47 and 2 Level 348,49 studies showed they were

not sufficient to establish a diagnosis of OSAS. Pediatric sleep

questionnaires were evaluated in 9 articles in children referred

for snoring, including 2 with Level 2 evidence,10,50 3 with Level

3 evidence,14,51 and 4 with Level 4 evidence.27,34,37,41 The 2 Level

2 studies showed low sensitivities for questionnaires to predict

polysomnographic evidence of OSAS with better specificities

but were still insufficient to differentiate primary snoring from

OSAS. Two of the 3 level 3 studies and all of the level 4 studies

showed insufficient correlation between sleep questionnaires

and PSGs.

The task force found that PSG in children is a reliable and

valid measure of the presence of OSAS. Test-retest reliability,

or consistency of results across multiple nights of polysomnographic

testing, was demonstrated in 1 Level 2,52 2 Level 3,18,53

and 1 Level 454 studies. There were no studies designed to test

interrater reliability for scoring PSGs in children. Test-retest validity

for PSG, or movement of various PSG parameters in the

parent and child have

been oriented to the sleep

laboratory in advance,

including, in some cases,

application of a limited

number of sensors to illustrate

the procedure to

the child; (c) when the

PSG technologist is experienced

and comfortable

in dealing with children

in the sleep laboratory

environment that is childfriendly;

and (d) when

the sleep specialist provides

specific guidance

and recommendations in

advance of the PSG with

regard to the child’s care

during the night.

Unattended testing outside

the sleep laboratory in

children has been used predominantly in research settings. There

is a paucity of research comparing it to traditional in-laboratory

attended sleep studies or other objective clinical outcomes, and

there are insufficient data upon which to base reliable clinical

recommendations for children at this time.

Obstructive sleep apnea syndrome should be diagnosed

based upon clinical and polysomnographic criteria. This parameter

is based on an extensive literature review conducted by the

Indications for PSG in Children task force.

The task force found that clinical evaluation alone does not

have sufficient sensitivity or specificity to establish a diagnosis

of OSAS. Clinical parameters such as history [4.2.1.1.1,

4.2.1.1.3, 4.2.1.1.4.1], physical examination [4.2.1.1.5], audio

or visual recordings [4.2.1.1.2], and standardized questionnaires

[4.2.1.1.3] did not consistently identify the presence or

absence of OSAS when compared with PSG. Snoring and other

nocturnal symptoms in 2 Level 1,8,9 4 Level 2,10-13 11 Level 3,14-

24 and 18 Level 425-42 studies showed inconsistent correlations

with respiratory parameters of PSG. Physical features of children

evaluated in 11 papers (2 Level 211,13; 3 Level 323,24,43; 6

Level 4)25,40,41,44-46 showed variable strengths of association with

respiratory PSG parameters with obesity demonstrating the

strongest association (see below). Polysomnographic parameters

correlated best with a combination of multiple signs and

Table 2—AASM levels of recommendations

Standard This is a generally accepted patient-care

strategy that reflects a high degree of clinical

certainty and generally implies the use of Level

1 evidence or overwhelming Level 2 evidence.

Guideline This is a patient-care strategy that reflects a

moderate degree of clinical certainty and implies

the use of Level 2 evidence or a consensus of

Level 3 evidence.

Option This is a patient-care strategy that reflects

uncertain clinical use and implies inconclusive or

conflicting evidence or conflicting expert opinion.

Adapted from Eddy6

Table 1—Levels of evidence5

1 Evidence provided by a prospective study in a broad spectrum of persons with the suspected condition,

using a reference (gold) standard for case definition, where test is applied in a blinded fashion, and

enabling the assessment of appropriate test of diagnostic accuracy. All persons undergoing the diagnostic test

have the presence or absence of the disease determined. Level 1 studies are judged to have a low risk of bias.

2 Evidence provided by a prospective study of a narrow spectrum of persons with the suspected condition,

or a well designed retrospective study of a broad spectrum of persons with an established condition (by

“gold standard”) compared to a broad spectrum of controls, where test is applied in a blinded evaluation,

and enabling the assessment of appropriate tests of diagnostic accuracy. Level 2 studies are judged to have a

moderate risk of bias.

3 Evidence provided by a retrospective study where either person with the established condition or controls are

of a narrow spectrum, and where the reference standard, if not objective, is applied by someone other

than the person that performed (interpreted) the test. Level 3 studies are judged to have a moderate to

high risk of bias.

4 Any study design where test is not applied in an independent evaluation or evidence is provided by

expert opinion alone or in descriptive case series without controls. There is no blinding or there may

be inadequate blinding. The spectrum of persons tested may be broad or narrow. Level 4 studies are

judged to have a very high risk of bias.

SLEEP, Vol. 34, No. 3, 2011 382 Practice Parameters—Aurora et al

also indicated for the diagnosis of sleep related hypoventilation

due to neuromuscular or chest wall deformities and congenital

central alveolar hypoventilation syndrome and in selected cases

of primary sleep apnea of infancy, with the realization that

some of these patients will be in a NICU and not have access

to polysomnography; these conclusions are based less on evidence

than on a consensus of expert opinion. Children should

be diagnosed with SRBDs by an integration of clinical evaluation

and PSG. In addition, certain clinical conditions, as delineated

above, are associated with a high prevalence of SRBD.

These patients should be screened for symptoms and signs of

SRBD and undergo PSG if present.

Three Level 4 studies74,105,106 in children demonstrated that

nap PSG is not as reliable as overnight PSG for identifying

SRBD [4.2.1.3] and underestimated the prevalence and severity

of SRBD, with sensitivities ranging from 69% to 75% and

specificities from 60% to 100%. This recommendation is based

on these limited studies and collective expert opinion using the

Rand/UCLA Appropriateness Method.

Four Level 2,52,107-109 8 Level 3,22,110-116 and 3 Level 4 studies35,117,118

[4.2.4.4, 4.2.4.6] showed subtle, nonspecific PSG

abnormalities in some infants who had experienced an ALTE.

The PSG findings were not predictive of recurrence of ALTE.

Studies of infants who eventually succumbed to sudden infant

death syndrome (SIDS) (4 Level 3)22,111,113,114 demonstrated PSG

abnormalities that were neither sufficiently distinctive nor predictive

to support routine use of PSG for children at risk for

SIDS. Finally, 2 low level studies109,116showed that infants who

had experienced an ALTE may be at increased risk to develop

SRBD. These infants, however, had other risk factors for

SRBD, such as a family history of SRBD or facial dysmorphology.

Clinical suspicion of SRBD in a patient with ALTE should

prompt consideration of PSG.

Adenotonsillectomy (AT) is commonly performed as a firstline

treatment of OSAS in children, yet the diagnosis of OSAS

is often based on clinical parameters alone.119 The task force

reviewed the literature to determine the clinical utility of PSG

to confirm the diagnosis of OSAS prior to AT. Whether or not

a PSG prior to AT has clinical utility is important for some of

the following issues (see review paper for a more complete

discussion):

(1) AT is a surgical procedure with a small risk of hemorrhage,

infection, upper airway compromise, and pain, and

should only be performed if necessary.

expected direction after a therapeutic intervention for OSAS,

was robust as demonstrated in all 45 studies [4.2.1.1.10].

Convergent validity, or whether PSG and an independent

measure both change consistently in the presence of OSAS,

was extensively evaluated, including objective [4.2.1.1.4.2]

and subjective sleepiness [4.2.1.1.4.1], radiographic evaluation

[4.2.1.1.6], neurocognitive and psychological evaluation

[4.2.1.1.7], blood pressure [4.2.1.1.8], and quality of life measures

[4.2.1.1.9]. Some, but not all, of these measures demonstrated

convergent validity with PSG.

Additionally, there was clinical consensus by experts that

the PSG is necessary to diagnose congenital central alveolar

hypoventilation syndrome, sleep related hypoventilation due

to chest wall disorders, and sleep related hypoventilations due

to neuromuscular disorder, for which there was also low level

evidence.55-63 There was also clinical consensus by experts that

PSG is necessary in selected cases to diagnose primary sleep

apnea of infancy when other medical disorders have been ruled

out. Patients with CCHS and primary sleep apnea of infancy

often present as neonates in the Neonatal Intensive Care Unit,

where PSG may not be available. These recommendations are

consistent with the recommendations outlined in the ICSD-2

Manual.64

Lastly, the task force identified certain conditions associated

with an elevated prevalence of SRBD including OSAS. The

clinician should consider PSG in children with the following

conditions if there is even the slightest suspicion of SRBD. A

high prevalence of SRBD has been reported in children with

obesity13,65-71 (13%67 to 78%65) [4.2.2.1], Down syndrome37,72-74

(57%37 to 100%74) ([4.2.2.8.1.1], Prader-Willi syndrome75-80

(93%75) [4.2.2.8.1.2], neuromuscular disorders55-63 (53% in

one study of children with Duchenne Muscular Dystrophy56)

[4.2.2.8.4], Chiari malformations and myelomeningocele81-84

(60% in one series of children with CM84) [4.2.2.8.4], and craniofacial

anomalies that obstruct the upper airway32,38,85-87 (48%

in children with achondroplasia,85 76% in a group of infants

with Pierre Robin sequence,86 and 50% to 91% in 2 small series

of craniofacial dysostoses32,87) [4.2.2.8.2]. Obesity was identified

as an independent risk factor for having SRBD. Furthermore,

SRBD was identified as an independent risk factor for

hypertension,20,88-96 suggesting that the clinician should evaluate

children who present with hypertension for the possibility of

underlying SRBD.

Children in the following categories have an intermediate

level of risk for OSAS: those with history of prematurity25,97-99

(prevalence of OSAS of 7.3%)97 [4.2.2.2], African American

race34,100-102 (conflicting data) [4.2.2.3], family history of

SRBD102,103 (sparse data) [4.2.2.4], and allergic rhinitis101,102,104

(not well defined) [4.2.2.5]. Children in these intermediate risk

groups ought to be queried for signs or symptoms of SRBDs,

and should undergo PSG if present.

Overall, the above data on SRBD prevalence and disease

associations included 1 Level 1,65 6 Level 2,13,86,88-90,100 17

Level 3,20,57,60,61,66,67,70,76,84,85,91-93,95,97,98,102 and 32 Level 4 studies.

25,32,34,37,38,55,56,58,59,62,63,68,69,71-75,77-83,87,94,96,99,101,103,104

In summary, high quality data demonstrate that PSG is indicated

for the diagnosis of OSAS in children both because clinical

parameters alone lack reliability to correctly classify disease

and because PSG is a valid and reliable clinical tool. PSG is

SLEEP, Vol. 34, No. 3, 2011 383 Practice Parameters—Aurora et al

lowing AT are better when PSG is routinely performed prior to

AT. The evidence taken as an aggregate indicates that preoperative

PSG has strong clinical utility prior to AT for treatment of

OSAS.

This recommendation is a logical extension of parameter

3.2.1. There are Level 2 and 3 studies documenting a high

prevalence of residual OSAS after AT. In 1 Level 2 study, residual

OSAS was detected in as many as 75% of non-obese

children,131 and in 1 Level 3 study,132 75% of a combined obese

and non-obese pediatric population had residual OSAS following

AT for OSAS. Although many patients had some degree

of residual obstruction, most had a considerable reduction in

the severity of the OSAS (postoperative results in the 2 studies

above showed 90%131 and 71%132 of the children had a postoperative

OAHI < 5). In 1 Level 2 study,130 which excluded

obese children, the rate of residual polysomnographic evidence

of OSAS was 10% to 28% (depending on the criteria used). Another

Level 2 study found that OSAS can recur 1 year postoperatively,

so patients should be reevaluated periodically.129 Given

the high prevalence of residual obstruction, clinicians should

evaluate children postoperatively for symptoms of OSAS and if

present, a PSG should be performed.

Incomplete resolution of OSAS was more common in children

with high preoperative AHI (exact cut-off not established

as norms and statistical methods varied from study to study)

(2 Level 2,129,130 1 Level 3132), obesity (2 Level 2,129,130 1 Level

3,132 3 Level 4101,133,134), craniofacial anomalies that obstruct the

upper airway (1 Level 3135 and 1 Level 438), and neurologic disorders

such as myelomeningocele (1 level 481) and Down syndrome

(1 Level 442), while absence of obesity and craniofacial

abnormalities (2 Level 3,132,136 1 Level 4137) and lower AHI (2

Level 2,129,130 1 Level 3132) favored a good outcome. Children

with neuromuscular disorders can have a mix of both obstructive

and central sleep apnea and require PSG following AT to

determine the need for CPAP or NIPPV as demonstrated in 2

level 481,83 studies. This recommendation is a logical extension

of 3.2.1. These populations are at increased risk for having residual

SRBD and are often difficult to reliably evaluate clinically.

(2) Clinical parameters may be unreliable for predicting

OSAS.

(3) Children with certain medical disorders are at higher surgical

risk (e.g., sickle cell anemia, HIV, coagulopathies, congenital

heart disease).

(4) Children with severe OSAS have a higher risk for certain

postoperative complications including respiratory compromise.

The task force identified 30 papers pertaining to the clinical

utility of PSG prior to AT. Twenty-three of these papers were

referenced previously as they demonstrated test-retest validity

of PSG in the setting of AT.

First the task force reviewed the literature to determine

whether PSG prior to AT correlated with symptoms or physical

features of SRBD. As detailed above, history and physical

examination were not always reliable predictors of SRBD in

children [4.2.1.1.1, 4.2.1.1.3, 4.2.1.1.4.1, 4.2.1.1.3, 4.2.1.1.5].

Three Level 3 papers18,23,43 showed the limitations of history and

physical examination for diagnosing OSAS in children specifically

scheduled for AT. In 1 Level 211 and 2 Level 426,41 studies,

the authors concluded that a negative PSG did not rule out

clinically significant SRBD that may respond to AT; however,

all 3 demonstrate that as one changes the cut-off of a polysomnographic

definition of OSAS to be more in-line with the recommendation

in the ICSD-2, the percentage of PSG-positive

subjects increases, improving the clinical utility of PSG.

To further establish clinical utility of PSG prior to AT, the

task force reviewed the literature to determine whether PSG

identified those children likely to develop perioperative complications.

Ten papers addressed the clinical utility of PSG for

assessment of perioperative risk of respiratory complications

related to AT in children. One Level 2,120 1 Level 3,121 and 4

Level 4 studies122-125 showed a positive correlation between

PSG measures of OSAS severity and postoperative respiratory

complications. In 1 study, respiratory complications occurred

as late as the first postoperative night124 and in another, as long

as 14 hours125after surgery. In 2 Level 4 studies,126,127 children

without significant comorbid diseases who had no or mild abnormalities

on preoperative PSG were likely to have an uncomplicated

postoperative course. Although in 2 Level 4 studies30,128

preoperative PSG did not identify those who later developed

perioperative complications, the majority of the evidence supports

the clinical utility of preoperative PSG for predicting

which children are at risk for postoperative respiratory compromise

or prolonged stay and will need postoperative monitoring.

Lastly, to establish clinical utility of PSG prior to AT the task

force examined whether the PSG could predict which children

were more likely to have residual OSAS following surgery.

Two Level 2 studies129,130 demonstrated that children with higher

preoperative AHIs had a greater likelihood of residual OSAS

following AT.

In summary, as delineated in practice parameter 3.2.1, PSG

is indicated for the diagnosis of SRBD in children. Logically

it follows that PSG is indicated to diagnose OSAS prior to AT

when OSAS is the primary indication for AT. There are data

indicating that history and physical examination alone have

limitations for predicting OSAS and that the preoperative AHI

can guide the physician in perioperative and postoperative

management. At this time, the task force was unable to identify

prospective studies addressing whether clinical outcomes folSLEEP,

Vol. 34, No. 3, 2011 384 Practice Parameters—Aurora et al

determine the timing and frequency of follow-up PSG. This

recommendation is a generally accepted patient care strategy.

PSG is useful for assessing optimal ventilator settings since

respiration worsens during sleep and wake ventilator settings

may not be adequate for sleep. There were no studies addressing

the use of PSG in the management of ventilator settings that met

inclusion criteria. This recommendation is based on consensus

expert opinion using the Rand/UCLA Appropriateness Method.

Nocturnal oximetry is generally sufficient to assess adequate

oxygenation. However, PSG can be useful for titrating supplemental

oxygen in patients who may hypoventilate and may be

at risk for developing central apneas or hypercarbia with supplemental

oxygen. There were no studies addressing this topic

that met inclusion criteria. This recommendation is based on

consensus expert opinion using the Rand/UCLA Appropriateness

Method.

One Level 3 study147 demonstrated clinical usefulness of

PSG as part of the evaluation to assess readiness for decannulation

in children with long-term tracheostomy [4.4.4]. This

recommendation is based on this study and on consensus expert

opinion using the Rand/UCLA Appropriateness Method.

In children with asthma, prevalence studies showed conflicting

low level evidence for increased risk of SRBD

([4.3.1.1]102,148). The data were too sparse to assess the clinical

utility of PSG in children with cystic fibrosis, although 1 Level

4 study149 demonstrated clinical utility of PSG to initiate and

titrate noninvasive ventilation [4.3.1.2]. There were no studies

addressing the clinical utility of PSG in children with unexplained

pulmonary hypertension [4.2.2.7] or bronchopulmonary

dysplasia [4.3.1.3]. Finally, a low level study150 of children

with kyphoscoliosis who could not undergo PFTs did not find

statistically significant evidence that preoperative polysomnography

could predict those at risk for prolonged postoperative

ventilation after scoliosis repair [4.3.2.1]. As with all children,

those with asthma, cystic fibrosis, unexplained pulmonary hyto

This is a rarely performed treatment for OSAS in children

with only limited data regarding efficacy. Two low level studies

evaluated children following rapid maxillary expansion

(RME). Significant residual disease remained after RME in 1

Level 3138 and 1 Level 4 study139 [4.4.3]. PSG was useful to

establish residual disease and the efficacy of staged treatment.

Given the paucity of evidence demonstrating the efficacy for

this new procedure, it is recommended that children treated

with rapid maxillary expansion have follow-up PSG. This recommendation

is based on consensus expert opinion using the

Rand/UCLA Appropriateness Method.

This is a relatively new treatment for OSAS in children with

limited studies available. One Level 286 and 1 Level 4 study40

used PSG to demonstrate clinical efficacy of dental devices in

children [4.4.3]. Given the paucity of evidence demonstrating

the efficacy for this new procedure, it is recommended that children

treated with a dental device have follow-up PSG. This recommendation

is based on consensus expert opinion using the

Rand/UCLA Appropriateness Method.

PSG was shown to be a valid measure to assess response to

therapy for SRBD. There were insufficient data on autotitration

PAP (APAP) in children to assess this mode of therapy. Four

papers (1 Level 2,140 3 Level 4141-143) demonstrated that PSG was

useful to determine optimal PAP settings in children and infants.

It was particularly important for children at risk for multiple

types of SRBD, such as those with neurologic disorders.

Five studies (1 Level 357 and 4 Level 456,144-146) evaluated or described

the use of PSG for titration of nocturnal intermittent

positive pressure ventilation (NIPPV) in children with SRBD

and neuromuscular disorders. These studies demonstrated either

clinical or physiologic improvement with NIPPV that was

titrated using PSG.

Growth and development should be considered in children

on chronic PAP treatment as symptoms may resolve or worsen

with significant changes in the child’s morphology. One Level 4

study146 [4.4.2] demonstrated that many children required pressure

changes (66%) in PAP level, even in the absence of interventions,

suggesting that PAP requirements might change with

growth and development. Clinical judgment should be used to

SLEEP, Vol. 34, No. 3, 2011 385 Practice Parameters—Aurora et al

participated in research supported by Sepracor and participated

in a speaking engagement for Forest Pharmaceuticals. Dr. Karippot

has received research support from Wyeth and is Medical

Director of Akane Sleep Solutions, Inc., a sleep disorders clinic

and laboratory. The other authors have indicated no financial

conflicts of interest.

1. American Thoracic Society. Standards and Indications for Cardiopulmonary

Studies in Children. Am J Respir Crit Care Med 1996;153:866-78.

2. American Academy of Pediatrics. Clinical practice guideline: Diagnosis

and management of childhood obstructive sleep apnea syndrome. Pediatrics

2002;109:704-12.

3. Aurora RN, Morgenthaler T. On the Goodness of Recommendations: The

Changing Face of Practice Parameters. Sleep In press.

4. Wise MS, Nichols CD, Grigg-Damberger MM, et al. Respiratory Indications

for Polysomnography in Children: An evidence-based review. Sleep

2010;TBD:TBD.

5. Edlund W, Gronseth G, So Y, Franklin G. Clinical Practice Guideline Process

Manual. 4th ed. St. Paul, MN: American Academy of Neurology,

2005.

6. Eddy DM, American College of P. A manual for assessing health practices

& designing practice policies : the explicit approach. Philadelphia, Pa.:

American College of Physicians, 1992.

7. Iber C, Ancoli-Israel S, Chesson A, Quan SF, for the American Academy

of Sleep Medicine. The AASM Manual for the Scoring of Sleep and Associated

Events: Rules, Terminology and Technical Specifications, 1st ed.

Westchester, IL: American Academy of Sleep Medicine, 2007.

8. Masters IB, Harvey JM, Wales PD, O’Callaghan MJ, Harris MA. Clinical

versus polysomnographic profiles in children with obstructive sleep

apnoea. J Paediatr Child Health 1999;35:49-54.

9. Chervin RD, Weatherly RA, Ruzicka DL, et al. Subjective sleepiness and

polysomnographic correlates in children scheduled for adenotonsillectomy

vs other surgical care. Sleep 2006;29:495-503.

10. Goodwin JL, Kaemingk KL, Fregosi RF, et al. Parasomnias and sleep

disordered breathing in Caucasian and Hispanic children - the Tucson

children’s assessment of sleep apnea study. BMC Med 2004;2:14.

11. Goldstein NA, Pugazhendhi V, Rao SM, et al. Clinical assessment of pediatric

obstructive sleep apnea. Pediatrics 2004;114:33-43.

12. Goodwin JL, Kaemingk KL, Fregosi RF, et al. Clinical outcomes associated

with sleep-disordered breathing in Caucasian and Hispanic children-

-the Tucson Children’s Assessment of Sleep Apnea study (TuCASA).

Sleep 2003;26:587-91.

13. Wing YK, Hui SH, Pak WM, et al. A controlled study of sleep related

disordered breathing in obese children. Arch Dis Child 2003;88:1043-7.

14. Brouillette R, Hanson D, David R, et al. A diagnostic approach to suspected

obstructive sleep apnea in children. The Journal of Pediatrics

1984;105:10-4.

15. Carroll JL, McColley SA, Marcus CL, Curtis S, Loughlin GM. Inability

of clinical history to distinguish primary snoring from obstructive sleep

apnea syndrome in children. Chest 1995;108:610-8.

16. Goldbart AD, Krishna J, Li RC, Serpero LD, Gozal D. Inflammatory mediators

in exhaled breath condensate of children with obstructive sleep

apnea syndrome. Chest 2006;130:143-8.

17. Kaditis AG, Finder J, Alexopoulos EI, et al. Sleep-disordered breathing in

3,680 Greek children. Pediatr Pulmonol 2004;37:499-509.

18. Nieminen P, Tolonen U, Lopponen H. Snoring and obstructive sleep apnea

in children: a 6-month follow-up study. Arch Otolaryngol Head Neck

Surg 2000;126:481-6.

19. Pagel JF, Snyder S, Dawson D. Obstructive sleep apnea in sleepy pediatric

psychiatry clinic patients: polysomnographic and clinical correlates.

Sleep Breath 2004;8:125-31.

20. Reade EP, Whaley C, Lin JJ, McKenney DW, Lee D, Perkin R. Hypopnea

in pediatric patients with obesity hypertension. Pediatr Nephrol

2004;19:1014-20.

21. Rimell FL, Rosen G, Garcia J. Full polysomnographic evaluation of the

infant airway. Arch Otolaryngol Head Neck Surg 1998;124:773-6.

22. Sawaguchi T, Franco P, Kato I, et al. From epidemiology to physiology

and pathology: apnea and arousal deficient theories in sudden infant death

syndrome (SIDS)--with particular reference to hypoxic brainstem gliosis.

Forensic Sci Int 2002;130 Suppl:S21-9.

pertension, bronchopulmonary dysplasia, kyphoscoliosis, or

chest wall deformity for whom there is a clinical suspicion of a

SRBD should undergo PSG.

Improvement in diagnostic accuracy and clinical utility of

PSG for evaluation of SRBD in children will require investigations

that address a wide range of pediatric populations using

adequate sample sizes and standardized methodology. Study

designs should account for changes in respiratory physiology

by age and maturation and should avoid bias through inclusion

of a broad spectrum of subjects with a range of severity from

normal to severe disease. Development of definitive and wellvalidated

normative and pathological respiratory PSG values

will help refine diagnosis and possibly treatment options in

children with SRBD. Improved research design and methodology

will also improve understanding of the earliest forms of

SRBD and the natural history of SRBD in children.

There is an urgent need for research clarifying the clinical utility

of polysomnography. For example, comparison of validated

and relevant outcomes in patients managed with and without

PSG would provide the most compelling evidence to evaluate

the value of PSG in managing children with suspected SRBDs.

Findings indicate that PSG may be particularly useful in the

evaluation of children with chronic health conditions such as obesity,

metabolic syndrome, overt or evolving hypertension, and

other conditions associated with cardiovascular risk. There is a

need for further investigation of SRBD in children with neurodevelopmental

and neuromuscular disorders, sickle cell anemia,

craniofacial disorders, and certain infants who experience ALTEs.

The clinical utility and cost effectiveness of testing outside

the sleep laboratory for certain groups of children with suspected

SRBD needs further investigation. Preliminary evidence

suggests that efforts to make the sleep laboratory experience

more child-friendly will improve the quality of data collected

as well as patient and family satisfaction.

Pediatric sleep medicine is a complex, dynamic, and multidisciplinary

field, and the sleep specialist involved with evaluation

and management of children faces an evolving landscape.

The medical literature regarding pediatric PSG is expanding

exponentially, and recording techniques and methods for digital

analysis are changing at a rapid pace. Superimposed on these

dynamic changes is the challenge of characterizing respiratory

sleep disorders and the impact of SRBD on behavior and cognition

in the developing child. Performance of PSG using standardized

and developmentally appropriate methods has strong

clinical utility in the diagnosis and management of SRBD in

children. Accurate diagnosis and management of SRBD in children

is best accomplished through careful integration of polysomnographic

findings with the clinical evaluation.

The committee would like to thank Sharon Tracy, PhD and

Christine Stepanski, MS for their efforts in the development of

this manuscript.

This was not an industry supported study. Dr. Morgenthaler

has received research support from ResMed. Dr. Auerbach has

SLEEP, Vol. 34, No. 3, 2011 386 Practice Parameters—Aurora et al

49. Jacob SV, Morielli A, Mograss MA, Ducharme FM, Schloss MD, Brouillette

RT. Home testing for pediatric obstructive sleep apnea syndrome secondary

to adenotonsillar hypertrophy. Pediatr Pulmonol 1995;20:241-52.

50. Chau KW, Ng DK, Kwok KL, et al. Application of videotape in the screening

of obstructive sleep apnea in children. Sleep Med 2008;9:442-5.

51. Chervin RD, Weatherly RA, Garetz SL, et al. Pediatric sleep questionnaire:

prediction of sleep apnea and outcomes. Arch Otolaryngol Head

Neck Surg 2007;133:216-22.

52. Rebuffat E, Groswasser J, Kelmanson I, Sottiaux M, Kahn A. Polygraphic

evaluation of night-to-night variability in sleep characteristics and apneas

in infants. Sleep 1994;17:329-32.

53. Katz ES, Greene MG, Carson KA, et al. Night-to-night variability of

polysomnography in children with suspected obstructive sleep apnea. J

Pediatr 2002;140:589-94.

54. Li AM, Wing YK, Cheung A, et al. Is a 2-night polysomnographic

study necessary in childhood sleep-related disordered breathing? Chest

2004;126:1467-72.

55. Smith PE, Calverley PM, Edwards RH. Hypoxemia during sleep in Duchenne

muscular dystrophy. Am Rev Resp Dis 1988;137:884-8.

56. Suresh S, Wales P, Dakin C, Harris MA, Cooper DG. Sleep-related

breathing disorder in Duchenne muscular dystrophy: disease spectrum in

the paediatric population. J Paediatr Child Health 2005;41:500-3.

57. Mellies U, Dohna-Schwake C, Stehling F, Voit T. Sleep disordered breathing

in spinal muscular atrophy. Neuromuscul Disord 2004;14:797-803.

58. Quera Salva MA, Blumen M, Jacquette A, et al. Sleep disorders in

childhood-onset myotonic dystrophy type 1. Neuromuscul Disord

2006;16:564-70.

59. Santamaria F, V. AM, Parenti G, et al. Upper airway obstructive disease

in mucopolysaccharidoses: polysomnography, computed tomography and

nasal endoscopy findings. J Inherit Metab Dis 2007;30:743-9.

60. McGrath-Morrow SA, Sterni LM, McGinley B, Lefton-Grief MA, Rosquist

K, Lederman H. Polysomnographic values in adolescents with ataxia

telangiectasia. Pediatr Pulmonology 2008;43:674-9.

61. Khan Y, Heckmatt J. Obstructive apnoeas in Duchenne muscular dystrophy.

Thorax 1994;49:157-61.

62. Barbe F, Quera-Salva MA, McCann C, et al. Sleep-related respiratory

disturbances in patients with Duchenne muscular dystrophy. Eur Respir

J 1994;7:1403-8.

63. Kerr S, Kohrman M. Polysomnographic abnormalities in Duchenne Muscular

Dystrophy. J Child Neurol 1994;9:332-4.

64. American Academy of Sleep Medicine. International classification of

sleep disorders, 2nd ed.: Diagnositic and coding manual. Westchester, IL:

American Academy of Sleep Medicine, 2005.

65. Xu Z, Jiaqing A, Yuchan L, Shen K. A case-control study of obstructive

sleep apnea-hypopnea syndrome in obese and nonobese chinese children.

Chest 2008;133:684-9.

66. Kohler M, Lushington K, Couper R, et al. Obesity and risk of sleep related

upper airway obstruction in Caucasian children. J Clin Sleep Med

2008;4:129-36.

67. Beebe DW, Lewin D, Zeller M, et al. Sleep in overweight adolescents:

Shorter sleep, poorer sleep quality, sleepiness, and sleep-disordered

breathing. J Pediatr Psychol 2007;32:69-79.

68. Marcus CL, Curtis S, Koerner CB, Joffe A, Serwint JR, Loughlin GM.

Evaluation of pulmonary function and polysomnography in obese children

and adolescents. Pediatr Pulmonol 1996;21:176-83.

69. McKenzie SA, Bhattacharya A, Sureshkumar R, et al. Which obese children

should have a sleep study? Respir Med 2008;102:1581-5.

70. Chay OM, Goh A, Abisheganaden J, et al. Obstructive sleep apnea syndrome

in obese Singapore children. Pediatr Pulmonol 2000;29:284-90.

71. Kalra M, Inge T, Garcia V, et al. Obstructive sleep apnea in extremely

overweight adolescents undergoing bariatric surgery. Obes Res

2005;13:1175-9.

72. Dyken ME, Lin-Dyken DC, Poulton S, Zimmerman MB, Sedars E. Prospective

polysomnographic analysis of obstructive sleep apnea in down

syndrome. Arch Pediatr Adolesc Med 2003;157:655-60.

73. Levanon A, Tarasiuk A, Tal A. Sleep characteristics in children with

Down syndrome. J Pediatr 1999;134:755-60.

74. Marcus CL, Keens TG, Bautista DB, von Pechmann WS, Davidson Ward

SL. Obstructive sleep apnea in children with Down syndrome. Pediatrics

1991;88:132-9.

75. Lin HY, Lin SP, Lin CC, et al. Polysomnographic characteristics in patients

with Prader-Willi syndrome. Pediatr Pulmonology 2007;42:881-7.

23. Wang RC, Elkins TP, Keech D, Wauquier A, Hubbard D. Accuracy of

clinical evaluation in pediatric obstructive sleep apnea. Otolaryngol Head

Neck Surg 1998;118:69-73.

24. Xu Z, Cheuk DK, Lee SL. Clinical evaluation in predicting childhood

obstructive sleep apnea. Chest 2006;130:1765-71.

25. Greenfeld M, Tauman R, DeRowe A, Sivan Y. Obstructive sleep apnea

syndrome due to adenotonsillar hypertrophy in infants. Int J Pediatr Otorhinolaryngol

2003;67:1055-60.

26. Guilleminault C, Winkle R, Korobkin R, Simmons B. Children and nocturnal

snoring: evaluation of the effects of sleep related respiratory resistive

load and daytime functioning. Eur J Pediatr 1982;139:165-71.

27. Mallory GB, Jr., Fiser DH, Jackson R. Sleep-associated breathing disorders

in morbidly obese children and adolescents. J Pediatr 1989;115:892-7.

28. Marcus CL, Hamer A, Loughlin GM. Natural history of primary snoring

in children. Pediatr Pulmonol 1998;26:6-11.

29. Nanaware SK, Gothi D, Joshi JM. Sleep apnea. Indian J Pediatr

2006;73:597-601.

30. Pang KP, Balakrishnan A. Paediatric obstructive sleep apnoea: is a polysomnogram

always necessary? J Laryngol Otol 2004;118:275-8.

31. Pavone M, Paglietti MG, Petrone A, Crino A, De Vincentiis GC, Cutrera

R. Adenotonsillectomy for obstructive sleep apnea in children with Prader-

Willi syndrome. Pediatr Pulmonol 2006;41:74-9.

32. Pijpers M, Poels PJ, Vaandrager JM, et al. Undiagnosed obstructive sleep

apnea syndrome in children with syndromal craniofacial synostosis. J

Craniofac Surg 2004;15:670-4.

33. Preutthipan A, Suwanjutha S, Chantarojanasiri T. Obstructive sleep apnea

syndrome in Thai children diagnosed by polysomnography. Southeast

Asian J Trop Med Public Health 1997;28:62-8.

34. Rosen CL. Clinical features of obstructive sleep apnea hypoventilation

syndrome in otherwise healthy children. Pediatr Pulmonol 1999;27:403-9.

35. Rosen CL, Frost JD, Jr., Harrison GM. Infant apnea: polygraphic studies

and follow-up monitoring. Pediatrics 1983;71:731-6.

36. Sanchez-Armengol A, Fuentes-Pradera MA, Capote-Gil F, et al. Sleeprelated

breathing disorders in adolescents aged 12 to 16 years : clinical

and polygraphic findings. Chest 2001;119:1393-400.

37. Shott SR, Amin R, Chini B, Heubi C, Hotze S, Akers R. Obstructive sleep

apnea: Should all children with Down syndrome be tested? Arch Otolaryngol

Head Neck Surg 2006;132:432-6.

38. Sisk EA, Heatley DG, Borowski BJ, Leverson GE, Pauli RM. Obstructive

sleep apnea in children with achondroplasia: surgical and anesthetic

considerations. Otolaryngol Head Neck Surg 1999;120:248-54.

39. Southall DP, Talbert DG, Johnson P, et al. Prolonged expiratory apnoea: a

disorder resulting in episodes of severe arterial hypoxaemia in infants and

young children. Lancet 1985;2:571-7.

40. Villa MP, Bernkopf E, Pagani J, Broia V, Montesano M, Ronchetti R.

Randomized controlled study of an oral jaw-positioning appliance for the

treatment of obstructive sleep apnea in children with malocclusion. Am J

Respir Crit Care Med 2002;165:123-7.

41. Weatherly RA, Ruzicka DL, Marriott DJ, Chervin RD. Polysomnography

in children scheduled for adenotonsillectomy. Otolaryngol Head Neck

Surg 2004;131:727-31.

42. Wiet GJ, Bower C, Seibert R, Griebel M. Surgical correction of obstructive

sleep apnea in the complicated pediatric patient documented by polysomnography.

Int J Pediatr Otorhinolaryngol 1997;41:133-43.

43. Shatz A. Indications and outcomes of adenoidectomy in infancy. Ann Otol

Rhinol Laryngol 2004;113:835-8.

44. Lam YY, Chan EYT, Ng DK, et al. The correlation among obesity, apneahypopnea

index, and tonsil size in children. Chest 2006;130:1751-6.

45. Tauman R, O’Brien LM, Ivanenko A, Gozal D. Obesity rather than severity

of sleep-disordered breathing as the major determinant of insulin

resistance and altered lipidemia in snoring children. Pediatrics

2005;116:e66-73.

46. Zhang XW, Li Y, Zhou F, Guo CK, Huang ZT. Comparison of polygraphic

parameters in children with adenotonsillar hypertrophy with

vs without obstructive sleep apnea. Arch Otolaryngol Head Neck Surg

2007;133:122-6.

47. Lamm C, Mandeli J, Kattan M. Evaluation of home audiotapes as an abbreviated

test for obstructive sleep apnea syndrome (OSAS) in children.

Pediatr Pulmonol 1999;27:267-72.

48. Sivan Y, Kornecki A, Schonfeld T. Screening obstructive sleep apnoea

syndrome by home videotape recording in children. Eur Respir J

1996;9:2127-31.

SLEEP, Vol. 34, No. 3, 2011 387 Practice Parameters—Aurora et al

100. Stepanski E, Zayyad A, Nigro C, Lopata M, Basner R. Sleep-disordered

breathing in a predominantly African-American pediatric population. J

Sleep Res 1999;8:65-70.

101. Morton S, Rosen C, Larkin E, Tishler P, Aylor J, Redline S. Predictors of

sleep-disordered breathing in children with a history of tonsillectomy and/

or adenoidectomy. Sleep 2001;24:823-9.

102. Redline S, Tishler P, Schluchter M, Aylor J, Clark K, Graham G. Risk Factors

for Sleep-disordered Breathing in Children. Am J Respir Crit Care

Med 1999;159:1527-32.

103. Ovchinsky A, Rao M, Lotwin I, Goldstein NA. The familial aggregation

of pediatric obstructive sleep apnea syndrome. Arch Otolaryngol Head

Neck Surg 2002;128:815-8.

104. McColley SA, Carroll J, Curtis S, Loughlin GM, Sampson HA. High

Prevalence of Allergic Sensitization in Children with Habitual Snoring

and Obstructive Sleep Apnea. Chest 1997;111:170-3.

105. Marcus CL, Keens TG, Davidson Ward SL. Comparison of nap and overnight

polysomnography in childr