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S3 Guideline

Somnologie 2017 · 21:290–301https://doi.org/10.1007/s11818-017-0136-2Published online: 7 November 2017© The Author(s) 2017. This article is an openaccess publication.

Geert Mayer1 · Michael Arzt2 · Bert Braumann3 · Joachim H. Ficker4 · Ingo Fietze5 ·Helmut Frohnhofen6 · Wolfgang Galetke3 · Joachim T. Maurer7 · Maritta Orth7 ·Thomas Penzel5 · Hans Pistner8 · Winfried Randerath9 · Martin Rösslein10 ·Helmut Sitter11 · Boris A. Stuck11

1 Schwalmstadt-Treysa, Deutschland2 Regensburg, Deutschland3 Köln, Deutschland4Nürnberg, Deutschland5 Berlin, Deutschland6 Essen, Deutschland7Mannheim, Deutschland8 Erfurt, Deutschland9 Solingen, Deutschland10 Freiburg, Deutschland11Marburg, Deutschland

German S3 GuidelineNonrestorative Sleep/SleepDisorders, chapter “Sleep-Related Breathing Disorders inAdults,” short versionGerman Sleep Society (DeutscheGesellschaft für Schlafforschung undSchlafmedizin, DGSM)

Managing Editor: Dr. rer. nat. Martina Bögel,Hamburg

This is an English translation of the pub-lished German pocket guideline “S3-LeitlinieNicht erholsamer Schlaf/Schlafstörungen– Kapitel Schlafbezogene Atmungsstörun-gen bei Erwachsenen – Kurzversion”Deutsche Gesellschaft für SchlafforschungundSchlafmedizin (DGSM)2017.A complete list of references can be found inthe original publication of the S3 guideline:Deutsche Gesellschaft für Schlafforschungund Schlafmedizin (2017) S3-Leitlinie Nichterholsamer Schlaf/Schlafstörungen – Kapitel„Schlafbezogene Atmungsstörungen“. Som-nologie 20 (Suppl s2):S97–S180 (https://doi.org/10.1007/s11818-016-0093-1).

Contents

1. What’s new?2. Classification of sleep-related

breathing disorders2.1 Obstructive sleep apnea2.2 Central sleep apnea2.3 Sleep-related hypoventilation/

sleep-related hypoxemia3. Diagnosis3.1 Diagnostic recommendations4. Obstructive sleep apnea—

recommendations4.1 Positive airway pressure therapies4.2 Non-positive airway pressure ther-

apies5. Perioperative management of pa-

tients with obstructive sleep ap-nea—recommendations

6. Diagnosis and treatment of centralsleep apnea—recommendations

7. Diagnosis and treatment ofsleep-related hypoventilation/hypoxemia—recommendations

1. What’s new?

4 Within the past 20 years the preva-lence of obstructuve sleep apnea(OSA) has increased by 14–55%.

4 Sleep-related breathing disorders(also termed sleep-disordered breath-ing, SBD) are common in patientswith heart failure. They are alsoassociated with increased morbidityand mortality in subjectively non-hypersomnic patients.

290 Somnologie 4 · 2017

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http://dx.doi.org/10.1007/s11818-016-0093-1

http://dx.doi.org/10.1007/s11818-016-0093-1

Table 1 Diagnoses of sleep-related breathing disorders according to the International Classifi-cation of SleepDisorders Version 3 (ICSD-3; AASM2014)

Main category Subcategory ICD-10-CM

Obstructive sleepapnea

Obstructive sleep apnea in adults G47.33

Obstructive sleep apnea in children G47.33

Central sleep apnea Central sleep apnea with Cheyne–Stokes breathing R06.3

Central sleep apnea due to a medical cause withoutCheyne–Stokes breathing

G47.37

Central sleep apnea due to high-altitude periodicbreathing

G47.32

Central sleep apnea due to drugs or substances G47.39

Primary central sleep apnea G47.31

Primary central sleep apnea in children P28.3

Primary central sleep apnea in premature infants P28.4

Central sleep apnea due to therapy G47.39

Sleep-relatedhypoventilation

Obesity hypoventilation syndrome E66.2

Congenital central alveolar hypoventilation syndrome G47.35

Late-onset central hypoventilationwith hypothalamicdysfunction

G47.36

Idiopathic central alveolar hypoventilation G47.34

Sleep-related hypoventilation due to drugs or sub-stances

G47.36

Sleep-related hypoventilation due to a medical cause G47.36

Sleep-related hypoxia Sleep-related hypoxia G47.36

Isolated symptomsand normal variants

Snoring R06.83

Catathrenia

4 There is an association between OSAand malignant diseases.

4 Maternal OSA during pregnancy canharm the newborn.

4 Untreated sleep apnea increasescognitive decline in patients withdementia.

4 Patients with a high probability ofa sleep-related breathing disorderand a high accident risk shouldreceive diagnosis and initiation ofany required treatment as early aspossible.

4 Clinical examination should includeinspection of the nose, oral cavity,pharynx, and dental status, as wellas evaluation of facial skeleton mor-phology. A cephalometric radiographmay be obtained to establish facialbone morphology.

4 The “STOP-BANG” questionnairehas been incorporated into thediagnostic spectrum.

4 Polygraphy systems should only beused when there is a high pretestprobability of diagnostic confirma-

tion and for determining the severityof a sleep-related breathing disorder.

4 In cardiovascular disease patientswithout typical symptoms of a sleep-related breathing disorder, simplifiedsystems with 1–3 channels can beused.

4 Questions addressing OSA should beincluded in preoperative assessmentsof case history.

4 In case of suspected undiagnosedOSA a diagnostic sleep work-upshould be performed; however,the urgency of surgery must beweighed against the necessity/typeof sleep medicine diagnostics on anindividual basis.

4 The technical possibilities for tele-monitoring have improved consider-ably during recent years. Telemedicalcare of patients with a positive airwaypressure device is now technicallypossible through nightly recording oftreatment-relevant parameters.

4 Algorithms have been developed for

jthe management of patients withsuspected obstruction of the upperairways (. Fig. 1)

jthe management of patientswith cardiovascular diseases andsleep-related breathing disorders(. Fig. 2)

jthe treatment of patients with OSA(. Fig. 3)

jthe management of patients withsuspected central sleep apnea(. Fig. 4)

2. Classification

Sleep-related breathing disorders mani-fest exclusively or primarily during sleep.They disrupt sleep and thus impair itsrestorative function. Characteristic pat-terns of disturbed breathing are apneasand hypopneas with or without pharyn-geal obstruction, and hypoventilation.Depending on the type of breathing dis-order, it may be accompanied by hypox-emia, or cause hypercapnia and acidosis.

The International Classification ofSleep Disorders Version 3 (ICSD-3)distinguishes between five diagnosticcategories, the names of which are basedon the patterns of disordered breathingduring sleep or the underlying pathome-chanism (. Table 1). Within these fivecategories, ICSD-3 contains descriptionsof 18 diseases.

Early diagnosis and treatment, e. g.,of OSA, reduces the risk of accidentsand improves quality of life. Currentlyit is assumed that untreated OSA leadsto increased healthcare costs. In con-trast, effective treatment of OSA repre-sents a cost-efficient measure in terms ofhealthcare economics.

2.1 Obstructive sleep apnea

OSA is characterized by apneas and hy-popneas, which are caused by partialor complete collapse of the upper air-ways. According to ICSD-3, an obstruc-tive apnea is diagnosed when the breath-ing disorder cannot be explained by anyother sleep disorder or medical condi-tion, or by the use of drugs or othersubstances, and an apnea–hypopnea in-dex (AHI) >15/h (each event ≥10s) sleeptime or an AHI ≥5/h sleep time in com-

Somnologie 4 · 2017 291

S3 Guideline

Table 2 Diagnostic instruments for thedifferent categoriesof sleep-relatedbreathingdisorders

Question-naires

Perfor-manceand vigi-lance tests

1–3-channelpolygraphy

4–6-channelpolygraphy

Polysomno-graphy


(+) (+) (+) + +

Central sleep apnea (+) (+) (+) +


(+) +

Sleep-relatedhypoxemia

(+) +

+ use recommended, (+) use possible under particular conditions, no entry the method is neitherrecommended nor rejected, i. e., there is no evidence for the method or it is not possible or it iseconomically nonviable

Table 3 Questionnaires and instruments used for vigilance diagnostics.The validated instru-ments assess complaints, impairments towellbeing, symptoms, and various behavioral patterns

ESS Berlin Q STOP-BANG Waist toheight

PVT,Osler,DASS

MSLT/MWT


(+) (+) (+) (+) (+) (+)

Central sleep apnea (+) (+)


(+)

Sleep-relatedhypoxemia

(+)

+ use recommended, (+) use possible under particular conditions, no entry the method is neitherrecommended nor rejected, i. e., there is no evidence for the method or it is not possible or it iseconomically nonviable

bination with a typical clinical pathologyor relevant comorbidity is present.

Clinical pathology: Daytime sleepi-ness up to the extent of involuntarilyfalling asleep is the main clinical symp-tom of OSA. However, some affected pa-tients exhibit no sleepiness, do not con-sider it to be a symptom of disease or donot explicitly notice it. Daytime sleepi-ness reducesproductivity and, during thecourse of disease, also impairs cognitiveability, social compatibility, and qualityof life, for example. Sleeping partnersreport breathing arrests. The most im-portant diagnostic parameter is the AHI,which reports the number of apneas andhypopneasperhourofsleep. TheAHIob-jectifies the diagnosis and, together withthe clinical symptoms and comorbidities,determines the severity of OSA. An AHI>15/h and <30/h is defined as moderate,an AHI >30/h as severe OSA.

2.2 Central sleep apnea

This group of sleep-related breathingdisorders is characterized by dysregula-tion of respiratory control mechanismsand/or transfer of impulses to the tho-racic skeleton. In central apnea, despiteopen or passively collapsed upper air-ways, there is no respiratory airflowand, consequently, effective ventilationdoes not occur. For the entire durationof the suspended airflow, there is noinspiratory respiratory effort. In centralhypopneas, respiratory effort and airfloware reduced. In contrast to OSA, thereare no signs of paradoxical breathing.

Central sleep apnea is subdividedinto hypercapnic and non-hypercapnicforms. Hypercapnic breathing disordersare characterized by reduced respiratorydrive, or transfer to or action uponthe muscles of respiration (e. g., neuro-muscular diseases). In non-hypercapnicforms of central apnea, respiratory drive

is usually increased and/or increasedchemosensitivity is present (e. g., centralsleep apnea at high altitude, central sleepapnea with or without Cheyne–Stokesbreathing in cardio-/cerebrovasculardiseases and renal insufficiency).

2.3 Sleep-related hypoventilation/sleep-related hypoxemia

In contrast to ICSD-2, ICSD-3 differen-tiates between sleep-related hypoventila-tion and sleep-related hypoxemia. Sleep-related hypoventilation is differentiatedinto six separate entities, whereas nosubclassification is suggested for sleep-related hypoxemia. According to ICSD-3, sleep-related hypoxemia is presentwhen polysomnography or nocturnalpulse oximetry documents an oxygensaturation ≤88% lasting for at least 5 minin the absence of sleep-related hypoven-tilation, i. e., no hypercapnia is present.Sleep-related hypoxemia is usually a re-sult of a general medical or neurologicaldisease, and cannot be explained bya sleep-related breathing disorder alone.Some patients with sleep-related hypox-emia also exhibit hypoxemia during theday.

3. Diagnosis

Diagnosis of sleep-related breathingdisorders is a prerequisite to initiationof efficient, target-oriented, economictreatments with few side effects. Thediagnostic instruments are oriented tothe pathophysiology, consequences, andcomorbidities of sleep-related breath-ing disorders. They serve to define theseverity of the disorder and a patient’scomorbidities, and should be able toestimate the extent of the consequences.They include recording of case his-tory, self-rating questionnaires, in- andoutpatient multichannel devices, videorecording, and clinical laboratory di-agnostic tests, as well as instrument-based and non-instrument-based per-formance tests (. Tables 2 and 3). Aloneor in combination, all of the employeddiagnostic instruments serve to establishdiagnosis and monitor the effects oftreatment. Beyond this, they are nec-


Table 4 Recommended channels for cardiorespiratory polysomnography.The table presentsthe functions to be assessed, the corresponding biosignal, the technical requirements, and thetechnical specifications in termsof optimal sampling rate and filter settings

Function Parameter Technicalrequirements

Optimal sam-pling rate

Filter

Sleep EEG, EOG Electrodes 500 Hz 0.3–35 Hz

EMG Electrodes 500 Hz 10–100Hz

Breathing Oronasal airflow Nasal pressurecannula, thermistor

100 Hz 0.1–15 Hz

Respiratory effort Induction plethys-mography

100Hz 0.1–15 Hz

Oxygen saturation SaO2 25 Hz –

Carbon dioxidesaturation

tcPaCO2 25 Hz –

Snoring Microphone 500Hz –

Cardiac ECG Electrodes 500 Hz 0.3–70 Hz

Movement EMG tibialismuscle Electrodes 500 Hz 10–100Hz

Body position Position sensor 1 Hz –

Video Video camera 5 Hz –

EEG electroencephalogram, EOG electrooculogram, EMG electromyogram, ECG electrocardiogram,SaO2 oxygen saturation, tcPaCO2 transcutaneous measurement of carbon dioxide partial pressure

essary for sociomedical evaluation andassessment.

Depending on the particular case sce-nario, the diagnostic methods may beapplied in combination, simultaneouslyor sequentially, complementarily or ex-clusionarily, with different demands interms of time, personnel, organization,and materials.

Themost importantdiagnostic instru-ment and the gold standard reference forsleep medicine diagnostics in the sleeplaboratory is supervised cardiorespira-tory polysomnography (PSG; . Table 4).Recording and evaluation of the PSGshould be performed according to theAASM criteria (version 2.3).

For diagnosis of sleep-related breath-ingdisorders, simplifiedportable systemsare available. Using 4–6 channels, thesecan measure breathing-related parame-ters without recording sleep electroen-cephalograms (EEGs).

3.1 Diagnostic recommendations

The sleep-related breathing disorders al-gorithms (. Figs. 1, 2, 3 and 4) and thedecision paths represent a guide to selec-tionofparticulardiagnostic instruments.

Non-instrument-based diagnostics4 For evaluation of the nasal struc-

tures relevant to airflow, clinicalexamination of the nose should beperformed, which may also includeendoscopy (C).

4 Examination of the oral cavity andpharynx is highly relevant and shouldbe performed (B).

4 If therapy with a mandibular ad-vancement device (MAD) is con-sidered, the possible mandibularprotrusion and dental status shouldbe assessed, which can be comple-mented by a panoramic radiogram(PSA, panoramic x ray; B).

4 Thediagnostic workup ofOSA shouldinclude evaluation of facial skeletonmorphology for orientation (B). Thismay include a lateral cephalometricradiograph (Lat Ceph) in order toassess, e. g., the posterior airwayspace (PAS).

4 To detect skeletal abnormalities,a cephalometric radiograph may berecommended. The PAS should bemeasured extending from the inferiorborder of the mandible. For distancesbelow 10mm, a narrowed airwaycan be assumed. Further confirma-tion might be obtained from three-dimensional imaging of the upperairway or by performing transnasalvideoendoscopy. Adequate dentition

is a prerequisite for modeling ofa MAD, with at least eight loadableteeth or equivalent implants in themaxilla and mandible or an equiva-lent implant supply. In this scenario,a panoramic radiogram should bemade and evaluated by a dentistexperienced in sleep medicine (B).

4 For differential diagnosis of thecauses of OSA, individual patientsshould be offered dental and spe-cialist radiographic examination byqualified sleep medicine dentists, or-thodontists, or oral and maxillofacialsurgeons, including cephalometricradiography to investigate the pos-sibility of treatment with a MAD orcorrective jaw osteotomy.

Instrument-based diagnostics4 After assessing the abovementioned

pretest probability, instrument-baseddiagnostics can be divided into thefollowing three categories: pre-liminary diagnostics, confirmatorydiagnostics, differential diagnos-tics (C).

Polysomnography4 PSG in the sleep laboratory mon-

itored and supervised by qualifiedsleep medicine personnel is recom-mended as the gold standard andreference method (A).

4 PSG should be performed accordingto current guidelines. This includesrecording of sleep EEG, EOG, EMG,and ECG; oronasal airflow; snoring;respiratory effort; oxygen saturation;body position; and a video (A;. Table 4).

4 Videometric analysis should beperformed for diagnosis of parasom-nias and sleep movement disorders,and for differential diagnostic dis-crimination from several types ofepilepsy (A).

4 In cases with a low pretest proba-bility or suspicion of sleep diseasesother than OSA by medical history,PSG is indicated for the differentialdiagnosis (A).


S3 Guideline

Table 5 Clinical guidelines formanual CPAP titration

1. Adequate patient information, instruction, and adaptation of therapy

2. Titration of the CPAP pressure at which apneas, hypopneas, RERAs, and snoring no longeroccur

3. Commence titrationwith 4mbar (CPAP), or IPAP 8/EPAP 4mbar (bilevel)

4. Max. CPAP: 15mbar, max. IPAP: 20mbar (bilevel), IPAP/EPAP difference: min. 4, max. 10mbar

5. Where necessary, increase the pressure in 1-mbar increments with a time interval of at least5min

6. Pressure is increased when at least two OSAs or three hypopneas or five RERAs or 3min of loudsnoring occur

7. Change to bilevel in cases of intolerance to CPAP or pressure >15mbar

8. Therapeutic goal: RDI <5/h, min. oxygen saturation>90%

9. Optimal titration: RDI <5/h for at least 15min, including REM sleep and no arousals

10. Good titration: RDI ≤10/h or 50% reduction of baseline in cases with a pretreatment RDI<15/h, including occurrence of REM sleep and reduction of waking reactions

11. Adequate titration: RDI >10/h, but a reduction by 75% of the baseline value; particularly inpatients with severe OSAS or in patients with optimal titration in whom no REM sleep occurs

12. Unacceptable titration: fulfills none of the abovementioned criteria; and

13. A second titration night is necessary when the criteria for optimal/good titration are notfulfilled during the first night

CPAP continuous positive airway pressure, IPAP inspiratory positive airway pressure, EPAP expiratorypositive airway pressure, RERA respiratory effort related arousal, RDI respiratory disturbance index,REM rapid eye movement,OSA obstructive sleep apnea, OSAS OSA syndrome

Polygraphy for sleep-related breathingdisorders4 Polygraphy systems with a reduced

number of channels can be usedprovided they include at least onemeasurement of oxygen saturation,oronasal airflow, respiratory effort,heart or pulse rate, and body posi-tion (A). Such systems should onlybe used when there is a high pretestprobability of obtaining diagnosticconfirmation or for assessment of theseverity of sleep-related breathingdisorders (A).

4 Polygraphy systems for diagnosisof sleep-related breathing disordersshould be applied by specializedsleep medicine physicians, whocan assess and evaluate the pretestprobability, the symptoms, and thecomorbidities (A).

4 In general, polygraphy should not beused as a substitute for PSG for thediagnosis of sleep-related breathingdisorders in patients with relevantcomorbidities (A). The recordedsignals should be scored visually bytrained personnel. Evaluation byso-called automatic scoring alone iscurrently not recommended (A).

4 For diagnosis of sleep-related breath-ing disorders by exclusion, car-diorespiratory PSG is recommended;polygraphy is not sufficient (A).

4 Neither polygraphy nor PSG issufficient to clarify hypercapnicrespiratory failure (A).

4 Disease course and treatment canbe monitored polygraphically. Inpatients with an unclear responseto therapy, patients with a highcardiovascular risk, and patients withother sleep-impairing diseases, PSGmonitoring may be necessary (C).

Reduced monitoring for sleep-relatedbreathing disorders4 Polygrams fulfilling fewer than all

of the abovementioned criteria cangive an indication of the existenceof a sleep-related breathing disorderand increase the pretest probability.Polygraphy is not, however, recom-mended as a stand-alone method fordiagnosis of sleep-related breathingdisorders (A).

4 In the presence of cardiovasculardiseases that increase the risk ofsleep-related breathing disorders(arterial hypertension, heart failure,atrial fibrillation, cerebrovascular

disease) and the absence of alltypical symptoms, a single- or two-channel registration is possible. If thisregistration supports the presence ofOSA, further diagnostic workup withpolygraphy or PSG is indicated (C).

4. Obstructive sleepapnea—recommendations

The algorithm for treatment of patientswith OSA is shown in . Fig. 3. Clinicalguidelines formanualCPAP-titration aregiven in . Table 5.

4.1 Positive airway pressuretherapies

4 Continuous positive airway pressure(CPAP) therapy is the gold standardfor treatment of OSA syndrome (A).

4 CPAP therapy should be adminis-tered for moderate and severe sleepapnea (AHI >15/h; A).

4 In cases of mild sleep apnea (AHI≤15/h) with a cardiovascular riskand/or daytime fatigue, CPAP therapycan be considered (C).

4 For initial titration, structured patienttraining should take place (B).

4 Therapeutic decisions regarding theCPAP treatment mode should bemade by a physician qualified in sleepmedicine (A).

4 Minimal time should elapse betweentitration of the respiratory ther-apy and provision of a therapeuticdevice (B).

4 It is recommended that the selectionof the device, mask, and additionalsupportive aids, as well as the initialfitting, be performed by personnelqualified in sleep medicine (C).

4 Initiation of CPAP therapy or a mod-ified positive airway pressure treat-ment should be performed in a sleeplab with polysomnographic monitor-ing (A).

4 The final adjustments should beperformed with the same mask anddevice that the patient will receive forhome use.

4 Whenever clinically possible, bileveltherapy should always be precededby a therapeutic trial with CPAP orautomatic CPAP (APAP) (B).


4 APAP and CPAP are of equal valuefor titration of treatment and long-term therapy of OSA (A).

4 APAP should not be used to treatin central sleep apnea or nocturnalhypoventilation (B).

4 The first therapeutic monitoringshould occur within the first 6 weeksand be based on clinical examination;additional polygraphy should beperformed with at least 6 channels.Subsequent treatment should bemonitored at least annually (B).

4 Polygraphic or polysomnographicmonitoring should be performed inpatients with subjective complaints,or clinical or technical problems (A).

The clinical guidelines for manual CPAPtitration are summarized in . Table 5.

CPAP-intolerant patients4 For patients, who cannot be treated

with CPAP, other types of respiratorysupport or other suitable treatmentsshould be employed (A).

Patients with dementia4 In patients with mild or moderate

dementia and OSA, an attempt ofCPAP treatment should be made.

4.2 Non-positive airway pressuretherapies

Weight reduction4 Weight reduction strategies should be

recommended as supportive therapyto all overweight patients (A).

Mandibular advancement devices4 MADs may be an alternative to

positive airway pressure therapy inpatients with mild to moderate OSA(AHI ≤30/h). This is particularlyrelevant for patients with a body massindex (BMI) < 30 kg/m2 and a lifetimehistory of sleep apnea (A).

4 In patients with a high AHI and/orBMI >30 kg/m2, a MAD can be con-sidered where positive airway pres-sure therapy cannot be used despiteuse of all supportive measures (C).

4 MADs should be fitted by personnelwith dental and sleep medicineexpertise (A).

4 The effect of MAD therapy should beregularly monitored, e.g., annually,by physicians qualified in sleepmedicine (A).

Drug-based treatments4 Drug treatment of OSA cannot be

recommended (A).4 Modafinil (off-label) treatment can

be considered for residual daytimesleepiness due to OSA in patients onCPAP therapy, provided other causeshave been excluded (C).

Oxygen therapy4 Nocturnal oxygen therapy should

not be used as the sole treatment forOSA (A).

Therapies to increase muscle tone4 Surface electrical stimulation to

increase muscle tone should not beperformed (B).

4 Non-electrical methods and my-ofunctional exercises can be consid-ered in individual cases (B).

Positional therapy4 For patients with mild to moderate

position-dependent OSA, therapyto prevent sleeping in the supineposition can be considered when noother treatments recommended inthis guideline is applicable or wherethese are not adequately tolerated (C).

Surgical interventions4 Surgery to improve nasal breathing

should be considered in patients withimpaired nasal breathing resulting inCPAP intolerance (B).

4 In patients with tonsillar hypertrophyand oropharyngeal obstruction,tonsillectomy should be performed,particularly when an alternativetherapy (CPAP, MAD) is not possibleor not sufficiently tolerated (A).Tonsillectomy may be combined withuvulopalatopharyngoplasty (C).

4 In the absence of anatomic abnor-malities, neurostimulation of thehypoglossal nerve can be used inpatients with moderate to severeOSA when positive airway pressuretherapy meeting the abovenamedcriteria cannot be employed. Neu-

rostimulation should only be usedin case of CPAP intolerance or in-effectiveness with AHI 15–50/h and≤class I obesity, provided no con-centric obstruction is documented insleep endoscopy (B).

4 In the presence of appropriateanatomic findings with a smallmandible and narrow facial skeleton(PAS <10mm on a cephalometric ra-diograph), advancement of the max-illa and/or mandible (bimaxillary/maxillomandibular advancement)should be considered, particularlywhen an alternative therapy (CPAP,MAD) is not possible or is insuffi-ciently tolerated (A).

4 Muscle-resecting surgery to the softpalate is not recommended (A).

4 Several other surgical interventionsmay be expedient, depending on theanatomic findings (C).

5. Perioperativemanagement ofpatients with obstructive sleepapnea—recommendations

4 Questions addressing OSA should beincluded in preoperative assessmentsof medical history (B).

4 In case of suspected undiagnosedOSA a diagnostic sleep work-upshould be performed; however, thepriority of the surgical proceduremust be weighed against the neces-sity/type of sleep medicine diagnosticworkup on an individual basis (B).

4 In the presence of OSA requiringtreatment, a previously titrated CPAPtherapy should be continued in theperioperative phase; in the absence ofa previously titrated CPAP therapy,initiation CPAP treatment should beconsidered, provided permissible bythe priority of surgery (B).

4 The selection of the type of anesthesia,as well as the type and duration ofpotentially necessary postoperativemonitoring, should be orientedtoward the type and the seriousnessof surgery, the perioperative analgesicrequirements, the severity of the(assumed) breathing disorder, and thepatient’s individual risk constellation,


S3 Guideline

Table 6 Diagnostic criteria of obesity hy-poventilation syndrome

a. Hypercapnia (daytime PaCO2 >45mmHg)

b. Body mass index >30 kg/m2

c. Hypoventilation is not primarily caused byanother disease

including sleep apnea-associatedcomorbidities (B).

6. Diagnosis and treat-ment of central sleepapnea—recommendations

The algorithm for management of pa-tients with suspected central sleep apneais shown in . Fig. 4.

Diagnosis

4 When diagnosis of central sleepapnea has been confirmed, possiblegeneral medical, pharmacological,and neurological causes should beinvestigated (A).

Treatment of central sleep apneain patients with heart failure withpreserved left ventricular ejectionfraction (HFpEF)

4 In HFpEF patients (left ventricularejection fraction, LVEF, >45%), CPAPtherapy or adaptive servoventilation(ASV) should be used to treat centralsleep apnea (B).

4 In HFpEF patients (LVEF >45%),oxygen therapy can be used to treatsymptomatic central sleep apneawhere CPAP or, in the presence of thecorrect indication, ASV therapy hasfailed (C).

Treatment of central sleep apneain patients with heart failure withreduced left ventricular ejectionfraction (HFrEF)

4 For treatment of central sleep apneain HFrEF patients, the heart failureshould be treated according to currentguidelines (A).

4 In patients with moderate to severecentral sleep apnea and symptomatic

Table 7 Indications for initiation of noninvasive ventilation

Obesity hypoventilation syndrome

– Nocturnal transcutaneouslymeasured CO2 level under CPAP therapy >55mmHg for at least5min

or

– Nocturnal oxygen saturation<90% for at least 10min

Diseases with obstruction of the lower airways

– Hypercapnia while awake (PaCO2 ≥50mmHg)

or

– Hypercapnia while asleep (PaCO2 ≥55mmHg or ΔPtcCO2 ≥10mmHg compared to normocap-nic awake-state)

Neuromuscular or chest wall diseases

– Hypercapnia while awake (PaCO2 ≥45mmHg)

or

– Hypercapnia while asleep (PaCO2 ≥50mmHg or ΔPtcCO2 ≥10mmHg compared to normocap-nic awake-state)

HFrEF (LVEF ≤45%), ASV therapyshould not be performed (A).

4 In selected patients with symptomaticmoderate to severe central sleepapnea and HFrEF (LVEF ≤45%),therapy with CPAP can be consid-ered (C).

4 In patients with symptomatic moder-ate to severe central sleep apnea andHFrEF (LVEF ≤45%), therapies forwhich there are no randomized long-term studies, e. g., unilateral stimula-tion of the phrenic nerve and oxygentherapy, should only be appliedwithin prospective studies (B).

Treatment of central sleep apneain patients with heart failure

4 Alternative therapies such as bilevelin spontaneous time (ST) modus, ac-etazolamide, or theophylline shouldnot be used to treat normo- orhypocapnic central sleep apnea inpatients with heart failure (B).

Recommendations for centralsleep apnea due to periodicbreathing at high altitude

4 Acetazolamide can be recommendedin healthy individuals to reducecentral apneas/periodic breathingat high altitude and to improvenocturnal oxygen saturation at highaltitude (C).

4 Combined therapy comprising ac-etazolamide and CPAP can be rec-ommended to prevent worsening ofcentral sleep apnea/periodic breath-ing at high altitude in patients withpreviously diagnosed sleep-relatedbreathing disorders (C).

Recommendations for centralsleep apnea due to medications,drugs, or substances

4 In opioid-induced sleep apnea a re-duction in opioid dosage should beconsidered (B).

4 Positive airway pressure therapiesshould be applied on an individualbasis in opioid-induced sleep apnea,and their efficiency should be assessedpolysomnographically (A).

4 In individual cases, positive airwaypressure therapies and oxygen ad-ministration may be combined (C).Therapy initiation and monitor-ing should include capnography inaddition to polysomnography (A).

Recommendations for idiopathiccentral sleep apnea

4 Treatment can be performed withnoninvasive ventilation therapyor as spontaneous breathing witha background frequency (C).


Suspected obstruction of the upperairways or impairments of vigilance

Caused by medical, psychiatric,or psychological disease in need

of optimization?

Check specifictreatment options

yes

no

yes

yes

yes

yes

no

no

no

nono

no

no

yes

yesyes

Define the pretest probabilityof OSA (daytime sleepiness

and breathing pausesand snoring)

High pretest probability?

OSA?

PSG for differentialdiagnosis

Central sleep apnea?

Polygraphy of cardio-respiratory parameters

Obstructive AHI >15/h?

Risk of nocturnal hypoventilation?

Treat OSA and hypoventilation OSA therapy

Hypercapnia while awake or asleep(daytime blood gas analysis, andnighttime capnometry and PSG)?

Proceed to CSA

Other sleep disorder? Sleep medicinecounseling

Specific therapy

0

1

2

3

4

5

6

7

8

9 10

1416

171513

12

11

Fig. 18 Algorithm formanagement of patients with suspected obstruction of the upper airways.Following exclusion ofmedical andpsychological diseases requiring optimization and in the presence of a highpretest probability, i.e., daytimesleepiness plusbreathing pauses plus snoring, polygraphy of cardiorespiratory parameters can be a sufficient diagnosticinstrument. In the case of a low pretest probability, polysomnography (PSG) is performed for differential diagnosis.(AHI apnea–hypopnea index,OSA obstructive sleep apnea,CSA central sleep apnea)


S3 Guideline

Primary disease: arterialhypertonia, heart failure,

atrial fibrillation, CNS disease

0

31

9

11

12

5131

14

7

8

10

2

4

5

6

Symptoms of sleep-related breathing

disorders?

Monitor for sleep-relatedbreathing disorders using

reduced systems with1–3 channels

Sleep-relatedbreathing disorder

suspected?

Polysomnography fordifferential diagnosis

Treat primary disease and repeatsleep-related diagnostics where

appropriate

Other sleep disorder?No sleep medicine

diseaseOSA? CSA?

TreatCSA Specific

therapy

High pretest probability(snoring AND sleeping partner-

reported breathing disorderAND daytime sleepiness)?

Six-channel polygraphy

OSA confirmed?

Treat OSA

yes

yesyes

yesno

no

no

no

no no no

yes

yes

yes

Fig. 28 Algorithmformanagementofpatientswithcardiovasculardiseases.Around50%ofpatientswithcardiovasculardis-ease are also affected by a sleep-related breathing disorder. Therefore, in asymptomatic cardiovascular patients,monitoringfor sleep-related breathing disorders can be performedwith simplified systemswith 1–3 channels. If symptoms of sleep-re-lated breathing disorders are present, polygraphy or polysomnography is indicated. (CNS central nervous system,OSA ob-structive sleep apnea,CSA central sleep apnea)


OSAS requiring treatment

Suspected dysmorphology andpathogenetically relevant anatomicabnormalities in the upper airways?

0

1

4

5

7

98

CPAP/APAP116

10

14

yes

yes

no

no

no

no

Attempt at CPAP/APAP or MAD

Effective?

Effective?

Effective?

AHI ≤30/h?

CPAP/APAP or MAD

Optimization of therapy** Optimization of therapy**

Monitor therapy

Residual daytimesleepiness?

Off-label modafinilpossible**

yes

yes

yes

yes

3219

12

13

Attempt atCPAP/APAP

no

no

Attempt at bilevel/auto-bilevel**

bilevel/auto-bilevel**

15

16

17

18

yes

noPossible correction(e.g., surgery)

Persistent OSASrequiring treatment?*

Possible sleep medicine counselingand individualized recommendations

concerning different treatmentmodalities

Fig. 38 Algorithm for treatment of patients with obstructive sleep apnea.*Patient training, behavioral recommendations,sleepmedicine counselling; in overweight patients, weight reduction should be attempted in parallel. **In patients with anapnea–hypopnea index (AHI) ≤30/h and lifelong obstructive sleep apnea (OSA), positional therapy can be considered if noother therapy is possible or tolerated.Mandibular advancement devices (MAD) can alsobe considered inpatientswith severesleepapneawhodonottolerateorrefusecontinuouspositiveairwaypressure (CPAP),or inwhomCPAPtherapycannotbeuseddespite utilisation of all supportmeasures.Where positive airway pressure therapies orMAD fail, in the absence of anatomicabnormalities and the presence of an AHI of 15–50/h, neurostimulation of the hypoglossal nerve (NSHG) can be used up toclass I obesity, provided there is no concentric obstruction of the airways. (OSASobstructive sleep apnea syndrome,APAP au-tomatic CPAP)


S3 Guideline

0Suspected CSA

Polygraphy orpolysomnography

Sleep-related breathingdisorder confirmed?

OSA? Continue to OSA algorithm

Heart failure?

Guideline-conform treatmentof heart failure

EF ≤ 45 % ?

Sleep medicine counseling;in exceptional cases with

clear symptoms, attempt atCPAP

Renal insufficiency, CNS disease,other comorbidities?

Optimization of treatmentfor primary disease

Idiopathic CSA

yes

yes

yes

yes

yes

yes

yes

yes

yesyes

yes

yes

no

no

no

nono

no

no

no

no

Polysomnography fordifferential diagnosis*

CSA ?

Opioid-induced sleep apnea?

Consider weaning ordosage reduction

Persistent CSA? Persistent CSA?

Persistent CSA?

CPAP

Effective?

Effective?

CPAP

ASV

ASV

Sleep medicine counseling

Sleep medicine counseling

1

27

6252

16

17

15

10

13

14

11

12

18

19

20

23

22

2124

2

3

4

5

6

7

8

9

Counseling

no no no

Fig. 48 Algorithm formanagement of patients with suspected central sleep apnea.*Upon unclear findings in polygraphy,polysomnography isperformedfordifferentialdiagnosis. (CSAcentral sleepapnea,CPAPcontinuouspositiveairwaypressure,ASV adaptive servoventilation,CNS central nervous system,OSA obstructive sleep apnea, EF ejection fraction)

Recommendations for centralsleep apnea due to therapy

4 Known triggers (e. g., over-treat-ment or split nights) should beeliminated (A).

4 In patients with central sleep apneadue to therapy who require treatmentand who are normo- or hypocap-nic, therapy should be switched toASV (B).

7. Diagnosis and treatment ofsleep-related hypoventilation/sleep-related hypoxemia

Diagnostic recommendations

4 In the presence of clinical indicationsof sleep-related hypoventilationor predisposing primary disease,diagnosis should be performedvia nocturnal arterial or capillaryblood gas analysis, or nocturnalmeasurement of transcutaneous orend-tidal CO2. For diagnosis of

obesity hypoventilation syndrome,a daytime blood gas analysis isrequired (. Table 6). Sleep-relatedhypoxemia should be diagnosed bynocturnal oximetry in combinationwith measurement of CO2 during thenight (A).

4 In patients with BMI >30 kg/m2 andsymptoms of a sleep-related breath-ing disorder, the awake-state venousbicarbonate, or arterial or capillarypCO2, or transcutaneous or end-tidal CO2 should be measured inorder to exclude the simultaneous


presence of sleep-related hypoventi-lation (. Table 6; A).

4 Transcutaneous capnometry is rec-ommended as the most sensitivemethod for demonstrating the pres-ence of sleep-related hypercapnia.This can be performed in combina-tion with polygraphy or PSG (C).

4 In patients with neuromuscular orchest wall diseases, sleep-relatedhypoventilation should be ruled outin candidates for ventilation therapywith a vital capacity <50% (A).

4 PSG is the gold standard for diagnosisof exclusion and differential diagnosisof sleep-related breathing disordersin the context of sleep-related hy-poventilation or hypoxemia (A).

Treatment

4 In patients with obesity hypoventi-lation, an attempt at CPAP therapywith CO2 monitoring can be under-taken (C).

4 If nocturnal hypoventilation persistsunder CPAP therapy, noninvasivepressure-support ventilation (withoutor with target volume) should beinitiated (B).

4 Oxygen therapy alone is not rec-ommended in patients with obesityhypoventilation syndrome (A).

4 After utilisation of all other weight-reduction strategies in patients withobesity hypoventilation syndrome,bariatric surgery can be consid-ered (B).

Indications for initiation ofnoninvasive ventilation

4 In patients with symptomatic ob-struction of the lower airways, orneuromuscular or chest wall diseaseswith hypercapnia in the awake-state(PaCO2 ≥50mmHg for diseases withobstruction of the lower airways or≥45mmHg in neuromuscular orchest wall diseases) or while asleep(PaCO2 ≥55mmHg or ≥50mmHg,respectively, or ΔPtcCO2 ≥10mmHgcompared normocapnic awake-state),initiation of noninvasive ventilationis recommended (. Table 7; A).

Corresponding address

Prof. Dr. med. G. MayerSchwalmstadt-Treysa, [email protected]

Acknowledgement. Various different specialistmedical societies and patient self-help groups wereinvolved in development of the original version ofthe guideline (see Somnologie 20, Suppl s2:97–180,https://doi.org/10.1007/s11818-016-0093-1).

OpenAccess. Thisarticle isdistributedunderthetermsof the Creative CommonsAttribution 4.0 InternationalLicense (http://creativecommons.org/licenses/by/4.0/), which permits unrestricteduse, distribution,and reproduction in anymedium, provided yougiveappropriate credit to the original author(s) and thesource, providea link totheCreativeCommons license,and indicate if changesweremade.


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