German S3 Guideline Nonrestorative Sleep/Sleep Disorders, chapter “Sleep-Related Breathing Disorders in Adults,” short version

Erratum to:
 Somnologie 2017 ·21:290–301
 https://doi.org/10.1007/s11818-017-0136-2
 There is a mistake on p. 295, left column under “Mandibular advancement devices.” The first entry should read correctly:

Perioperative management of patients with obstructive sleep apnea-recommendations 6. Diagnosis and treatment of central sleep apnea-recommendations 7.
Diagnosis and treatment of sleep-related hypoventilation/ hypoxemia-recommendations 1. What's new? 4 Within the past 20 years the prevalence of obstructuve sleep apnea (OSA) has increased by 14-55%. 4 Sleep-related breathing disorders (also termed sleep-disordered breathing, SBD) are common in patients with heart failure. They are also associated with increased morbidity and mortality in subjectively nonhypersomnic patients. There is an association between OSA and malignant diseases. 4 Maternal OSA during pregnancy can harm the newborn. 4 Untreated sleep apnea increases cognitive decline in patients with dementia. 4 Patients with a high probability of a sleep-related breathing disorder and a high accident risk should receive diagnosis and initiation of any required treatment as early as possible. 4 Clinical examination should include inspection of the nose, oral cavity, pharynx, and dental status, as well as evaluation of facial skeleton morphology. A cephalometric radiograph may be obtained to establish facial bone morphology. 4 The "STOP-BANG" questionnaire has been incorporated into the diagnostic spectrum. 4 . 1) j the management of patients with cardiovascular diseases and sleep-related breathing disorders (. Fig. 2) j the treatment of patients with OSA (. Fig. 3) j the management of patients with suspected central sleep apnea (. Fig. 4)

Classification
Sleep-related breathing disorders manifest exclusively or primarily during sleep. They disrupt sleep and thus impair its restorative function. Characteristic patterns of disturbed breathing are apneas and hypopneas with or without pharyngeal obstruction, and hypoventilation. Depending on the type of breathing disorder, it may be accompanied by hypoxemia, or cause hypercapnia and acidosis. The International Classification of Sleep Disorders Version 3 (ICSD-3) distinguishes between five diagnostic categories, the names of which are based on the patterns of disordered breathing during sleep or the underlying pathomechanism (. Table 1). Within these five categories, ICSD-3 contains descriptions of 18 diseases.
Early diagnosis and treatment, e. g., of OSA, reduces the risk of accidents and improves quality of life. Currently it is assumed that untreated OSA leads to increased healthcare costs. In contrast, effective treatment of OSA represents a cost-efficient measure in terms of healthcare economics.

Obstructive sleep apnea
OSA is characterized by apneas and hypopneas, which are caused by partial or complete collapse of the upper airways. According to ICSD-3, an obstructive apnea is diagnosed when the breathing disorder cannot be explained by any other sleep disorder or medical condition, or by the use of drugs or other substances, and an apnea-hypopnea index (AHI) >15/h (each event ≥10 s) sleep time or an AHI ≥5/h sleep time in com-  bination with a typical clinical pathology or relevant comorbidity is present. Clinical pathology: Daytime sleepiness up to the extent of involuntarily falling asleep is the main clinical symptom of OSA. However, some affected patients exhibit no sleepiness, do not consider it to be a symptom of disease or do not explicitly notice it. Daytime sleepiness reduces productivity and, during the course of disease, also impairs cognitive ability, social compatibility, and quality of life, for example. Sleeping partners report breathing arrests. The most important diagnostic parameter is the AHI, which reports the number of apneas and hypopneasperhourofsleep. The AHI objectifies the diagnosis and, together with the 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.

Central sleep apnea
This group of sleep-related breathing disorders is characterized by dysregulation of respiratory control mechanisms and/or transfer of impulses to the thoracic skeleton. In central apnea, despite open or passively collapsed upper airways, there is no respiratory airflow and, consequently, effective ventilation does not occur. For the entire duration of the suspended airflow, there is no inspiratory respiratory effort. In central hypopneas, respiratory effort and airflow are reduced. In contrast to OSA, there are no signs of paradoxical breathing.
Central sleep apnea is subdivided into hypercapnic and non-hypercapnic forms. Hypercapnic breathing disorders are characterized by reduced respiratory drive, or transfer to or action upon the muscles of respiration (e. g., neuromuscular diseases). In non-hypercapnic forms of central apnea, respiratory drive is usually increased and/or increased chemosensitivity is present (e. g., central sleep apnea at high altitude, central sleep apnea with or without Cheyne-Stokes breathing in cardio-/cerebrovascular diseases and renal insufficiency).

Sleep-related hypoventilation/ sleep-related hypoxemia
In contrast to ICSD-2, ICSD-3 differentiates between sleep-related hypoventilation and sleep-related hypoxemia. Sleeprelated hypoventilation is differentiated into six separate entities, whereas no subclassification is suggested for sleeprelated hypoxemia. According to ICSD-3, sleep-related hypoxemia is present when polysomnography or nocturnal pulse oximetry documents an oxygen saturation ≤88% lasting for at least 5 min in the absence of sleep-related hypoventilation, i. e., no hypercapnia is present. Sleep-related hypoxemia is usually a result of a general medical or neurological disease, and cannot be explained by a sleep-related breathing disorder alone. Some patients with sleep-related hypoxemia also exhibit hypoxemia during the day.

Diagnosis
Diagnosis of sleep-related breathing disorders is a prerequisite to initiation of efficient, target-oriented, economic treatments with few side effects. The diagnostic instruments are oriented to the pathophysiology, consequences, and comorbidities of sleep-related breathing disorders. They serve to define the severity of the disorder and a patient's comorbidities, and should be able to estimate the extent of the consequences. They include recording of case history, self-rating questionnaires, in-and outpatient multichannel devices, video recording, and clinical laboratory diagnostic tests, as well as instrumentbased and non-instrument-based performance tests (. Tables 2 and 3). Alone or in combination, all of the employed diagnostic instruments serve to establish diagnosis and monitor the effects of treatment. Beyond this, they are nec- Depending on the particular case scenario, the diagnostic methods may be applied in combination, simultaneously or sequentially, complementarily or exclusionarily, with different demands in terms of time, personnel, organization, and materials.
The most important diagnostic instrument and the gold standard reference for sleep medicine diagnostics in the sleep laboratory is supervised cardiorespiratory polysomnography (PSG; . Table 4). Recording and evaluation of the PSG should be performed according to the AASM criteria (version 2.3).
For diagnosis of sleep-related breathing disorders, simplified portable systems are available. Using 4-6 channels, these can measure breathing-related parameters without recording sleep electroencephalograms (EEGs).

Diagnostic recommendations
The sleep-related breathing disorders algorithms (. Figs. 1, 2, 3 and 4) and the decision paths represent a guide to selection of particular diagnostic instruments. 4 For evaluation of the nasal structures relevant to airflow, clinical examination of the nose should be performed, which may also include endoscopy (C). 4 Examination of the oral cavity and pharynx is highly relevant and should be performed (B). 4 If therapy with a mandibular advancement device (MAD) is considered, the possible mandibular protrusion and dental status should be assessed, which can be complemented by a panoramic radiogram (PSA, panoramic x ray; B). 4 The diagnostic workup of OSA should include evaluation of facial skeleton morphology for orientation (B). This may include a lateral cephalometric radiograph (Lat Ceph) in order to assess, e. g., the posterior airway space (PAS). 4 To detect skeletal abnormalities, a cephalometric radiograph may be recommended. The PAS should be measured extending from the inferior border of the mandible. For distances below 10 mm, a narrowed airway can be assumed. Further confirmation might be obtained from threedimensional imaging of the upper airway or by performing transnasal videoendoscopy. Adequate dentition is a prerequisite for modeling of a MAD, with at least eight loadable teeth or equivalent implants in the maxilla and mandible or an equivalent implant supply. In this scenario, a panoramic radiogram should be made and evaluated by a dentist experienced in sleep medicine (B). 4 For differential diagnosis of the causes of OSA, individual patients should be offered dental and specialist radiographic examination by qualified sleep medicine dentists, orthodontists, or oral and maxillofacial surgeons, including cephalometric radiography to investigate the possibility of treatment with a MAD or corrective jaw osteotomy. 4 After assessing the abovementioned pretest probability, instrument-based diagnostics can be divided into the following three categories: preliminary diagnostics, confirmatory diagnostics, differential diagnostics (C). . Table 4). 4 Videometric analysis should be performed for diagnosis of parasomnias and sleep movement disorders, and for differential diagnostic discrimination from several types of epilepsy (A). 4 In cases with a low pretest probability or suspicion of sleep diseases other than OSA by medical history, PSG is indicated for the differential diagnosis (A).  4 Polygrams fulfilling fewer than all of the abovementioned criteria can give an indication of the existence of a sleep-related breathing disorder and increase the pretest probability. Polygraphy is not, however, recommended as a stand-alone method for diagnosis of sleep-related breathing disorders (A). 4 In the presence of cardiovascular diseases that increase the risk of sleep-related breathing disorders (arterial hypertension, heart failure, atrial fibrillation, cerebrovascular disease) and the absence of all typical symptoms, a single-or twochannel registration is possible. If this registration supports the presence of OSA, further diagnostic workup with polygraphy or PSG is indicated (C).

Obstructive sleep apnea-recommendations
The algorithm for treatment of patients with OSA is shown in . Fig. 3. Clinical guidelines for manual CPAP-titration are given in .

Non-positive airway pressure therapies
Weight reduction 4 Weight reduction strategies should be recommended as supportive therapy to all overweight patients (A). 4 MADs may be an alternative to positive airway pressure therapy in patients with mild to moderate OSA (AHI ≤30/h). This is particularly relevant for patients with a body mass index (BMI) < 30 kg/m 2 and a lifetime history of sleep apnea (A). 4 In patients with a high AHI and/or BMI >30 kg/m 2 , a MAD can be considered where positive airway pressure therapy cannot be used despite use of all supportive measures (C). 4 MADs should be fitted by personnel with dental and sleep medicine expertise (A). 4 The effect of MAD therapy should be regularly monitored, e.g., annually, by physicians qualified in sleep medicine (A). 4 Drug treatment of OSA cannot be recommended (A). 4 Modafinil (off-label) treatment can be considered for residual daytime sleepiness due to OSA in patients on CPAP therapy, provided other causes have been excluded (C).

Drug-based treatments
Oxygen therapy 4 Nocturnal oxygen therapy should not be used as the sole treatment for OSA (A).
Therapies to increase muscle tone 4 Surface electrical stimulation to increase muscle tone should not be performed (B). Positional therapy 4 For patients with mild to moderate position-dependent OSA, therapy to prevent sleeping in the supine position can be considered when no other treatments recommended in this guideline is applicable or where these are not adequately tolerated (C). 4 Surgery to improve nasal breathing should be considered in patients with impaired nasal breathing resulting in CPAP intolerance (B). 4 In patients with tonsillar hypertrophy and oropharyngeal obstruction, tonsillectomy should be performed, particularly when an alternative therapy (CPAP, MAD) is not possible or not sufficiently tolerated (A). Tonsillectomy may be combined with uvulopalatopharyngoplasty (C). 4 In the absence of anatomic abnormalities, neurostimulation of the hypoglossal nerve can be used in patients with moderate to severe OSA when positive airway pressure therapy meeting the abovenamed criteria cannot be employed. Neu-rostimulation should only be used in case of CPAP intolerance or ineffectiveness with AHI 15-50/h and ≤class I obesity, provided no concentric obstruction is documented in sleep endoscopy (B). 4 In the presence of appropriate anatomic findings with a small mandible and narrow facial skeleton (PAS <10 mm on a cephalometric radiograph), advancement of the maxilla and/or mandible (bimaxillary/ maxillomandibular advancement) should be considered, particularly when an alternative therapy (CPAP, MAD) is not possible or is insufficiently tolerated (A). 4 Muscle-resecting surgery to the soft palate is not recommended (A). 4 Several other surgical interventions may be expedient, depending on the anatomic findings (C). 4 Questions addressing OSA should be included in preoperative assessments of medical history (B). 4 In case of suspected undiagnosed OSA a diagnostic sleep work-up should be performed; however, the priority of the surgical procedure must be weighed against the necessity/type of sleep medicine diagnostic workup on an individual basis (B). 4 In the presence of OSA requiring treatment, a previously titrated CPAP therapy should be continued in the perioperative phase; in the absence of a previously titrated CPAP therapy, initiation CPAP treatment should be considered, provided permissible by the priority of surgery (B). 4 The selection of the type of anesthesia, as well as the type and duration of potentially necessary postoperative monitoring, should be oriented toward the type and the seriousness of surgery, the perioperative analgesic requirements, the severity of the (assumed) breathing disorder, and the patient's individual risk constellation, including sleep apnea-associated comorbidities (B).

Diagnosis and treatment of central sleep apnea-recommendations
The algorithm for management of patients with suspected central sleep apnea is shown in . Fig. 4.   Fig. 1 8 Algorithm for management of patients with suspected obstruction of the upper airways. Following exclusion of medical and psychological diseases requiring optimization and in the presence of a high pretest probability, i.e., daytime sleepiness plus breathing pauses plus snoring, polygraphy of cardiorespiratory parameters can be a sufficient diagnostic instrument. In the case of a low pretest probability, polysomnography (PSG) is performed for differential diagnosis. Recommendations for central sleep apnea due to therapy