Current Concepts of Sleep Apnea Surgery E-Book

• Herausgeber: Thieme
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Veröffentlichungsjahr: 2019

Beschreibung

A key new reference dedicated to the surgical management of sleep-disordered breathing...

The importance of unobstructed respiration in sleep, and the long-term risks of sleep apnea, cannot be overemphasized. The therapeutic efficacy of the widely prescribed "gold standard," CPAP, is compromised by low patient acceptance and compliance.

In light of the limits of CPAP and other forms of conservative therapy (e.g., mandibular advancement devices), there is a growing tendency to explore and expand the role of surgery in the treatment of severe sleep apnea. New insights and developments in pathophysiology, surgical techniques, and implants have opened the way to increased success in treating sleep apnea surgically.

This new work by leading international specialists provides a detailed, evidence-based approach to selected advanced surgical techniques, beginning with patient selection criteria, discussion of indications for and against surgery, choice of procedure (also in combinations), and more.

Key Features:

• Systematic, practice-oriented approach to examination, diagnosis, and treatment
• Step-by-step description of surgical concepts and techniques
• Superbly illustrated with full-colored photographs and drawings
• Focus on those procedures that have been shown to be successful in specific situations
• Discussion of outcomes, success rates, risks, and potential complications; where evidence-based data are not available, expert opinion is provided

Current Concepts of Sleep Apnea Surgery will be welcomed by residents, fellows, and board-certified surgeons in otorhinolaryngology and head and neck surgery.

This book includes complimentary access to a digital copy on https://medone.thieme.com.

Leseprobe

To access the additional media content available with this e-book via Thieme MedOne, please use the code and follow the instructions provided at the back of the e-book.

Current Concepts of Sleep Apnea Surgery

Thomas Verse, MD

Professor of OtorhinolaryngologyDirector of Department of Otorhinolaryngology–Head and Neck SurgeryAsklepios Clinic HarburgAsklepios Campus Hamburg of Semmelweis UniversityHamburg, Germany

Nico de Vries, MD, PhD

Professor of OtolaryngologyDepartment of Otorhinolaryngology–Head and Neck SurgeryOLVG HospitalDepartment of Oral KinesiologyACTA AmsterdamAmsterdam, The NetherlandsDepartment of Otorhinolaryngology–Head and Neck SurgeryUniversity of AntwerpAntwerp, Belgium

281 illustrations

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ISBN 978-3-13-240119-8

Also available as an e-book:eISBN 978-3-13-240263-8

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Contents

Videos

Preface

Contributors

1Introduction and History of Sleep Apnea Surgery

1.1 Introduction

1.2 A Short History of Surgery for Sleep-Disordered Breathing: From the Uvula Crusher to the Stimulation of the Hypoglossus Nerve

1.2.1 Antiquity

1.2.2 Renaissance

1.2.3 19th Century

1.2.4 20th Century

1.2.5 Palatal Surgery

1.2.6 Lower Pharyngeal Airway Procedures

1.2.7 Devices for the Tongue Base Suspension

1.2.8 Laryngeal Obstructive Sleep Apnea

1.2.9 Multilevel Surgery

1.2.10 Hypoglossal Stimulation

1.2.11 Maxillofacial Surgery

1.2.12 Final Remark

2Pathophysiology

2.1 Epidemiology

2.1.1 Introduction

2.1.2 Definitions

2.1.3 Signs and Symptoms Suggestive of Obstructive Sleep Apnea

2.1.4 Age and Gender Bias

2.1.5 Symptoms of OSA in Older Subjects

2.1.6 Symptoms in Overlap Syndrome

2.1.7 Focused History

2.1.8 Screening Questionnaires and Clinical Prediction Models

2.1.9 Consequences

2.1.10 Conclusions

2.2 Causes of Obstructive Sleep Apnea

2.2.1 Introduction

2.2.2 Anatomic Causes of Obstructive Sleep Apnea

2.2.3 Nonanatomic Causes of Obstructive Sleep Apnea

3Diagnosis of Sleep-Disordered Breathing

3.1 History Taking

3.1.1 Conclusion

3.2 Clinical Evaluation of Patients with (Suspected) Sleep-Disordered Breathing

3.2.1 Introduction

3.2.2 Anamnesis

3.2.3 General Evaluation

3.2.4 Upper Airway Evaluation

3.2.5 Limitations

3.2.6 Conclusion

3.3 Sleep Studies

3.3.1 Differential Diagnosis in Sleep-Related Breathing Disturbances

3.3.2 Clinical Investigations

3.3.3 Computer-Based Tests of Vigilance and Attention

3.3.4 Evaluation of Sleep and Breathing Disturbances During Sleep

3.3.5 Parameters of Sleep Studies

3.3.6 Case Reports

3.4 Topo Diagnosis of Obstruction Site(s)

3.4.1 Awake Nasopharyngoscopy

3.4.2 Drug-Induced Sleep Endoscopy

3.4.3 Upper Airway Imaging in Sleep-Disordered Breathing

3.4.4 Analysis of Snoring Sounds

4Nonsurgical Treatment: Lifestyle, Weight Loss, Positional Therapy, Mandibular Advancement Devices, Continuous Positive Airway Pressure, Multimodality Treatment

4.1 Introduction

4.2 Lifestyle Intervention

4.2.1 Didgeridoo and Physical Therapy

4.2.2 Alcohol, Tobacco, and Sedative Abstinence, Sleep Hygiene

4.3 Positional Therapy

4.4 Oral Appliances

4.4.1 Mechanism of Action

4.4.2 Outcomes

4.4.3 Side Effects

4.4.4 Patient Selection

4.5 Continuous Positive Airway Pressure

4.6 Multimodality Treatment

5Surgical Principles

5.1 Patient Selection

5.1.1 Introduction

5.1.2 Continuous Positive Airway Pressure Washout

5.2 How to Score and Compare Surgical Results with Those of Nonsurgical Treatment

5.2.1 Introduction

5.2.2 How to Compare the Different Treatment Options?

5.2.3 Formulas

5.2.4 Percentage of TST during which CPAP Must Be Used to Meet Sher’s Success Criteria

5.2.5 Percentage of TST during which CPAP Must Be Used to Reduce AHI to Below 10

5.2.6 Percentage of TST during which CPAP Must Be Used to Reduce AHI to Below 5

5.2.7 Percentage of TST during which CPAP Must Be Used to Reduce AHI by a Certain Percentage

5.2.8 Discussion

5.3 How to Measure Clinical Success

5.3.1 Surgical Success

5.3.2 Success in Conservative Treatment

5.3.3 AHI Defines OSA Severity

5.3.4 Clinical Endpoints in OSA

5.3.5 Literature

5.4 Combination Therapy for Sleep-Disordered Breathing

5.4.1 Combination of CPAP and Other Noninvasive Treatment Options

5.4.2 Combination of Different Types of Oral Appliance Therapy

5.4.3 Combination of Oral Appliance Therapy and Surgery

5.4.4 Combination of Positional Therapy and Other Noninvasive Treatment Options

5.4.5 Combination of Positional Therapy and Surgery

5.4.6 Conclusion

6Pediatric Obstructive Sleep Apnea

6.1 Diagnosis

6.1.1 Introduction

6.1.2 Prevalence

6.1.3 Clinical Finding

6.1.4 Physical Examination

6.1.5 Diagnostic Workup

6.2 Treatment

6.2.1 Introduction

6.2.2 Medical Intervention

6.2.3 Oral Appliances

6.2.4 Surgical Interventions

6.2.5 Anesthesia and Positioning

6.2.6 Operative Technique/Operative Steps

6.2.7 Complications (Including Measures for Specific Complications)

6.2.8 Postoperative Care (Including Medication and Drainage)

6.2.9 Outcome (Including EBM Data for AHI and ESS)

6.2.10 Other Pediatric Obstructive Sleep Apnea Surgeries

7Nose

7.1 Introduction

7.2 Pathophysiology

7.2.1 Nasal Breathing during Wakefulness

7.2.2 Nasal Breathing during Sleep

7.2.3 Theories, How an Increase in Nasal Resistance Can Induce Airway Collapse

7.3 Conservative Treatment of the Nose

7.3.1 Drugs

7.4 Nasal Surgery

7.4.1 Nasal Surgery for Snoring

7.4.2 Nasal Surgery for Obstructive Sleep Apnea

7.4.3 Nasal Surgery to Improve Positive Airway Pressure Treatments

8Surgery in Adults

8.1 Minimally Invasive Surgery

8.1.1 Interstitial Radiofrequency in the Soft Palate

8.1.2 Palatal Implants and Other Stiffening Procedures

8.1.3 Uvulopalatoplasty

8.2 Invasive Procedures

8.2.1 Palate and Tonsils

8.2.2 Tongue Base

8.2.3 Larynx and Trachea

8.3 Maxillofacial Surgeries

8.3.1 Introduction

8.3.2 Distraction Osteogenesis Maxillary Expansion

8.4 Multilevel Surgery

8.4.1 Definition

8.4.2 Indications, Contraindications, and Patient Selection

8.4.3 Diagnostic Workup

8.4.4 Specific Risks, Patient Information, and Consent

8.4.5 Anesthesia and Positioning

8.4.6 Equipment

8.4.7 Operative Technique/Steps

8.4.8 Complications

8.4.9 Postoperative Care

8.4.10 Outcomes

9Bariatric Surgery

9.1 Definition

9.2 Indications, Contraindications, and Patient Selection

9.3 Diagnostic Workup

9.4 Specific Risks, Patient Information, Consent

9.5 Anesthesia and Positioning

9.6 Equipment

9.7 Operative Technique/Operative Steps

9.8 Complications (Including Measures for Specific Complications)

9.9 Postoperative Care (Including Medications and Drainage)

9.10 Outcomes (Including Data for Apnea–Hypopnea Index and Epworth Sleepiness Scale)

10Postoperative Care and Follow-Up

10.1 Perioperative Care and Follow-Up: Anesthesiologist’s Aspects

10.1.1 Introduction

10.1.2 Perioperative Complications of OSA

10.1.3 Preoperative Management of Patients with OSA

10.1.4 Intraoperative Management of Patients with OSA

10.1.5 Postoperative Management of Patients with OSA

10.1.6 Outpatient Surgery for Patients with OSA

10.1.7 Conclusion

10.2 Perioperative Management: Surgeon’s Perspective

10.2.1 Introduction to OSA

10.2.2 Definition of OSA

10.2.3 Prevalence of OSA

10.2.4 Clinical Symptoms Suggesting Presence of OSA

10.2.5 General Clinical Signs Suggesting Presence of OSA

10.2.6 Head- and Neck-Specific Clinical Signs Suggesting Presence of OSA

10.2.7 Surgical Groups

10.2.8 Methods of OSA Screening

10.2.9 Treatment of OSA

10.2.10 Intraoperative Management

10.2.11 Postoperative Management

10.2.12 Postoperative Follow-Up

10.3 Follow-Up

10.3.1 Definition

10.3.2 Follow-Up for Outcome Measurements

10.3.3 Follow-Up in Active and Passive Implants for Sleep Apnea

Index

Videos

Video 6.1: Argon plasma coagulation technique for tonsillotomy.

Video 8.1: Z-palatopharyngoplasty (Z-PPP) technique.

Video 8.2: Relocation—uvulopalatopharyngoplasty (UPPP) in obstructive sleep apnea (OSA).

Video 8.3: Expansion sphincter pharyngoplasty (ESP) evolutive technique.

Video 8.4: Implantation of selective upper airway stimulation.

Video 8.5: Primary collapse of the epiglottis in an adult male.

Video 8.6: Three-dimensional planning of maxillomandibular advancement surgery in an OSA patient.

Video 8.7: Operative procedure of maxillomandibular advancement surgery in an OSA patient.

Video 8.8: Distraction osteogenesis maxillary expansion (DOME).

Preface

Obstructive sleep apnea (OSA) is one of the most frequent and common diseases all over the globe. In 1981, both continuous positive airway pressure (CPAP) and uvulopalatopharyngoplasty (UPPP) were introduced in the treatment of OSA. That year marked the birth of modern sleep medicine. We have since learnt a lot about the pathophysiology of OSA. Today, there is a variety of treatment modalities for OSA, snoring and related disturbances including conservative (i.e., diet, behavior therapy, positional treatments), medical device treatment (i.e., oral devices, CPAP), and operative treatments. After a period that was characterized by the search for the optimal single treatment, we today know that often a combination of different treatment modalities provides the best results.

Sleep apnea surgery is a relatively young discipline that is developing rapidly. Surgical procedures aimed to treat sleep apnea need to be selected in awareness of the individual underlying pathology, pathophysiology and anatomy, and severity of the disease, and comorbidities must also be taken into account. The first part of the book is designed to provide the reader with fundamental knowledge about the pathophysiology and diagnosis of OSA and to give a practical approach on how to choose the best treatment(s) for every individual case.

The second part concentrates on surgical approaches to treat OSA. Both of us have performed sleep apnea surgery for decades and witnessed, and to a certain extent influenced, the development of sleep apnea surgery for many years. Today, there are too many surgeries or modifications to include in one book. Therefore, we have discussed those techniques that work best in our hands. Leading experts in the field of surgery from all over the world have contributed as coauthors for specific topics and surgical techniques. Of course, there are other modifications of sleep surgeries that might work well or come up in future. However, we are convinced that this book provides a variety of effective surgical treatments that will help successfully treat the biggest part of the clinical cases. The easy-to-read text is accompanied by figures and videos of best quality, and the readers are provided with a variety of solutions for their sleep surgery cases. We very much hope that this book will become a helpful tool in sleep apnea surgery.

Thomas Verse, MDNico de Vries, MD, PhD

Contributors

José Enrique Barrera, MD, FACS

Associate Professor

Uniformed Services University

Bethesda, Maryland, USA

Clinical Associate Professor

University of Texas Health Sciences Center

Medical Director

Texas Facial Plastic Surgery and ENT

San Antonio, Texas, USA

Annemieke Beelen, MD

Department of Otorhinolaryngology–Head and Neck Surgery

OLVG Hospital

Amsterdam, The Netherlands

Chiara Bellini, MD

Department of Otolaryngology–Head and Neck Surgery

Head-Neck and Oral Surgery Unit

G.B. Morgagni-L. Pierantoni Hospital

Forli, Italy

Linda B. L. Benoist, MD

Department of Otorhinolaryngology and Head and Neck Surgery

Erasmus University Medical Center

Rotterdam, The Netherlands

Jolien Beyers, MD

Faculty of Medicine and Health Sciences

University of Antwerp

Antwerp, Belgium

Department of ENT, Head and Neck Surgery

Antwerp University Hospital UZA

Edegem, Belgium

Marc Blumen, MD

Head, Department of Otolaryngology/Sleep and Breathing

Centre Medical Veille-Sommeil

Paris, France

Marina Carrasco-Llatas, Md, PhD

ENT Consultant

Hospital Universitario Dr. Peset

Valencia, Spain

Alessandra Castrogiovanni, MD

Clinic for Pneumology and Allergology

Center of Sleep Medicine and Respiratory Care

Bethanien Hospital

Solingen, Germany

Khai Beng Chong, MD

Department of Otorhinolaryngology

Tan Tock Seng Hospital

Tan Tock Seng, Singapore

Marijke Dieltjens, MBS, PhD

Department of ENT, Head and Neck Surgery

Antwerp University Hospital UZA

Edegem, Belgium

Mohamed Salah El-Rashwan, MD

Department of Otolaryngology

Suez Canal University Teaching Hospitals

Ismailia, Egypt

Michael Friedman, MD, FACS

Department of Otolaryngology–Head and Neck Surgery

Division of Sleep Surgery

Rush University Medical Center

Department of Otolaryngology

Advanced Center for Specialty Care

Advocate Illinois Masonic Medical Center

Chicago, Illinois, USA

Christian Guilleminault, DM, MD, DBIOL

Professor

Department of Psychiatry and Behavioral Sciences

Stanford University School of Medicine

Stanford, California, USA

Evert Hamans, MD, PhD

ENT surgeon

Department of Otorhinolaryngology

Hospital Network Antwerp

Antwerp, Belgium

Clemens Heiser, MD, Prof.

Provisional Medical Director

Head of Sleep Laboratory

Department of Otorhinolaryngology, Head and Neck Surgery

Klinikum Rechts der Isar

Technical University of Munich

Munich, Germany

Simon Herkenrath, MD

Clinic for Pneumology and Allergology

Center of Sleep Medicine and Respiratory Care

Bethanien Hospital

Solingen, Germany

PD Dr. med. habil. Michael Herzog

Chief Doctor

Clinic for ENT diseases, Head and Neck Surgery

Carl-Thiem-Klinikum Cottbus gGmbH

Cottbus, Germany

Aarnoud Hoekema, MD, DMD, PhD

Oral and Maxillofacial Surgeon

Department of Oral and Maxillofacial Surgery

Tjongerschans Hospital

Heerenveen, The Netherlands

Department of Oral Kinesiology

Academic Centre for Dentistry Amsterdam (ACTA)

MOVE Research Institute Amsterdam

University of Amsterdam and VU University Amsterdam

Amsterdam, The Netherlands

Department of Oral and Maxillofacial Surgery

Academic Medical Center (AMC)

Amsterdam, The Netherlands

Department of Oral and Maxillofacial Surgery

University Medical Center Groningen

Groningen, The Netherlands

Jan de Lange, MD

Maxillofacial Surgeon

Chairman, Department of Maxillofacial Surgery

University of Amsterdam

Amsterdam, The Netherlands

Hsin-Ching Lin, MD, FACS, FICS

Professor and Chairman

Department of Otolaryngology

Sleep Center and Robotic Surgery Center

College of Medicine, Chang Gung University

Kaohsiung Chang Gung Memorial Hospital

Kaohsiung City, Taiwan

Stanley Yung-Chuan Liu, MD, DDS

Assistant Professor of Otolaryngology

Co-Director, Sleep Surgery Fellowship Stanford University School of Medicine

Stanford, California, USA

Peter van Maanen, MD, PhD

Department of Otorhinolaryngology–Head and Neck Surgery

OLVG Hospital

Amsterdam, The Netherlands

Andrea Marzetti, MD

Department of Otolaryngology

San Carlo di Nancy Hospital

Rome, Italy

OA Dr. med. Joachim T. Maurer

Deputy Hospital Director

University ENT Clinic Mannheim

Head of Sleep Medical Center

Mannheim, Germany

Giuseppe Meccariello, MD

Department of Otolaryngology–Head and Neck Surgery

Head-Neck and Oral Surgery Unit

G.B. Morgagni-L. Pierantoni Hospital

Forli, Italy

Carla Miltz, MD

Clinic for Pneumology and Allergology

Center of Sleep Medicine and Respiratory Care

Bethanien Hospital

Solingen, Germany

Filippo Montevecchi, MD

Department of Otolaryngology–Head and Neck Surgery

Head-Neck and Oral Surgery Unit

G.B. Morgagni-L. Pierantoni Hospital

Forli, Italy

Edward B. Pang

Student, Otolaryngology

Asia Sleep Centre

Paragon, Singapore

Kathleen A. Pang

Student, Otolaryngology

Asia Sleep Centre

Paragon, Singapore

Kenny P. Pang, FRCSEd, FRCSI(OTO)

Consultant, Otolaryngology

Asia Sleep Centre

Paragon, Singapore

Dirk Pevernagie, MD, PhD

Director

Center for Sleep Medicine

Kempenhaeghe Foundation

Heeze, The Netherlands

Department of Internal Medicine

Faculty of Medicine and Health Sciences

Ghent University

Ghent, Belgium

Prof. Dr. med. Wolfgang Pirsig

Professor Emeritus for Otorhinolaryngology

University of Ulm

Ulm, Germany

Anne-Lise Poirrier, MD

Rhinology and Facial Plastic Surgery

University Hospital of Liege

Liège, Belgium

Robert Poirrier, MD

Sleep Center, Department of Neurology

University Hospital of Liege

Liège, Belgium

Christel de Raaff, MD

Department of Surgery

Albert Schweitzer Hospital

Dordrecht, The Netherlands

Winfried J. Randerath, MD

Clinic for Pneumology and Allergology

Center of Sleep Medicine and Respiratory Care

Bethanien Hospital

Solingen, Germany

Madeline Ravesloot, MD, PhD, MSc

Department of Otorhinolaryngology–Head and Neck Surgery

OLVG Hospital

Amsterdam, The Netherlands

Martin Roesslein, MD

Department of Anesthesiology and Critical Care Medicine

University Medical Center

Freiburg, Germany

Kerstin Rohde†, MD

Private Practice

Hamburg, Germany

Jim Smithuis, MD, PhD

Department of Otorhinolaryngology–Head and Neck Surgery

OLVG Hospital

Amsterdam, The Netherlands

Ullrich Sommer, MD

Clinic for ENT Diseases

Helios University Clinic Wuppertal

Wuppertal, Germany

PD Dr. med. Armin Steffen

Managing Senior Physician

Department of Otolaryngology

University Hospital Schleswig-Holstein

Lübeck, Germany

Boris A. Stuck, MD

Clinic for ENT Diseases

Philipps-Universität Marburg

Marburg, Germany

Olivier M. Vanderveken, MD, PhD

Faculty of Medicine and Health Sciences

University of Antwerp

Antwerp, Belgium

Department of ENT, Head and Neck Surgery

Antwerp University Hospital UZA

Edegem, Belgium

Johan Verbraecken, MD, PhD

Pulmonologist and Medical Coordinator

Department of Pulmonary Medicine

Multidisciplinary Sleep Disorders Centre

Antwerp University Hospital UZA

Edegem, Belgium

Thomas Verse, MD

Professor of Otorhinolaryngology

Director of Department of Otorhinolaryngology–Head and Neck Surgery

Asklepios Clinic Harburg

Asklepios Campus Hamburg of Semmelweis University

Hamburg, Germany

Claudio Vicini, MD

Department of Otolaryngology–Head and Neck Surgery

Head-Neck and Oral Surgery Unit

G.B. Morgagni-L. Pierantoni Hospital

Forli, Italy

Nico de Vries, MD, PhD

Professor of Otolaryngology

Department of Otorhinolaryngology–Head and Neck Surgery

OLVG Hospital

Department of Oral Kinesiology

ACTA Amsterdam

Amsterdam, The Netherlands

Department of Otorhinolaryngology–Head and Neck Surgery

University of Antwerp

Antwerp, Belgium

Anneclaire Vroegop, MD

Faculty of Medicine and Health Sciences

University of Antwerp

Antwerp, Belgium

Department of ENT, Head and Neck Surgery

Antwerp University Hospital UZA

Edegem, Belgium

Bart van Wagensveld, MD

Department of Bariatric Surgery

Quro Obesity Center

Dubai, United Arab Emirates

David White, MD

Professor of Medicine, Part Time

Harvard Medical School

Boston, Massachusetts

Audrey Jung-Sun Yoon, MD

Orthodontist

Stanford, California, USA

Clinical Faculty, Lecturer

Section of Pediatric Dentistry

University of California Los Angeles

Los Angeles, California, USA

Honorary Assistant Professor

Orthodontics, Faculty of Dentistry

The University of Hong Kong

Sai Wan, Hong Kong

1 Introduction and History of Sleep Apnea Surgery

Abstract

Symptoms and surgical procedures for snoring and obstructive sleep apnea (OSA) are known from antiquity especially from Greece, where uvulas were crushed, nasal polyps removed, and fine needles thrust into the belly of Dionysius to stop his OSA-originated sleep. In the Renaissance, caustic methods were introduced by Arabian physicians of the Middle Ages and snares were installed to reduce obstructive tissues of the upper airways. In addition, guillotine-like devices for uvulectomy and tonsillotomy were developed and used until the 20th century. In 1878, Meyer added the effective adenoidectomy to the procedures for sleep-disordered breathing, while in 1969 Kuhl et al proved tracheostomy to be an effective therapy to heal even severe OSA. With the development of modern sleep medicine in the 1970s, palatal surgery, tongue base techniques, maxillofacial procedures, and multilevel surgery enabled a tailored treatment of the patients which for the moment is culminating in the successful hypoglossal nerve stimulation procedure.

Keywords: sleep surgery, history, obstructive sleep apnea, snoring

1.1 Introduction

David White

This book has been written to describe which patients with obstructive sleep apnea (OSA) can be identified as appropriate candidates for upper airway surgery, to describe in detail the various procedures available, and to discuss how a particular surgery can be selected for a given patient. Upper airway surgery, in general, assumes that the primary cause of OSA is an anatomically small pharyngeal airway and that the surgical procedure can adequately correct this anatomical abnormality to allow for unobstructed breathing during sleep. It has been known for years that abnormal pharyngeal anatomy is an important part of OSA pathophysiology and this will be discussed further. However, the success or failure of upper airway surgery to reduce or eliminate disordered breathing is likely dependent on a number of variables only some of which relate to anatomy. These include:

• The severity of the anatomical abnormality.

• The site or sites, severity, and configuration of collapse and their proper identification.

• The role and importance of nonanatomical traits in the pathogenesis of OSA in a particular patient.

The role of abnormal anatomy in the pathogenesis of OSA has been well described over the years. Haponik et al1 were the first to suggest this possibility when they demonstrated a smaller pharyngeal airway lumen in OSA patients compared with a control group using CT scanning in 1982. This led to numerous assessments of pharyngeal anatomy in OSA patients using a variety of imaging techniques including cephalometry, acoustic reflection, CT scanning, and MRI. The work of Richard Schwab2,3 using MRI for the past 10 to 15 years has convincingly demonstrated that the upper airway lumen is smaller and that certain tissue structures are larger in OSA patients compared with various control groups. These enlarged structures include the tongue, the lateral pharyngeal walls, the parapharyngeal fat pads, and the soft palate/uvula among others. However, virtually all such imaging has been conducted during wakefulness when pharyngeal muscles are active, making pure assessment of anatomy difficult. Ultimately Isono et al4 studied patients during neuromuscular blockade and found the pressure-area plots of patients with OSA to be quite different from controls, indicating a clear anatomic deficiency in the apnea patients.

In addition to studies directly assessing pharyngeal anatomy, metrics of pharyngeal collapsibility obtained during sleep have been used for the past 30 years to quantify the severity of the anatomic abnormality. Alan Schwartz and colleagues5,6 at Johns Hopkins developed the methods to quantify the critical closing pressure (Pcrt) that can be measured with and without pharyngeal muscle activity (active versus passive Pcrt). This metric has proved quite valuable as a physiologic measure of the severity of the anatomic abnormality and has been used widely. However, no measure of anatomy whether quantified awake or asleep, with or without muscle activity, or using imaging or physiologic techniques has correlated well with the severity of OSA.7 Indeed some patients without OSA have a similar or more collapsible airway than many OSA patients.8 Patients with a very high passive Pcrt (above 2–3 cm H2O) generally have more severe OSA than those with a lower Pcrt (−2 to 0 cm H2O). However, there remains huge variability in the apnea–hypopnea index (AHI) at any measured level of pharyngeal collapsibility.7,8 This failure to predict apnea severity can be interpreted in a number of ways. First, AHI may be a poor measure of OSA severity. Second, Pcrt may be a less quantitative assessment of the pure anatomy than originally thought. However, third, and most likely, is the fact that anatomy is not the entire explanation for the presence or severity of OSA. Other physiologic traits are likely important as well and these will be addressed later. That being said, anatomy is the most important trait in the majority of OSA patients, and OSA is likely to resolve if surgery can completely correct the anatomic deficiency yielding a minimally collapsible airway (Pcrt below −6 or −7 cm H2O).8 However, this is often difficult.

Recognizing that anatomy is not often the entire explanation for the presence of OSA, it is not surprising that the techniques described earlier for quantifying pharyngeal anatomy/collapsibility have not proved very useful in predicting who will and will not respond to upper airway surgery. Again, this may reflect our inability to adequately quantify collapsibility or the importance of nonanatomic traits. However, considerable effort has been put into at least identifying the site(s) of collapse as clearly as possible and directing the surgery at the appropriate site(s). Not surprisingly, assessing the site of collapse during sleep, generally using drug-induced sleep endoscopy (DISE), has proved the most fruitful.9 However, in the author’s opinion, no study has combined DISE and measurement of Pcrt to predict surgical outcomes, and such a study is needed as both the site of collapse and the severity of collapsibility seem likely to dictate surgical success.

It has become evident over the past 10 to 15 years that nonanatomical traits are important in OSA pathogenesis.10,11,12 Most evidence suggests that there are four phenotypic traits that dictate who will and will not develop OSA. As outlined earlier, anatomy is one such trait. The others include:

•The upper airway response: This is the ability of the pharyngeal dilator muscles to respond to standard stimuli (airway negative pressure and rising PCO2) during sleep. Conceptually, virtually all patients with OSA breathe normally while awake with little difficulty maintaining a patent upper airway. Thus pharyngeal dilator muscles can compensate for even the most anatomically deficient airway during wakefulness.13 It is the failure of this compensatory muscle activation during sleep that leads to airway collapse in most patients. However, there is considerable variability in the responsiveness of these muscles during sleep. In some patients these muscles can activate quickly during sleep yielding stable respiration despite considerable airway collapsibility. In other patients with a minimally abnormal airway, the muscles cannot compensate during sleep and airway collapse occurs rapidly. Thus, variability in upper airway muscle responsiveness importantly dictates who does and who does not develop sleep apnea.

•Arousal threshold to respiratory stimulation: Based on what has been said earlier, when there is deficient pharyngeal anatomy, upper airway muscles must respond during sleep to open the airway if apneas or hypopneas are to be prevented. However, the stimuli to the upper airway muscles (increasingly negative airway pressure and rising PCO2) develop slowly after the onset of airway obstruction.14 Thus the individual must stay asleep long enough for these stimuli to reach adequate levels to activate the dilator muscles and restore airway patency. If the individual awakens from sleep before the required level of muscle activation has been reached, stable breathing during sustained periods of sleep will become difficult to achieve. Thus a high respiratory arousal threshold may help prevent disordered breathing by allowing pharyngeal dilator muscles adequate time to activate. On the other hand, individuals with a low respiratory arousal threshold will readily awaken shortly after each episode of airflow obstruction and therefore cycle between sleep and wake.

•Loop gain (ventilatory control instability):Loop gain is an engineering term used to describe the gain of any system controlled by feedback loops. Respiratory control is very much a feedback-controlled system designed primarily to control arterial PCO2. Loop gain is most easily understood as the respiratory response to a disturbance divided by that disturbance, i.e., response/disturbance. A high loop gain is characterized by a large respiratory response to a small disturbance. In such a case, a small increase in PCO2 leads to a large increase in ventilation to correct it. When this occurs, ventilation can become unstable with waxing and waning between hyperpnea and hypopnea/apnea. Thus individuals with a high loop gain have a tendency toward unstable respiratory control.15 If that same individual has a collapsible upper airway, then small airway obstructions can lead to large ventilatory overshoots, which leads to the next obstructive event.

Thus, although upper airway anatomy is fundamentally important in the pathogenesis of OSA, it is far from the entire cause of this disorder.

The fact that sleep apnea has a multifactorial cause should not deter efforts focused primarily on improving pharyngeal anatomy such as upper airway surgery. As stated previously, if the anatomy can be adequately addressed, the other traits generally become unimportant. It is when surgery is unsuccessful or only partially successful that the other contributors to OSA need to be considered. Currently if surgery does not lead to an adequate reduction in AHI, doctors revert to standard approaches to apnea management, i.e., continuous positive airway pressure (CPAP), mandibular advancing devices, or further surgery; all approaches again focus on correcting the anatomy. An alternative approach would be to recognize that improving anatomy increases the potential role of the nonanatomic traits described before and makes therapies focused on these other traits more likely to be successful. As an example, two recently completed but unpublished studies (oral communication from Dr. Scott Sands in September 2017) indicate that the single most important trait distinguishing OSA patients who failed pharyngeal surgical procedures versus being cured was a particularly high loop gain, not badly abnormal anatomy. This would suggest, although the studies have not been performed, that treating this high loop gain in the surgical failures with acetazolamide or nocturnal oxygen might well turn failures into successes.

In conclusion, upper airway surgery in appropriately selected OSA patients is a viable therapy focused on correcting deficient pharyngeal anatomy, the primary cause of sleep apnea. Thus, if the anatomic defect is not too great, the site and type of surgery are correct, and the other nonanatomic traits are not terribly abnormal, surgery should be successful. However, when surgery is not successful, continuing to address only anatomy may not be in the best interest of the patient and efforts to improve the other traits may yield surprisingly good results. Such an approach, however, will require further research before it is broadly accepted.

1.2 A Short History of Surgery for Sleep-Disordered Breathing: From the Uvula Crusher to the Stimulation of the Hypoglossus Nerve

Wolfgang Pirsig

1.2.1 Antiquity

Observations about symptoms and surgical procedures to influence snoring and OSA are transmitted from antiquity. Let us start with the so-called “Sleeping Lady of Malta,” a 5,000-year-old terracotta sculpture from the Stone Age in the Hypogeum of Malta. She looks like a snoring woman suffering from obesity and hypersomnia.

In Greek mythology, the family of the Gods of the Underworld is associated with sleep in a fascinating interrelationship: Nyx (night) is the mother of the twins Hypnos (sleep) and Thanatos (death), and Morpheus (dreams) is the son of Hypnos. Detailed observations on the multiple facets of sleep-disordered breathing (SDB) were documented by the ancient Greeks and Romans, not only as to medical aspects but also in the Greco–Roman literature. Albert Esser (1885–1972) gave us an inspiring insight into these ancient sources about SDB.16 Snoring may be caused by exogenous factors such as excessive eating and drinking, supine position, dropping of the lower jaw, or an epidemic disease of the nose. Esser also cites endogenous or constitutional factors that induce snoring such as age, small children and old people, or the pyknic or plethoric sleeper with a well-fed neck. In the ancient literature there are some detailed observations of the characteristics of the snoring sounds, including the extremely loud and interrupted snoring and the apneic snoring combined with a stop of breath. The main inspiratory type of snoring was recognized, as were the respiratory effort and body movements associated with snoring.

Comparable body dimensions as “The Sleeping Lady of Malta” can be supposed for Dionysius (360–305 BC), tyrant of Heraclea on the Euxine (Black Sea). He loved eating and Athenaeus (“Deipnosophistae” ca. 200 AD) transmitted Dionysius’ wish on how to die: “One thing for my own self I desire - and this seems to me the only death that is a happy dying - to lie on my back with its many rolls of fat, scarce uttering a word, gasping for breath, while I eat and say ‘I am rotting away in pleasure.’”17 Athenaeus also reported that the physicians prescribed that he should get some fine needles, exceedingly long, which they thrust through his ribs and belly whenever he happened to fall into a very deep sleep. Now up to a certain point under the flesh, completely calloused as it was by fat, the needle caused no sensation; but if the needle went through so far as to touch the region which was free of fat, then he would be thoroughly aroused. At last Dionysius was choked by his own fat.18

In the 1980s, 2,300 years later, a modern form of bariatric surgery was applied in the United States to successfully treat obesity-related OSA.19 A study about 330 patients who were successfully treated by bariatric surgery was published by Kleinhans and Verse.20

Hippocrates (460–359 BC), clearly described how a nasal polyp causes snoring 2,400 years ago: “When the polyp comes from the nose, hanging down the middle cartilages like a uvula, softly expanding with expiration outside the nose, retracting with inspiration, it causes a croaky voice and snoring during sleep.”21 Hippocrates surgically treated the polyps with loops or using the sponge method which was nicely depicted by Baldewein22 (▶Fig. 1.1).

In the past, uvula pathology appears tos have been a common cause of different symptoms among them those associated with SDB. As the access to the uvula is easy, no wonder it became the scapegoat being sacrificed for all types of diseases for thousands of years as first documented in the Indian Sushruta 3,000 years ago. Hippocrates clearly recommended when to crush the uvula (Prognostic XXII): “It is dangerous to cut away or lance the uvula while it is red and enlarged, … Where, however, … forming what is called ‘the grape,’ that is when the front of the uvula is enlarged and vivid, while the upper part is thinner, it is safe to operate.”

Early instruments to amputate the uvula were excavated in Roman tombs. Usually they were manufactured from bronze. The forceps for crushing the uvula, termed staphylagra, is shown in ▶Fig. 1.2. It was buried in about 275 AD and found in a physician’s tomb in Paris.23

Fig. 1.1(a, b) Baldewein’s drawing of Hippocrates’ technique for removal of nasal polyps in snorers.22

Fig. 1.2 Staphylagra for crushing the uvula, bronze, Roman period (Milne, 1907; ▶Table 32.3)

1.2.2 Renaissance

In his book, Wund Artzney oder Artzneyspiegell, Ambroise Paré (1510–1590) mentioned that the swollen uvula causes prevention of sleep, coughing, and fear of being choked.24 This can be stopped by cauterizing it using nitric acid or a snare. The snare is depicted on a woodcut on page 267 of the book. In 1608, the same type of snare like that of Paré and a ligature carried on the outside of the ring was applied by Wilhelm Fabry von Hilden (1560–1634) to amputate the extremely long uvula disturbing respiration and eating in a noble man. The resected uvula and the snare in action are naturally shown in ▶Fig. 1.3.25

Thomas Bartholin (1616–1680) reported about a guillotine-knife type of uvulotome, but indicated that it was originally devised by a Norwegian peasant, Canute de Thorbern. This instrument is described and depicted by Johann Scultetus (1595–1645) from Ulm in his German book edition of 1666 (Scultetus 1666 p. 19–22 and Tabula IX Fig. I and Fig. II).26 Canute de Thorbern’s uvulotome (▶Fig. 1.4) later became the precursor of the tonsil guillotine for the rapid excision of the tonsils.

1.2.3 19th Century

In the 19th century several milestones were set in the field of medicine. César Jean Legallois (1812) described the neuronal influence on breathing and the heart. John Cheyne (1818) and William Stokes (1854) found connections between heart disorders and irregular breathing with central apneas.27,28 The poet Charles Dickens (1812–1870) gave excellent symptomatic descriptions of OSA in the character of Joe, (the little fat boy), and in the obese Samuel Pickwick in his continuing booklet papers (The Posthumes Papers of the Pickwick Club).29,30 In 1877, Sir Henry Broadbent (1835–1907), less poetically but meticulously, described an OSA: “When a person, especially advanced in years, is lying on his back in heavy sleep and snoring loudly, it very commonly happens that every now and then the inspiration fails to overcome the resistance of the pharynx, of which stridor or snoring is the audible sign, and there will be perfect silence through two, three or four respiratory periods, in which there are ineffectual chest movements; finally air enters with a loud snort, after which there are several compensatory deep inspirations …”.31

Concepts and instruments for sleep surgery relating to adenotomy, uvulectomy, tonsillotomy, tracheostomy, and nasal surgery were published in the second half of 19th century.

Hans Wilhelm Meyer (1824–1895) from Copenhagen, scholarly studied the adenoids and their symptoms, especially their impact on children during sleep.32 His descriptions of the symptoms (hearing problems, mouth breathing, sleep disturbance, snoring, floppy features, and sleepiness in children) are still valid today, and also his experience about the positive outcome after adenotomy as to snoring, sleep quality, and daytime sleepiness.

Thorbern’s uvular guillotine was modified for the use as tonsillotome in the 19th century by Philip Syng Physick (1828), William B. Fahnestock (1832), Morrel Mackenzie (1880), and Albert Mathieu (1883) (▶Fig. 1.5a, b). The Fahnestock-type tonsil guillotine still remained in use until the 1950s for tonsillotomy. Several casuistics about tonsillotomy for snoring children can be found in the 19th century. One example is the case report of Dr. Friedrich Betz about a 3-year-old boy: “… as sometimes snoring is caused by hypertrophic tonsils … In such a case, snoring can be reduced by amputation of the tonsils, or according to the circumstances can radically be healed.”33 However, the polysomnographic evidence that hypertrophic tonsils cause OSA in children who can be healed by adenotonsillectomy was shown not before 1965 when several centers in France, United States, and Canada published their results.34,35

In the just founded Lancet of 1848, tracheostomy for snoring in patients with epilepsy, severe drunkenness, and apoplexy was published by Marshall Hall (1790–1857).36 But it took more than 120 years before Wolfgang Kuhlo and colleagues from Freiburg im Breisgau polysomnographically proved that SDB due to a Pickwickian syndrome could be healed (▶Fig. 1.6).37

Fig. 1.3 Woodcut of the uvula resected (p. 93); snare resecting the uvula (p. 98).25

Fig. 1.4 Canute de Thorbern’s uvulotome in Scultetus 1666, Table IX.26

By the end of the 19th century, nasal surgery was also indicated in children and adults to improve their sleep quality and reduce snoring. Krieg successfully performed a submucous septal resection in a girl with obstructed nose, snoring, and attacks of suffocation during sleep.38 Cline published a case study of the relief of excessive daytime sleepiness following nasal surgery, and Wells reported an increase of daytime vigilance in 8 of 4010 patients after nasal surgery.39,40

1.2.4 20th Century

In the 19th century, insomnia, sleep apnea, and narcolepsy had been described; however, any type of documentation of sleep phenomena was lacking. In 1928, Hans Berger (1873–1941), a psychiatrist from Jena, registered the electrical activity of the human brain at the surface of the head and named the method electroencephalography.41 Thus, some sleep phenomena could be monitored continuously. However, sleep research was not actively pursued until the early 1950s when Nathaniel Kleitmann (1895–1999) and Eugene Aserinsky (1921–1998) first registered rapid eye movements (REMs) during sleep by means of electro-oculography in 1953.42 The pattern of sleep was differentiated in non–rapid eye movement (non-REM) and REM phases with regular cyclical periods. In 1973, sleep apnea as a syndrome was first described by Guilleminault et al.43 This group also established a sleep clinic at Stanford University. Until the late 1970s, mostly physiologists, neurologic and psychiatric specialists in their sleep laboratories diagnosed SDB using electroencephalographic (EEG) recordings, while pulmonary and intern departments investigated cardiopulmonary parameters. In the late 1970s, the diagnostics and treatments of SDB were taken over by interdisciplinary university sleep centers such as at Stanford, Detroit, Cleveland in the United States, Bologna in Italy, and Freiburg im Breisgau, Munich, and Marburg in Germany. In the 1980s, surgical disciplines were also integrated in these sleep centers.

Fig. 1.5(a, b) Mathieu-type tonsil guillotine, steel plated, designed in 1883, collection Pirsig.

Fig. 1.6 Polysomnographies before and following tracheotomy.37

The 1980s paved the way for new methods to treat SDB with device options, namely CPAP, oral appliances, and electrostimulation. Colin E. Sullivan, pneumologist from Sidney, has been an outstanding pioneer. In 1981, he published with his group the reversal of OSA by nasal CPAP.44

In 1982, German psychiatrist Karlheinz Meier-Ewert proved in a self-experiment over 9 months that an oral appliance functioning according to the principle of the Esmarch movement of the mandible could keep the upper airway open during sleep (1984 Munich Poster).45

The 1980s also saw otorhinolaryngologists and maxillofacial surgeons being inventive in developing new approaches for sleep surgery with varying degrees of success according to the level of the obstruction of the upper airway.

1.2.5 Palatal Surgery

Palatoplasty with a partial uvulectomy for loud snoring was first performed in 1964 by Takenosuke Ikematsu in Japan. He published his results in 152 patients in 1964.46

In 1977, Quesada et al from Barcelona proved by polysomnography that they could delete or reduce obstructive apneas by partial resection of the soft palate, uvulectomy, and tonsillectomy in patients with Pickwickian syndrome.47 In 1981, Shiro Fujita’s publication of uvulopalatopharyngoplasty (UPPP) spurred a new era in the surgical treatment of SDB.48 This rather invasive technique with several side effects was modified in many countries until the end of the century. The enthusiasm about UPPP decreased after Sher’s meta-analysis about UPPP showing that its overall positive efficacy was only 40%.49 Furthermore, Sher recognized that the success rate of sleep surgery also depends on the level of pharyngeal obstruction during sleep. In 1978, Hill et al had already studied the complex pattern of collapse of the pharyngeal walls during OSAs using fiberoptic and electromyographic (EMG) studies.50 During 1980s, the diagnostic tools of acoustic information in snoring noises, such as flexible nasopharyngoscopy, pharyngeal pressure measurements, and Müller maneuver during wakefulness, did not deliver the expected results to predict the levels of pharyngeal obstruction during sleep. Croft and Pringle (1991) introduced DISE to improve the detection of the proper levels for upper airway surgery in the daily work.51

Several modifications of the “standard UPPP” tried to improve the outcome of the palatal surgery, starting with Powell’s uvulopalatal flap (1996). In chronological order the following modifications were published: extended uvulopalatal flap (EUPF 2003), lateral pharyngoplasty (LP 2003), Z-palatoplasty (ZPP 2004), Han-UPPP (2005), expansion sphincter pharyngoplasty (ESP 2007), microdebrider-assisted extended uvulopalatoplasty (MEUP 2008), relocation pharyngoplasty (rPP 2009), Z-palatopharyngoplasty (Z-PPP 2010), and soft palate webbing flap (SPWF 2015). Details about the improvements, side effects, and references of these modifications, published after a mean follow-up of 10 months have recently been reported.52

1.2.6 Lower Pharyngeal Airway Procedures

Many invasive and less invasive procedures to achieve an enlargement of the pharyngeal tube at the tongue base level have been published. One principle was to reduce the amount of tongue base tissue and other procedures aimed to shift the tongue and/or surrounding tissues toward anteriorly. The first transoral tongue base resection was described by Djupesland et al in 1987.53 By 1992, Djupesland published the technique of palatopharyngoglossoplasty.54 In 1991, Fujita et al reported about the midline glossectomy using the laser.55 Chabolle performed the most extended tongue base reduction via an external approach and presented the results in 1999.56 In the same year, the feasibility of interstitial radiofrequency (RFQ) surgery of the tongue base as minimally invasive surgical therapy was first investigated in 15 OSA patients by Powell et al.57

Surgery on the hyoid bone to widen the upper airway for OSA was described by Kaya in 1984.58 Two years later Riley et al combined hyoid myotomy-suspension with inferior sagittal osteotomy of the mandible to treat OSA.59 This last technique has been modified by the Stanford group in 1994 under the term hyoid suspension, although it is a hyoidthyroidpexia.60 A less invasive modification, also applicable under local anesthesia, was introduced by Hörmann et al in 2001.61

1.2.7 Devices for the Tongue Base Suspension

By 1992, Faye-Lund et al verified the idea of tongue suspension by fixing the tongue base at the chin with homologous fascia lata, but this technique proved to involve great expense.62 The idea of tongue base suspension regained actuality in the 21st century in the form of some minimally invasive systems: the first invention of the Influ-ENT Repose system was published by DeRowe et al.63 Other existing medical devices for tongue suspension are lateral hyoid expansion (Aspire), Tongue anchor (Aspire), Advance system (Aspire), Flour-of-mouth Attracting System (Apneon), Pavad, and ReVent.

1.2.8 Laryngeal Obstructive Sleep Apnea

Laryngeal structures relatively rarely cause OSA in comparison to soft palate, tonsils, and tongue. In 1981, Olsen et al reported a case of OSA due to a laryngeal cyst in an infant, which was healed after removal of the cyst.64 In 1987, Zalzal et al described that newborns, especially preterm, with laryngeal abnormalities and presenting laryngomalacia needed procedures such as epiglottoplasty.65 In adults, a floppy epiglottis is the most common reason for laryngeal OSA and can be treated by laser surgery.66

1.2.9 Multilevel Surgery

The pathophysiological concept of a two level–pharyngeal collapse (retropalatal and retrolingual) proved to be too simplified and was replaced by a dynamic multiple level collapse concept, reflecting the complex pattern of collapsibility of the whole upper airway during sleep. This concept was especially successful in treating patients with SDB intolerant of nasal CPAP. Multilevel surgery for OSA was first performed in 1985 in Chicago by Caldarelli et al.67 They showed an increased positive outcome by adding a tongue retaining device and palatopharyngoplasty to nasal surgery in comparison to the success rate of the three methods alone. The step of treating OSA by surgical procedures of the nose, soft palate, tongue, mandible, and maxilla was published by Waite et al in 1989.68 Following Fujita’s division of the pharynx into three levels, Riley et al in 1993 termed this type of treatment as multilevel surgery, which is now achieved in all combinations of the single procedures.69,70

1.2.10 Hypoglossal Stimulation

In 1988, Miki et al found significant reduction in OSA in six patients who were electrically stimulated with surface electrodes in the submental region.71 This observation triggered a new effective treatment modality for patients with OSA rejecting CPAP or other therapies. The enormous progress and the efficacy of this new nerve stimulation method was recently published in the prospective cohort study—the STAR trial of 2017, reporting the successful stimulation of the hypoglossal nerve at follow-up after 48 months72 (see ▶Fig. 1.7).

Fig. 1.7 Tools for hypoglossal nerve stimulation with Inspire.

1.2.11 Maxillofacial Surgery

Since the 1980s, maxillomandibular advancement (MMA) has proved to be the most successful surgical option after tracheotomy in the treatment of OSA and was especially performed in patients with craniofacial deformities. This procedure was either performed on the mandible or maxilla or on both facial bones, and also in combination with above-mentioned procedures. By 1972, Cosman and Crikelair reported two cases of respiratory difficulty associated with micrognathia that responded to mandibular advancement, respectively, with hyoid advancement.73

Kuo et al performed mandibular advancement in three patients with OSA in 1979.74 In 1989, Waite et al published their results of maxillomandibular advancement surgery in 23 patients with OSA. In 1992, McCarthy et al introduced osteogenesis especially in infants with grossly retropositioned mandible or midface distraction.75 The enthusiasm about the initially good results had been dampened because follow-up showed partial recurrence of the malformation during growth.

1.2.12 Final Remark

The years of the 1980s were the “golden decade of therapy for SDB,” sleep surgery included. In the meantime, SDB had increasingly been recognized as a widespread disease with multidisciplinary aspects. Its many symptomatic facets in children and adults probably are the reason why patients with SDB often were not adequately diagnosed and treated in the past. Some surgical procedures started rather radical and turned into less invasive versions, while others disappeared. Since the beginning of the 21st century new devices have been integrated into sleep surgery. The enormous progress as to research, diagnostics, and treatment modalities in sleep medicine in the past 30 years is not only the result of technical improvements, but also of the increasingly interdisciplinary cooperation worldwide, the exchange of knowledge, and the growing World Wide Web. To be a witness of this development was an inspiring experience for the author as an otorhinolaryngologist who had performed adenotonsillectomies and tracheotomies in the 1970s without knowing that some of these patients suffered from OSA. In 1985, the author joined the group of sleep medicine to understand more of this fascinating specialty.

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2 Pathophysiology

Abstract

Obstructive sleep apnea (OSA) is diagnosed more frequently now than in the past. The characteristics of this potentially life-threatening disorder are (socially) disturbing snoring, excessive daytime sleepiness, disturbed concentration and memory, personality changes as well as cardiovascular, metabolic, and cognitive morbidities. Snoring is usually the cardinal symptom, but is aspecific, while the disorder can be suspected based on a thorough history taking (and physical-technical examination). In high-risk populations, OSA can contribute to the course of the underlying disorder, and influence its outcome. Due to its high prevalence and multiple interactions with most organ systems, OSA is a huge burden for the healthcare systems worldwide which deserves explicit attention.

Keywords: epidemiology, prevalence, apnea, fatigue, sleepiness, nocturia, prediction, consequences, comorbidities, hypertension, stroke, arrhythmias, coronary artery disease, metabolic, cognitive, obesity, chronic heart failure

2.1 Epidemiology

Johan Verbraecken

2.1.1 Introduction

Epidemiological studies provide strong evidence that sleep-disordered breathing (SDB), especially OSA, is highly prevalent not only in the general population (▶Table 2.1), but also in specific patient categories with obesity,1,2 systemic hypertension,3,4 cardiovascular disease,5,6,7,8 diabetes mellitus,9,10,11 metabolic syndrome,12 and endocrinopathies.9,13 Often patients with SDB suffer from excessive daytime sleepiness, though other symptoms can be present as well, while some others remain asymptomatic. In some cases, patients express fatigue, tiredness, or lack of energy rather than sleepiness itself, which can be related to a comorbid medical disorder, but can also be the cardinal symptom of OSA.14,15,16,17