Materiały źródłowe

• #1 Pathophysiology of Pediatric Obstructive Sleep Apnea

  https://pmc.ncbi.nlm.nih.gov/articles/PMC2645256/

  Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. The pathophysiology of OSA in children is a complex interaction between an airway predisposed toward collapse and neuromuscular compensation. Anatomic measures of the airway lumen, soft tissue, and skeleton are of critical importance to the development of OSA, although they do not completely account for the pattern of sleep-disordered breathing. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Arousal from sleep contributes to ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.

• #2 Pathophysiology of Pediatric Obstructive Sleep Apnea

  https://pmc.ncbi.nlm.nih.gov/articles/PMC2645256/

  The essential feature of obstructive sleep apnea (OSA) in children is increased upper airway resistance during sleep. Airway narrowing may be due to craniofacial abnormalities and/or soft tissue hypertrophy. The resultant breathing patterns during sleep are highly variable, but include obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. […] The pathophysiology of OSA in children is a complex interaction between an airway predisposed toward collapse and neuromuscular compensation. […] Arousal from sleep contributes to ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep.

• #3 Pediatric Obstructive Sleep Apnea – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557610/

  Pediatric obstructive sleep apnea (OSA) is a childhood disorder in which there is upper airway dysfunction causing complete or partial airway obstruction during sleep leading to decreased oxygen saturation or arousals from sleep. It can have dramatic effects on childhood behavior, neurodevelopment, metabolism, and overall health. Early recognition, evaluation, and treatment are important to prevent long-term consequences. […] Obstructive sleep apnea, 95% of diagnosed sleep apnea, is due to complete collapse of the upper airway or partial collapse, resulting in arousal from sleep or 3% or more oxygen desaturation. Anything that can decrease airway diameter or integrity can contribute to OSA, including anatomic, genetic, or neuromuscular issues. […] The four main features that contribute to OSA are obesity, lymphoid hyperplasia, craniofacial abnormalities, and neuromuscular dysfunction. All of these abnormalities provide increased extrinsic factors that can lead to upper airway compression or collapsibility. Obesity causes fat deposits to surround the upper airway and increase extrinsic pressure that causes collapse. The presence of lymphoid hyperplasia causes tonsillar and adenoid obstruction of the airway, and the increased relaxation during sleep allows these to become significantly more problematic. Neuromuscular dysfunction can be seen in both central and obstructive causes of sleep apnea. This is most often seen in cases like Down syndrome, where there is hypotonia, which contributes to increased susceptibility of the airway to collapse. Additionally, patients with craniofacial abnormalities, including those with Crouzon, Pierre-Robin, or Apert syndromes, as well as those with cleft lip or palate, are at an increased risk. The presence of alteration of the normal airway anatomy as well as features such as micrognathia, micro or macroglossia, and midface hypoplasia all contribute to decreased posterior oropharynx space and the increased incidence of pediatric OSA.

• #4 Obstructive sleep apnea syndrome in children: Epidemiology, pathophysiology, diagnosis and sequelae

  https://www.e-cep.org/journal/view.php?number=2010531001

  The prevalence of pediatric obstructive sleep apnea syndrome (OSAS) is approximately 3% in children. Adenotonsillar hypertrophy is the most common cause of OSAS in children, and obesity, hypotonic neuromuscular diseases, and craniofacial anomalies are other major risk factors. […] The main risk factors for OSAS in adults are obesity and male sex, which are related to the propensity for repetitive upper airway collapse. In younger children, the major risk factor for the development of OSAS is adenotonsillar hypertrophy. […] It is suggested that central ventilatory drive is increased during childhood and then declines gradually with age. This increased central ventilatory drive during sleep accounts for the increased upper airway reflexes and tone in children, resulting in less collapsibility than in adults.

• #5 Pediatric Obstructive Sleep Apnea – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557610/

  The incidence of pediatric OSA peaks between 2 to 8 years of age due to the increased growth of tonsils and adenoids relative to the size of the upper airway in this age group. Risk factors for early-onset OSA include prematurity, Down syndrome, African American race, and daycare attendance. The severity can be increased in those with obesity, tobacco exposure, and reduced family income. […] Diagnosis of sleep apnea is made by measuring the apneic events during sleep. […] If there is adenotonsillar hypertrophy, the most effective treatment is adenotonsillectomy (AT). This is recommended for most patients with an AHI more than 9 events/hour and those with mild or moderate disease with significant symptoms. […] If identified and managed promptly, patients will not suffer long-term consequences or complications of pediatric OSA.

• #6 Pediatric Obstructive Sleep Apnea – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557610/

  Pediatric obstructive sleep apnea (OSA) is a childhood disorder in which there is upper airway dysfunction causing complete or partial airway obstruction during sleep leading to decreased oxygen saturation or arousals from sleep. It can have dramatic effects on childhood behavior, neurodevelopment, metabolism, and overall health. Early recognition, evaluation, and treatment are important to prevent long-term consequences. […] Obstructive sleep apnea, 95% of diagnosed sleep apnea, is due to complete collapse of the upper airway or partial collapse, resulting in arousal from sleep or 3% or more oxygen desaturation. Anything that can decrease airway diameter or integrity can contribute to OSA, including anatomic, genetic, or neuromuscular issues. […] The four main features that contribute to OSA are obesity, lymphoid hyperplasia, craniofacial abnormalities, and neuromuscular dysfunction. All of these abnormalities provide increased extrinsic factors that can lead to upper airway compression or collapsibility. Obesity causes fat deposits to surround the upper airway and increase extrinsic pressure that causes collapse. The presence of lymphoid hyperplasia causes tonsillar and adenoid obstruction of the airway, and the increased relaxation during sleep allows these to become significantly more problematic. Neuromuscular dysfunction can be seen in both central and obstructive causes of sleep apnea. This is most often seen in cases like Down syndrome, where there is hypotonia, which contributes to increased susceptibility of the airway to collapse. Additionally, patients with craniofacial abnormalities, including those with Crouzon, Pierre-Robin, or Apert syndromes, as well as those with cleft lip or palate, are at an increased risk. The presence of alteration of the normal airway anatomy as well as features such as micrognathia, micro or macroglossia, and midface hypoplasia all contribute to decreased posterior oropharynx space and the increased incidence of pediatric OSA.

• #7 Update on paediatric obstructive sleep apnoea – Dehlink – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/6511/6228

  Obstructive sleep apnoea (OSA) is one of the most common causes of sleep-disordered breathing (SDB) in children. […] The low grade systemic inflammation and increased oxidative stress seen in this condition are believed to underpin the development of these OSA-related morbidities. […] Although the aetiologies of paediatric OSA are multiple, they can be broadly classified into conditions which result in intrinsic upper airway narrowing and those that result in increased upper airway collapsibility. […] Adenotonsillar hypertrophy is currently the most common example of the former. […] To understand upper airway collapsibility, researchers have modeled the upper airway as a Starling resistor, essentially a rigid tube with a collapsible segment, the collapsible segment being the pharynx bordered by rigid upstream (nasal passages) and downstream (trachea) segments.

• #8 Obstructive sleep apnea syndrome in children: Epidemiology, pathophysiology, diagnosis and sequelae

  https://www.e-cep.org/journal/view.php?number=2010531001

  In obese children, excessive deposition of fat tissue within the muscles and tissue surrounding the upper airway leads to reduced airway size and increased airway resistance. […] Genetic risk factors have been identified in the development of OSAS. […] The pathophysiology of cardiovascular complications is as follows: intermittent upper airway obstruction during sleep in OSAS patients that have induced an exaggeration of continuous negative intrathoracic pressure swings, leading to a second series of sustained alterations of blood pressure and endothelial function, and eventually changes in cardiac structure and function occurs probably via oxidative stress and increased sympathetic tone. […] Pediatric OSAS has been commonly overlooked and underdiagnosed by both parents and clinician until now.

• #9 Current Concepts in Pediatric Obstructive Sleep Apnea

  https://www.mdpi.com/2227-9067/10/3/480

  In young healthy children, the main etiology of OSA is related to adenoid and/or tonsillar hypertrophy. However, other factors such as malocclusion or other causes of inflammation such as allergic rhinitis and asthma may also play a significant role. […] Obesity is increasingly more prevalent in the pediatric population and is a significant risk factor for OSA especially in the adolescent group. […] Comprehensive sleep history and thorough physical examination to screen for OSA in children are inadequate for a definitive diagnosis of OSA. […] Despite the extensive clinical description of symptoms and signs of OSA, the sensitivity and specificity of these parameters are limited in predicting polysomnography-confirmed OSA. […] Attempts to develop different screening tools have resulted in limited sensitivity and specificity. In-laboratory polysomnography (PSG) remains the gold standard for diagnosing pediatric sleep-disordered breathing.

• #10 Pediatric Obstructive Sleep Apnea – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557610/

  Pediatric obstructive sleep apnea (OSA) is a childhood disorder in which there is upper airway dysfunction causing complete or partial airway obstruction during sleep leading to decreased oxygen saturation or arousals from sleep. It can have dramatic effects on childhood behavior, neurodevelopment, metabolism, and overall health. Early recognition, evaluation, and treatment are important to prevent long-term consequences. […] Obstructive sleep apnea, 95% of diagnosed sleep apnea, is due to complete collapse of the upper airway or partial collapse, resulting in arousal from sleep or 3% or more oxygen desaturation. Anything that can decrease airway diameter or integrity can contribute to OSA, including anatomic, genetic, or neuromuscular issues. […] The four main features that contribute to OSA are obesity, lymphoid hyperplasia, craniofacial abnormalities, and neuromuscular dysfunction. All of these abnormalities provide increased extrinsic factors that can lead to upper airway compression or collapsibility. Obesity causes fat deposits to surround the upper airway and increase extrinsic pressure that causes collapse. The presence of lymphoid hyperplasia causes tonsillar and adenoid obstruction of the airway, and the increased relaxation during sleep allows these to become significantly more problematic. Neuromuscular dysfunction can be seen in both central and obstructive causes of sleep apnea. This is most often seen in cases like Down syndrome, where there is hypotonia, which contributes to increased susceptibility of the airway to collapse. Additionally, patients with craniofacial abnormalities, including those with Crouzon, Pierre-Robin, or Apert syndromes, as well as those with cleft lip or palate, are at an increased risk. The presence of alteration of the normal airway anatomy as well as features such as micrognathia, micro or macroglossia, and midface hypoplasia all contribute to decreased posterior oropharynx space and the increased incidence of pediatric OSA.

• #11 Childhood Sleep Apnea, Pediatric Obstructive Sleep Apnea (OSA)

  https://my.clevelandclinic.org/health/diseases/14312-obstructive-sleep-apnea-in-children

  Childhood sleep apnea is a common condition that causes a pause in your childs breathing pattern while they sleep. Your childs breathing changes due to an obstruction or blockage in their airway or because their brain isnt communicating with their breathing muscles. […] An obstruction or blockage in your childs airways causes obstructive childhood sleep apnea. A miscommunication from your childs brain to the muscles in your childs airway causes central sleep apnea. Sometimes the use of a CPAP machine may cause a more complex sleep apnea. […] Blockages or obstructions caused by obstructive sleep apnea can be the result of: Enlarged tonsils or adenoids. These are glands located in the back of your throat. They can get bigger if your child has an infection or inflammation. A genetic trait can make their glands larger than normal.

• #12 Pediatric Obstructive Sleep Apnea – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557610/

  Pediatric obstructive sleep apnea (OSA) is a childhood disorder in which there is upper airway dysfunction causing complete or partial airway obstruction during sleep leading to decreased oxygen saturation or arousals from sleep. It can have dramatic effects on childhood behavior, neurodevelopment, metabolism, and overall health. Early recognition, evaluation, and treatment are important to prevent long-term consequences. […] Obstructive sleep apnea, 95% of diagnosed sleep apnea, is due to complete collapse of the upper airway or partial collapse, resulting in arousal from sleep or 3% or more oxygen desaturation. Anything that can decrease airway diameter or integrity can contribute to OSA, including anatomic, genetic, or neuromuscular issues. […] The four main features that contribute to OSA are obesity, lymphoid hyperplasia, craniofacial abnormalities, and neuromuscular dysfunction. All of these abnormalities provide increased extrinsic factors that can lead to upper airway compression or collapsibility. Obesity causes fat deposits to surround the upper airway and increase extrinsic pressure that causes collapse. The presence of lymphoid hyperplasia causes tonsillar and adenoid obstruction of the airway, and the increased relaxation during sleep allows these to become significantly more problematic. Neuromuscular dysfunction can be seen in both central and obstructive causes of sleep apnea. This is most often seen in cases like Down syndrome, where there is hypotonia, which contributes to increased susceptibility of the airway to collapse. Additionally, patients with craniofacial abnormalities, including those with Crouzon, Pierre-Robin, or Apert syndromes, as well as those with cleft lip or palate, are at an increased risk. The presence of alteration of the normal airway anatomy as well as features such as micrognathia, micro or macroglossia, and midface hypoplasia all contribute to decreased posterior oropharynx space and the increased incidence of pediatric OSA.

• #13 Pediatric Obstructive Sleep Apnea > Fact Sheets > Yale Medicine

  https://www.yalemedicine.org/conditions/pediatric-obstructive-sleep-apnea

  Sleep apnea is a condition in which the muscles at the back of the throat intermittently relax too much, partially or completely blocking the airway. […] Obstructive sleep apnea affects 3 to 6 percent of children and is associated with repetitive narrowing of the airways, which is the breathing tube from the mouth and the nose down to the lungs, explains Yale Medicine’s Craig A. Canapari, MD, director of the Pediatric Sleep Medicine Program. […] Obesity is a common factor associated with obstructive sleep apnea in adults. In children, however, the most common cause of the problem is enlarged tonsils and adenoids. […] Additional causes of obstructive sleep apnea in children include „low airway tone as in cerebral palsy or Down syndrome,” Dr. Canapari notes. […] If your child has obstructive sleep apnea, your physician may recommend removal of the tonsils (tonsillectomy) or adenoids (adenoidectomy), or both.

• #14 Childhood Sleep Apnea: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1004104-overview

  Childhood sleep apnea differs from adult obstructive sleep apnea in that adults with sleep apnea frequently present with hypersomnia, whereas children often demonstrate short attention spans, emotional lability, and behavioral problems. […] For most children, enlargement of the tonsils and/or adenoid is the proximate cause for the development of obstructive sleep apnea. […] The contribution of the various anatomical nasopharyngeal structures to Pcrit and the interactions between these structures that lead to upper airway patency or obstruction during sleep are of obvious importance in increasing the understanding of the pathophysiology of obstructive sleep apnea in children. […] The static pressure and/or area relationships of the passive pharynx were endoscopically measured in 14 children with obstructive sleep apnea and in 13 healthy children under general anesthesia with complete paralysis, and it was determined that children with obstructive sleep apnea closed their airways at the level of enlarged adenoids and tonsils at low positive pressures, whereas healthy children required subatmospheric pressures to induce upper airway closure. […] Thus, both congenital and acquired anatomic factors clearly play a significant role in the pathogenesis of pediatric obstructive sleep apnea.

• #15 Update on paediatric obstructive sleep apnoea – Dehlink – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/6511/6228

  Obstructive sleep apnoea (OSA) is one of the most common causes of sleep-disordered breathing (SDB) in children. […] The low grade systemic inflammation and increased oxidative stress seen in this condition are believed to underpin the development of these OSA-related morbidities. […] Although the aetiologies of paediatric OSA are multiple, they can be broadly classified into conditions which result in intrinsic upper airway narrowing and those that result in increased upper airway collapsibility. […] Adenotonsillar hypertrophy is currently the most common example of the former. […] To understand upper airway collapsibility, researchers have modeled the upper airway as a Starling resistor, essentially a rigid tube with a collapsible segment, the collapsible segment being the pharynx bordered by rigid upstream (nasal passages) and downstream (trachea) segments.

• #16 Update on paediatric obstructive sleep apnoea – Dehlink – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/6511/6228

  Disturbances in Pcrit are believed to play a key role in OSA pathogenesis. […] Children with OSA have been found to have significantly more collapsible upper airways with elevated (i.e., less negative) Pcrit during sleep than children without OSA. […] Increased upper airway collapsibility can be caused either by conditions leading to a decrease in muscle tone in the upper airway, such as cerebral palsy, neuromuscular disorders, or inflammatory conditions affecting the upper airways, such as allergic rhinitis and asthma. […] The concurrent presence of adenotonsillar hypertrophy and obesity appears to facilitate the emergence of OSA. […] The consequent excessive daytime sleepiness from OSA is likely to impact on physical activity, which in turn favours more weight gain. […] Furthermore, OSA and obesity might also be linked via an imbalance between leptin and ghrelin, two hormones crucial in regulating satiety and hunger.

• #17

  https://journals.lww.com/prcm/fulltext/2021/05020/paediatric_obstructive_sleep_apnoea_.3.aspx

  Other structural factors increasing the risk of developing childhood OSA include craniofacial skeletal dysmorphologies in the mandible and maxilla. […] The UA size is mainly determined by static pharyngeal mechanics, neuromuscular tone, and luminal pressure, with multiple studies reporting children with OSA having higher positive critical closing pressures of the pharynx (Pcrit), with airways collapsing easily in mild inspiratory negative pressures. […] This indicates that other neuromuscular factors may play an integral role, with the passive Pcrit and mean airway closing pressure (Pclose) being 25 cm H2O and 7.4 cm H2O, respectively, in normal children, compared with 5 cm H2O and 2 cm H2O in children with OSA, indicating problems with neuromuscular compensation. […] Intermittent hypoxia and re-oxygenation episodes induced by OSA stimulate tissue necrosis, oxidative stress, and macrophage infiltration, resulting in localized inflammation and consequent systemic inflammation due to circulating cytokines released by proinflammatory immune cells. […] Indeed, studies have shown that proinflammatory markers, such as tumour necrosis factor alpha (TNF-), interleukin (IL)-17, IL-23, and C-reactive protein (CRP), are significantly increased in children with OSA.

• #18 Childhood Sleep Apnea: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1004104-overview

  In addition, in contrast to adults, some children exhibit a variation of obstructive sleep apnea termed obstructive hypoventilation (OH). Children with obstructive hypoventilation demonstrate periods of hypercapnia that occur in the absence of discrete respiratory events that fulfill the criteria for apnea or hypopnea. […] The ability to maintain upper airway patency during the normal respiratory cycle is the result of a delicate equilibrium between the forces that promote airway closure and dilation. […] The 4 major predisposing factors for upper airway obstruction are the following: Anatomic narrowing, Abnormal mechanical linkage between airway dilating muscles and airway walls, Muscle weakness, Abnormal neural regulation. […] Obstructive apnea and hypopnea are related to upper airway obstruction. Upper airway obstruction may occur at one or more levels, including the nasopharynx, mouth, velopharynx, retroglossal region, hypopharynx, and larynx.

• #19 Childhood Sleep Apnea: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1004104-overview

  In addition, in contrast to adults, some children exhibit a variation of obstructive sleep apnea termed obstructive hypoventilation (OH). Children with obstructive hypoventilation demonstrate periods of hypercapnia that occur in the absence of discrete respiratory events that fulfill the criteria for apnea or hypopnea. […] The ability to maintain upper airway patency during the normal respiratory cycle is the result of a delicate equilibrium between the forces that promote airway closure and dilation. […] The 4 major predisposing factors for upper airway obstruction are the following: Anatomic narrowing, Abnormal mechanical linkage between airway dilating muscles and airway walls, Muscle weakness, Abnormal neural regulation. […] Obstructive apnea and hypopnea are related to upper airway obstruction. Upper airway obstruction may occur at one or more levels, including the nasopharynx, mouth, velopharynx, retroglossal region, hypopharynx, and larynx.

• #20 Pathophysiology of Pediatric Obstructive Sleep Apnea | CoLab

  https://colab.ws/articles/10.1513%2Fpats.200707-111MG

  Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. […] However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.

• #21 Pathophysiology of Pediatric Obstructive Sleep Apnea | CoLab

  https://colab.ws/articles/10.1513%2Fpats.200707-111MG

  Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. […] However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.

• #22 Pathophysiology of Pediatric Obstructive Sleep Apnea

  https://pmc.ncbi.nlm.nih.gov/articles/PMC2645256/

  The essential feature of obstructive sleep apnea (OSA) in children is increased upper airway resistance during sleep. Airway narrowing may be due to craniofacial abnormalities and/or soft tissue hypertrophy. The resultant breathing patterns during sleep are highly variable, but include obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. […] The pathophysiology of OSA in children is a complex interaction between an airway predisposed toward collapse and neuromuscular compensation. […] Arousal from sleep contributes to ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep.

• #23 Pathophysiology of Pediatric Obstructive Sleep Apnea

  https://pmc.ncbi.nlm.nih.gov/articles/PMC2645256/

  The essential feature of obstructive sleep apnea (OSA) in children is increased upper airway resistance during sleep. Airway narrowing may be due to craniofacial abnormalities and/or soft tissue hypertrophy. The resultant breathing patterns during sleep are highly variable, but include obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. […] The pathophysiology of OSA in children is a complex interaction between an airway predisposed toward collapse and neuromuscular compensation. […] Arousal from sleep contributes to ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep.

• #24 Pathophysiology of Pediatric Obstructive Sleep Apnea | CoLab

  https://colab.ws/articles/10.1513%2Fpats.200707-111MG

  Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. […] However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.

• #25 Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01496-3

  In recent years, a number of studies have shown that a low respiratory arousal threshold may be an important endotype of OSAS. […] In ventilatory control, loop gain is a measure of respiratory instability, which refers to unstable ventilatory chemoreflex control and is recognized as a key pathophysiological feature that contributes to OSAS. […] Increased pharyngeal dilator muscle activity in OSAS patients compared with matched controls has been interpreted as evidence of a neuromuscular protective compensatory reflex in response to anatomical compromise in OSAS.

• #26 Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01496-3

  In recent years, a number of studies have shown that a low respiratory arousal threshold may be an important endotype of OSAS. […] In ventilatory control, loop gain is a measure of respiratory instability, which refers to unstable ventilatory chemoreflex control and is recognized as a key pathophysiological feature that contributes to OSAS. […] Increased pharyngeal dilator muscle activity in OSAS patients compared with matched controls has been interpreted as evidence of a neuromuscular protective compensatory reflex in response to anatomical compromise in OSAS.

• #27 Update on paediatric obstructive sleep apnoea – Dehlink – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/6511/6228

  OSA has been shown to be associated with leptin resistance and increased ghrelin levels, which could favour obesity. […] There is emerging evidence that OSA is a disease with chronic low grade systemic inflammation and increased oxidative stress which likely lead to the end organ morbidities described above. […] The mechanisms underlying these imbalances are not fully understood, but some interesting findings have been made recently. […] OSA and obesity seem to mutually amplify the systemic inflammatory pathways, for instance monocyte chemoattractant protein 1 and plasminogen activator-inhibitor 1 levels have been found to be significantly raised in obese OSA children compared with body mass index (BMI)-matched obese children without OSA. […] It is postulated that this induction of inflammatory cascades along with increased oxidative stress gives rise to the morbidities associated with OSA.

• #28 You Cannot Hit Snooze on OSA: Sequelae of Pediatric Obstructive Sleep Apnea

  https://www.mdpi.com/2227-9067/9/2/261

  Pediatric obstructive sleep apnea (OSA) has been shown to not only affect the quality of sleep, but also overall health in general. Untreated or inadequately treated OSA can lead to long-term sequelae involving cardiovascular, endothelial, metabolic, endocrine, neurocognitive, and psychological consequences. The physiological effects of pediatric OSA eventually become pathological. […] Pediatric obstructive sleep apnea (OSA) has adverse effects as a result of disruption of sleep and abnormal ventilation. Long term, if untreated, pediatric OSA can lead to adverse cardiovascular, endothelial, metabolic, endocrine, neurocognitive, and psychological outcomes that affect quality of life. […] Untreated or inadequately treated OSA in children can lead to systemic and pulmonary hypertension, postural orthostatic hypertension syndrome, cardiac arrhythmias, coronary artery changes, and cerebrovascular changes.

• #29

  https://journals.lww.com/prcm/fulltext/2021/05020/paediatric_obstructive_sleep_apnoea_.3.aspx

  Other structural factors increasing the risk of developing childhood OSA include craniofacial skeletal dysmorphologies in the mandible and maxilla. […] The UA size is mainly determined by static pharyngeal mechanics, neuromuscular tone, and luminal pressure, with multiple studies reporting children with OSA having higher positive critical closing pressures of the pharynx (Pcrit), with airways collapsing easily in mild inspiratory negative pressures. […] This indicates that other neuromuscular factors may play an integral role, with the passive Pcrit and mean airway closing pressure (Pclose) being 25 cm H2O and 7.4 cm H2O, respectively, in normal children, compared with 5 cm H2O and 2 cm H2O in children with OSA, indicating problems with neuromuscular compensation. […] Intermittent hypoxia and re-oxygenation episodes induced by OSA stimulate tissue necrosis, oxidative stress, and macrophage infiltration, resulting in localized inflammation and consequent systemic inflammation due to circulating cytokines released by proinflammatory immune cells. […] Indeed, studies have shown that proinflammatory markers, such as tumour necrosis factor alpha (TNF-), interleukin (IL)-17, IL-23, and C-reactive protein (CRP), are significantly increased in children with OSA.

• #30

  https://journals.lww.com/prcm/fulltext/2021/05020/paediatric_obstructive_sleep_apnoea_.3.aspx

  Other structural factors increasing the risk of developing childhood OSA include craniofacial skeletal dysmorphologies in the mandible and maxilla. […] The UA size is mainly determined by static pharyngeal mechanics, neuromuscular tone, and luminal pressure, with multiple studies reporting children with OSA having higher positive critical closing pressures of the pharynx (Pcrit), with airways collapsing easily in mild inspiratory negative pressures. […] This indicates that other neuromuscular factors may play an integral role, with the passive Pcrit and mean airway closing pressure (Pclose) being 25 cm H2O and 7.4 cm H2O, respectively, in normal children, compared with 5 cm H2O and 2 cm H2O in children with OSA, indicating problems with neuromuscular compensation. […] Intermittent hypoxia and re-oxygenation episodes induced by OSA stimulate tissue necrosis, oxidative stress, and macrophage infiltration, resulting in localized inflammation and consequent systemic inflammation due to circulating cytokines released by proinflammatory immune cells. […] Indeed, studies have shown that proinflammatory markers, such as tumour necrosis factor alpha (TNF-), interleukin (IL)-17, IL-23, and C-reactive protein (CRP), are significantly increased in children with OSA.

• #31 Update on paediatric obstructive sleep apnoea – Dehlink – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/6511/6228

  OSA has been shown to be associated with leptin resistance and increased ghrelin levels, which could favour obesity. […] There is emerging evidence that OSA is a disease with chronic low grade systemic inflammation and increased oxidative stress which likely lead to the end organ morbidities described above. […] The mechanisms underlying these imbalances are not fully understood, but some interesting findings have been made recently. […] OSA and obesity seem to mutually amplify the systemic inflammatory pathways, for instance monocyte chemoattractant protein 1 and plasminogen activator-inhibitor 1 levels have been found to be significantly raised in obese OSA children compared with body mass index (BMI)-matched obese children without OSA. […] It is postulated that this induction of inflammatory cascades along with increased oxidative stress gives rise to the morbidities associated with OSA.

• #32 You Cannot Hit Snooze on OSA: Sequelae of Pediatric Obstructive Sleep Apnea

  https://www.mdpi.com/2227-9067/9/2/261

  Hypertension in pediatric OSA is due to multifactorial pathogenesis. Recurrent hypoxemia and hypercapnia in pediatric OSA lead to activation of the sympathetic nervous system with consequent increases in catecholamine levels, which persist during the daytime and contribute to the development of hypertension. […] Elevated plasma P-selectin levels, a marker of platelet activation, was noted in children with OSA. The activation of P-selectin is mediated by inflammatory processes linked to atherogenesis. Additionally, hypoxemia and sleep fragmentation secondary to OSA can promote both sympathetic activity and reaction oxygen species (ROS) formation, which further cause platelet activation and upregulation of adhesion molecules, respectively. These data support the postulation that pediatric OSA can promote the onset of atherosclerosis and subsequent CAD.

• #33 You Cannot Hit Snooze on OSA: Sequelae of Pediatric Obstructive Sleep Apnea

  https://www.mdpi.com/2227-9067/9/2/261

  The mechanisms that lead to endothelial dysfunction are multifactorial. Intermittent hypoxia during sleep in children with OSA leads to systemic low-grade inflammatory processes with worsening oxidative stress, leading to interactions of endothelial, platelet, and inflammatory cells. […] Evidence suggests that untreated OSA increases the risk and incidence of insulin resistance, dyslipidemia, growth hormone dysfunction, and other metabolic disorders in children. The bidirectional association between OSA and obesity plays a role in the development of metabolic and endocrine syndromes. […] Untreated and unmanaged pediatric OSA has been linked with significant neurocognitive sequelae. The hypoxemia and hypercapnia that results from airway obstruction during sleep leads to oxidative stress and neuronal injury within the brain, particularly the hippocampus and cerebral cortex.

• #34 Obstructive sleep apnea syndrome in children: Epidemiology, pathophysiology, diagnosis and sequelae

  https://www.e-cep.org/journal/view.php?number=2010531001

  In obese children, excessive deposition of fat tissue within the muscles and tissue surrounding the upper airway leads to reduced airway size and increased airway resistance. […] Genetic risk factors have been identified in the development of OSAS. […] The pathophysiology of cardiovascular complications is as follows: intermittent upper airway obstruction during sleep in OSAS patients that have induced an exaggeration of continuous negative intrathoracic pressure swings, leading to a second series of sustained alterations of blood pressure and endothelial function, and eventually changes in cardiac structure and function occurs probably via oxidative stress and increased sympathetic tone. […] Pediatric OSAS has been commonly overlooked and underdiagnosed by both parents and clinician until now.

• #35 You Cannot Hit Snooze on OSA: Sequelae of Pediatric Obstructive Sleep Apnea

  https://www.mdpi.com/2227-9067/9/2/261

  The mechanisms that lead to endothelial dysfunction are multifactorial. Intermittent hypoxia during sleep in children with OSA leads to systemic low-grade inflammatory processes with worsening oxidative stress, leading to interactions of endothelial, platelet, and inflammatory cells. […] Evidence suggests that untreated OSA increases the risk and incidence of insulin resistance, dyslipidemia, growth hormone dysfunction, and other metabolic disorders in children. The bidirectional association between OSA and obesity plays a role in the development of metabolic and endocrine syndromes. […] Untreated and unmanaged pediatric OSA has been linked with significant neurocognitive sequelae. The hypoxemia and hypercapnia that results from airway obstruction during sleep leads to oxidative stress and neuronal injury within the brain, particularly the hippocampus and cerebral cortex.

• #36 Reduced Regional Grey Matter Volumes in Pediatric Obstructive Sleep Apnea | Scientific Reports

  https://www.nature.com/articles/srep44566

  Pediatric OSA is associated with cognitive risk. […] We assessed the presence of neuronal injury, measured as regional grey matter volume, in 16 OSA children (8 male, 8.12.2 years, AHI:11.15.9 events/hr), and 200 control subjects (84 male, 8.22.0 years), 191 of whom were from the NIH-Pediatric MRI database. […] Significant grey matter volume reductions appeared in OSA throughout areas of the superior frontal and prefrontal, and superior and lateral parietal cortices. […] Thus, pediatric OSA subjects show extensive regionally-demarcated grey matter volume reductions in areas that control cognition and mood functions, even if such losses are apparently independent of cognitive deficits. […] Since OSA disease duration in our subjects is unknown, these findings may result from either delayed neuronal development, neuronal damaging processes, or a combination thereof, and could either reflect neuronal atrophy or reductions in cellular volume (neurons and glia).

• #37 Reduced Regional Grey Matter Volumes in Pediatric Obstructive Sleep Apnea | Scientific Reports

  https://www.nature.com/articles/srep44566

  Earlier animal studies from our laboratory clearly showed that intermittent hypoxia and sleep fragmentation, primary characteristics of OSA, induce discernible neuronal cell losses in several brain regions. […] The present study aimed to assess the presence of potential injury to neuronal areas measured as reduced grey matter volume in a group of pediatric OSA patients relative to a large set of comparable control subjects. […] These regional brain changes were not correlated with the severity of respiratory disturbance during sleep and there were no trends indicative of an association with cognitive ability, as determined from the DAS-GCA scores. […] Since determining OSA disease duration is not practically possible, subjects may have experienced OSA for several years, and these findings may either reflect delayed neuronal development or disease induced neuronal damage.

• #38 Sleep apnoea in the child

  https://www.racgp.org.au/afp/2015/june/sleep-apnoea-in-the-child

  Obstructive sleep apnoea (OSA) is a condition causing repetitive episodes of upper airway obstruction during sleep, leading to hypoxia and/or sleep disturbance. OSA affects 15% of children and has important implications for learning, behaviour and cardiovascular health. […] The most common cause of OSA in childhood is enlargement of the tonsils and adenoids. Tonsils and adenoids grow most quickly in the pre-school years, and the adenoids are large in some children even in the latter part of the first year of life. Enlargement of lymphoid tissue in the confined space of the pharynx can result in airway obstruction during sleep, with relaxation of the dilating muscles of the pharynx contributing to the obstruction. […] Obesity, when present, does increase the risk of OSA, affecting up to 50% of overweight and obese children, compared with 15% of the general paediatric population.

• #39 Update on paediatric obstructive sleep apnoea – Dehlink – Journal of Thoracic Disease

  https://jtd.amegroups.org/article/view/6511/6228

  Disturbances in Pcrit are believed to play a key role in OSA pathogenesis. […] Children with OSA have been found to have significantly more collapsible upper airways with elevated (i.e., less negative) Pcrit during sleep than children without OSA. […] Increased upper airway collapsibility can be caused either by conditions leading to a decrease in muscle tone in the upper airway, such as cerebral palsy, neuromuscular disorders, or inflammatory conditions affecting the upper airways, such as allergic rhinitis and asthma. […] The concurrent presence of adenotonsillar hypertrophy and obesity appears to facilitate the emergence of OSA. […] The consequent excessive daytime sleepiness from OSA is likely to impact on physical activity, which in turn favours more weight gain. […] Furthermore, OSA and obesity might also be linked via an imbalance between leptin and ghrelin, two hormones crucial in regulating satiety and hunger.

• #40 Childhood Sleep Apnea, Pediatric Obstructive Sleep Apnea (OSA)

  https://my.clevelandclinic.org/health/diseases/14312-obstructive-sleep-apnea-in-children

  Muscle tone changes. Certain genetic conditions, like Down syndrome or cerebral palsy, can cause muscle tone changes in your childs head and neck. Your child may have a normal muscle tone during the day but their muscle tone decreases at night, allowing tissue to come closer together and block the airway. […] Bone structure abnormalities. A narrow facial bone structure like a small jaw or an overbite can affect your childs air intake. […] Childhood sleep apnea treatment varies based on the cause and severity. Their healthcare provider will focus on clearing your childs airways. Treatment options could include: Surgery: Surgery may be necessary to remove enlarged tonsils or adenoids or repair structural abnormalities of your childs head and neck to create more room in their airway. […] If your child develops complex sleep apnea after treatment for obstructive sleep apnea, their healthcare provider may suggest changing the airflow pressures on their CPAP machine or refitting the mask to your childs face. Most often, CPAP airflow pressures are too high or too low. Almost all symptoms of complex sleep apnea improve with adjusted therapy.

• #41 How to Treat Sleep Apnea in Children | Cedars-Sinai

  https://www.cedars-sinai.org/blog/pediatric-obstructive-sleep-apnea.html

  Sleep apnea is a condition where breathing stops or slows for periods during sleep. […] Obstructive sleep apnea, the type discussed here, occurs when the airway is partly or fully blocked for some period during sleep. […] There are two reasons children may have obstructive sleep apnea. The first occurs when there’s not enough space in the back of the throat for air to flow easily into their windpipe to get into their lungs. This is commonly caused by large tonsils or adenoids but can also be caused by craniofacial disorders. […] The second is often caused by neuromuscular problems, where the child doesn’t have normal muscle tone and the back of the throat collapses as they try to breathe. […] Children with Down syndrome are more at risk, with an estimated 53% to 76% having sleep apnea.

• #42 Pediatric obstructive sleep apnea – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/pediatric-sleep-apnea/symptoms-causes/syc-20376196

  Pediatric obstructive sleep apnea is caused by muscles in the back of the throat relaxing and blocking the upper airway. In children, this leads to pauses in breathing that last about twice as long as the typical breath. […] When breathing stops, this triggers the brain to wake up so that the airway can open again. This makes it hard to get enough rest. […] Various conditions can raise the risk of the upper airway becoming blocked during sleep. Commonly, enlarged tonsils in the back of the mouth and enlarged adenoids in the back of the nose can cause a blockage. Other possible causes include being born with a birth defect related to the shape of the face or head and certain health conditions.

• #43 Pediatric Obstructive Sleep Apnea > Fact Sheets > Yale Medicine

  https://www.yalemedicine.org/conditions/pediatric-obstructive-sleep-apnea

  Sleep apnea is a condition in which the muscles at the back of the throat intermittently relax too much, partially or completely blocking the airway. […] Obstructive sleep apnea affects 3 to 6 percent of children and is associated with repetitive narrowing of the airways, which is the breathing tube from the mouth and the nose down to the lungs, explains Yale Medicine’s Craig A. Canapari, MD, director of the Pediatric Sleep Medicine Program. […] Obesity is a common factor associated with obstructive sleep apnea in adults. In children, however, the most common cause of the problem is enlarged tonsils and adenoids. […] Additional causes of obstructive sleep apnea in children include „low airway tone as in cerebral palsy or Down syndrome,” Dr. Canapari notes. […] If your child has obstructive sleep apnea, your physician may recommend removal of the tonsils (tonsillectomy) or adenoids (adenoidectomy), or both.

• #44 Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01496-3

  In recent years, a number of studies have shown that a low respiratory arousal threshold may be an important endotype of OSAS. […] In ventilatory control, loop gain is a measure of respiratory instability, which refers to unstable ventilatory chemoreflex control and is recognized as a key pathophysiological feature that contributes to OSAS. […] Increased pharyngeal dilator muscle activity in OSAS patients compared with matched controls has been interpreted as evidence of a neuromuscular protective compensatory reflex in response to anatomical compromise in OSAS.

• #45 Pathophysiology of Pediatric Obstructive Sleep Apnea | CoLab

  https://colab.ws/articles/10.1513%2Fpats.200707-111MG

  Sleep-disordered breathing is a common and serious cause of metabolic, cardiovascular, and neurocognitive morbidity in children. The spectrum of obstructive sleep-disordered breathing ranges from habitual snoring to partial or complete airway obstruction, termed obstructive sleep apnea (OSA). Breathing patterns due to airway narrowing are highly variable, including obstructive cycling, increased respiratory effort, flow limitation, tachypnea, and/or gas exchange abnormalities. As a consequence, sleep homeostasis may be disturbed. Increased upper airway resistance is an essential component of OSA, including any combination of narrowing/retropositioning of the maxilla/mandible and/or adenotonsillar hypertrophy. […] However, in addition to anatomic factors, the stability of the upper airway is predicated on neuromuscular activation, ventilatory control, and arousal threshold. During sleep, most children with OSA intermittently attain a stable breathing pattern, indicating successful neuromuscular activation. At sleep onset, airway muscle activity is reduced, ventilatory variability increases, and an apneic threshold slightly below eupneic levels is observed in non-REM sleep. Airway collapse is offset by pharyngeal dilator activity in response to hypercapnia and negative lumenal pressure. Ventilatory overshoot results in sudden reduction in airway muscle activation, contributing to obstruction during non-REM sleep. Arousal from sleep exacerbates ventilatory instability and, thus, obstructive cycling. Paroxysmal reductions in pharyngeal dilator activity related to central REM sleep processes likely account for the disproportionate severity of OSA observed during REM sleep. Understanding the pathophysiology of pediatric OSA may permit more precise clinical phenotyping, and therefore improve or target therapies related to anatomy, neuromuscular compensation, ventilatory control, and/or arousal threshold.

• #46 Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01496-3

  In recent years, a number of studies have shown that a low respiratory arousal threshold may be an important endotype of OSAS. […] In ventilatory control, loop gain is a measure of respiratory instability, which refers to unstable ventilatory chemoreflex control and is recognized as a key pathophysiological feature that contributes to OSAS. […] Increased pharyngeal dilator muscle activity in OSAS patients compared with matched controls has been interpreted as evidence of a neuromuscular protective compensatory reflex in response to anatomical compromise in OSAS.

• #47 Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome | Signal Transduction and Targeted Therapy

  https://www.nature.com/articles/s41392-023-01496-3

  In recent years, a number of studies have shown that a low respiratory arousal threshold may be an important endotype of OSAS. […] In ventilatory control, loop gain is a measure of respiratory instability, which refers to unstable ventilatory chemoreflex control and is recognized as a key pathophysiological feature that contributes to OSAS. […] Increased pharyngeal dilator muscle activity in OSAS patients compared with matched controls has been interpreted as evidence of a neuromuscular protective compensatory reflex in response to anatomical compromise in OSAS.

• #48

  https://journals.lww.com/prcm/fulltext/2021/05020/paediatric_obstructive_sleep_apnoea_.3.aspx

  Other structural factors increasing the risk of developing childhood OSA include craniofacial skeletal dysmorphologies in the mandible and maxilla. […] The UA size is mainly determined by static pharyngeal mechanics, neuromuscular tone, and luminal pressure, with multiple studies reporting children with OSA having higher positive critical closing pressures of the pharynx (Pcrit), with airways collapsing easily in mild inspiratory negative pressures. […] This indicates that other neuromuscular factors may play an integral role, with the passive Pcrit and mean airway closing pressure (Pclose) being 25 cm H2O and 7.4 cm H2O, respectively, in normal children, compared with 5 cm H2O and 2 cm H2O in children with OSA, indicating problems with neuromuscular compensation. […] Intermittent hypoxia and re-oxygenation episodes induced by OSA stimulate tissue necrosis, oxidative stress, and macrophage infiltration, resulting in localized inflammation and consequent systemic inflammation due to circulating cytokines released by proinflammatory immune cells. […] Indeed, studies have shown that proinflammatory markers, such as tumour necrosis factor alpha (TNF-), interleukin (IL)-17, IL-23, and C-reactive protein (CRP), are significantly increased in children with OSA.

• #49

  https://journals.lww.com/prcm/fulltext/2021/05020/paediatric_obstructive_sleep_apnoea_.3.aspx

  Other structural factors increasing the risk of developing childhood OSA include craniofacial skeletal dysmorphologies in the mandible and maxilla. […] The UA size is mainly determined by static pharyngeal mechanics, neuromuscular tone, and luminal pressure, with multiple studies reporting children with OSA having higher positive critical closing pressures of the pharynx (Pcrit), with airways collapsing easily in mild inspiratory negative pressures. […] This indicates that other neuromuscular factors may play an integral role, with the passive Pcrit and mean airway closing pressure (Pclose) being 25 cm H2O and 7.4 cm H2O, respectively, in normal children, compared with 5 cm H2O and 2 cm H2O in children with OSA, indicating problems with neuromuscular compensation. […] Intermittent hypoxia and re-oxygenation episodes induced by OSA stimulate tissue necrosis, oxidative stress, and macrophage infiltration, resulting in localized inflammation and consequent systemic inflammation due to circulating cytokines released by proinflammatory immune cells. […] Indeed, studies have shown that proinflammatory markers, such as tumour necrosis factor alpha (TNF-), interleukin (IL)-17, IL-23, and C-reactive protein (CRP), are significantly increased in children with OSA.

• #50 You Cannot Hit Snooze on OSA: Sequelae of Pediatric Obstructive Sleep Apnea

  https://www.mdpi.com/2227-9067/9/2/261

  Hypertension in pediatric OSA is due to multifactorial pathogenesis. Recurrent hypoxemia and hypercapnia in pediatric OSA lead to activation of the sympathetic nervous system with consequent increases in catecholamine levels, which persist during the daytime and contribute to the development of hypertension. […] Elevated plasma P-selectin levels, a marker of platelet activation, was noted in children with OSA. The activation of P-selectin is mediated by inflammatory processes linked to atherogenesis. Additionally, hypoxemia and sleep fragmentation secondary to OSA can promote both sympathetic activity and reaction oxygen species (ROS) formation, which further cause platelet activation and upregulation of adhesion molecules, respectively. These data support the postulation that pediatric OSA can promote the onset of atherosclerosis and subsequent CAD.

• #51 Childhood Sleep Apnea: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1004104-overview

  Obstructive sleep apnea (OSA) in children is characterized by episodic upper airway obstruction that occurs during sleep. The airway obstruction may be complete or partial. […] Three major components of obstructive sleep apnea have been identified: episodic hypoxia, intermittent hypercapnia, and sleep fragmentation. […] The mechanisms of obstruction, adverse effects of obstructive sleep apnea, diagnostic criteria, and recommended treatment options are different in children from those in adults. […] Important recent advances in the understanding of the underlying pathophysiological mechanisms of obstructive sleep apnea in children have been coupled with improved approaches to the diagnosis and management of obstructive sleep apnea. […] Disordered breathing during sleep is a hallmark of obstructive sleep apnea syndrome. Breathing abnormalities include apnea (cessation of air flow) and hypopnea (decreased air flow).

• #52 Pediatric Obstructive Sleep Apnea > Fact Sheets > Yale Medicine

  https://www.yalemedicine.org/conditions/pediatric-obstructive-sleep-apnea

  Sleep apnea is a condition in which the muscles at the back of the throat intermittently relax too much, partially or completely blocking the airway. […] Obstructive sleep apnea affects 3 to 6 percent of children and is associated with repetitive narrowing of the airways, which is the breathing tube from the mouth and the nose down to the lungs, explains Yale Medicine’s Craig A. Canapari, MD, director of the Pediatric Sleep Medicine Program. […] Obesity is a common factor associated with obstructive sleep apnea in adults. In children, however, the most common cause of the problem is enlarged tonsils and adenoids. […] Additional causes of obstructive sleep apnea in children include „low airway tone as in cerebral palsy or Down syndrome,” Dr. Canapari notes. […] If your child has obstructive sleep apnea, your physician may recommend removal of the tonsils (tonsillectomy) or adenoids (adenoidectomy), or both.

• #53 Pediatric Obstructive Sleep Apnea – OpenAnesthesia

  https://www.openanesthesia.org/keywords/pediatric-obstructive-sleep-apnea/

  Most pediatric patients with obstructive sleep apnea syndrome (OSAS) will not have undergone formal testing nor have a formal diagnosis of OSAS; however, those with severe OSAS may have a sensitivity to opioid medications. […] While multiple factors predispose to OSAS, adenotonsillar hypertrophy and obesity are the major risk factors in otherwise healthy pediatric patients. […] Pediatric OSAS is primarily caused by adenotonsillar hypertrophy and obesity, but craniofacial abnormalities and neuromuscular diseases can also cause OSAS. […] Anatomic obstruction can be due to airway narrowing from adenotonsillar hypertrophy or decreased space in the posterior oropharynx due to craniofacial abnormalities. Airway obstruction in pediatric OSAS patients under anesthesia is more likely to occur at the level of the tonsils and adenoids compared to the soft palate in adults.

• #54 Pediatric Obstructive Sleep Apnea – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557610/

  The incidence of pediatric OSA peaks between 2 to 8 years of age due to the increased growth of tonsils and adenoids relative to the size of the upper airway in this age group. Risk factors for early-onset OSA include prematurity, Down syndrome, African American race, and daycare attendance. The severity can be increased in those with obesity, tobacco exposure, and reduced family income. […] Diagnosis of sleep apnea is made by measuring the apneic events during sleep. […] If there is adenotonsillar hypertrophy, the most effective treatment is adenotonsillectomy (AT). This is recommended for most patients with an AHI more than 9 events/hour and those with mild or moderate disease with significant symptoms. […] If identified and managed promptly, patients will not suffer long-term consequences or complications of pediatric OSA.

• #55 Obstructive sleep apnea syndrome in children: Epidemiology, pathophysiology, diagnosis and sequelae

  https://www.e-cep.org/journal/view.php?number=2010531001

  The prevalence of pediatric obstructive sleep apnea syndrome (OSAS) is approximately 3% in children. Adenotonsillar hypertrophy is the most common cause of OSAS in children, and obesity, hypotonic neuromuscular diseases, and craniofacial anomalies are other major risk factors. […] The main risk factors for OSAS in adults are obesity and male sex, which are related to the propensity for repetitive upper airway collapse. In younger children, the major risk factor for the development of OSAS is adenotonsillar hypertrophy. […] It is suggested that central ventilatory drive is increased during childhood and then declines gradually with age. This increased central ventilatory drive during sleep accounts for the increased upper airway reflexes and tone in children, resulting in less collapsibility than in adults.

• #56 Pediatric Obstructive Sleep Apnea – OpenAnesthesia

  https://www.openanesthesia.org/keywords/pediatric-obstructive-sleep-apnea/

  OSAS patients have altered neuromuscular responses to changes in airway pressures. Unlike in adults, children can maintain their airway opening and often do not have full collapse, leading to a low-flow breathing pattern that characteristically leads to hypercarbia. […] Hypotonia in diseases such as Trisomy 21 predisposes patients to airway collapse due to neuromuscular dysfunction and airway obstruction from macroglossia. Obesity also predisposes to airway collapse due to increased pressure from excess tissues around the airway. […] Chronic inflammatory disorders such as sinusitis, allergic rhinitis, and asthma as well as environmental smoke exposure are all associated with elevated inflammatory markers and airway collapse in OSAS. […] Genetic predisposition has been demonstrated in family cohort studies. African American children are at 3.5 times higher risk for OSAS than other populations.

• #57 Childhood Sleep Apnea: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1004104-overview

  In addition, in contrast to adults, some children exhibit a variation of obstructive sleep apnea termed obstructive hypoventilation (OH). Children with obstructive hypoventilation demonstrate periods of hypercapnia that occur in the absence of discrete respiratory events that fulfill the criteria for apnea or hypopnea. […] The ability to maintain upper airway patency during the normal respiratory cycle is the result of a delicate equilibrium between the forces that promote airway closure and dilation. […] The 4 major predisposing factors for upper airway obstruction are the following: Anatomic narrowing, Abnormal mechanical linkage between airway dilating muscles and airway walls, Muscle weakness, Abnormal neural regulation. […] Obstructive apnea and hypopnea are related to upper airway obstruction. Upper airway obstruction may occur at one or more levels, including the nasopharynx, mouth, velopharynx, retroglossal region, hypopharynx, and larynx.

• #58 Childhood Sleep Apnea: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1004104-overview

  Childhood sleep apnea differs from adult obstructive sleep apnea in that adults with sleep apnea frequently present with hypersomnia, whereas children often demonstrate short attention spans, emotional lability, and behavioral problems. […] For most children, enlargement of the tonsils and/or adenoid is the proximate cause for the development of obstructive sleep apnea. […] The contribution of the various anatomical nasopharyngeal structures to Pcrit and the interactions between these structures that lead to upper airway patency or obstruction during sleep are of obvious importance in increasing the understanding of the pathophysiology of obstructive sleep apnea in children. […] The static pressure and/or area relationships of the passive pharynx were endoscopically measured in 14 children with obstructive sleep apnea and in 13 healthy children under general anesthesia with complete paralysis, and it was determined that children with obstructive sleep apnea closed their airways at the level of enlarged adenoids and tonsils at low positive pressures, whereas healthy children required subatmospheric pressures to induce upper airway closure. […] Thus, both congenital and acquired anatomic factors clearly play a significant role in the pathogenesis of pediatric obstructive sleep apnea.

• #59 Pediatric Obstructive Sleep Apnea (OSA) | Diagnosis & Treatment

  https://www.cincinnatichildrens.org/health/o/obstructive-sleep-apnea

  Pediatric obstructive sleep apnea can share symptoms with attention deficit hyperactivity disorder (ADHD). Because of this, some children with pediatric OSA are misdiagnosed as having ADHD. Some children may have both conditions. Pediatric obstructive sleep apnea can also sometimes worsen ADHD symptoms. […] Its important to treat pediatric obstructive sleep apnea as soon as possible. Treating it early can help the child maintain normal growth and development. […] A childs treatment plan depends on whats causing the pediatric obstructive sleep apnea. Treatments may include: […] If enlarged tonsils and adenoids are causing the condition, your doctor will recommend removing them. This surgery is called an adenoidectomy or tonsillectomy. […] A CPAP machine provides air pressure that keeps the throat from closing during sleep. Your child will wear a small mask over their nose during sleep. A CPAP machine may be helpful when surgery is not possible.

• #60 Pathophysiology of Pediatric Obstructive Sleep Apnea: Putting It All Together | SpringerLink

  https://link.springer.com/chapter/10.1007/978-1-60761-725-9_11

  This chapter aims to amalgamate the various intermediate phenotypes involved in pediatric obstructive sleep apnea (OSA) to explain the clinical expression of the disease: habitual snoring, obstructive hypoventilation, upper airway resistance syndrome (UARS), and OSA. […] Understanding the individual determinants of the pathophysiology of the pediatric OSA may lead to a more personalized approach to therapy and improved outcomes in the future.

• #61 (PDF) Much Ado about Sleep: Current Concepts on Mechanisms and Predisposition to Pediatric Obstructive Sleep Apnea

  https://www.academia.edu/82669728/Much_Ado_about_Sleep_Current_Concepts_on_Mechanisms_and_Predisposition_to_Pediatric_Obstructive_Sleep_Apnea

  Obstructive sleep apnea is a common disorder characterized by repetitive upper airway narrowing during sleep with resulting hypoxemia, hypercapnia, sympathetic activation, and sleep disruption. Early intervention in children suspected to have OSA is essential to reduce the risk of developing more severe OSA as adults.

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