Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4566_Библиотеки_им_академика_М_И_Перельмана
.pdf
Development of breathing and sleep
a)
https://t.me/medicina_free
Breathing
S
aO
2
ECG
Healthy/mature
physiological apnoea
S
aO
2
HR
b) Airway/lung
problems
S
aO
2
HR
c) Vagal
mechanisms
HR
S
aO
2
Figure 1. The sequence of apnoea, bradycardia and desaturation. a) Physiological apnoea, no
desaturation or bradycardia. b) Short apnoea with rapid desaturation due to airway closure, low
FRC, ventilation/perfusion mismatch, intrapulmonary shunts and tachycardia. c) Apnoea with
bradycardia due to vagal and/or trigeminal inhibition during swallowing, obstruction or reflux.
HR: heart rate. Reproduced and modified from Simonds et al. (2012) with permission.
causes such as seizures, cardiac diseases, bacterial infection, metabolic disorders
and central hypoventilation. For higher-risk BRUEs, subsequent investigations could
include cardiorespiratory function, blood gases and PSG/polygraphy (PG).
BRUEs should not be ignored; they may cause severe hypoxia, even if the link
with sudden infant death syndrome (SIDS) is controversial. If there are no serious
underlying conditions, the risk of SIDS is certainly low, but the long-term outcome for
these infants is yet to be determined.
Further reading
• Carroll JL (2003). Developmental plasticity in respiratory control. J Appl Physiol; 94: 375–389.
• Cherniack NS (2006). Cardiopulmonary integration: the dark side. Respiration; 73: 733–734.
• Cohen G, et al. (2005). Development of chemoreceptor responses in infants. Respir Physiol
Neurobiol; 149: 233–242.
• Darnall RA (2010). The role of CO2 and central chemoreception in the control of breathing in
the fetus and the neonate. Respir Physiol Neurobiol; 173: 201–212.
374
ERS Handbook: Respiratory Sleep Medicine
Development of breathing and sleep
https://t.me/medicina_free
• Gauda EB, et al. (2004). Maturation of peripheral arterial chemoreceptors in relation to
neonatal apnea. Semin Neonatol; 9: 181–194.
• Hunt CE, et al. (2004). Cardiorespiratory events detected by home memory monitoring and
one-year neurodevelopmental outcome. J Pediatr; 145: 465–471.
• Katz-Salamon M (2004). Delayed chemoreceptor responses in infants with apnea. Arch Dis
Child; 89: 261–266.
• Lorch SA, et al. (2011). Epidemiology of apnea and bradycardia resolution in premature infants.
Pediatrics; 128: e366–e373.
• Poets CF, et al. (1991). Arterial oxygen saturation and breathing movements during the first
year of life. J Dev Physiol; 15: 341–345.
• Praud JP (2010). Upper airway reflexes in response to gastric reflux. Paediatr Respir Rev; 11:
208–212.
• Rampogal S, et al. (2022). Brief resolved unexplained events: a new diagnosis, with implications
for evaluation and management. Eur J Pediatr; 181: 463–470.
• Simonds AK, et al., eds (2012). ERS Handbook Respiratory Sleep Medicine. Sheeld, European
Respiratory Society.
Acknowledgement
This is an update of the ERS Handbook of Respiratory Sleep Medicine first edition chapter
‘Development of breathing and sleep and physiopathology of apnoea in the first years of life’, by
Gary Cohen, Miriam Katz-Salamon and Ha Trang.
375ERS Handbook: Respiratory Sleep Medicine
Sleep disordered breathing
https://t.me/medicina_free
in children
Refika Ersu and Ha Trang
OSAS
OSAS aects 2–5% of the paediatric population. Partial or total obstruction of the
upper airway results in obstructive apnoeas and hypopnoeas during sleep, with or
without associated desaturation, hypercapnia and sleep fragmentation. It is thought
that there is a continuum between normal state and OSAS, which is the complete
clinical presentation of the disorder. Intermediate presentations include 1) primary
snoring, which is chronic snoring without associated apnoea or arterial desaturation,
and 2) upper airway resistance syndrome (UARS), characterised by inspiratory
respiratory eorts during sleep, identified using oesophageal pressure, but without
typical apnoea or hypopnoea. It is currently thought that primary snoring may not
have adverse eects on health. In contrast, UARS, which is dicult to identify in
current practice, may progress towards complications if undiagnosed.
Epidemiology
The prevalence of OSAS in children is estimated to range 0.7–10.3%, with peak
incidence at 5–10 years of age. An estimated prevalence of 6.4% in children aged
1–6 years and of 3.7% in children aged 7–12 years has been reported. The prevalence
of OSA is unknown in infants and toddlers. OSAS has been shown to occur equally in
girls as in boys.
∼8–10% of children snore regularly. However, not all children who snore have OSAS.
Infants can snore without apnoea.
There are no large, controlled, longitudinal studies relating the natural history of
OSAS in children. It is not known whether childhood OSAS evolves into adult OSAS,
Key points
• Childhood OSAS is underrecognised.
• Snoring is not predictive of the presence of OSAS.
• PSG is an important tool for diagnosing OSAS.
• Paediatric rules for scoring sleep and respiration of PSG should be used.
• Paediatric criteria for OSAS diagnosis should be used.
• Hypoventilation is more severe in NREM sleep than in REM sleep in CCHS.
376
ERS Handbook: Respiratory Sleep Medicine
SDB in children
https://t.me/medicina_free
or whether there are two dierent diseases. It has been shown that some infants
who previously presented with spells and obstructive apnoea were diagnosed with
OSAS during later childhood. Longitudinal studies have shown complete resolution of
OSAS, particularly in female children, during the transition to late adolescence or early
adulthood, suggesting that childhood and adolescent OSAS may be distinct entities,
and that adolescent OSAS is likely to persist into adulthood. Obesity and male sex
were consistent key risk factors for OSAS incidence.
Pathophysiology
Factors underlying the development of OSAS in children are primarily associated
with reduced patency of the upper airway. The main causes are enlarged tonsils
and/or adenoids. However, the pathophysiological mechanisms are multiple and
intertwined:
• Abnormal craniofacial skeleton, ranging from major malformations (such as Pierre
Robin sequence, Crouzon syndrome, Apert syndrome or achondroplasia), to milder
abnormalities that do not fall within a labelled syndrome. The latter may be a
moderate hypoplasia of the middle third of the face with arched palate and narrow
nasal cavity, or a narrow oropharyngeal cavity, with or without a retrognathia and
a lingual retrusion.
• Abnormal craniofacial and pharyngeal so tissue, resulting in reduction of the
upper airway size, enlargement of lymphoid tissues (e.g. tonsils and adenoids),
cervical fat accumulation (e.g. obesity), increased upper airway collapsibility, nasal
obstruction, etc.
• Neuromuscular dysfunction, in the broadest sense of the term, including impaired
neurological control of breathing or upper airway muscle tone, etc.
Genetic and environmental factors have been identified in the predisposition for
OSAS. The abnormalities are oen numerous and complex. It is not always easy to
determine which abnormalities are causes and which are consequences of OSAS.
Clinical presentation
The clinical presentation of OSAS diers with age. Symptoms are dominated by
respiratory diculties at night in all age groups – snoring during sleep, breathing
pauses, laboured breathing or mouth breathing.
Infants and younger children (1–6 years of age) oen struggle to remain awake at sleep
times and adopt unusual positions during sleep, such as prone with the neck extended.
Parents complain of sleep problems (restless sleep, frequent body movements,
night sweats and frequent nocturnal awakenings) or secondary enuresis. Morning
sluggishness and occasional daytime fatigue are reported. Sometimes, nonrespiratory
symptoms can be misleading; impaired attention or concentration, hyperactivity,
behavioural problems, all oen manifest as altering academic performance.
In older children (pre-adolescent and adolescent), loud snoring and breathing
diculties are common. They may report daytime hypersomnolence, resulting in
daytime naps, irritability, and impaired concentration and attention. Hypersomnolence
is a dicult symptom to assess in children, as typical subjective assessments using
questionnaires may be not applicable in this age group. Occasionally, patients may
report morning headaches.
Clinical assessment should include a general paediatric evaluation and a comprehensive
examination of craniofacial segments and oropharynx (clinical assessment in children
is covered further in chapter 17.4 of this Handbook).
377ERS Handbook: Respiratory Sleep Medicine
SDB in children
https://t.me/medicina_free
Confirming OSAS
PSG
PSG is an important tool that helps: confirm or exclude OSAS; determine the severity
of the disorder allowing treatment strategy decisions to be adjusted accordingly;
exclude other possible causes of sleepiness. It important to use paediatric scoring
and diagnostic sleep study criteria when managing children suspected of OSA. A
review of sleep and respiratory rules for PSG in children has been published by
the American Academy of Sleep Medicine. The technical and scoring details of
paediatric PSG are discussed further in chapter 17.4 of this Handbook.
Young children, typically infants or toddlers, may demonstrate sustained obstruction
of breathing during sleep with hypercapnia and/or hypoxaemia, but without typical
apnoea or hypopnoea. This pattern is termed ‘obstructive hypoventilation’ and is
defined as sleep-related hypoventilation associated with partial airway obstruction.
Diagnosis of UARS is not performed in routine practice, as it requires invasive
measurement of oesophageal pressure. Further evaluation of noninvasive techniques
of diagnosis is needed.
OSAS is therefore is confirmed with either an elevated AHI or obstructive hypoventilation in conjunction with an appropriate history and associated clinical features.
Are there alternative diagnostic procedures for OSAS beyond PSG? Snoring is highly
associated with OSAS. However, the presence of snoring does not always imply OSAS,
and its intensity is not correlated with OSAS severity. In the same way, thee absence of
snoring does not exclude OSAS. Breathing pauses may not be recognised by parents,
as they are predominant in REM sleep, which oen occurs late at night. A limited
number of paediatric sleep questionnaires are available; some only explore respiratory
symptoms (the Brouillette questionnaire), and others explore many domains, such as
sleep quality, hypersomnolence and behaviour (the Pediatric Sleep Questionnaire).
Some sleep questionnaires are generally in accordance with PSG results, but are not
able to dierentiate children with primary snoring from those with OSA, nor are they
able to measure the severity of OSA. The ESS, which is widely used in adults, has
been modified and adapted for children by changing the nature of diurnal activities.
However, this questionnaire is yet to be validated in large paediatric populations and
no consensus exists on the cut-o score in children.
Nocturnal home oximetry
Nocturnal home oximetry is typically considered positive when the graphics show
bursts of desaturations occurring during one or many periods of 10–30 min overnight.
A positive oximetry result may be relatively specific for OSA, but a negative oximetry
result does not exclude the disorder. Oximetry can be used as a screening tool in
selected populations, but there is no evidence to suggest that oximetry alone can
replace PSG for OSA diagnosis.
Respiratory PG
Respiratory polygraphy (PG) is a system of overnight recordings of respiratory
parameters without neurological parameters, meaning sleep periods and sleep stages
cannot be determined. Few studies have assessed the validity of respiratory PG for
the diagnosis of OSA in children. The cut-o value of the frequency of apnoeas and
hypopnoeas for diagnosing OSAS with respiratory PG in children is aected by its
technical specifications and the setting of the study (attended in-laboratory versus
unattended at home). Depending on these measures, PG may overestimate or
underestimate the AHI. There is currently no evidence to suggest that ambulatory
378
ERS Handbook: Respiratory Sleep Medicine
SDB in children
https://t.me/medicina_free
diagnostic techniques have the acceptable degree of diagnostic accuracy to replace
PSG. These techniques need to be assessed in larger paediatric populations.
Associated complications
OSAS adversely aects neurocognition and behaviour, the heart and circulation, and
growth and metabolism, resulting in increased morbidity in aected children.
Neurocognition and behaviour
The eects of OSAS on neuropsychological and cognitive function have gained a great
deal of attention. Early studies reported learning diculties or school problems and it
has since been widely acknowledged that neurocognitive deficits are highly prevalent
in children with OSAS. These children demonstrate memory and attention impairment,
executive function impairment and a lower intellectual quotient than controls. They
may also present with behavioural disorders, and various degrees of hyperactivity
and aggressiveness, which sometimes evolves into attention-deficit hyperactivity
disorder (ADHD). These disorders cause a deterioration in learning abilities and school
performance. Importantly, neurocognitive deficits are found to be more pronounced
in children with more severe OSAS. Moreover, they are not only found in children with
identified OSAS, but are also seen in those with primary snoring, i.e. without identified
apnoeas or hypopnoeas. Tonsillectomy significantly improves cognition and behavior of
children.
Dierent factors underlying brain deficits have been suggested: hypoxaemia and
especially repeated hypoaxemic swings overnight, causing ischaemic injury in
vulnerable brain regions including the cerebellum and hippocampus, with the
additional negative eect of sleep fragmentation.
Whilst a number of studies have shown that OSAS is associated with cognitive and
behavioral disorders in children >2 years of age, there are no such studies in infants
and toddlers.
The heart and circulation
In early cases of OSAS, cor pulmonale with HF was a presenting symptom. Now, pulmonary
hypertension (PH) may be more commonly asymptomatic. Recent studies have shown
that children with OSAS may have systemic hypertension (both diurnal and nocturnal
SBP and DBP). More discrete abnormalities can also be observed: loss of wake–sleep
modulation of BP (which is mediated by the autonomic nervous system), le ventricular
remodelling and endothelial abnormalities. Cardiovascular abnormalities correlate with
the desaturation index, suggesting a role for repeated hypoxaemic episodes.
Growth and metabolism
Failure to thrive was a presenting symptom of childhood OSAS in early reports.
Resolution of OSAS results in a significant growth rebound. It has been hypothesised
that failure to thrive may be caused by a reduction in the release of the growth
hormone, caused by sleep fragmentation, or increased energy expenditure during
sleep relating to repeated inspiratory eorts against upper airway obstruction. It is
unclear whether OSA is associated with insulin resistance in children.
Conclusion
OSAS is common in children. However, it is still under-recognised and undertreated. There remain a number of unaddressed questions about pathophysiology,
complications, diagnosis and treatment of OSAS in children. Controlled, longitudinal,
large-scale studies are required in order to improve understanding of and care for
OSAS in children.
379ERS Handbook: Respiratory Sleep Medicine
SDB in children
https://t.me/medicina_free
Sleep hypoventilation syndromes
Sleep hypoventilation syndromes include a wide variety of disorders that aect central
control of breathing and/or respiratory mechanics. Alveolar hypoventilation is caused
by inadequate ventilation and results in increased P
Treatment aims to provide ventilation support through use of NIV, targeting primary
and concomitant hypoxaemia.
aCO
2
disease when possible.
Congenital central hypoventilation syndrome
Congenital central hypoventilation syndrome (CCHS) is the result of congenital failure
of autonomic control of breathing. The incidence of CCHS is estimated to be one in
200 000. >90–92% of patients with CCHS harbour PHOX-2B mutations, the most
frequent being polyalanine expansions. Treatment is currently supportive through
lifelong ventilatory support.
CCHS typically presents at birth. Neonates with CCHS demonstrate repeated apnoeas,
cyanosis during sleep, bradycardia and, despite severe hypoxaemia, fail to increase
their breathing. PSG shows severe alveolar hypoventilation during sleep with shallow
breathing and a slow respiratory rate. Hypoventilation is most severe during sleep,
particularly during NREM sleep, when control of breathing depends almost exclusively
on the central CO2 level. The hallmark feature of CCHS is an absent or markedly
reduced central hypercapnic ventilatory response (HCVR). Ventilatory deficit persists
throughout life. With increasing age, most patients can breathe spontaneously while
awake. However, 5–10% of them also require ventilatory support during the daytime.
Milder CCHS can be diagnosed during childhood or even adulthood, and typically manifests
with cyanotic apnoea spells, unexplained convulsions that are resistant to treatment, a
normal EEG, and the ability to breath-hold for prolonged periods. These presentations
have been associated with short expansion mutations containing 25 alanine repeats.
Neuromuscular conditions
In contrast to CCHS, ventilatory drive is usually well preserved in neuromuscular
disorders. Instead, alveolar hypoventilation occurs as the patient’s respiratory
muscles are weakened and cannot withstand the work of breathing. In Duchenne
muscular dystrophy, congenital muscular dystrophies and myopathies, inspiratory
and expiratory muscle weakness usually progress in tandem. In spinal muscular
atrophy, expiratory muscle weakness may initially outstrip expiratory muscle
weakness. Scoliosis and upper airway obstruction can add to the mechanical load.
Hypoventilation first occurs in REM sleep, then progresses to NREM sleep and
finally to diurnal hypoventilation if the vicious cycle is not addressed. A FVC of
<60% predicted and a raised serum bicarbonate level are simple screening tools for
nocturnal hypoventilation, and are probably more useful than direct measurements
of respiratory muscle strength.
Cough peak flow is a useful measure of cough ecacy. Children over ∼10 years of age
with a cough peak flow of <270 L·min−1 are at risk of diculty clearing secretions, and
have an increased rate of chest infections.
Sleep studies should be carried out annually in children with a vital capacity of
<60% pred, as well as in those who have lost ambulation or who have symptoms of
nocturnal hypoventilation, such as poor sleep quality, frequent awakenings, morning
headaches, concentration problems or sleepiness during the day, and loss of appetite
at breakfast time. The frequency of sleep study performance should increase if
380
ERS Handbook: Respiratory Sleep Medicine
SDB in children
https://t.me/medicina_free
symptoms progress or lung function changes rapidly. As a minimum, S
end-tidal CO2 tension (P
characterised into central and obstructive by multichannel respiratory monitoring.
) should be monitored; respiratory events can be better
ETCO
2
aO
2
and P
tcCO
/
2
Arousals can either be detected with full PSG or through measurement of autonomic
surrogates, e.g.heart rate variation. Oximetry alone is not sucient to fully exclude
nocturnal hypoventilation, but an overnight oxygen saturation (S
who has slept well and who is entirely asymptomatic makes significant nocturnal
) of ≥93% in a child
pO
2
hypoventilation, requiring ventilatory support, unlikely.
The treatment for children with symptomatic nocturnal hypoventilation is positive
pressure ventilation, usually NIV.
It is worth noting that until recently, children with neuromuscular disorders who
have received treatment have been symptomatic. This changed in recent years with
the development of new drugs that either improve secondary pathophysiological
consequences or modify the underlying genetic defect.
Further reading
• Aurora RN, et al. (2011). Practice parameters for the respiratory indications for PSG in children.
Sleep; 34: 379–388.
• Birnkrant DJ, et al. (2018). Diagnosis and management of Duchenne muscular dystrophy,
part 2: respiratory, cardiac, bone health, and orthopaedic management. Lancet Neurol; 17:
347–361.
• Chan KC, et al. (2019). How OSA evolves from childhood to young adulthood: natural history
from a 10-year follow-up study. Chest; 156: 120–130.
• Flotats-Bastardas M, et al. (2020). New therapeutics options for pediatric neuromuscular
disorders. Front Pediatr; 8: 583877.
• Hull J, et al. (2012). Guideline for respiratory management of children with neuromuscular
weakness. Thorax; 67: Suppl. 1, i1–i40.
• Kaditis AG, et al. (2016). Obstructive sleep disordered breathing in 2- to 18-year-old children:
diagnosis and management. Eur Respir J; 47: 69–94.
• Maloney MA, et al. (2018). Congenital central hypoventilation syndrome: diagnosis and
management. Expert Rev Respir Med; 12: 283–292.
• Redline S, et al. (2007). The scoring of respiratory events in sleep: reliability and validity. J Clin
Sleep Med; 3: 169–200.
• Riha RL, et al. (2023). ERS technical standards for using type III devices (limited channel
studies) in the diagnosis of sleep disordered breathing in adults and children. Eur Respir J; 61:
2200422.
• Trang H, et al. (2005). The French Congenital Central Hypoventilation Syndrome Registry:
general data, phenotype, and genotype. Chest; 127: 72–79.
• Weese-Mayer D, et al. (2010). An ocial ATS clinical policy statement: congential central
hypoventilation syndrome. Am J Respir Crit Care Med; 181: 626–644.
• Wise MS, et al. (2011). Executive summary of respiratory indications for polysomnography in
children: an evidence-based review. Sleep; 34: 389–398.
Acknowledgement
This is an update of the ERS Handbook of Respiratory Sleep Medicine first edition chapter ‘Sleep
disordered breathing in children’, by Ha Trang and Anita K. Simonds.
381ERS Handbook: Respiratory Sleep Medicine
Comorbid respiratory
https://t.me/medicina_free
disorders in children
Stijn Verhulst and Brigitte Fauroux
A comorbid respiratory disease can aggravate sleep problems and SDB in children.
However, the relationship between SDB and the comorbid respiratory disease may
be complex, justifying individualised analysis and management, as illustrated in this
chapter, which discusses the interaction between certain respiratory disorders and
sleep in children.
Asthma
OSA and asthma are common respiratory disorders in children. They share common
risk factors, such as obesity, gastro-oesophageal reflux disease (GORD) and
allergic rhinitis. The two conditions are also interrelated: OSA can increase airway
inflammation and may consequently be associated with poor asthma control, and
asthma is associated with an increase in respiratory eort and intrathoracic pressure
swings, which may increase the collapsibility of the upper airways, contributing to
the development and worsening of OSA. These high intrathoracic pressure swings
may also provoke or exaggerate gastro-oesophageal reflux (GOR), which is a common
risk factor. Finally, the overnight respiratory symptoms of OSA and asthma share
similarities, such as laboured breathing, arousals, reduced sleep duration and poor
sleep quality.
It is important to distinguish nonrespiratory sleep disturbances from SDB. Asthma
and SDB are associated with nonrespiratory sleep disturbances, such as reduction
in total sleep time, abnormalities in sleep architecture with a reduction in REM
sleep, and an increase in light sleep, sleep fragmentation and nocturnal awakenings.
Importantly, asthma medications such as corticosteroids and β2-agonists may also
impair sleep quality.
Key points
• There is an interaction between sleep, SDB and several chronic respiratory
disorders during childhood.
• There is a bidirectional relationship between asthma and OSA in children.
• Allergic rhinitis can contribute to OSA.
• Lung disease and other complications in CF can impact sleep.
• Infants with BPD can present with various sleep problems.
382
ERS Handbook: Respiratory Sleep Medicine
Comorbid respiratory disorders in children
https://t.me/medicina_free
Although children with asthma are more likely to develop snoring and OSA, the
prevalence of OSA in asthmatic children seems to be relatively low and is rarely severe.
Rather than a causal association between asthma and SDB, which implies temporality
and directionality, the relationship appears to be bidirectional.
In terms of treatment, adenotonsillectomy seems to be associated with an improvement
in asthma control. Local corticosteroids and/or leukotriene agonists have been shown
to have a beneficial eect on moderate residual OSA aer adenotonsillectomy. Both
asthma and SDB require appropriate and individualised treatment.
Allergy
Allergic rhinitis is a common inflammatory disorder of the nasal airways characterised
by nasal itching, rhinorrhea, nasal congestion and/or sneezing. Allergic rhinitis has
been shown to be associated with SDB and OSA, reduced total sleep time, poor sleep
quality, night sweating, nocturnal enuresis and daytime dysfunction.
A systematic review and meta-analysis concluded that sleep duration was similar
between patients with allergic rhinitis and controls. However, patients with
allergic rhinitis had significantly poorer subjective sleep quality (evaluated via
a questionnaire), used more sleep medication (questionnaire), and had a lower
subjective (questionnaire) and objective (PSG) sleep eciency. It should be noted
that the overall quality of evidence ranged from low to very low, suggesting that
conclusions should be made with caution.
In terms of treatment, like asthma, local nasal corticosteroids and/or leukotriene
agonists have been shown to have a beneficial eect on mild OSA and on moderate
residual OSA aer tonsillectomy, and may thus be beneficial for SDB symptoms in
patients with allergic rhinitis.
Cystic fibrosis
Although cystic fibrosis (CF) is generally considered to be a respiratory disease, it
aects multiple organ systems. Initial studies that assessed sleep issues in CF focused
on respiratory problems: nocturnal hypoxia, alveolar hypoventilation and the risk of
airway obstruction from nasal polyps. Treatment evaluations included long-term
oxygen (O2) therapy or NIV in cases of nocturnal hypercapnia.
In more recent studies, patients with a better preserved lung function were included,
permitting a greater focus on sleep patterns and sleep quality. Reduced sleep duration
and poor sleep quality have been found to be very common, and it is thought that they
can be explained by chronic pain and cough, frequent stools, GOR, nasal obstruction
or sinusitis, and drugs, such as corticosteroids or β-agonists. In teenagers, poor
sleep hygiene, sleep debt and poor sleep quality are associated with depression, poor
academic performance, and reduced physical activity and quality of life. Restless legs
syndrome is also common in adult patients with CF. Although these sleep problems
seem more important in patients with a low lung function, they may also be observed
in patients with preserved lung function.
It is possible that the consequences of poor sleep may exaggerate the multi-organ
morbidity of CF, such as pain, inflammation, susceptibility to infection, and glucose
intolerance; however, these aspects are largely under-evaluated. Sleep problems
in many patients with CF are dominated by non-SDB problems. Whilst reduced
sleep duration and poor sleep quality are extremely common, they are also largely
overlooked. Sleep should be evaluated on a routine basis in CF with prospective
383ERS Handbook: Respiratory Sleep Medicine
Соседние файлы в папке Библиотека им академика М.И. Перельмана