Treatment and Prognosis of The Obesity Hypoventilation Syndrome - UpToDate

Treatment and prognosis of the obesity hypoventilation syndrome - UpToDate 02/01/21 18.
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Treatment and prognosis of the obesity

hypoventilation syndrome
Author: Thomas J Martin, MD
Section Editor: M Safwan Badr, MD
Deputy Editor: Geraldine Finlay, MD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2020. | This topic last updated: Aug 19, 2020.
INTRODUCTION
Obesity hypoventilation syndrome (OHS; "pickwickian syndrome") exists when an obese

individual (body mass index [BMI] >30kg/m2) has awake alveolar hypoventilation (arterial
carbon dioxide tension [PaCO2] >45 mmHg) which cannot be attributed to other
conditions (eg, neuromuscular disease). Untreated OHS is a progressive disorder that is
associated with significant morbidity such that prompt recognition and treatment is
critical.
The treatment and prognosis of OHS are reviewed here. The clinical manifestations,
diagnosis, complications, and pathogenesis of OHS are discussed separately. (See "Clinical
manifestations and diagnosis of obesity hypoventilation syndrome" and "Epidemiology
and pathogenesis of obesity hypoventilation syndrome".)
FIRST LINE THERAPY
Noninvasive positive airway pressure (PAP) together with weight loss are the initial first
line therapies for patients with OHS [1]. A comprehensive and multidisciplinary approach
utilizing experts in obesity, sleep, and pulmonary medicine is recommended.
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Treatment and prognosis of the obesity hypoventilation syndrome - UpToDate 02/01/21 18.12
Positive airway pressure — All patients with OHS have some form of sleep disordered
breathing, typically obstructive sleep apnea (OSA; 90 percent) or sleep-related
hypoventilation (10 percent), warranting treatment with noninvasive PAP. PAP therapy
should not be delayed while the patient tries to lose weight. Selection of the appropriate
mode of PAP (eg, continuous PAP [CPAP], bilevel PAP [BPAP], volume cycled or hybrid
modes of noninvasive ventilation) [2] and approach to initiating PAP therapy in patients
with OHS are described in detail separately. (See "Noninvasive positive airway pressure
therapy for the obesity hypoventilation syndrome".)
Similar to patients with OSA who do not have OHS, patients with OHS have better
outcomes when adherence to CPAP is adequate [3]. (See "Adherence with continuous
positive airway pressure (CPAP)".)
Obesity hypoventilation plus obstructive sleep apnea (continuous positive airway

pressure) — CPAP is the typical mode chosen for treatment for OHS plus OSA, while BPAP,
usually in the spontaneous–timed mode, is indicated in those who fail CPAP. (See
"Noninvasive positive airway pressure therapy for the obesity hypoventilation syndrome",
section on 'Obesity hypoventilation and obstructive sleep apnea'.)
Obesity hypoventilation plus sleep-related hypoventilation (bilevel positive airway

pressure) — Patients with OHS and sleep-related hypoventilation are generally initially
managed with BPAP. (See "Noninvasive positive airway pressure therapy for the obesity
hypoventilation syndrome", section on 'Obesity hypoventilation and sleep-related
hypoventilation'.)
Weight loss and lifestyle modifications — All patients with OHS should begin a weight
loss program. Weight loss improves alveolar ventilation (sometimes normalizing the
awake arterial carbon dioxide tension [PaCO2] and arterial oxygen tension [PaO2]),
reduces the risk of cardiorespiratory complications (eg, pulmonary arterial hypertension
and left ventricular function), improves nocturnal oxyhemoglobin saturation, decreases
the frequency of respiratory events (ie, apneas, hypopneas) during sleep if the patient has
coexisting OSA, and improves pulmonary function [4-11]. These benefits appear to occur
regardless of whether the weight loss was due to lifestyle modification (ie, diet, exercise)
or surgery. (See 'Additional treatments targeted at weight loss' below.)
Weight loss should be supervised and controlled. Rapid, unsupervised weight loss is
discouraged because it is generally not sustained and may have serious side effects (eg,
cholelithiasis). There are no reliable predictors of the exact amount of weight that must be
lost to ameliorate nocturnal upper airway dysfunction and cardiorespiratory failure in
OHS. Individuals with OHS are usually morbidly obese (ie, more than 50 percent above
ideal body weight), and clinical experience suggests that weight loss of more than 100
pounds is often needed before clinically significant improvement is seen.
All patients with OHS should make lifestyle modifications to lose weight. Lifestyle
modifications refer to various combinations of dietary change, exercise, and behavioral
modification, which are described in detail separately. (See "Obesity in adults: Dietary
therapy" and "Obesity in adults: Role of physical activity and exercise" and "Obesity in
adults: Behavioral therapy".)
Individuals with OHS may have more difficulty maintaining long term weight loss than
persons with uncomplicated obesity because of exercise limitations related to their
chronic respiratory failure. Thus, while lifestyle modifications are necessary in patients
with OHS, they are seldom sufficient [12] to achieve and maintain a degree of weight loss
that satisfactorily improves alveolar ventilation and sleep-related breathing disorders [13].
Thus, patients should be educated in weight loss interventions that produce significant
and sustained weight loss of 25 to 30 percent of body weight (eg, bariatric surgery) [1].
(See 'Additional treatments targeted at weight loss' below.)
Compared with positive airway pressure therapy, lifestyle modification alone is less
effective at improving symptoms, polysomnographic parameters, hypercapnia, and some
pulmonary function measurements [14].
SECOND LINE THERAPY
Second line therapies are reserved for patients with OHS who fail or do not tolerate first
line therapies (ie, noninvasive positive airway pressure [PAP] and weight loss measures).
Bariatric surgery is also an option for those who wish to discontinue or reduce the need
for PAP therapy. In general, these are only considered after aggressive attempts have
been made to optimize PAP therapy. In general, these therapies are suboptimal and
associated with increased risk of adverse effects. Choosing among them depends upon
factors including severity of OHS, degree of obesity, likelihood of efficacy or adverse
effects, and patient preferences.
Treatments targeted at obesity hypoventilation and sleep disordered breathing
Tracheostomy — Since the introduction of noninvasive PAP therapy, tracheostomy for

treatment of OHS is now rarely necessary. Tracheostomy itself (without ventilation
through the device) may be effective in patients with OHS and coexisting OSA because it
relieves upper airway obstruction during sleep with subsequent improvement in alveolar
ventilation and the arterial carbon dioxide tension (PaCO2) during wakefulness [15].
However, not all patients return to eucapnia following tracheostomy because upper
airway obstruction is just one factor responsible for alveolar hypoventilation in this
population; other factors (eg, decreased respiratory compliance and ventilatory muscle
strength) are unaltered by tracheostomy. In keeping with this hypothesis is our experience
and available data, which suggest that, despite tracheostomy placement, most patients
still require nocturnal ventilation for residual OSA through the device [16].
Tracheostomy alone cannot be used to treat OHS with sleep-related hypoventilation

unless the tracheostomy is also used for nocturnal ventilation.
In addition to the typical risk and complications [17-20], tracheostomy in the obese
individual is technically more difficult because debulking of excess adipose tissue may be
required in order to securely insert a standard tracheostomy tube [21,22]. In addition, it
may be associated with a higher risk of tube displacement [17,20]. (See "Overview of
tracheostomy".)
The role of tracheostomy and other surgical procedures (eg, maxillomandibular

advancement) sometimes used in the treatment of OSA have not been rigorously tested in
patients with OHS and are discussed separately. (See "Surgical treatment of obstructive
sleep apnea in adults", section on 'Global upper airway procedures'.)
Additional treatments targeted at weight loss — For patients in whom lifestyle

modifications are insufficient (see 'Weight loss and lifestyle modifications' above) and/or
for patients who either want to discontinue or do not tolerate noninvasive PAP, referral to
a bariatric expert is appropriate. Weight loss medications are potentially harmful and
often insufficient, so we believe that they should only be used on a case-by-case basis
after a careful evaluation of the potential benefits and risks to the individual patient.
Bariatric surgery — For morbidly obese patients with OHS, considerable attention has
been directed towards bariatric surgery, since lifestyle modifications alone are generally
insufficient and pharmacological therapy is of uncertain efficacy and safety [23]. Although
no study has specifically enrolled patients with OHS, improvements in gas exchange, OSA,
and indices of pulmonary hypertension have been reported in obese individuals
undergoing bariatric surgery [4,6-8,10,11,24]. However, patients with OHS may be
excluded from surgery due to the presence of comorbid conditions (eg, pulmonary
hypertension or severe morbid obesity itself). Additionally, the response to bariatric
surgery (degree of weight loss, improvement in OSA, improvement in physiologic
parameters) is dependent on both individual patient variables and surgical technique.
Thus, complete resolution of OHS and freedom from PAP therapy is not uniform. The
indications, contraindications, techniques, and complications of bariatric surgery and the
preoperative evaluation of OSA prior to bariatric surgery, including recommendations on
consultation with a sleep expert and/or repeat polysomnography, are reviewed in detail
separately. (See "Bariatric operations for management of obesity: Indications and
preoperative preparation" and "Bariatric procedures for the management of severe
obesity: Descriptions" and "Surgical risk and the preoperative evaluation and
management of adults with obstructive sleep apnea".)
Patients should continue their noninvasive PAP therapy pre- and postoperatively. Inability
to tolerate PAP therapy prior to bariatric surgery may necessitate a temporary
tracheostomy either prior to or at the time of bariatric surgery [25]. Even with optimal
titration of nocturnal noninvasive PAP preoperatively, patients with sleep-disordered
breathing may be at further risk for hypoventilation postoperatively due to the effects of
surgery, general anesthesia, or medications, such that empiric adjustments to PAP
settings may be needed for a short period. Postoperative management of patients with
obesity and OSA is discussed separately. (See "Bariatric surgery: Postoperative and long-
term management of the uncomplicated patient" and "Postoperative management of
adults with obstructive sleep apnea".)
Medication — Pharmacologic therapy for weight loss should only be administered in

patients with OHS who fail diet and exercise measures. However, many of the approved
weight loss medications may initially only achieve weight loss of 5 to 10 kg over 3 to 12
months before the weight loss plateaus, which is typically not enough to improve or
eliminate awake hypoventilation. In addition, most patients regain their weight if the
medications are discontinued. Indications, efficacy, and adverse effects of weight loss
pharmacotherapy are discussed separately. (See "Obesity in adults: Drug therapy".)
THERAPIES OF LIMITED VALUE OR ASSOCIATED WITH HARM
Oxygen alone — Oxygen should not be administered as the sole therapy for OHS. This is
because oxygen may increase hypercapnia, as demonstrated in two studies of stable
newly diagnosed untreated patients with OHS [26,27]. In addition, although supplemental
oxygen will treat sleep-related hypoxemia, it does not address the pathophysiologic
contributors to awake alveolar hypoventilation, including altered chemoresponsiveness,
nocturnal upper airway occlusion, and impaired respiratory mechanics.
In situations in which a patient with OHS requires supplemental oxygen (eg, for comorbid
chronic obstructive pulmonary disease, severe nocturnal desaturations unresponsive to
noninvasive positive airway pressure therapy [PAP]), it should be used concurrently with
optimally titrated PAP therapy. Monitoring the need for oxygen is important since
hypercapnia may improve, and diurnal oxygen requirements may decrease with
adherence to PAP therapy [28].
If supplemental oxygen is necessary and the patient cannot tolerate PAP, the patient
should be carefully monitored (clinically and/or with polysomnography) to detect potential
adverse effects of hypercapnia on hemodynamics and symptoms. (See "Mechanisms,
causes, and effects of hypercapnia", section on 'Oxygen-induced hypercapnia' and "The
evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic
respiratory failure", section on 'Administration of oxygen'.)
Respiratory stimulants — Respiratory stimulants (ie, progestins and acetazolamide) are

adjunctive therapies that are a last resort for patients who continue to have serious
alveolar hypoventilation despite PAP therapy and weight loss. If prescribed, it should be
done on a trial basis only in conjunction with optimally titrated PAP.
Progestins (eg, medroxyprogesterone) alone have been shown to improve but not to
eliminate awake hypercapnia and hypoxemia in patients with OHS [29,30], while
acetazolamide has been shown to improve alveolar ventilation in patients with OHS
[15,31,32]. However these agents do not affect all of the pathogenic contributors to OHS,
in particular the recurrent upper airway collapse that occurs during sleep in patients who
have coexisting obstructive sleep apnea (OSA) [33-37] or the altered respiratory mechanics
[38]. Leaving these contributors untreated typically results in undertreatment of OHS. In
addition, progestins and acetazolamide have potentially serious side effects (eg,
electrolyte disturbance, venous thromboembolism) [39,40]. The respiratory stimulant

theophylline has not been studied in patients with OHS. (See "Management of obstructive
sleep apnea in adults", section on 'Pharmacologic'.)
SUPPORTIVE THERAPIES
Avoidance of alcohol and sedatives — Patients with OHS should be advised to avoid
alcohol, benzodiazepines, opiates, muscle relaxants, and barbiturates. Failure to abstain
from these agents may mitigate the impact of positive pressure therapy. If any of these
agents is considered imperative in the treatment of an individual with OHS, clinical
monitoring is warranted to evaluate the impact of the medication on symptoms and
arterial gas exchange. Polysomnography may be a useful adjunct to help assess nocturnal
ventilation and adequacy of therapy. (See "Management of obstructive sleep apnea in
adults", section on 'Alcohol avoidance' and "Management of obstructive sleep apnea in
adults", section on 'Concomitant medications'.)
Treatment of comorbid conditions — Routine treatment of comorbid conditions and the

prevention of complications are also necessary in all patients with OHS. Comorbid
conditions that impair ventilation or reduce the ventilatory response to hypoxemia or
hypercapnia are likely to contribute to the impairment caused by obesity. As a result, the
clinician should make an effort to identify and treat comorbid conditions, including:
● Chronic obstructive pulmonary disease (COPD) - Treatment of coexisting COPD

includes the cessation of smoking and the prescription of inhaled bronchodilators
and, possibly, inhaled corticosteroids. Supplemental oxygen benefits patients with
hypercapnic COPD but should not be administered in OHS without co-prescribing
positive airway pressure (PAP) since it can worsen alveolar hypoventilation. The
diagnosis and management of COPD are reviewed separately. (See "Chronic
obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and
staging" and "Stable COPD: Initial pharmacologic management" and "Long-term
supplemental oxygen therapy".)
● Hypothyroidism – Hypothyroidism may contribute to the chronic ventilatory failure of

OHS by decreasing chemoresponsiveness, causing obstructive sleep apnea (OSA; due
to macroglossia and/or upper airway dilator muscle dysfunction), or causing either a
myopathy or neuropathy that affects the respiratory muscles [41-44]. These
consequences of hypothyroidism may be improved with thyroid hormone

replacement. In cases of subclinical hypothyroidism, which is characterized by mild
elevation of serum thyroid stimulating hormone (<10 mU/L) and a normal free T4
level, we prefer to monitor these patients (eg, every six months) for the development
of overt hypothyroidism using clinical examination and thyroid function tests. (See
"Treatment of primary hypothyroidism in adults".)
FOLLOW-UP
The therapeutic goals for patients with OHS include [45]:
● Normalization of the arterial carbon dioxide tension (PaCO2) during wakefulness and
sleep (ie, PaCO2 <45 mmHg).
● Elimination of oxyhemoglobin desaturation during wakefulness and sleep; to avoid

worsening hypercapnia, it is recommended that the provision of supplemental
oxygen during positive airway pressure (PAP) therapy be the minimum amount
required to maintain an oxyhemoglobin saturation of ≥90 percent.
● Relief of the symptoms of OHS (typically daytime hypersomnolence).
● Prevention of complications, including erythrocytosis, pulmonary hypertension, and

right heart failure.
● Treatment of underlying OSA (ie, elimination of obstructive and hypopnea events) or

sleep-related hypoventilation (ie, nonobstructive events).
● Improvement of sleep architecture and quality, reducing nocturnal work of breathing,

and providing respiratory muscle rest.
While there are no standard recommendations for the follow-up of patients undergoing
treatment for OHS, follow-up should include clinical evaluation of the response to
noninvasive PAP and/or weight loss (eg, every six months). Notably, duration of therapy,
and therefore follow-up, are typically indeterminate and often lifelong since the degree of
support may change over time depending upon factors including weight loss/gain,
medications, or the development or treatment of contributing comorbidities.
● Follow-up after noninvasive PAP – The follow-up of those treated with noninvasive PAP
is focused on ensuring adequate settings and compliance with therapy as well as the
evaluation of symptoms, repeating arterial blood gases (ABG), and, in select
circumstances, repeating polysomnography, the details of which are discussed
separately. (See "Initiation of positive airway pressure therapy for obstructive sleep
apnea in adults" and "Mode selection for positive airway pressure titration in adults
with obstructive sleep apnea", section on 'Follow-up' and "Noninvasive positive airway
pressure therapy for the obesity hypoventilation syndrome", section on 'Assessing
treatment response' and "Mode selection for positive airway pressure titration in
adults with obstructive sleep apnea".)
● Follow-up after weight loss - It is unusual that weight loss, even if significant,
eliminates the need for nocturnal ventilation. Thus, long term PAP is still typically
needed, but most patients have reduced PAP settings or can switch to continuous PAP
(CPAP) if originally receiving bilevel PAP (BPAP). Reassessment of OHS is performed
after significant weight loss has occurred (eg, usually within one to two years after
bariatric surgery). An ABG should be performed to examine the awake partial arterial
pressures of carbon dioxide (PaCO2) and oxygen (PaO2), as well as in-laboratory
polysomnography to assess for accurate PAP and supplemental oxygen settings so
that adjustments can be made if necessary. Early, rapid weight loss (typically 45 to 70
percent of excess body weight) during the first postoperative year after bariatric
surgery is often associated with improvement of OHS [46]. However, this has not been
universal and some patients have residual OSA despite amelioration of symptoms
[4,6,13,47-52]. Thus, discontinuation of noninvasive PAP therapy after weight loss
should not be performed unless polysomnography demonstrates that residual OSA
or hypoventilation warranting therapy is absent.
PROGNOSIS
Morbidity and mortality in untreated patients with OHS is high [53,54]. OHS tends to be
progressive if left untreated, with many patients developing cardiovascular complications
including pulmonary hypertension and right heart failure.
The main cause of death is generally from cardiovascular disease [54,55]. The impact of
therapy, particularly noninvasive positive airway pressure, on cardiovascular complications
and mortality is uncertain and appears limited based upon extrapolated data from
patients with obstructive sleep apnea (OSA). Even when sleep disordered breathing is
treated with positive airway pressure therapy, mortality in those with severe OHS remains
substantially worse than individuals with OSA alone [55]. (See "Obstructive sleep apnea
and cardiovascular disease in adults".)
Hospitalization rates are higher in OHS compared with eucapnic obese individuals [56],
and once hospitalized, patients with OHS are more likely to need intensive care unit
management, be intubated, and require long-term care at discharge [57].
Individuals with OHS have considerably worse health status and access more health care
resources compared to the general population, with differences apparent up to eight
years before a diagnosis is made [58].
The presence of significant awake hypoxemia at diagnosis and during PAP therapy has
been associated with a poor prognosis [59,60].
SUMMARY AND RECOMMENDATIONS
● Obesity hypoventilation syndrome (OHS; "pickwickian syndrome") exists when an

obese individual (body mass index [BMI] >30kg/m2) has awake alveolar
hypoventilation (arterial carbon dioxide tension [PaCO2] >45 mmHg), which cannot be
attributed to other conditions (eg, neuromuscular disease). (See 'Introduction' above
and "Clinical manifestations and diagnosis of obesity hypoventilation syndrome".)
● For patients with OHS, we recommend a comprehensive and multidisciplinary

approach targeted at the immediate initiation of noninvasive positive airway pressure
(PAP) together with lifestyle modifications for weight loss. (See 'Positive airway
pressure' above and "Noninvasive positive airway pressure therapy for the obesity
hypoventilation syndrome".)
● For patients with OHS who fail or do not tolerate first line therapies in whom
aggressive attempts have been made to optimize PAP therapy, options include
tracheostomy for the treatment of sleep disordered breathing and bariatric surgery or
rarely medication for weight loss. In general, these therapies are suboptimal and
associated with increased risk of adverse effects. Choosing among them depends
upon factors including severity of OHS, degree of obesity, medical comorbidities,
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likelihood of efficacy or adverse effects, and patient preferences. (See 'Weight loss
and lifestyle modifications' above and 'Second line therapy' above.)
● For patients with OHS in whom supplemental oxygen is indicated (eg, for significant
sleep-related oxyhemoglobin desaturation or for hypoxemic respiratory failure), we
suggest that it be administered in conjunction with noninvasive PAP, based upon the
rationale that supplemental oxygen alone may worsen hypercapnia. Oxygen should
not be administered as a sole therapy for OHS. Respiratory stimulants (ie, progestins
and acetazolamide) are adjunctive therapies that are a last resort for patients who
continue to have serious alveolar hypoventilation despite PAP therapy and weight
loss. However, such agents are typically minimally effective and are associated with
adverse effects. (See 'Therapies of limited value or associated with harm' above.)
● Patients with OHS should be advised to abstain from alcohol and sedatives (eg,
benzodiazepines, opiates, muscle relaxants, and barbiturates) which can contribute to
hypoventilation and mitigate the effects of PAP therapy. In addition, the clinician
should identify and treat comorbid conditions that may contribute to hypoventilation
(eg, chronic obstructive pulmonary disease and hypothyroidism) or can complicate
OHS (eg, pulmonary hypertension). (See 'Supportive therapies' above.)
● Patients with OHS should be followed clinically for their response to noninvasive PAP
and/or weight loss (eg, every six months). Notably, duration of therapy, and therefore
follow-up, are typically indeterminate and often lifelong since the degree of support
may change over time depending upon factors including weight loss/gain,
medications, or the development or treatment of contributing comorbidities. (See
'Follow-up' above and "Noninvasive positive airway pressure therapy for the obesity
hypoventilation syndrome", section on 'Assessing treatment response'.)
● Morbidity and mortality in untreated patients with OHS is high, with most deaths due
to cardiovascular complications including pulmonary hypertension and right heart
failure. The impact of therapy on cardiovascular complications and mortality is
uncertain. (See 'Prognosis' above.)
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Topic 7713 Version 28.0
Contributor Disclosures
Thomas J Martin, MD Nothing to disclose M Safwan Badr, MD Nothing to disclose Geraldine Finlay,
MD Consultant/Advisory Boards: LAM Board of directors, LAM scientific grant review committee for The
LAM Foundation.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
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Treatment and Prognosis of The Obesity Hypoventilation Syndrome - UpToDate

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Treatment and prognosis of the obesity hypoventilation syndrome - UpToDate 02/01/21 18.

Official reprint from UpToDate®

Treatment and prognosis of the obesity

Obesity hypoventilation syndrome (OHS; "pickwickian syndrome") exists when an obese

FIRST LINE THERAPY

Obesity hypoventilation plus obstructive sleep apnea (continuous positive airway

Obesity hypoventilation plus sleep-related hypoventilation (bilevel positive airway

SECOND LINE THERAPY

Treatments targeted at obesity hypoventilation and sleep disordered breathing

Tracheostomy — Since the introduction of noninvasive PAP therapy, tracheostomy for

Tracheostomy alone cannot be used to treat OHS with sleep-related hypoventilation

The role of tracheostomy and other surgical procedures (eg, maxillomandibular

Additional treatments targeted at weight loss — For patients in whom lifestyle

Medication — Pharmacologic therapy for weight loss should only be administered in

THERAPIES OF LIMITED VALUE OR ASSOCIATED WITH HARM

Respiratory stimulants — Respiratory stimulants (ie, progestins and acetazolamide) are

electrolyte disturbance, venous thromboembolism) [39,40]. The respiratory stimulant

Treatment of comorbid conditions — Routine treatment of comorbid conditions and the

● Chronic obstructive pulmonary disease (COPD) - Treatment of coexisting COPD

● Hypothyroidism – Hypothyroidism may contribute to the chronic ventilatory failure of

consequences of hypothyroidism may be improved with thyroid hormone

The therapeutic goals for patients with OHS include [45]:

● Elimination of oxyhemoglobin desaturation during wakefulness and sleep; to avoid

● Relief of the symptoms of OHS (typically daytime hypersomnolence).

● Prevention of complications, including erythrocytosis, pulmonary hypertension, and

● Treatment of underlying OSA (ie, elimination of obstructive and hypopnea events) or

● Improvement of sleep architecture and quality, reducing nocturnal work of breathing,

SUMMARY AND RECOMMENDATIONS

● Obesity hypoventilation syndrome (OHS; "pickwickian syndrome") exists when an

● For patients with OHS, we recommend a comprehensive and multidisciplinary

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3. Bouloukaki I, Mermigkis C, Michelakis S, et al. The Association Between Adherence to

6. Martí-Valeri C, Sabaté A, Masdevall C, Dalmau A. Improvement of associated

9. Lumachi F, Marzano B, Fanti G, et al. Hypoxemia and hypoventilation syndrome

10. Dávila-Cervantes A, Domínguez-Cherit G, Borunda D, et al. Impact of surgically-

16. Camacho M, Teixeira J, Abdullatif J, et al. Maxillomandibular advancement and

17. El Solh AA, Jaafar W. A comparative study of the complications of surgical

26. Wijesinghe M, Williams M, Perrin K, et al. The effect of supplemental oxygen on

32. Powers MA. Obesity hypoventilation syndrome: bicarbonate concentration and

37. Anttalainen U, Saaresranta T, Vahlberg T, Polo O. Short-term medroxyprogesterone

39. Vasilakis C, Jick H, del Mar Melero-Montes M. Risk of idiopathic venous

41. Martinez FJ, Bermudez-Gomez M, Celli BR. Hypothyroidism. A reversible cause of

44. Skatrud J, Iber C, Ewart R, et al. Disordered breathing during sleep in

45. Randerath W, Verbraecken J, Andreas S, et al. Definition, discrimination, diagnosis

47. Korenkov M, Shah S, Sauerland S, et al. Impact of laparoscopic adjustable gastric

55. Castro-Añón O, Pérez de Llano LA, De la Fuente Sánchez S, et al. Obesity-

57. Nowbar S, Burkart KM, Gonzales R, et al. Obesity-associated hypoventilation in

58. Jennum P, Kjellberg J. Health, social and economical consequences of sleep-

Topic 7713 Version 28.0

Conflict of interest policy

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