INTRODUCTION — Obesity hypoventilation syndrome (OHS) is defined as the presence of awake alveolar hypoventilation in an obese individual which cannot be attributed to other conditions associated with alveolar hypoventilation [1-3]. OHS is associated with increased cardiovascular morbidity and mortality. Consequently, early detection and treatment are crucial to minimize these adverse effects.
The clinical manifestations, diagnosis, and complications of OHS are reviewed here, while the pathogenesis and treatment are discussed separately. (See "Epidemiology and pathogenesis of obesity hypoventilation syndrome" and "Treatment and prognosis of the obesity hypoventilation syndrome" and "Noninvasive positive airway pressure therapy for the obesity hypoventilation syndrome".)
DEFINITION — OHS is defined by raised awake arterial pressure of carbon dioxide (PaCO2) levels in patients with obesity in whom alternative causes hypercapnia and hypoventilation have been excluded.
PROPOSED STAGING — However, it is now recognized that nocturnal hypoventilation precedes the development of awake hypercapnia, with earlier recognition and treatment of the problem potentially reducing the development of significant comorbid conditions. Recognizing this, a European Respiratory Society taskforce has proposed a staging schema for hypoventilation in patients with obesity (ie, body mass index [BMI] >30 kg/m2) [2]. Patients with obstructive sleep apnea (OSA) and no hypercapnia were considered stage 0. Stages I and II represented patients with obesity-associated sleep hypoventilation but normal awake PaCO2 and either serum bicarbonate <27 mmol/L (stage I) or >27mmol/L (stage II). Stages III and IV encompassed classically defined OHS patients with or without concurrent OSA. Those in stage IV were distinguished from stage III by the presence of significant cardiometabolic comorbidities.
RISK FACTORS — The major risk factor for OHS is obesity (body mass index [BMI] >30 kg/m2), in particular, severe obesity (BMI >50 kg/m2), where prevalence may be as high as 50 percent. However, not all patients with obesity develop OHS.
Risk factors in obese patients are poorly defined but may include [4-6]:
●Significant increase in waist:hip ratio (ie, central obesity)
●Reduced lung function due to obesity
●Reduced inspiratory muscle strength
●Severe obstructive sleep apnea (OSA; eg, apnea hypopnea index >30 events per hour)
Unlike OSA, male gender is not a risk factor for OHS [7-9]. However, women may present somewhat differently.
Patients with OHS usually present in the fifth and sixth decades of life.
CLINICAL MANIFESTATIONS — The clinical manifestations of OHS are nonspecific and reflect the manifestations of obesity, coexistent obstructive sleep apnea (OSA is present in 90 percent of OHS) or of OHS-related complications (eg, pulmonary hypertension).
Symptoms and signs — Patients with OHS are obese (body mass index [BMI] >30 kg/m2), hypersomnolent individuals. Ninety percent have at least some coexisting OSA (apnea-hypopnea index [AHI] >5 events per hour), with severe disease (eg, AHI >30 events per hour) seen in 70 percent of patients [10]. Symptoms and physical findings of OSA include daytime hypersomnolence, loud snoring, choking during sleep, resuscitative snorting, fatigue, impaired concentration and memory, a small oropharynx, and a thick neck [1,11]. The 10 percent of individuals with OHS who have coexistent sleep hypoventilation without significant OSA present similarly to those with the OHS-OSA phenotype, except witnessed apneas during sleep are less common [11]. They are also more likely to be older females [12,13]. However, standard history taking and questionnaires do not readily establish or exclude an OHS diagnosis [14]. The manifestations of OSA and nocturnal hypoventilation are provided in detail separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults" and "Central sleep apnea: Risk factors, clinical presentation, and diagnosis", section on 'Clinical findings'.)
Many patients with OHS present late in the course of their disease and have manifestations of endstage disease including [1,6,15-17]:
●Severe hypoxemic hypercapnic respiratory failure - While many patients present with chronic stable symptoms or chronic hypercapnic respiratory failure, about one-third of patients present with acute-on-chronic respiratory failure prompting hospital admission [15,17-21]. There is some evidence to suggest that women may present later than men and are more likely to present with acute-on-chronic respiratory failure [19,22]. Such patients are often misdiagnosed as having chronic obstructive pulmonary disease (COPD) or asthma, despite an absence of obstruction on pulmonary function testing [23]. Daytime hypoxemia and significant and sustained reductions in overnight oximetry (eg, peripheral saturation <80 percent) are features that are uncommon in OSA or obesity alone [24]. (See "Pulse oximetry" and "Home sleep apnea testing for obstructive sleep apnea in adults", section on 'Pulse oximetry'.)
●Right heart failure from pulmonary hypertension (dyspnea on exertion, elevated jugular venous pressure, hepatomegaly, and pedal edema) and less commonly, facial plethora from polycythemia.
Laboratory tests — OHS may be associated with the following findings:
●Elevated serum bicarbonate (>27 mEq/L) – Almost all patients with OHS have an elevated serum bicarbonate (venous and/or arterial), which is usually a clue that the patient is chronically hypercapnic. However, it is nonspecific since other etiologies can raise the bicarbonate level (eg, dehydration, medications) and it is not 100 percent sensitive since other conditions (eg, lactic acidosis, chronic hyperventilation) may lower the bicarbonate level.
This cut-off is based upon limited data. One observational study reported that a venous serum bicarbonate of >27 mEq/L had a 92 percent sensitivity for identifying awake hypercapnia in obese individuals, although specificity was significantly lower (50 percent) [25]. A bicarbonate level <27 mEq/L had 97 percent negative predictive value for excluding the diagnosis in this study. Another study reported a sensitivity of 85 percent and specificity of 89 percent in patients with levels >27 mEq/L when capillary blood gas samples were used [26].
●Hypercapnia (arterial pressure of carbon dioxide [PaCO2] >45 mmHg) – Consistent with the phenomenon of hypoventilation, all patients with OHS have hypercapnia on arterial blood gas analysis when awake and on room air. Although most patients with OHS present with chronic elevations in the PaCO2, about one-third have acute-on-chronic respiratory failure [17,20,21]. A raised bicarbonate (>27 mmol/L) or base excess (>3 mmol/L) in the absence of another cause for a metabolic alkalosis in an obese individual with a PaCO2 <45 mmHg may be an early indicator of OHS, warranting closer investigation [27,28]. (See "Arterial blood gases" and "Venous blood gases and other alternatives to arterial blood gases".)
●Hypoxemia (PaO2 <70 mmHg) – Hypoxemia is usually present. The calculated alveolar-arterial (A-a) oxygen gradient is classically normal, although a mild widening is not unusual related to ventilation-perfusion mismatching or coexistent parenchymal or vascular lung disease [29,30]. Severe nocturnal desaturation is also common (eg, peripheral saturation <80 percent).
●Polycythemia — Polycythemia due to recurrent hypoventilation- or OSA-associated hypoxemia is uncommon but may be present as a late manifestation.
Pulmonary function tests — Although findings of restriction are more commonly seen in obese patients with OHS than in eucapnic obese patients, they are nonspecific, and normal pulmonary function tests (PFTs) do not exclude the diagnosis. In general, PFTs are more useful for ruling out underlying causes of hypoventilation. (See 'Exclude other causes of hypercapnia and alveolar hypoventilation' below.)
In OHS a restrictive pattern on PFTs due to obesity is common, particularly in those with a higher BMI (eg, BMI >50 kg/m2); both forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) are reduced, while the FEV1/FVC ratio is preserved [31,32]. More commonly, a reduction in functional residual capacity and expiratory reserve volume is seen [32]. FVC values were found in one study to be lower in patients with OHS than OSA but the threshold was ill-defined [4]. (See "Overview of pulmonary function testing in adults" and "Chest wall diseases and restrictive physiology".)
Severe restriction is uncommon with obesity and may indicate another restrictive lung disorder.
Imaging and cardiac studies — In OHS, typical findings on chest radiograph include elevation of both hemidiaphragms due to the obese abdomen and the heart may be enlarged due to right ventricular hypertrophy or pericardial fat.
Evidence of right ventricle enlargement from pulmonary hypertension that complicates advanced OHS may be seen on electrocardiography (EKG) and echocardiography [33,34].
DIAGNOSTIC APPROACH — The diagnostic approach focuses on establishing awake (often daytime) hypoventilation in an obese patient in the absence of other causes of alveolar hypoventilation. Polysomnography with continuous nocturnal carbon dioxide monitoring is the gold standard for the evaluation of patients suspected of having obesity hypoventilation syndrome (OHS). Testing should be performed to characterize the type of underlying sleep disordered breathing (ie, OHS with or without coexisting obstructive sleep apnea [OSA]). (See 'Identify coexistent sleep disordered breathing' below.)
For patients who present with acute-on-chronic hypercapnic respiratory failure suspected to be due to OHS, immediate treatment with positive pressure therapy is appropriate to stabilize their clinical condition [17,19,21]. Once the patient has improved and is stable, a diagnostic evaluation can be initiated. The treatment of OHS is discussed separately. (See "Treatment and prognosis of the obesity hypoventilation syndrome" and "Noninvasive positive airway pressure therapy for the obesity hypoventilation syndrome".)
Suspecting obesity hypoventilation — A strong clinical suspicion for OHS is critical for the diagnosis. We typically initiate evaluation in obese patients (body mass index [BMI] >30 kg/m2) with suspected or known OSA (or sleep disordered breathing), particularly those with severe OSA (eg, apnea hypopnea index >60 events per hour, since the prevalence is high in this population).
We also initiate evaluation in obese individuals with or without OSA who have the following clinical features:
●Unexplained awake room air peripheral saturation (SpO2) ≤94 percent or an overnight nadir saturation <80 percent
●Unexplained dyspnea on exertion
●Symptoms and signs of pulmonary hypertension and/or right-sided heart failure (eg, elevated jugular venous pressure, hepatomegaly, and pedal edema)
●Facial plethora, which may indicate polycythemia
●A raised bicarbonate on venous blood sampling (see 'Laboratory tests' above)
Many of these features are more common in patients with OHS than in eucapnic obese individuals or in patients who have OSA alone [1,4,6,15-17,24,25,35].
Hypoventilation first becomes apparent during sleep in patients with obesity [2]. In one study, the prevalence of obesity-related sleep hypoventilation (ORSH) had a prevalence of 19 percent amongst 94 obese patients (BMI >40kg.m-2). These individuals experienced a rise in carbon dioxide (CO2) during sleep with a normal or raised bicarbonate during wakefulness while PaCO2 remained <45 mmHg [2]. Predictors of ORSH were awake oxygen saturation ≤93 percent, and a partial arterial pressure of carbon dioxide of ≥45 mmHg in the supine position [36]. These findings have led some experts to suggest that ORSH is a precursor to OHS. However, further studies are needed to confirm the evolution of ORSH to OHS.
Further details regarding the clinical manifestations of OHS are discussed above. (See 'Clinical manifestations' above.)
Indicators of chronic alveolar hypoventilation — In patients in whom OHS is suspected, the presence of chronic hypoventilation is usually inferred when a chronic respiratory acidosis (hypercapnic respiratory acidosis) on arterial blood gas analysis (ABG) is demonstrated together with compensatory metabolic alkalosis (ie, elevated bicarbonate).
●ABG – Whether an ABG should be obtained in all patients suspected of having OHS has been the subject of debate. We and others suggest that when the suspicion for OHS is strong, an ABG should be measured. ABGs should be performed while the patient is awake, sitting upright, and breathing room air (so that A-a oxygen gradient can be calculated). Where ABGs are difficult to obtain, venous blood sampling can be used as a surrogate for pH, PaCO2, and bicarbonate [37,38]. (See "Arterial blood gases" and "Venous blood gases and other alternatives to arterial blood gases".)
●Serum bicarbonate – For those in whom the suspicion is low to moderate (eg, <20 percent), obtaining serum bicarbonate is typically sufficient. Based upon the results we suggest the following:
•Bicarbonate level >27 mEq/L – An elevated bicarbonate level greater than 27 mEq/L, significantly increases the likelihood of OHS and an ABG should be done to investigate for the presence of chronic hypercapnic acidosis (partial pressure of arterial carbon dioxide [PaCO2] >45 mmHg). ABGs can also identify hypoxemia. Should chronic respiratory acidosis with compensatory metabolic alkalosis be identified, then OHS is likely, and if not identified then OHS is unlikely. Interpretation of acid-base disturbances and distinguishing acute, acute-on-chronic, and chronic hypercapnia (figure 1 and figure 2 and figure 3) are discussed separately (See "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure", section on 'Arterial blood gas analysis' and "Simple and mixed acid-base disorders", section on 'Respiratory acid-base disorders'.)
•Bicarbonate level is ≤27 mEq/L – If the bicarbonate level is ≤27 mEq/L, OHS is unlikely, particularly when the suspicion for OHS is low to moderate. An ABG is not absolutely necessary in this population. However, the approach in this population should be individualized. An ABG may be considered in obese patients with borderline elevations in bicarbonate, reduced oxygenation parameters, and suspected complex acid-base disturbance (eg, acute-on-chronic hypercapnia, triple acid-base disturbance), as well as in those in whom an ABG would facilitate excluding an alternate diagnosis.
Exclude other causes of hypercapnia and alveolar hypoventilation — For those in whom a chronic respiratory acidosis with compensatory metabolic alkalosis is found, additional testing is necessary to exclude other diseases that can cause or contribute to chronic alveolar hypoventilation or hypercapnia. Disorders that commonly co-exist with obesity that may contribute to hypercapnia include chronic obstructive pulmonary disease (COPD), restrictive lung disease (eg, neuromuscular weakness, severe interstitial lung disease, chest wall disease), hypothyroidism, electrolyte disturbances, and chronic sedative use [1,11]. Testing should be individualized but generally includes:
●Serum chemistries and electrolytes – Electrolyte disturbances that may exacerbate hypercapnia include hypophosphatemia, hypomagnesemia, and rarely, hypermagnesemia, hypokalemia, or hypercalcemia. If found, these should be corrected and the ABG repeated. (See "Hypomagnesemia: Clinical manifestations of magnesium depletion" and "Hypophosphatemia: Clinical manifestations of phosphate depletion".)
●Complete blood count – Chronic hypoxemia from underlying lung disease may be associated with polycythemia, which may be a useful tool to monitor response to therapy [31,39]. Although rare, an elevated eosinophil fraction on a complete blood count may be consistent with neuropathy from eosinophilic myalgia. (See "Hypereosinophilic syndromes: Clinical manifestations, pathophysiology, and diagnosis", section on 'Neurologic disease' and "Diagnostic approach to the patient with erythrocytosis/polycythemia", section on 'Causes of absolute polycythemia'.)
●Thyroid function tests – Hypothyroidism may contribute to the chronic ventilatory failure of OHS by decreasing chemo-responsiveness, causing OSA (due to macroglossia and/or upper airway dilator muscle dysfunction), or causing either a myopathy or neuropathy that affects the respiratory muscles [40-43]. (See "Laboratory assessment of thyroid function" and "Hypomagnesemia: Clinical manifestations of magnesium depletion" and "Hypophosphatemia: Clinical manifestations of phosphate depletion".)
●Pulmonary function tests – Pulmonary function tests (PFTs) including spirometry, lung volumes, diffusing capacity, and inspiratory and expiratory pressures may facilitate the identification and severity of a potential underlying lung disease and should be performed in the chronic stable state. (See "Overview of pulmonary function testing in adults" and "Tests of respiratory muscle strength".)
●Imaging – A chest radiograph should be performed to exclude parenchymal lung disease, chest wall disease, asymmetrical elevation of a hemidiaphragm (ie, diaphragm paralysis), and cardiomegaly.
●Other – Rarely, a toxicology screen (eg, concomitant benzodiazepine or narcotic use) or creatine phosphokinase (eg, contributing myositis) are obtained.
Further details regarding the evaluation of acute hypercapnia (table 1) are discussed separately (see "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure")
IDENTIFY COEXISTENT SLEEP DISORDERED BREATHING — Ideally, in-laboratory polysomnography (PSG) is performed in all patients suspected as having OHS, in whom a diagnosis of obstructive sleep apnea (OSA) or other sleep disordered breathing (SDB) does not already exist. However, many factors including third party payor issues, degree of obesity, and likelihood of OSA or sleep-hypoventilation determine what sleep test is chosen.
●Factors favoring in-laboratory PSG include morbid obesity (body mass index [BMI] >40 kg/m2), high likelihood of sleep-related hypoventilation (as CO2 monitoring is available only with in-center testing), heart failure, and significant daytime or nocturnal hypoxemia.
●Home sleep apnea testing (HSAT) is not ideal for rule out OHS as HSAT is best suited for uncomplicated, high probability obstructive sleep apnea cases. It should be noted that HSAT does not detect sleep-related hypoventilation, thus necessitating PSG with continuous nocturnal carbon dioxide monitoring. HSAT may be suitable in those with non-morbid obesity (BMI 30 to 40 kg/m2) in whom the likelihood of OSA is high or those in whom the issue of cost expressly prohibits PSG evaluation.
Although PSG or HSAT is not required to diagnose OHS, sleep testing distinguishes the 90 percent of patients with OHS who have coexistent OSA from the 10 percent of patients who have sleep-related hypoventilation alone [11,44]. Determining the type of SDB is important since it has implications for the type of therapy administered. Further details regarding diagnostic testing are provided separately. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnostic tests' and "Home sleep apnea testing for obstructive sleep apnea in adults" and "Central sleep apnea: Risk factors, clinical presentation, and diagnosis".)
Although, the apnea hypopnea index [AHI] is likely to be higher in OHS patients than those with eucapnic OSA, it doesn’t distinguish these groups [25,45]. However, patients with OHS tend to have severe OSA (eg, AHI >50/hour) [25,45,46] and usually have more profound oxygen desaturation during sleep than patients with OSA alone, spending a significantly larger part of sleep time with saturations <90 percent [45,47,48]. (See "Polysomnography in the evaluation of sleep-disordered breathing in adults".)
DIAGNOSIS — OHS is a diagnosis of exclusion that can be made when the following criteria are met:
●Obesity (body mass index [BMI] >30 kg/m2)
●Awake alveolar hypoventilation as indicated by a partial arterial pressure of carbon dioxide >45 mmHg
●Alternative causes hypercapnia and hypoventilation have been excluded (see 'Exclude other causes of hypercapnia and alveolar hypoventilation' above)
Although the majority also have sleep-disordered breathing (nocturnal obstructive and nonobstructive events), it is the awake (ie, typically daytime) hypoventilation that is critical for diagnosis.
The absence of an alternative cause of hypercapnic hypoventilation is an important requirement for the diagnosis of OHS. In clinical practice, patients frequently have additional diseases that cause acute and/or chronic hypercapnia. However, assessing the contributions of additional etiologies may be tricky and a matter of clinical judgement. If a potential contributing etiology is mild or considered unlikely to cause hypercapnia, then it is appropriate to diagnose OHS. In contrast, if a coexisting disease is severe and considered likely contributing to hypercapnia, OHS cannot be diagnosed with certainty. (See 'Exclude other causes of hypercapnia and alveolar hypoventilation' above and 'Differential diagnosis' below.)
Because symptoms are nonspecific, the diagnosis of OHS is frequently delayed. It is commonly misdiagnosed as asthma or chronic obstructive pulmonary disease [23] and some patients are not diagnosed until hospitalization for acute-on-chronic respiratory failure occurs. (See 'Symptoms and signs' above.)
DIFFERENTIAL DIAGNOSIS — The main competing diagnosis for the symptoms of OHS is obstructive sleep apnea (OSA). Apart from the presence of chronic respiratory acidosis with compensatory metabolic alkalosis, both disorders are often clinically indistinguishable from one another. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Clinical features'.)
Common etiologies for respiratory hypercapnia and alveolar hypoventilation are typically distinguished by history, examination, pulmonary function testing, imaging, and laboratory findings:
●Chronic obstructive pulmonary disease (COPD) – COPD may be identified in those with a smoking history, obstruction on pulmonary function tests, and imaging findings of emphysema. (See "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging".)
●Interstitial lung diseases (ILD) – ILD may be identified in those with imaging findings of parenchymal abnormalities and restriction on pulmonary function tests. (See "Approach to the adult with interstitial lung disease: Clinical evaluation" and "Approach to the adult with interstitial lung disease: Diagnostic testing".)
●Neuromuscular (NM) disorders – NM disorders may be identified by history (eg, weak cough), weakness on examination, and restrictive deficit and muscle weakness on lung function testing. Chest imaging may reveal an elevated hemidiaphragm to suggest diaphragmatic paralysis. (See "Respiratory muscle weakness due to neuromuscular disease: Clinical manifestations and evaluation".)
●Chest wall disorders – Such disorders (eg, kyphoscoliosis) may be obvious on clinical examination or on imaging. (See "Chest wall diseases and restrictive physiology".)
●Hypothyroidism – Hypothyroidism is typically evident on laboratory testing. (See "Clinical manifestations of hypothyroidism" and "Diagnosis of and screening for hypothyroidism in nonpregnant adults".)
●Chronic sedative use - Use of sedatives may be found on history or toxicology testing. (See "General approach to drug poisoning in adults".)
ASSESS COMPLICATIONS — All patients with obesity hypoventilation syndrome (OHS) should be assessed for common complications, many of which are shared with obesity alone (table 2) [49]. These are discussed in detail separately. (See "Overweight and obesity in adults: Health consequences" and "Treatment and prognosis of the obesity hypoventilation syndrome", section on 'Treatment of comorbid conditions'.)
Specifically, patients with OHS should be assessed for the following common complications:
●Mild to moderate pulmonary hypertension (PH) – Up to two-thirds of patients with OHS have PH. Thus, at diagnosis we typically perform an electrocardiogram and echocardiogram in this population to evaluate for PH, the details of which are discussed separately. (See "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Epidemiology, pathogenesis, and diagnostic evaluation in adults".)
●Cardiovascular and metabolic comorbidities – Conditions such as hypertension, congestive heart failure, and insulin resistance are all more common in patients with OHS than in patients with eucapnic obesity, and may be present three or more years prior to the diagnosis of OHS [4,49-51]. Thus, at the time of diagnosis we typically perform fasting bloods assessing plasma glucose, triglycerides, and cholesterol to ensure comorbid conditions have been identified and are being appropriately managed. A cross sectional study of stable OHS patients found cardiovascular morbidity risk was significantly higher in those with the predominantly sleep hypoventilation OHS phenotype despite these individuals exhibiting less severe nocturnal and awake gas exchange compared with those who had OHS and significant OSA [52].
The natural history and prognosis of OHS is discussed separately. (See "Treatment and prognosis of the obesity hypoventilation syndrome".)
SUMMARY AND RECOMMENDATIONS
●Obesity hypoventilation syndrome (OHS) is defined as the presence of awake alveolar hypoventilation (partial arterial pressure of carbon dioxide [PaCO2] >45 mmHg) in an obese individual (body mass index [BMI] >30 kg/m2), which cannot be attributed to other conditions associated with hypoventilation. (See 'Introduction' above and 'Diagnosis' above and 'Definition' above and 'Proposed staging' above.)
●The symptoms and clinical manifestations of OHS are nonspecific and are more reflective of the manifestations of obesity, coexistent obstructive sleep apnea (OSA; eg, hypersomnolence, snoring, witnessed apneas), or OHS-related complications (eg, pulmonary hypertension). Sleep-related desaturation and daytime hypoxemia are common. (See 'Clinical manifestations' above.)
●For those in whom OHS is strongly suspected (eg, morbidly obese patients with suspected or known OSA), we suggest that an arterial blood gas (ABG) be obtained to look for evidence of alveolar hypoventilation (ie, PaCO2 >45 mmHg). For those in whom the suspicion is low to moderate (eg, <20 percent), obtaining serum bicarbonate is typically sufficient; an elevated bicarbonate level >27 mEq/L, increases the likelihood of OHS and should prompt an ABG, while a bicarbonate level ≤27 mEq/L suggests that OHS is unlikely, and unless an alternate etiology or complex acid-base disturbance is suspected, an ABG is not usually indicated. For those in whom a chronic respiratory acidosis (PaCO2 >45 mmHg) with compensatory metabolic alkalosis is found, additional testing is necessary to exclude other diseases that can cause or contribute to chronic alveolar hypoventilation or hypercapnia. (see 'Diagnostic approach' above)
●For those with suspected OHS in whom a diagnosis of OSA does not already exist, in-laboratory polysomnography should ideally be performed based upon the rationale that 90 percent of patients with OHS have coexistent OSA of at least mild to moderate severity while the remainder have sleep-related hypoventilation only. Home sleep apnea testing may be a suitable alternative in those who do not have morbid obesity (ie, BMI 30 to 40 kg/m2) in whom the likelihood of OSA is high or those in whom cost is an issue. (See 'Identify coexistent sleep disordered breathing' above.)
●OHS is a diagnosis of exclusion (obesity and awake alveolar hypoventilation which cannot be attributed to other conditions associated with hypoventilation). Once diagnosed, all patients with OHS should be assessed for common complications, including pulmonary hypertension and cardiovascular disorders (table 2). (See 'Diagnosis' above and 'Differential diagnosis' above and 'Assess complications' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Paul Suratt, MD, who contributed to an earlier version of this topic review.
