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Obesity Hypoventilation Syndrome (OHS) is defined as a combination of obesity (BMI ≥ 30 kg/m2), daytime hypercapnia (PaCO2 > 45 mm Hg) and sleep disordered breathing (after ruling out other disorders that might cause alveolar hypoventilation).
People with OHS have impairments in respiratory mechanics including slight weakness in their respiratory muscles due to increased resistance of the rib cages. Furthermore, OHS is characterized by central resistance to leptin, a hormone which plays an important role in the stimulation of ventilation and control of metabolism, with consequent deterioration of respiratory control and cardiometabolic effects. Obesity-related physiological changes are heightened in the supine position, becoming relevant during the sleep. In fact, 85% of patients with OHS has obstructive sleep apnoea with long-lasting apnoea and hypopnoea and insufficient post-event ventilatory compensation, which contribute to diurnal hypoventilation. Central hypoventilation during REM sleep is prevalent in 15% of people with obesity hypoventilation syndrome.
These physiological changes could adversely affect pulmonary gas exchange with early-onset oxygen desaturation in combination with upper airway obstruction and hypoventilation.
Moreover, patients with OHS show an additional burden of comorbidities and increased mortality compared with normocapnic non-obese subjects and this will affect the management in ICU (Intensive Care Unit) or ward in case of Acute Hypercapnic Respiratory Failure (AHRF).
The Authors of this paper conducted a retrospective study with the aim to describe the ventilatory management and the outcome of subjects with OHS admitted to the ICU for AHRF.
Diagnostic workup for OHS included chest CT scan, pulmonary function test, overnight pulsossimetry and/or polysomnography and arterial blood gas samples (morning and daytime). Patients were diagnosed with OHS either before enrollment either during the study, with the date of OHS new diagnosis subsequently recorded. Patients admitted to ICU for other causes of acute hypercapnic respiratory failure, such as septic ore hemorrhagic shock, were excluded. 
The study included 115 subjects with OHS and 72% of the them had a concurrent Obstructive Sleep Apnoea Syndrome (OSAS) [median AHI 40, C.I. 25-62]. Fourteen subjects (37.8%) were diagnosed with OHS and treated with CPAP or home NIV before ICU admission.


Congestive heart failure (50%) and pulmonary embolism were the main cause of ICU admission in OHS patients. Cardiovascular comorbidities are frequent in obese patients and left-ventricular diastolic disfunction is a known complication of obesity, altogether with pulmonary hypertension. NIV use in these patients can improve pulmonary hemodynamic, by correction of hypoventilation. During the follow-up period, 37 subjects (32.1%) were admitted to the ICU for acute hypercapnic respiratory failure (PaCO2 at admission 51 mmHg, C.I. 48–53). Acute-on-chronic respiratory failure secondary to OHS without any identified precipitating factor occurred in the remaining 11 subjects (29.7%). In ICU, Noninvasive Ventilation (NIV) was used as first-line ventilatory support for 36 patients (97.2%) and succeeded in 33 of them (91.7%), with a median time to correct hypercapnic acidosis with NIV was 2.9 days (1-3). Causes of NIV failure were worsening of mental status (two patients); developing of severe hypoxemia due to acute respiratory distress syndrome (one patient). One patient was ventilated invasively from the begin and 3 subjects (2.7%) were switched to invasive mechanical ventilation after NIV failure. Only one patient died in the ICU, but cause of death was metastatic cancer, not respiratory failure.

Key Points

- ICU stay was not associated with a worse outcome and NIV proved to be effective in treating respiratory acidosis in nearly 90% patients (median time to correct acidosis: 2.9 day). This should discourage early intubation when possible.
- Low Vital Capacity (VC) at the time of the diagnosis was found to be an independent factor associated with ICU admission for AHRF and could be a surrogate of OHS severity.

Limits of the study
- Including only patients with a diagnosis of OHS established according the methods chosen, the Authors may have create a selection and information bias and underestimating the real prevalence of OHS in the ICU; moreover, being retrospective design made the evaluation of OHS and cardiovascular comorbidities more difficult.
- The monocentric design and the small sample size with a relatively low number of events (ICU admissions or deaths) make the study underpowered.
- The Authors were unable to show that an ICU stay is a risk factor for the long-term outcome due to the lack of power of the study.