Adapted de Pépin, Borel, Tamisier, Lévy

Severe obesity BMI > 30 kg/m2 and diurnal PaCO2 > 45 mmHg

In the absence of other known cause of hypoventilation

Mortality is increased compared to “simple obesity” suggesting specific cardiovascular morbidity

Nowbar. Am J Med 2004

OR 4.0

Adjusting for age sex BMI

Compared with eucapnic morbidly obese patients and eucapnic patients with sleep-disordered breathing, patients with OHS have increased health care expenses and are at higher risk of developing serious cardiovascular disease leading to early mortality.

Despite the significant morbidity and mortality associated with this syndrome, diagnosis and institution of effective treatment occur late in the course of the syndrome.

Mokhlesi B, Kryger MH, Grunstein RR. Assessment and management of patients with obesity hypoventilation syndrome. Proc Am Thorac Soc. 2008

This is believed to be the ideal treatment for OHS. Respiratory insufficiency, pulmonary hypertension and sleep disorders

[Dixon JB 2012] can be reversed if patients achieve a normal weight, although only a few maintain a significant weight reduction for a long period.

Although bariatric surgery has been tested as an alternative treatment for OSA patients with extreme obesity, there are still some doubts about the benefit of this kind of therapy [Dixon JB 2012].

Less data are available in the case of OHS especially as regards the long-term consequences. [Douglas C, 2012]

Moreover, bariatric surgery can be an alternative for only a minority of OHS patients due to the morbidity and mortality inherent in the surgical procedure itself

Douglas C. OSA and Weight Loss: Review. Sleep Disord. 2012

Behaviorally , diet and pharmacologically weight loss in OSA

Surgically induced weight loss in OSA

Surgical vs Conventional Therapy for Weight Loss Treatment of OSA – BODY WEIGHT

Dixon JBM, JAMA 2012

Surgical vs Conventional Therapy for Weight Loss Treatment of OSA – Apnea-Hypopnea Index

Dixon JBM, JAMA 2012

Adapted from Randerath W

“I have lost that tendency to sleepiness which made me think of the fat boy in Pickwick. My color is very much better and my ability to work is greater.“

William H. Taft, Präsident der USA 1909-1913

NIV consists of the application of intermittent positive pressure ventilation, normally with bilevel positive pressure, using nasal or naso-oral masks.

NIV can improve nocturnal hypercapnia by: increasing alveolar ventilation,

preventing obstructive events,

improving leptin action (or preventing the resulting central hypoventilation) and

providing more efficient direct muscular repose.

Several series of cases and one RCT on 37 patients with mild hypercapnia [Borel 2012] have shown improvements: in the clinical picture, arterial blood gases and sleep

disorders with this treatment [Massa, 2001].

A reduction in days of hospital admission has been observed in longitudinal studies [Berg G 2001].

NIV decreases mortality in a series of patients treated with NIV, compared with other studies in which patients were not treated or refused treatment [Pepin 2012].

Borel et al, Chest 2012. RCT – 19 NIV (BiPAP) vs 18 Controls

Daytime PCO2

Sat mean

Respiratoryarousal

Sat < 90%

CPAP prevents obstructive events in patients with OHS but the PaCO2 is not normalized in all patients.

Only one RCT has evaluated the clinical, PaCO2 and polysomnographic improvements in CPAP vs. NIV in 36 OHS patients selected for their favorable response to an initial night of CPAP treatment [Piper 2007].

More RCTs are need !

Piper AJ et Randomized trial of CPAP vs bi-level support in the treatment of Obesity Hypoventilation Syndrome without severe nocturnal desaturation. Thorax 2008;63:395

This is the only RCT comparing NIV vs CPAP in 36 OHS patients who respond to an initial night with CPAP treatment.

The follow up was 3 months and there were no differences in gas exchange, sleepiness and QL.

The weakness of this study is the selection of patients (no severe nocturnal desaturation)

Piper AJ, al. RCT: CPAP vs bi-level in OHS without severe nocturnal desaturation. Thorax 2008

Piper at al Thorax 63; 395-401

Exclusion CriteriaPatients with persisting hypoventilation during initial CPAP Trial

SpO2

HR

SpO2

HR

SpO2

HR

Hypercapnic OSA

SpO2

HR

SpO2

HR

SpO2

HR

Hypercapnic OSA & OHS

Hypercapnic OSA

SpO2

HR

SpO2

HR

SpO2

HR

Hypercapnic OSA & OHS

Hypercapnic OHS

Hypercapnic OSA

SpO2

HR

SpO2

HR

SpO2

HR

Hypercapnic OSA & OHS

Hypercapnic OSA

SpO2

HR

SpO2

HR

SpO2

HR

10% of Patients with OHS have no co-existent OSA1,2,3

1. Kessler et al. Chest 2001; 120:369-71

2. Perez de Llano et al . Chest 2005; 128: 587-594

3. Mohhlesi et al. Sleep Breath 2007; 11: 117-24

Nowbar et al Am J Med 2004; 116: 58-9

Budweiser et al J Intern Med 2007; 261:375-383

3%

9%

23%

20%

Does NIV (Bilevel) Influence Survival ?

Conclusão : (n=36) Este estudo sugere uma relação entre obesidade e restrição pulmonar e aponta para um impacto positivo da cirurgia bariátricana Função Respiratória .

IMC = 59,5 kg/m2IAH = 76,8SaO2 mínima = 67 %SaO2 média = 83 %

IMC = 27,8 kg/m2IAH = 2SaO2 mínima = 94SaO2 média = 95

Conclusões: Frequência elevada de Distúrbio Respiratório do Sono

em doentes candidatos a cirurgia de obesidade

Limitação da predição de Distúrbio Respiratório do Sono com base na apresentação clínica

Face ao risco cirúrgico destes doentes o rastreio sistemático com recurso a estudo do sono parece mandatório

A resolução do Distúrbio Respiratório do Sono com a

redução do peso é expectável na maioria dos doentes.

Hybrid Mode Combine the advantages of pressure and

volume pre-set Target volume set based on ideal body weight Automatic adjustment of inspiratory pressure

(range setting) Difference between target VT and actual VT

modifies inspiratory pressure Changes of inspiratory pressure (1 cmH2O/min) Constant VT

ST AVAPS

PaCO2 (kPa) 6.1±0.9* 6.4±0.8*

PaO2 (kPa) 9.3±1.2 8.9±0.9

Weight 142±28* 139±29*

BMI 50±7 48±9*

ESS (/24) 7±5* 6±5*

SRI-SS (/100) 58±14* 66±19*

Mean IPAP 23.2±3.1 21.5±5.0

Mean Vte 671±158 634±144

Mean Vte/kg ideal wgt 10.4±2.4 10.0±1.4

Compliance (hr/day) 5.7±1.9 4.2±2.9

Follow up data

*pre-post p<0.05

ST AVAPS

PaCO2 (kPa) 6.1±0.9* 6.4±0.8*

PaO2 (kPa) 9.3±1.2 8.9±0.9

Weight 142±28* 139±29*

BMI 50±7 48±9*

ESS (/24) 7±5* 6±5*

SRI-SS (/100) 58±14* 66±19*

Mean IPAP 23.2±3.1 21.5±5.0

Mean Vte 671±158 634±144

Mean Vte/kg ideal wgt 10.4±2.4 10.0±1.4

Compliance (hr/day) 5.7±1.9 4.2±2.9

Follow up data

*pre-post p<0.05