Previously undiagnosed obesity hypoventilation syndrome

There are approximately 300 million obese individuals (body mass index (BMI) 30 kg/m² or higher) worldwide,¹ and in the UK nearly one quarter of all adults are classified as clinically obese.² Obesity hypoventilation syndrome (OHS) describes a subgroup of obese individuals who develop chronic daytime hypercapnia (arterial carbon dioxide tension (Paco₂) >6 kPa) and hypoxia (arterial oxygen tension (Pao₂) <8 kPa) in the absence of chronic obstructive pulmonary disease (COPD).³,⁴ Presentation is usually indolent, with symptoms arising due to hypercapnia and sustained hypoventilation (hypersomnolence, alterations in cognitive function, headache, peripheral oedema, hypertension, congestive cardiac failure).⁵ At Southend Hospital we have noticed an increase in acute admissions in obese individuals with type II respiratory failure of initially unknown cause in whom a diagnosis of OHS was eventually made.

We collected data on 11 patients (seven men) diagnosed with OHS from 1996 to 2005 from the respiratory disease register. Patients with possible overlap syndrome were excluded (smokers with forced expiratory volume in 1 s/forced vital capacity (FEV₁/FVC) ratio <70%). Patient demographics, lung function and Epworth sleep score (ESS) were documented. The results of initial sleep studies on air were analysed. Initial management was recorded and follow‐up data were reviewed regarding ESS, blood gases, long‐term use of continuous positive airway pressure (CPAP) or non‐invasive ventilation (NIV, using bi‐level pressure support ventilation).

The mean (SD) age of the 11 patients was 59 (12) years and the mean (SD) BMI was 52.7 (16.6) kg/m² (range 37–102). Two patients were current smokers, one an ex‐smoker and eight were never smokers. Seven patients were hypertensive, three were known to have hypothyroidism (two on treatment) and two had asthma. Only two cases presented before 2002 and nine after 2002. Eight presented to the A&E with type II respiratory failure of unknown cause, with a mean (SD) pH of 7.25 (0.15), mean Pao₂ 11.6 (4.0) kPa and mean (SD) HCO₃⁻ 34.9 mmol/1 (4.5). Three patients presented to respiratory outpatients.

All patients had increasing shortness of breath; in two the breathlessness was gradual (over 4–6 months), in six cases the breathlessness was only present in the preceding 3–4 weeks, and in three the symptoms were acute, starting only days before admission. These three patients also had evidence of a respiratory infection. All patients had a normal chest radiograph on admission. None of the patients had a diagnosis of OHS made until reviewed by a respiratory physician.

Sleep studies showed a mean (SD) apnoea/hypopnoea index score of 33 (22)/h and oxygen desaturations 39 (37)/h. The range of the mean nocturnal oxygen saturation was 66–89.9%. The mean ESS was 15 on presentation (range 5–22), mean (SD) FEV₁ was 1.53 (0.52) l and mean (SD) FEV₁/FVC ratio was 77 (6)%. In the eight patients presenting to A&E, six required NIV, one CPAP and one did not require intervention acutely. One patient has required treatment with NIV long‐term and eight others were managed on CPAP. One patient died due to non‐compliance with treatment. One has improved with weight loss alone. Only the patient with asthma has subsequently decompensated and developed acute type II respiratory failure.

At follow up the mean ESS was 3 (range 0–10). Blood gases on air had improved with a mean (SD) pH of 7.46 (0.10), mean (SD) Paco₂ 5.94 (1.15) kPa, mean Pao₂ 8.59 (1.38) kPa, and mean HCO₃⁻ 28.6 (4.1).

Decompensated OHS is often not recognised in A&E. In our study a diagnosis of OHS as the cause of respiratory failure was not appreciated until referral to a respiratory physician had been made. The presentation of OHS is very non‐specific, but should be considered in obese patients who have increasing shortness of breath, have never smoked, and have type II respiratory failure and a normal chest radiograph.