Obesity and its associated co morbidities, including the metabolic syndrome, are increasingly recognised as a major challenge for healthcare systems worldwide.1 Moreover, younger patients are presenting with higher body mass index (BMI).2 We describe a 21 year old morbidly obese (BMI > 50) Caucasian female presenting with symptoms of snoring, disrupted sleep with frequent arousals, morning headaches with debilitating daytime somnolence, and ventilatory failure, meeting criteria for a diagnosis of the overlapping syndromes of combined obstructive sleep apnoea (OSA) and obesity hypoventilation syndrome (OHS).3 We highlight effective treatments available, and how they impact on the patient’s quality of life.

Case

A 21 year old female was referred for respiratory assessment by her GP with a suspected diagnosis of OSA. She reported excessive levels of daytime somnolence, frequent night-time wakening with arousals, nocturia, witnessed apnoeas and loud snoring for the past three years. She reported morning headaches and shortness of breath on walking (breathless at 50m on the flat). She had been overweight since childhood. She had no other medical history of note, and was on no medication, in particular no sedatives, analgesics, or respiratory suppression medication

She was morbidly obese (weighing 133kg, height of 160cm (BMI 52kg/m2). She was cyanotic at rest, with baseline oxygen saturations of 87% on room air. Pulmonary and cardiovascular examination revealed clear lung fields and a non-displaced apex beat, but a raised jugular venous pressure, loud pulmonary second heart sound, and bilateral pitting peripheral oedema to mid-shins, consistent with cor-pulmonale.

Routine blood tests were unremarkable. An electrocardiogram demonstrated right axis deviation with right heart strain. Her chest radiograph demonstrated right heart  enlargement and central pulmonary venous congestion.

Transthoracic echocardiogram showed dilated pulmonary arteries, dilated right ventricle, and flattened septum (features consistent with elevated right heart pressures).

Arterial blood gas (ABG) measurement on room air showed a pH 7.33 [normal7.35-7.45], PaO2  6.8 kPa [normal>12.0kPa], PaCO2 9.1 kPa [normal4-6kPa], Bicarbonate 35.9 [normal22-28], with oxygen saturations of 83%, consistent with acute on chronic ventilatory failure. ABG measurement on room air after two minutes of voluntary hyperventilation showed a normal carbon dioxide level, indicating her respiratory failure was due to hypoventilation, and not due to intrinsic lung pathology. Overnight non-invasive TOSCA monitoring by earlobe probe (non-invasive continuous recording of capillary oxygen and carbon dioxide levels) performed on room air demonstrated 118 desaturations (> 4% drop in oxygen saturations) per hour (normal < 10 per hour), with mean oxygen saturations 59% (normal > 90%); mean carbon dioxide level was 8.2kPa (normal < 6 kPa). These findings indicate severe repetitive nocturnal obstructive desaturations, consistent with obstructive sleep apnoea, and severe nocturnal hypoventilation.

The cause of her ventilatory failure was obesity hypoventilation syndrome (OHS), the diagnosis of which requires a BMI > 30kg/m2, a PaCO2 > 6kPa at rest (in the absence of a respiratory cause), and the presence of sleep disordered breathing6.

A trial and titration of non-invasive ventilation (NIV) over three nights, using overnight TOSCA monitoring, was undertaken to treat her OHS. Final titration values on her NIV or bilevel positive airway pressure (BiPAP) were an inspiratory positive airway pressure (IPAP) of 25 cm H20 and expiratory positive airway pressure (EPAP) of 13 cmH20 on room air, reducing desaturations to 6.7 events per hour, improved O2 saturations of 93.5% and mean estimated CO2 readings of 7.2kPa.

The patient felt ‘energised’, delighted with this improvement, had a much better quality of sleep, waking more refreshed without headaches, and resolution of daytime somnolence. Moreover, treatment of obesity needs to focus on sustained weight loss, ie. the root of the problem. She was encouraged to use the improvement in her energy to address weight, and through NIV, exercise and diet, she lost almost 30kg, and BMI is 41kg/m 218 months later.

Discussion

Severe obesity is challenging for doctors and patients.

OSA and associated daytime tiredness can result in a downward spiral, leading to worsening overweight. We recommend pulse oximetry in the community evaluation of obese patients. Dietary measures, improving energy levels via non-invasive ventilation (NIV), and bariatric surgery can reverse the spiral.5

OHS will increasingly be seen as a complication of obesity, in younger patients, with markedly increased cardiovascular risk, compounding that related to Obesity /Obstructive Sleep Apnoea alone.6,7 Vigilance is required in clinical evaluation of young severely obese patients.

References

1. World Health Organization: Obesity and overweight. Fact Sheet No 311.Available from: http://www.who.int/mediacentre/factsheets/fs311/en/index.html
2. The Report of the National Taskforce on Obesity. DOHC Ireland 2005
3. Kaw R et al. Determinants of hypercapnia in obese patients with obstructive sleep apnea: a systematic review and meta-analysis of cohort studies. Dept of Hospital Medicine, Medicine Institute, Cleveland Clinic, Cleveland, OH, USA. Chest 2009 Sep; 136(3): 787-96.
4. Olson AL, Zwillich C. The obesity hypoventilation syndrome. University of Colorado Health Sciences Center, Division of Pulmonary Sciences and Critical Care Medicine, Denver, 80262, USA. The Am J Med 2005; 118:948–56
5. Zammit C et al. Obesity and respiratory diseases. Sleep and Ventilation Unit, Department of Respiratory Medicine, North Middlesex University Hospital, London, UK. Int J Gen Med. 2010; 3: 335-343.
6. Berg G et al. The use of health-care resources in obesity-hypoventilation syndrome. Sleep Disorders Centre, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba. Chest 2001; 120:377–83
7. Nowbar S et al. Obesity-associated hypoventilation in hospitalized patients: Prevalence, effects, and outcome. University of Colorado Health Sciences Center, Denver, Colorado, USA. Am J Med 2004; 116:1–7

Full author details: Dr Michael O'Callaghan: GP Trainee, TCD/HSE GP Scheme, AMNCH, Tallaght, D24; Dr Liam Regan: GP Trainee, TCD/HSE GP Scheme, AMNCH, Tallaght, D24; Dr Eddie Moloney MD FRCPI FCCP: Consultant Respiratory Physician / Senior Lecturer in Medicine, Trinity College Dublin; Dr Brendan O' Shea, TCD HSE GP Training Scheme & Lecturer at Dept Public Health and Primary Care, Trinity College Dublin.; Dr Barry Boland: General Practitioner, Monasterevin, Co Kildare.