A 47-year-old woman presented to the-Sleep clinic with exertional breathlessness, snoring, choking, witnessed apnoeas and daytime somnolence. Past history included Idiopathic Juvenile Arthritis, diagnosed at age 8, since when she had been taking prednisolone. Her body mass index was 29 kg/m² and Epworth Sleepiness Score (ESS) 21/24. She had a small pharynx on direct inspection. Chest radiograph (Figure 1) and CT scan chest (Figure 2) showed significant chest wall deformity secondary to multiple osteoporotic rib fractures, presumably from long-term corticosteroids. Lung function showed a restrictive defect with reduced lung volumes. Sleep study (Figure 3 and Table 1) identified severe Obstructive Sleep Apnoea (OSA) with 4% oxygen desaturation index (ODI) of 165/hr with blood gas of pH 7.36, pO2 8.7, pCO2 6.3, bicarbonate 26, due to a combination of OSA, weight and chest wall deformity. The OSA was likely to be caused by her excess weight and small pharynx.

Figure 1: Chest X-ray showing chest wall deformity secondary to osteoporotic multiple rib fractures (patient consent obtained for all images).

Figure 2: CT scan chest confirming significant chest wall deformity secondary to multiple rib fractures compounded by increased BMI, both secondary to longterm corticosteroid therapy.

Figure 3: Summary graph of the sleep study (Pre CPAP therapy) of the patient showing oxygen desaturation index of 165/hour, mean oxygen saturation 86%.

Table 1: Oxygen desaturation index of 165/hour, mean oxygen saturation 86%.

She was commenced on Continuous Positive Airway Pressure (CPAP) therapy for OSA, fixed pressure 10 cm H2O. This improved her sleep quality so much, she hardly moved over night and consequently awoke with significant early morning joint stiffness, from which she took hours during the daytime to recover. She therefore limited CPAP use (average 0.3hr/night); her symptoms persisted and ESS remained 21.

Autoset CPAP was then tried to see if its variable pressure caused more arousals, allowing increased movement during the night; it did not. She also tried an alarm waking her every 90 minutes or 4 hourly intervals, to allow stretching of her joints, but she found it difficult to get back to sleep. Over time, she developed a regime of split night CPAP use: using CPAP between 1:00- 2:00 am and then again from 6:00 am in the morning to achieve an average compliance of 3.6 hours/night. This has improved her OSA-related symptoms as well as the joint discomfort caused by overnight immobility. Investigations performed with this split night CPAP regime showed improved ESS (5) and ODI, 16/hour (Figure 4). There are no case reports of similar CPAP limitations due to joint problems. One report describes a 10 year old with arthrogryposis and OSA, but does not mention similar CPAP issues [1]. Split-night diagnostic -CPAP titration studies have been described previously, but not split-night CPAP therapy [2]. This novel approach may be useful in patients with joint stiffness caused by immobility in deep sleep with CPAP [3].

Figure 4 Pulse oximetry of the same patient using split night CPAP. Oxygen Desaturation Index is improved to 16/hour, mean oxygen saturation of 92%. The time when CPAP is not used in hours 2, 3 and 4 is clearly seen.

Some patients with arthritis may find their joints are stiff from overnight immobility when they use CPAP successfully for the treatment of OSA. It may be helpful for these people to use split- night CPAP therapy as a way of partially treating OSA and allowing some nocturnal joint movement.