Obstructive sleep apnoea in extremely obese patient

Anthropometry: Height 175 cm Weight 170 kg BMI: 55.51 kg/m2
Physical examination: hyperstenic, exogenous obesity, eupnoea, oropharyngeal patency Mallampati grade 4, varices of lower limbs and chronic trophic skin changes
Blood gases:
- Saturation by pulse oximetry: 93%
- Arterial blood gases: pH 7.430 pCO₂ 5.94 kPa pO₂ 8.01 kPa, SaO₂ 92.0%, cHCO₃ 29.10 mmol/L – mild hypoxaemia, with no hypercapnia, with bicarbonates retention suggestive for night-time hypoventilation
Spirometry and body plethysmography: no ventilatory impairment, mild decrease of FVC, TLC on lower limit (Figure 1)
Epworth sleepiness scale: 12 points - a questionnaire for evaluation of daytime sleepiness (Figure 2) - 10 and more points indicate severe daytime sleepiness

Chest X-ray: no infiltration in parenchyma, accentuated hilar shadows (Figure 3)
Polysomnography: severe obstructive sleep apnoea of apnoeic-hypopnoeic index 113.1 episodes/h, with severe desaturations of average saturation in REM sleep 75% and 82% in NREM sleep, with desaturation index 105 episodes/h, time in saturation below 90% was 374 min, with hypoventilation in 28.8% of sleep, with disrupted sleep with reduction of slow wave sleep and REM sleep, with snoring (29.1% of sleep duration). Dominant type of respiratory episodes was mixed apnoeic episodes that start as central due to absence of respiratory centre activity and continue as obstructive (Figure 4 and 5).

Patient was treated with continuous positive airway pressure with oronasal mask (Figure 6). Effective therapeutic pressure was 18 cmH₂O. At this pressure we attained reduction of apnoeic-hypopnoeic index from 113.1 to 6.4 episodes/h. (Figure 7), reduction of desaturation index from 105 to 5.1 episodes/h, increase of average saturation from 75% in REM and 82% in NREM to 95.5%, reduction of time under 90% saturation from 374 min to 54 s (Figure 8).
In arterial blood gases we observed increase of pO₂ from 8.01 to 9.87 kPa, decrease of pCO₂ from 5.94 to 5.37 kPa, decrease of bicarbonates from 29.10 to 25.80 mmol/L and increase of saturation from 92% to 95.8%.
Subjectively patient reported being completely refreshed after night sleep, he denied any breathlessness.

Severe obstructive sleep apnoea

Follow-up: After 7 months of using CPAP patient was examined. Compliance of CPAP use was 5 hours per night, residual apnoeic-hypopnoeic index was 2.9 episodes/h. Patient was feeling incomparably better in terms of reduction of daytime sleepiness, he lost weight but he was unable to tell how many kilograms.

Sleep apnoea refers to repetitive episodes of cessation of air flow during sleep for at least 10 seconds; hypopnoea is an episode of flattened breathing followed by desaturation and/or arousal. Indicator of sleep apnoea severity is the apnoeic-hypopnoeic index (AHI), i. e. number of episodes per hour. The majority of respiratory episodes are obstructive in which partial or complete collapse of pharynx occurs due to a loss of muscle tone during sleep. Respiratory effort is still present. In central sleep apnoea loss of airflow is a result of respiratory centre inactivity, thoracic and abdominal movements are not present. In mixed sleep apnoea the episode starts as central apnoea and continues as obstructive.

An episode of obstructive apnoea or hypopnoea leads to an increase of inspiratory effort, deepening of negative intrathoracic pressure, acute hypoxaemia and hypercapnia. These changes activate sympathetic nervous system and together with brain cortex result in an arousal from sleep. In arousal, muscle tone in pharynx rises, airways reopen with short compensatory hyperventilation, blood gases are normalized, and one can hear explosive snoring sounds (Figure 4).
In frequent cyclic repetition of these changes, chronic intermittent hypoxia, sustained sympathicotonia and sleep fragmentation develop. These chronic consequences cause typical symptoms and complications (Figures 9 and 10).

Obesity, mainly central obesity, contributes to OSA mainly by peripharyngeal deposition of fat tissue, possibly by infiltration of submucosa by fat cells. Obesity reduces functional residual capacity and caudal traction on upper airway structures from mediastinal, rib cage and cervical strap muscle attachments which substantially increase pharyngeal collapsibility.

This patient was diagnosed with severe obstructive sleep apnoea and his subjective symptoms and objective findings were consistent with literary data. Patient was treated with continuous positive airway pressure with excellent objective and subjective effect. Furthermore, weight loss is inevitable part of treatment plan for such patient.