Obstructive sleep apnoea and psychiatry — structured clinical viva

High pretest OSA in a man with schizophrenia, major SGA-related weight gain, EDS, snoring/apnoeas, and hypertension. The request for stronger night sedation is the wrong vector — sedatives may worsen SDB and respiratory risk. Clozapine is likely still indicated for psychosis; the airway and metabolic problems need concurrent management.[1][2][5]

1. Probability and framing. STOP-BANG domains all lighting up; OSA is common in SMI clinical samples and under-detected. Daytime sleepiness may be mislabelled as negative symptoms or clozapine sedation alone.[1][3]

2. Why not more benzodiazepines. Sedating/hypnotic drugs can adversely affect SDB physiology; observational data link benzodiazepines with acute respiratory failure risk in OSA. Night sedation does not stent the airway.[5][6]

3. Investigations. Refer sleep medicine for PSG/HSAT pathway; metabolic panel, ECG as clozapine protocol; document EDS and near-miss risk. Partner history is essential.[3][4]

4. Definitive care. If moderate–severe OSA: PAP first-line, weight management, alcohol/smoking cessation support, positional strategies as advised. Continue clozapine if psychosis requires it; do not sacrifice relapse prevention for cosmetic weight goals without a plan.[4][7]

5. Adherence in psychosis. Mask paranoia, tactile sensitivity, chaotic routines, depression, and cost undermine CPAP — psychiatry owns motivational support, carer involvement, and liaison with sleep technicians for mask desensitisation.[4][2]

6. Monitoring and safety. Weight, BMI, glucose, lipids; reassess OSA after further weight change. Advise against driving if EDS until assessed; document. SAVE one-liner: hard CV primary endpoint neutral — still treat symptoms and cardiometabolic risk holistically.[7][8]