Title : Opioid induced hypoventilation and sleep related hypoxemia in a patient on buprenorphine naloxone an underrecognized problem.
Abstract:
This is a 68-year-old male patient, BMI of 25 kg/m2, with past medical history of hypertension, diabetes and CKD stage III. He has a history of cervical laminectomy and chronic back pain on maintenance opioid therapy with Buprenorphine- Naloxone at a dose of 20mg daily for the last 10 years. Other medications notable for Gabapentin 100mg daily and Trazodone 50mg at night. Patient is a former smoker with a 45-pack year history, he otherwise denies alcohol intake or illicit drug use. He was diagnosed with obstructive sleep apnea prior to seeing us in the sleep medicine clinic. No outside baseline sleep study was available; however, he was inconsistently using his auto-adjusting CPAP (APAP) of 10-20 cm of water. A recent PAP generated data showed an elevated residual AHI of 11 events/hr and he had moderate day time sleepiness, with an Epworth Sleepiness Score of 13/24. The plan was to improve adherence and continue APAP. A home sleep apnea test was ordered which showed an REI of 9.6 and SpO2 <88% for >50% of the night in the absence of respiratory events, this was done without APAP.
Work up for nocturnal hypoxemia showed normal pulmonary mechanics and normal diffusion on pulmonary function test. Patient had normal resting and exertional SpO2 levels. CT chest angiogram did not show emphysema, no visible arterio-venous malformations. CXR did not show evidence of hemidiaphragm. ECHO revealed diastolic dysfunction, no shunt. ABG revealed pH of 7.39, PaCO2 of 63 mmHg and PaO2 67 mmHg on room air. Calculated A-a gradient was normal. Serum bicarbonate levels was chronically elevated to 38 mmol/L.
Patient was recently hospitalized two months ago for acute on chronic hypercapnic respiratory failure, superimposed by an RSV infection, where he was discharged on oxygen of 3LPM during the day and bled into his APAP at night. Patient during subsequent clinical follow-up had endorsed that his oxygen saturation improves to normal with deep breathing. Given the significant concerns of hypoventilation an in-lab sleep titration polysomnogram with transcutaneous (TCO2) monitoring was performed. His baseline TCO2 values in a semi-recumbent position with HOB elevation to 45 degrees was 60-69 mmHg, with a respiratory rate of 10-12 breaths per minute. On BPAP Spontaneous mode with pressure support of 10 cmH20, TCO2 remained elevated above 70 mmHg. Adaptive Servo Ventilation (ASV) was used briefly due to intermittent central apneas, that were mostly sleep wake transitional and due to BPAP intolerance, per our lab protocol. ASV showed the lowest exhaled tidal volumes and persistently elevated TCO2 values. The patient was subsequently transitioned to Volume Assured Pressure Support (EPAP 13 cmH2O, minimum PS 5 cmH2O, maximum PS 15 cmH2O, inspiratory time (Ti) minimum 0.3 seconds, Ti maximum 1.7, Target Va 6cc/kg with rate at 12 breaths per minute) and showing normalization in the TCO2 values to 40 mmHg. This case serves as an educational resource to help improve recognition on how chronic maintenance doses of buprenorphine- naloxone, a highly potent opioid can have profound respiratory effects, including substantial hypoventilation and sleep- related hypoxemia and not just central apneas, Biot’s breathing that are already well-established side effects, which has important clinical implications.
