Opioid-induced Central Sleep Apnea Syndrome, a Case Study

Case Report

Austin J Sleep Disord. 2015;2(1): 1008.

Opioid-induced Central Sleep Apnea Syndrome, a Case Study

Torabi-Nami M1,2*, Mehrabi S2,3, Borhani- Haghighi A4,1 and Derman S5

1Department of Neuroscience, Shiraz University of Medical Sciences, Shiraz, Iran

2Sleep Disorders Laboratory, Shiraz University of Medical Sciences, Shiraz, Iran

3Division of Pulmonology, Department of Internal Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

4Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran

5Sleep Disorders Unit, American Hospital, Koç Foundation, Istanbul, Turkey

*Corresponding author: Mohammad Torabi Nami, Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz 71348-14336, Iran

Received: January 12, 2015; Accepted: February 20, 2015; Published: February 24, 2015


Although not as prevalent as obstructive causes of sleep disorderedbreathing, central sleep apnea syndrome (CSAS) is a serious condition requiring close medical attention. The increasing rates of opium addiction as well as the frequent use of opioid analgesics have turned opioid-induced CSA to a more frequently encountered medical scenario in our sleep medicine practice. Here, we report a case with typical presentation of opium-induced CSAS, who referred to us with excessive daytime sleepiness characterized by irresistible need for daytime naps and cognitive lapses. The clinical characteristics, confirmation of diagnosis in polysomnography followed by the suggested care to such a patient are the focus of the present case study.

Keywords: Central sleep apnea; Hypopnea; Polysomnography; Opioidinduced; Excessive daytime sleepiness


The majority of adult patients who undergo evaluation in sleep centers suffer from obstructive sleep apnea (OSA) and the diagnosis is usually confirmed based on the overnight polysomnography [1]. Although central sleep apnea (CSA) is not as prevalent as the obstructive type, we tend to see increasing number of such patients of which some report opioid abuse or extensive use of opioid analgesics. Excessive daytime sleepiness (EDS) is often the chief complaint of these patients when referred to the sleep clinic [2]. Clinicians need to be well-versed about the clinical significance of central sleep apnea syndrome as well as its opioid-induced type upon evaluating or referring suspected cases. When the diagnosis is confirmed, entering drug cessation programs, pharmacotherapy as indicated, close medical follow up, and possibly the use of continuous positive airway pressure (CPAP) are amongst the therapies controversially advocated in the literature [2,3].

Case Presentation

Presenting illness

N.A, a 55year-old male was evaluated with the chief complaint of excessive daytime sleepiness (EDS) and frequent pauses in breath during sleep over the past 5 years. The patient’s problem along with continued sleep snoring were aggravated over the last 6 months prior to presentation to our sleep clinic. Although the patient reported EDS, his Epworth Sleepiness scales score marginally higher than normal (10/24). He further complained of unrefreshed morning wake ups with problem in maintaining nocturnal sleep since long.

The patient had been going to bed between 11pm and 12 am and waking up between 7 am to 8 am. With a self-reported short sleep latency of almost 5 min, and the average total sleep time (TST) of 7-8 hours, he complained of frequent nocturnal awakening with unknown trigger. He however had no problem returning back to sleep easily. The patient had unintentional, irresistible 2 to 3 naps each for nearly 1.5 hours during the day, feeling temporarily refreshment upon awakening. The patient reported no typical symptom for narcolepsy, restless legs syndrome or post-traumatic stress disorder (PTSD) but revealed symptoms compatible with parasomnia such as sleep walking, sleep talking and nightmares disorder.

Clinical history

He reported 3 motor vehicle accidents and several near accidents secondary to his excessive somnolence over the past 2 years. The patient’s past medical history was positive for coronary artery disease (CAD) stable on medical therapy, hyperlipidemia, hypertension and cardiac arrhythmias (over the past 2 years), whereas unremarkable for thyroid disease, chronic obstructive pulmonary disease (COPD), asthma, allergy, and diabetes. Six months prior to presentation, the patient experienced a cerebral transient ischemic attack (TIA) with instant recovery and no significant sequelae.

He has been a 30 pack/year cigarette smoker with decreased smoking since the TIA occurred. The patient has been inhaling opium for more than 5 years while decided to cease opium inhalation since 5 months prior to presentation. He therefore entered the methadone maintenance therapy (MMT) under a psychiatrist’s care receiving 30- 50 mg methadone PO/d for two months after which he switched to use opium tincture instead of methadone. He has been using high doses of opium tincture (5-6 mL/day), often beyond the prescribed regimen, over the last three months prior to his current presentation to our sleep center. The history was negative for alcohol or other substance abuse. His medication history included Clopidogrel 75mg PO QD, Atorvastatin 4o mg PO QD, Aspirin 80 mg PO QD, Nitrocantin 6.4 mg PO QD, Sodium Valproate 200 mg BID and Opium tincture 5-6 mL/d.

The family history was insignificant for OSA or other sleep disorders. On physical examination, he was found to have a BMI of 33.5, neck circumference of 39cm and an oropharyngeal Mallampati score of 2. The patient had a decreased motor power and hyperreflexia in his left lower extremity. No other remark in general and neurological examination was noted.

Evaluations and results

Given the severity of his symptoms (i.e. EDS and sleep disorderedbreathing complaints), he underwent polysomnography (PSG) (using the SOMNO screen System and the DOMINO analysis software) at our sleep disorders laboratory. His overnight PSG study revealed a total sleep time (TST) of 06h: 19min and the total time in bed (TIB) of 07h: 20min (sleep efficiency of 86%). Study showed a non-rapideye movement (NREM) sleep latency of less than 20 min and rapideye- movement (REM) latency of 33 min. Sleep stages analysis are summarized in Table 1. The patient was found to be continuously snoring with the snore index and snore fraction of 558.68 and 71.7%, respectively. He had 539 apnea events with an apnea-hypopnea index (AHI) of 77. Most flow limitations (41 events with the index 6.3) occurred during NREM sleep (Table 2). Central sleep apnea events were found quite frequent throughout the study except in stage W (wakefulness). There were frequent O2 desaturation episodes (n=159) with the desaturation index of 25.49, the baseline SpO2 of 82% and the nadir SpO2 of 57% during some central and mixed apnea events mainly in NREM sleep. Desaturation- and respiratoryrelated microarousals constituted 53% and 20% of all arousals during the study, respectively. There were no significant findings to suggest periodic leg-movement during sleep (PLMS).