We describe the case of a 67-year-old asymptomatic man who was referred to our hospital for abnormal laboratory results. He was incidentally found to have a massive empyema without underlying bronchopulmonary pneumonia. Following thoracentesis, he was diagnosed with chronic Streptococcus anginosus empyema. Therapeutic thoracentesis and treatment with tissue plasminogen activator and deoxyribonuclease failed to resolve the empyema, and there was residual loculated pleural fluid that was surrounded by a thick rind. The patient was referred to thoracic surgery for decortication of the pleural space via video-assisted thoracoscopic surgery. At 2-month follow-up, the patient had complete re-expansion of the lung tissue.

Introduction Observational research demonstrates a strong association between nightmares, insomnia, and sleep apnea in veterans with posttraumatic stress disorder (PTSD), supportive of the notion of a “complex sleep disturbance”. Relations between sleep disturbances and PTSD are often bi-directional and disturbed sleep affects non-sleep PTSD outcomes. We aimed to examine relationships between nightmares, respiratory events, CPAP use, and insomnia in trauma-exposed veterans with frequent nightmares. Methods Three weeks of app-based daily sleep diaries and weekly insomnia severity index (ISI) reports were collected from 41 veterans with a history of trauma and frequent nightmares. Relationships between weekly nightmares (total number), CPAP use, sleep efficiency, and ISI scores were analyzed using linear regression with standard errors adjusted for clustering of weeks within participants. Of the 41 participants, a subset of 15 participants completed 6-9 nights of at-home objective sleep measurements (Sleep Profiler) to examine the relationship between apnea events and nightmare awakenings. Measurements involved EEG integrated with airflow, respiratory effort, oxygen saturation, and actigraphy with event marker for real-time reporting of nightmares preceding awakenings. Results 41 veterans (mean age 48 (SD=16), 30% female) participated. Higher prior week ISI score predicted reduced CPAP adherence (β=-.53, p=.005). In turn, increased frequency and duration of CPAP use was associated with a significant increase in sleep efficiency the same week (β=.53, p=.018 and β=.56, p=.026, respectively). Analysis of respiratory events indicates that 20 of the 64 nightmare awakenings (31%) were preceded (i.e., within seconds of awakening) by apnea or hypopnea events. Of these 20, 11 events were reported by participants with a diagnosis of OSA and a CPAP device. Amongst these 11 events, 7 (64%) occurred on nights during which the participant reported use of their CPAP. Conclusion Analyses demonstrated statistically significant and clinically meaningful relationships among insomnia, nightmares, respiratory events and CPAP adherence in our sample, highlighting their interrelationships in trauma subjects. These data support the hypothesis that OSA contributes to nightmare experiences by demonstrating an immediate temporal relationship between apnea/hypopnea events and nightmare awakenings, and they underscore the importance of detecting and adequately treating sleep apnea for the treatment of nightmares in veterans. Support (if any)

No abstract

Introduction Hypoglossal nerve stimulation (HNS) is an efficacious option for treating moderate to severe obstructive sleep apnea (OSA). However, there is sparse evidence regarding tolerance and adherence to HNS therapy in patients with a diagnosis of insomnia. Report of case(s) A 57-year-old man with well-controlled depression presented for evaluation for HNS therapy. He had been diagnosed with moderate OSA with an apnea-hypopnea index of 22/hour, intolerant of continuous positive airway pressure and mandibular advancement device. He underwent uvulopalatopharyngoplasty without significant improvement. At the time of initial evaluation, he denied history of insomnia and prior sleep aid use. He subsequently underwent successful HNS device implantation and activation. One week after HNS initiation, the patient reported new symptoms of significant difficulty with sleep onset and inability to fall back asleep, which was worse than his untreated OSA symptoms. Device interrogation did not reveal any hardware problems. Adjustments to start delay, pause time and device configuration with awake endoscopy did not improve tolerance. Subsequently, the patient disclosed a remote history of insomnia, which was treated with multiple hypnotics in addition to cognitive-behavioral therapy for insomnia (CBTi) and had resolved. He was diagnosed with recurrent chronic insomnia, for which eszopiclone was initiated without significant improvement. He eventually agreed to CBTi, with partial improvement in device tolerance and improvement in insomnia symptoms. Conclusion This case highlights that HNS therapy adherence can be affected by prior history of, or a current diagnosis of insomnia. Our patient had a predisposition for insomnia that was well controlled prior to HNS therapy initiation. The onset of recurrent insomnia with HNS activation suggests that HNS was a precipitating factor for his now chronic insomnia. Although there is insufficient evidence to suggest whether history of insomnia should affect the decision to initiate HNS therapy, this case illustrates the importance of screening for insomnia at pre-implant evaluation. Our center is now routinely screening for a history of insomnia to identify patients who may benefit from treatment prior to HNS implantation. Larger studies are needed to explore a possible relationship between insomnia and HNS adherence. Support (if any):

Introduction Obstructive sleep apnea (OSA) and narcolepsy are both causes of excessive daytime sleepiness (EDS). OSA is a more prevalent diagnosis, but it can coexist with narcolepsy and confound diagnosis. We present a case of a delayed diagnosis of type 2 narcolepsy in a patient with known OSA. Report of case(s) A 31-year-old man with depression treated with sertraline and prior history of severe OSA diagnosed at an outside facility presented to our clinic for residual excessive daytime sleepiness. He demonstrated adequate adherence to continuous positive airway pressure (CPAP) of 13 cmH2O over a period of one year, good sleep hygiene and adequate sleep duration. He reported vivid dreams and sleep paralysis in the past, but none recently. There was no history of a delayed sleep phase. He denied hypnagogic or hypnopompic hallucinations or cataplexy. An in-lab polysomnogram (PSG) followed by multiple sleep latency test (MSLT) was ordered for further evaluation. Sertraline was held 2 weeks prior to the study. Overnight PSG on CPAP showed adequate treatment of OSA on CPAP pressures of 13–16 cmH2O. MSLT showed 3/5 sleep-onset rapid eye movement periods with a mean sleep latency of 5.8 minutes. A diagnosis of coexisting type 2 narcolepsy was made. Treatment was initiated with modafinil; however, his symptoms of EDS persisted and he was changed to methylphenidate with subsequent improvement. Conclusion The case above highlights the importance of maintaining a broad differential when investigating the etiology of EDS. In particular, patients with narcolepsy often experience a significant delay between onset of symptoms and receiving a diagnosis. Diagnosis can be confounded by a lack of classic symptoms and/or the presence of another sleep-related breathing disorder, as in the patient above. Residual EDS can be seen in patients with adequately treated OSA. There is sparse data regarding the co-prevalence of narcolepsy as the etiology of residual EDS in adequately treated OSA. Patients should still be screened for symptoms suggestive of narcolepsy. Persistence of EDS symptoms in young adults with adequately treated OSA should raise suspicion for another sleep-related disorder and merits further investigation. Support (if any):