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Background: Following a SARS-CoV-2 infection, symptoms such as fatigue, shortness of breath, or thoracic pain may persist for months after the illness (long-COVID). We investigated the prevalence of sleep-related breathing disorders (SRBD) in long-COVID. Patients and Methods: Long-COVID patients who underwent inpatient rehabilitation and received diagnostic polysomnography or polygraphy were included in this retrospective data analysis. Result(s): 70 patients (33 women) were included, 4 with pre-existing obstructive sleep apnea (OSA). Among the remaining 66 patients, 22 (33%) had SRBD (4 with central sleep apnea and 18 with OSA). Thus, overall SRBD prevalence was 26/70 (37%). Patients with SRBD were significantly older and showed a higher proportion of men. In addition, SRBD patients were more likely to require oxygen therapy, noninvasive ventilation, or invasive ventilation as part of their COVID-19-related hospitalisation prior to rehabilitation. View inline Conclusion(s): In Long-COVID, SRBD prevalence in our sample is 33% and 37%, respectively, which is higher than average. The diagnostic portfolio in Long-COVID should therefore include screening for the presence of SRBD. SRBD patients show a more intensive need for therapy in the context of their COVID-19-associated hospitalization, although this may be attributed to older age.
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SESSION TITLE: Uncommon Presentations and Complications of Chest Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: The correlation between long-haul Coronavirus 2019 (COVID-19) and sleep disorders remains poorly understood. In this report, we present a case of newly diagnosed central sleep apnea (CSA) and symptoms starting after a COVID-19 infection as part of a long-haul COVID-19 presentation. CASE PRESENTATION: A 69-year-old male presented to a sleep medicine clinic for evaluation of hypersomnia. He had a history of hypertension and pulmonary embolism. He contracted COVID-19 eight months prior to his presentation. He was not hospitalized, but received Remdesivir and prednisone. He complained of long-haul COVID-19 symptoms since his infection which included headaches, fatigue, cough, dyspnea, anosmia, poor appetite, dysgeusia, and memory impairment. He also started noticing nocturnal apneic episodes that frightened him and woke him up from sleep. His symptoms started after his infection and were not present prior. He went to the emergency department for evaluation and no etiology was identified. He was then referred to sleep medicine for further evaluation. A home sleep apnea test was done and showed severe sleep apnea with an Apnea-Hypopnea Index of 35.7 events per hour. His sleep apnea was predominantly central with a central apnea index of 15.3 events per hour. Cardiac testing showed no evidence of ischemia or cardiomyopathy with an ejection fraction of 52%. A CT angiogram showed no evidence of PE. Brain MRI showed no acute abnormalities. He was started on positive airway pressure therapy but could not tolerate it so he was sent for a phrenic nerve stimulator implantation. DISCUSSION: Long-term sequelae of COVID-19 infection have been increasingly recognized. However, the etiology and pathophysiology is poorly understood (1). Symptoms of long-haul COVID-19 include fatigue, dyspnea, cognitive manifestations, thrombosis and sleep disturbances (1). Sleep apnea was found in some studies to be a risk factor for severe COVID-19 illness and worse outcomes (2). The relationship between COVID-19 and sleep apnea in the post-viral syndrome remains unknown. Only few case reports have found obstructive sleep apnea as a new diagnosis and a possible cause of fatigue in post COVID-19 infection (3). There is no report of a relationship between CSA and COVID-19 in the literature. It is hypothesized that long-COVID can lead to brainstem dysfunction and dysautonomia, which can affect the ventilatory control mechanisms and lead to an unstable respiration (4–6). Our patient's nocturnal symptoms started after his infection as part of long-haul COVID-19. While we cannot determine if CSA was a result of COVID-19 infection or not, it is important to evaluate for sleep disordered breathing (SDB) in patients presenting with long-COVID symptoms to better understand the association. CONCLUSIONS: More research is need to better understand the correlation between SDB and long-haul COVID-19. Reference #1: 1. Mehandru S, Merad M. Pathological sequelae of long-haul COVID. Nat Immunol. 2022 Feb;23(2):194–202. 2. Miller MA, Cappuccio FP. A systematic review of COVID-19 and obstructive sleep apnoea. Sleep Medicine Reviews. 2021 Feb;55:101382. Reference #2: 3. Koczulla AR, Stegemann A, Gloeckl R, Winterkamp S, Sczepanski B, Boeselt T, et al. Newly detected rapid eye movement associated sleep apnea after coronavirus disease 2019 as a possible cause for chronic fatigue: two case reports. J Med Case Reports. 2021 Dec;15(1):211. 4. Barizien N, Le Guen M, Russel S, Touche P, Huang F, Vallée A. Clinical characterization of dysautonomia in long COVID-19 patients. Sci Rep. 2021 Dec;11(1):14042. Reference #3: 5. Yong SJ. Persistent Brainstem Dysfunction in Long-COVID: A Hypothesis. ACS Chem Neurosci. 2021 Feb 17;12(4):573–80. 6. White DP. Pathogenesis of Obstructive and Central Sleep Apnea. Am J Respir Crit Care Med. 2005 Dec;172(11):1363–70. DISCLOSURES: No relevant relationships by Amer Als ekh Mousa No relevant relationships by University of Arizona at Banne Institute No relevant relationships by Joyce Lee-Iannotti No relevant relationships by Anas Rihawi No relevant relationships by Amr Salem No relevant relationships by Mohanad Soliman No relevant relationships by Kristen Trimble
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Introduction: The hypothalamus plays a crucial role in regulating vital functions and circadian rhythms. Both the tumor involving the hypothalamic area and its treatment can lead to hypothalamic dysfunction, resulting in disturbances in sleep-wake patterns, sleep fragmentation, and increased daytime sleepiness. We describe two patients with craniopharyngioma who came to our attention due to the occurrence of episodes characterized by psychomotor slowing and afinalistic limb movements, temporal and spatial disorientation, psychomotor agitation, and oneiric stupor like episodes diagnosed as severe sleep disturbances. Case reports: Patient 1 is a 19-year-old male diagnosed with surgically treated craniopharyngioma. Subsequently, episodes of psychomotor slowing, afinalistic movements of the upper limbs diagnosed as seizures in another neurological center appeared;antiepileptic treatment was started without improvement. At the first examination in our center, excessive daytime sleepiness (EDS), fragmented nighttime sleep, episodes characterized by bimanual automatic gestures occurring during drowsy state, hypnagogic hallucinations, and sudden loss of muscle tone while awake were recognized. Actigraphy demonstrated irregular bedtimes, frequent nocturnal activity, and inappropriate daytime rest episodes. The Epworth Sleepiness Scale (ESS) showed subjective EDS (ESS=19). At PSG, hypersomnolence, severe sleep-related breathing disorder (SRBD), and no interictal and ictal seizure abnormalities were found. A BiPAP NIV was started, and antiepileptic therapy was discontinued. In the following months, PSG revealed marked improvement in SRBD and 1 SOREMP, and the MSLT a mean SOL of 6 min and 10 sec and 3 SOREMPs. These data allowed the diagnosis of secondary narcolepsy, and treatment with pitolisant was initiated with clinical improvement and reduced daytime sleepiness (ESS=9). Patient 2 is a 12-year-old male, surgically treated for craniopharyngioma at the age of 4 years, who developed episodes of myoclonic jerks, temporal and spatial disorientation, and psychomotor agitation during the lockdown period for COVID-19 emergency. Surmising paroxysmal epileptic episodes, the patient was hospitalized. The anamnestic data collection revealed a sleep-wake rhythm dysregulation, fragmented nighttime sleep, EDS, oneiric stupor-like episodes during which the patient performed simple automatic gestures mimicking daily-life activity, and severe impairment of alertness. The Long-term video-EEG, including polygraphic measurements, showed destruction of the wake-NREM sleep-REM sleep boundaries, episodes of undetermined state of vigilance, and concurrence of elements typical of different sleep stages. Moreover, a severe SRBD (AHI 19/h) has been observed. The MRI showed a volumetric increase in the post-surgical interpeduncular fossa and right paramedian cysts. Therefore, a multifactorial therapeutic plan including sleep hygiene and slow-release melatonin was started with improvement in nighttime sleep, but EDS persisted. Surgical treatment of cyst fenestration improved sleep-wake rhythm and behavior;BiPAP NIV was initiated with very poor adherence. Discussion: We aim to focus on sleep disorders as a possible complication of tumors involving the hypothalamic region. Our cases highlight that the clinical manifestation of these dysfunctions can be challenging to diagnose and can lead to misdiagnosis and inappropriate treatment that can harm patients' health and the quality of life of patients and their families. Conclusion: These findings support the need to incorporate comprehensive sleep assessment in survivors from childhood brain tumors involving the suprasellar/hypothalamic region.
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Introduction: Central sleep apnea (CSA) is a rare disorder caused by a reduction of airflow and ventilatory effort during sleep. CSA is rarely idiopathic and associated with medical conditions including heart failure, opioid medications, treatment emergent and high-altitude periodic breathing. At higher altitudes, hypoxemia induces periodic breathing with periods of deep and rapid breathing alternating with central apnea. Patients with high-altitude periodic breathing experience fragmented sleep, poor sleep quality, excessive daytime sleepiness, morning headaches and witnessed apnea. We discuss a patient with obstructive sleep apnea (OSA) who developed new-onset central sleep apnea after relocating to a higher altitude location. Report of Cases: A 75-year-old male with a history of moderate obstructive sleep apnea well controlled on CPAP for eight years, with no known cardiovascular or pulmonary disease, presented with new-onset excessive daytime sleepiness. He had recently relocated to an area in the Colorado mountains (7000 ft elevation) from his previous home in Los Angeles (sea level). His residual apneahypopnea index (r-AHI) displayed on his CPAP machine increased to 7-14/ hr from his normal of 1-2/hr after his relocation. Review of his compliance data revealed his central apnea index was elevated, contributing to his high r-AHI. A one-night nocturnal oximeter was mailed to the patient to use while on CPAP. Data revealed oxygen desaturation to less than 88% for about 2 hours of the night, worse during the early morning hours. The patient was advised to undergo a polysomnography and adaptive servo-ventilation titration if significant central sleep apnea was present. The patient declined due to concern about the COVID-19 pandemic. Supplemental nocturnal oxygen was initiated at 2L/min with normalization of the r-AHI. Conclusion: Patients with OSA who experience worsening symptoms or increased r-AHI despite excellent compliance with PAP therapy should be considered for repeat polysomnography or titration study. While it is expected that high-altitude central sleep apnea will improve with acclimatization, nocturnal supplemental oxygen in addition to PAP therapy is indicated for patients with high-altitude central sleep apnea to diminish hypoxemia and improve residual AHI and sleep quality.
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Introduction: Obstructive sleep apnea (OSA) is the most common sleep-related breathing disorder. It is a multi-factorial disease with a variety of identified causes including age, male gender, obesity, craniofacial and upper airway abnormalities. We would like to describe a patient who had severe OSA following application of Halo traction, which significantly improved following the removal of the device. Report of Cases: 14-year-old male with medical history of spina bifida, chiari malformation s/p decompression, shunted hydrocephalus and severe scoliosis, was admitted to the hospital for anterior spinal discectomy L2-S1 and Halo application with traction for scoliosis. He previously had nocturnal polysomnogram (NPSG) in 2017 that demonstrated very mild mixed apnea with an apnea hypopnea index (AHI) of 5.5. Because central apneas were very brief and clustered in REM, family elected to repeat a study rather than treat. In 2019, he had a follow up study with complaints of snoring and thirst, and this demonstrated an AHI of 21 with 29 brief central apneas and 72 hypopneas, 1 obstructive apnea. He had a T&A and turbinate ablation and due to the global pandemic did not undergo repeat sleep study. During admission for his anterior spinal discectomy and Halo, he demonstrated persistent night time hypoxia. A split night sleep study showed evidence of severe OSA with pretreatment AHI of 94.4, oxygen nadir 86%. Continuous positive airway pressure (CPAP) was initiated at 5 cm of water and titrated to 11 cm of water. On CPAP of +11 severe obstructive events continued with an AHI of 40.6, oxygen nadir 92%. A bilevel positive airway pressure (BIPAP) titration study the subsequent night started at pressures of 12/6 and titrated to 21/9 with respiratory rate of 12 yet demonstrated AHI of 51, oxygen nadir 89%. Study transitioned to average volume assisted pressure support (AVAPS) with IPAP max of 26, IPAP minimum of 12 EPAP of 9, tidal volume of 175ml, rate of 12 with inadequate control of his obstructive events with an AHI of 24.8, minimum oxygen saturations of 91. While hospitalized, he remained on AVAPS with normal capillary blood gases. Halo traction was removed 2 weeks following his surgery with plan was to send him home on AVAPS and repeat NPSG in 6 weeks. However, as a result of COVID pandemic/Philips recall, CPAP was the only device available for home use, so CPAP therapy at +8 cm was trialed overnight, demonstrating oxygen nadir of 92% and a normal capillary blood gas in the morning. Patient was then discharged home on CPAP of +8 cm of water. He returned back to sleep center for a BIPAP titration study to re-establish BIPAP/AVAPS settings, as his inpatient sleep study had shown severe OSA. During the sleep study, he was started on BIPAP 12/6 and he remained on it throughout the night with 0 central and 0 obstructive events. As he did well, he was advised to continue CPAP +8 with plans to repeat the sleep study off CPAP. In clinic follow up, he reported mild skin breakdown and occasionally waking unrefreshed. Conclusion: As our patient did significantly better following the removal of Halo traction device, it is likely that Halo traction device caused fixed over flexion of the cervical spine that resulted in decrease in his airway diameter, which further worsened during his sleep, and caused severe OSA.