Explore the vast range of titles available.

Application for ESRA Abstract Prizes: I apply as an Anesthesiologist (Aged 35 years old or less)Background and AimsA 25-year-old male presented following a motor vehicle accident with multiple right-sided rib fractures, pulmonary contusion, a small pneumothorax, and thoracolumbar spine fractures (figures 1, 2). Due to the extent of his injuries, emergency spinal fusion was indicated. On admission, he was hemodynamically stable but had hypoxemia (SpO2 95% on 50% Venturi mask, 91% on room air), tachypnea, dyspnea, and severe inspiratory pain.MethodsTo optimize analgesia and limit respiratory depression, an ultrasound-guided erector spinae plane (ESP) block was performed at the T8 level. General anesthesia included sevoflurane (1–1.2%) and fentanyl (250 µg). Surgery lasted two hours. Postoperatively, pain relief and oxygenation improved significantly (figure 3).ResultsMild pain (VAS 2/10) recurred after 20 hours, and a continuous ESP block was initiated using ropivacaine 2% (6 ml/h), maintained for 60 hours. Upon completion, oxygen saturation on room air was 96%. The patient was discharged on postoperative day 5.Abstract P220 Figure 1Vertebrae fracture[Image Omitted. See PDF.]Abstract P220 Figure 2Rib fractures[Image Omitted. See PDF.]Abstract P220 Figure 3Spine fusion, small right pneumothorax, ESP catheter[Image Omitted. See PDF.]ConclusionsTo our knowledge, this is the first case describing the use of an ESP block for thoracolumbar spinal fusion in a patient with rib fractures and hypoxemia. In such scenarios, the ESP block offers not only effective analgesia but also prevention of respiratory complications such as atelectasis, pneumonia, and worsening hypoxemia. It facilitates timely surgical intervention, reduces morbidity, and shortens hospitalization.

Introduction While sleep disorders are implicated in atrial fibrillation (AF), the interplay and overlap of these disorders in AF risk remains unclear and a risk stratification challenge. Sleep-based clusters associated with AF can account for this complexity and translate to actionable approaches to identify at-risk patients. We hypothesized discrete phenotypes of symptoms and polysomnography (PSG)-based data differ in relation to incident AF. Methods Cleveland Clinic patients (age>18) who underwent PSG 11/27/2004-12/30/2015 were retrospectively examined. Clusters were identified using latent class analysis of 23 symptoms (e.g. related to sleep disordered breathing (SDB), sleepiness, REM intrusion, NREM parasomnias), Epworth Sleepiness Scale (ESS) score, and 24 measures of SDB and sleep architecture from PSG reports. Outcome was 5-year incident AF. Cox-proportional hazards models were adjusted for age, sex, race, body mass index, cardiovascular disease and risk factors, tobacco use, chronic obstructive pulmonary disease, anti-arrhythmic medication use, and positive airway pressure use. Results The sample included 43,433 patients: age 51.8±14.5, 51.9% (n=22,548) male, 74.4% (n=32,313) White, 7.3% (n=3,151) with baseline AF, and 4.3% (n=1,875) developed 5-year incident AF. Five clusters were identified and ranked by strength of AF association: 1) Hypoxemic (n=3,245): highest %time SaO2< 90% (T90), 2) Apneas+Arousals (n=4,592): most witnessed apneas, highest apnea hypopnea index (AHI), highest arousal index, least hypopneas, 3) Short sleep+NREM (n=6,126): shortest sleep time, longest REM latency, lowest %REM, 4) Hypopneas (n=2,661): most hypopneas, 5) Long sleep+REM (n=26,809): longest sleep time, shortest REM latency, highest %REM. Compared to ‘Long sleep+REM’, ‘Hypoxemic’ had 47% higher AF risk (HR=1.47,95%CI=1.27-1.69), and ‘Hypopneas’ did not differ (HR=1.05,95%CI=0.86-1.28). Conclusion Of five clusters identified, the ‘Hypoxemic’ subtype conferred the strongest AF risk with the highest degree of hypoxemia (highest T90, lowest minimum and mean SaO2), maximum end-tidal CO2, heart rate, and ESS score. Consistent with prior evidence of hypoxemia as an AF driver and cardiovascular risk of the sleepy phenotype, this constellation of symptoms and physiologic alterations illustrates risk in the clinical setting, providing potential value as a risk prediction tool. Future investigation should focus on external validation of these findings. Support (if any) Cleveland Clinic Neurological Institute Center for Outcomes Research & Evaluation Pilot Grant, Transformative Research Resource Development Award

Please confirm that an ethics committee approval has been applied for or granted: Not relevant (see information at the bottom of this page)Background and Aims With the SARS-CoV-2 pandemic, regional anesthesia techniques gained more impact because of the need to avoid airway manipulation. To assure a fast recovery and ambulation, prilocaine was used more frequently due to its fast onset and lower duration of action.MethodsWe describe a case of methemoglobinemia in a patient submitted to a uterine aspiration after an abortion during the first trimester.ResultsThe patient weighted 50kg and had a medical history of ulcerative colitis medicated with sulfasalazine. She was anesthetized with spinal anesthesia with 60mg of hyperbaric prilocaine. After 17 minutes of the spinal technique the oxygen saturation dropped from 98-99% to 90% and a bluish discoloration on her lips was detected. With the assumption of a case of methemoglobinemia associated with prilocaine administration, methylene blue 1mg/kg was administered (50mg). The procedure was terminated, and she was admitted for surveillance. The case resolved with no complications.ConclusionsMethemoglobinemia is a rare complication associated with prilocaine. Normally higher doses are associated with the development of this syndrome. Sulfasalazine and other drugs administration may enhance the probability of the occurrence of methemoglobinemia. Methylene blue is an effective antidote for methemoglobinemia due to its own oxidizing properties.

Introduction Congenital central hypoventilation (CCHS) is a rare disorder due to impairment of autonomic nervous system clinically defined by a significantly reduced or abolished ventilatory response to hypercapnia and hypoxemia in the absence of pulmonary, neuromuscular, or cardiac disease. There is limited knowledge on associated respiratory manifestations and sleep-disordered breathing in children with the MECP2 duplication syndrome. Although sleep-disordered breathing and nocturnal hypoventilation are currently not well recognized in these children, we present a case of a patient with MECP2 mutation and congenital hypoventilation syndrome. Report of case(s) 24-week-old male born full-term via c-section presented with recurrent respiratory problems, laryngeal cleft, dysphagia, snoring and apneic episodes. Previous genetic work up showed chromosome 15q11.2 microdeletion. Past medical history was significant for neonatal ICU stay for respiratory distress immediately following birth. Tonsils are 1+ on exam. PSG showed profound central sleep apnea (CAI 300/h) with average apneic episodes lasted for 7 seconds and very significant periodic breathing (88%) and mild obstructive apnea. Mild hypoxemia was also seen with SpO2 in low 90s without any significant hypercapnia. Bradypnea with resp rate 10-20/m was seen. PHOX2B gene testing was negative. Genetic testing with SNP array showed MECP2 duplication syndrome. His development is delayed, currently at the age of 20 months, including cognitive, speech and motor function for which he is on therapy. Tracheostomy was recommended, however family preferred to continue with non-invasive ventilation while awaiting diaphragmatic pacing. Conclusion Respiratory manifestations in MECP2 duplication syndrome patients are common, with important impact and even a possible fatal outcome. Although sleep-disordered breathing and nocturnal hypoventilation is currently not cited as an important symptom in these children, there have been several case reports of CCHS associated with this. PSG should be considered in patients with MCEP2 duplication syndrome for timely diagnosis. Different treatment modalities (ENT surgery, CPAP and NIV) can be applied successfully to treat respiratory conditions associated with MECP2 duplication syndrome. Support (if any)

Abstract Introduction The current gold standard for a definitive diagnosis of OSA is an in-center Polysomnography (PSG). Home Sleep Apnea Testing(HSAT) has become an important tool in identifying high-risk populations. One of the limitations of the study is the lack of Electroencephalographic (EEG) data. This prevents the inclusion of Respiratory Effort Related Arousals (RERAs). We attempted to identify the patients whose HSAT showed an REI of less than 5 but are at risk for having sleep apnea based on the presence of airflow and thoraco-abdominal fluctuations. Methods Patients in this study were those that underwent HSAT from September 2016 till June of 2019. The studies reviewed and interpreted by board certified Sleep Specialists. Studies were done using nox-T3 sleep monitor and Nomad portable Home Sleep Testing type III devices-Both are type 3 Portable Monitors. Only those patients whose REI in their HSAT less than 5 were included in this study. All these patients had multiple airflow fluctuations in their HSAT that raised the suspicion for the presence of RERAs. None of these patients had significant hypoxemia in the HSAT.Airflow fluctuations were defined by the presence of fluctuations in the signal in the airflow channel along with increasing thoracoabdominal channels. Those patients with REI of less than 5 and without airflow fluctuations were excluded from the study. Results A total of 178 patients were recommended to undergo an in-center polysomnogram. Of those, 92 patients completed their polysomnogram with 59 patients ending up with a diagnosis of sleep apnea while 33 did not suggesting a false negative rate of 64.13%. Of those who were positive, 39 were females while 20 were males. Both groups did not differ significantly. Females had a median BMI of 32.9(28.19 for males), a median ESS of 11(8 in males) and a median RDI of 14.8(13.25). Conclusion Our study shows that both Home Sleep apnea testing can have a high proportion of false-negative results in patients exhibiting thoraco-abdominal and airflow fluctuations. The interpreting physicians should understand the limitations of the HSAT and should have a low threshold to recommend an in-center polysomnogram. Support None.

Introduction The apnea-hypopnea index (AHI) is used as a generic index to quantify both central sleep apnea (CSA) and obstructive sleep apnea (OSA) syndromes. Patterns of oxygenation abnormalities seen in CSA and OSA may be key to understanding differing clinical impacts of these disorders. Oxygen desaturation and resaturation slopes and durations in OSA and CSA were compared between OSA and CSA patients. Methods Polysomnographic data of patients aged 18 years or older with diagnosis of OSA and CSA, at University of Iowa Hospitals and Clinics, were analyzed and demographic data were collected. Oximetric changes during hypopneas and apneas were studied for desaturation/resaturation durations and desaturation/resaturation slopes. Desaturation and resaturation slopes were calculated as rate of change in oxygen saturation (ΔSpO2/Δtime). Comparison of hypoxemia-based parameters between patients with OSA and CSA was performed using unpaired t-test. Results 32 patients with OSA with median AHI of 15.4 (IQR 5.1 to 30.55) and median ODI of 15.47 (IQR 9.50 to 29.33) were compared to 15 patients with CSA with a median AHI of 20.4 (IQR 12.6 to 47.8) and median ODI of 27.56 (IQR 17.99 to 29.57). The mean number of desaturation and resaturation events was not significantly different between patients with OSA and CSA (OSA - 106.81±87.93; CSA - 130.67±76.88 with a p-value 0.1472). 4/15 CSA patients had Cheyne-Stokes breathing, 2/15 had treatment emergent central sleep apnea, 1/15 had methadone-associated CSA and for 8/15, no etiologies for CSA were found. Mean desaturation durations was significantly longer in OSA (20.84 s ± 5.67) compared to CSA (15.94 s ± 4.54) (p=0.0053) and consequently the desaturation slopes were steeper in CSA than OSA (-0.35%/sec ±0.180 vs. -0.243 ± 0.073; p=0.0064). The resaturation duration was not significantly longer in OSA (9.76 s ± 2.02) than CSA (9.057 s ± 2.17) (p=0.2857). Differences between desaturation duration and slopes between CSA and OSA persisted during REM and NREM sleep, and in supine sleep. Conclusion As compared to OSA, patients with CSA have different patterns of desaturations and resaturations with lesser hypoxic burden with CSA. This may have implications on the clinical outcomes seen between these two disorders. Support (if any):

IntroductionHypoxemia, acute respiratory distress syndrome and coagulopathy are common issues experiences by pts with severe COVID-19 disease.1 The aim of this study was to evaluate the efficacy of anticoagulation therapy in COVID-19 patients.MethodsThis is a retrospective observational study for patients admitted to a busy district hospital during the peak period of the COVID-19 pandemic. All patients aged >18 with suspected or confirmed RT-PCR COVID-19 and raised D-Dimer were included in this study. Data including demographics, comorbidities, and effects of anticoagulation on mortality were examined.ResultsA total of 628 pts with more males (n = 365; 58.1%), and 48.7% >75 years were included in the study. 27.9% were obese (BMI ≥ 30); and 25% were overweight (BMI 25 – 29.9). 448/628 (71.3%) had a positive swab for coronavirus and a further 70 patients (11.1%) had probable infection based on clinic-radiological suspicion. Nearly half (n = 311; 49.5%) of the patients had hypertension and a quarter (n = 166; 26.4%) had diabetes. A total of 226 (36%) pts died of which 85.8% (n = 194) had a positive swab compared to 12.8% (n = 29) with negative swab. This was statistically significant with a p-value of 0.001. Patients with a raised D-dimer 150/628 (23.8%) received therapeutic dose anticoagulation and 408/628 (64.9%) received prophylaxis or no anticoagulation. 53 patients (22.5%) of those who received treatment dose died compared to 183 (77.5%) who received prophylactic dose or no anticoagulation due to comorbidities. This was statistically significant (p value 0.02).Abstract S99 Table 1Association of swab PCR with Anticoagulants, D-Dimer in Mortality Variables Mortality with SWAB p-value Positive (n= 236) Negative (n= 41) n % n % Anticoagulant Yes 20687.33892.70.32 No 3012.737.3 Treatment Dose Anticoagulant Yes 5322.51639.00.02* No 18377.52561.0ConclusionTherapeutic anticoagulation significantly reduces mortality in COVID-19 patients with a high D-dimer.ReferenceKlok F, Kruip M, van der Meer N, et al. Incidence of thrombotic complications in critically ill ICU patients with COVID-19. Thromb Res 2020 Apr 10. [Epub ahead of print]

Introduction Individuals who travel to high altitude experience variable levels of poor sleep quality and sleep disordered breathing, which can have neurocognitive and other systemic impacts. Past studies by our group and others have shown that the apnea hypopnea index (AHI) increases, and nocturnal oxygen saturation decreases at higher altitude. This may change over time with acclimatization to environmental hypoxemia. The aim of this study was to examine the trajectory and variability in high altitude sleep disordered breathing effects in healthy young adult volunteers. Methods Twenty healthy volunteers were recruited from a local university (35% women), mean age 23.5(20.0, 32.2) years and BMI of 30.0(28.0, 35.9) kg/m2. Peripheral Arterial tonometry based home sleep apnea tests (HSAT; WatchPat One) was performed on all subjects at sea level up to three days prior to transportation via car to high altitude (3800m White Mountain Research Center - Barcroft Station, CA). Participants continued HSAT testing for three consecutive nights at high altitude sleeping in any position, without oxygen, acetazolamide, or use of any other medications impacting sleep or breathing. Mixed effects modeling was used to compare sleep parameters across nights. Results Subjects' characteristics: median (IQR)[range] age 23(20,32)[19,39] years, BMI 30(28, 36)[23,48] kg/m2, 35% women. AHI at altitude night 1 (67±4 events/hour) was significantly higher than sea level (7±4 events/hour; P< 0.001). Mean sleep SpO2 at altitude night 1 (79±1%) was significantly lower than sea level (95±1%; P< 0.0001). There was no statistically significant change in AHI or mean sleep SpO2 on nights 1-3; however substantial variability was noted between individual trajectories. Conclusion Healthy young adults exhibit severe Sleep Disordered Breathing when traveling to high altitude. Despite acclimatization, the severity of Sleep Disordered Breathing remained relatively unchanged overall. However substantial differences in individual trajectories were apparent. Larger studies are needed to understand how differences in genetics, sex, and other factors might impact Sleep Disordered Breathing at altitude. In addition, the impacts of (or tolerances to) altitude are likely to be broadly informative towards Sleep Disordered Breathing, hypoxemia, and other areas. Support (if any) N/A

Introduction Obstructive Sleep Apnea (OSA) is a widespread and heterogeneous sleep disorder. Studies have identified reproducible subtypes of OSA based on patient-reported symptoms that have different cardiovascular outcomes. Prior data showed similar apnea-hypopnea index (AHI) across subtypes; however, other physiological characteristics have not been comprehensively compared among these subtypes. Methods 1,285 participants from the Sleep Apnea Global Interdisciplinary Consortium (SAGIC) with moderate-severe OSA (AHI≥15) were included. Differences in traditional and novel physiological traits were compared among the Disturbed Sleep (n=183 [14.2%]), Minimally Symptomatic (n=581 [45.2%]), and Excessively Sleepy (n=521 [40.5%]) subtypes using analysis of covariance (ANCOVA) adjusted for age, sex, BMI and race/ethnicity. Measures included AHI and other respiratory event indices, hypoxic burden, oxygen characteristics, sleep/wake amounts, electroencephalogram (EEG) spectral characteristics, including metrics related to the odds ratio product (ORP; a validated index of sleep depth ranging from 0.0 [deep sleep] to 2.5 [full wakefulness]), arousal intensity, and heart rate response to arousal. Results Compared to other subtypes, the Disturbed Sleep subtype demonstrated increased wakefulness (more wake time [p< 0.001] and wake after sleep onset [p=0.001]), higher beta frequency EEG power (14.33-20.0 Hz [p=0.025] and 20.33-35.0 Hz [p=0.004]), and less deep sleep (higher average [p=0.001] and NREM-specific [p=0.044] ORP, less time with ORP from 0.50-0.75 [p=0.004] and 0.75-1.00 [p=0.015], and more time from 2.20-2.25 [p=0.017] and 2.25-2.50 [p=0.0005]). The Excessively Sleepy subtype had more severe hypoxemia, including greater hypoxic burden (p=0.002) and lower average SpO2 (p=0.002) and minimum SpO2 (p=0.0002) compared to other subtypes. Conclusion Differences in physiological characteristics, including ORP-related traits, were observed among symptom subtypes. Results suggest that characteristics indicative of increased wakefulness may distinguish those with the Disturbed Sleep subtype, whereas more severe hypoxemia may characterize the Excessively Sleepy subtype. Future investigations into underlying molecular causes of symptom subtypes, particularly the Excessively Sleepy, are warranted given evidence of associations with outcomes such as cardiovascular disease. Support (if any) SAGIC Investigators (Ayas N, Chen NH, Cistulli P, de Chazal P, Gislason TG, Han F, Hirsch-Allen AJ, Keenan BT, Li QY, Magalang UJ, Maislin G, Mazzotti DR, McArdle N, Mindel J, Pack AI, Penzel T, Schwab RJ, Singh B, Sutherland K); NIH P01 HL094307

Abstract Introduction Approximately 25% of all strokes are cryptogenic in nature, and about 50% of all young patients with cryptogenic stroke are found to have patent foramen ovale (PFO), which is known to be the most common cause of right-to-left shunting (RTLS). Studies have shown a 2.2-fold increase in right-to-left shunt in patients with OSA and PFO, compared to patients with PFO alone. Hence, increasing the risk of cardio-embolic stroke in such patients. We present a case series of 3 patients with PFO that had embolic stroke at a young age and were found to have comorbid OSA, the likely exacerbating factor of a RTLS. Methods A 38-year old female, a 59-year old male, and a 27-year old female presented with stroke-like symptoms without clear vascular pathology. Upon further work-up, all were found to have PFO with RTLS. Subsequently, these patients were referred for sleep evaluation, and each one was found to severe REM-related OSA with prominent oxygen desaturations. All three patients were started on PAP therapy for control of their OSA. Two out of the 3 patients opted for PFO closure, and the 3rd patient opted for anti-platelet therapy alone. He has had no recurrence of TIA/stroke after 12 years so far. Results These cases illustrate a correlation between right-to-left shunting and severe REM-related OSA, through possible elevation of right-sided pressure due to nocturnal desaturations/hypoxemia. Hence, it is worth consideration that the increased right-sided pressure induced by apneic events in sleep may be a potential exacerbating factor in producing stroke-like symptoms sooner in patients with PFO than in patients with PFO who are without OSA. Conclusion It may be beneficial to assess young patients with stroke due to PFO, for comorbid OSA as a cause of the RTLS. This would help to prevent recurrent stroke in such patients and improve quality of life. Support No financial support.