Literatura académica sobre el tema "Overnight oxygen saturation"

IntroductionSickle cell disease (SCD) is one of the most common inherited diseases worldwide. It is associated with lifelong morbidity and reduced life expectancy. Hydroxyurea (HU) has been shown to reduce the frequency and severity of vaso-occlusive episodes in SCD. Hypoxaemia and intermittent nocturnal oxygen desaturations occur frequently in children with SCD and contribute to the associated morbidity, including risk of cerebrovascular disease.ObjectiveTo evaluate the effect of HU on oxygen saturation (SpO2) overnight and on daytime SpO2 spot checks in children with SCD.MethodsA retrospective review of children with SCD and respiratory problems who attended two UK tertiary sickle respiratory clinics and were treated with HU. Longitudinal data were collected from 2 years prior and up to 3 years after the commencement of HU.ResultsForty-three children, 23 males (53%) with a median age of 9 (range 1.8–18) years were included. In the 21 children who had comparable sleep studies before and after starting HU, mean SpO2 was higher (95.2% from 93.5%, p=0.01) and nadir SpO2 was higher (87.2% from 84.3%, p=0.009) when taking HU. In 32 of the children, spot daytime oxygen saturations were also higher (96.3% from 93.5%, p=0.001).ConclusionChildren with SCD had higher oxygen saturation overnight and on daytime spot checks after starting HU. These data suggest HU may be helpful for treating persistent hypoxaemia in children with SCD pending more evidence from a randomised clinical trial.

Abstract Premature death and cardiac abnormalities are described in individuals with sickle cell disease (SCD), but the mechanisms are not well characterized. We tested the hypothesis that cardiac abnormalities in children with SCD are related to sleep-disordered breathing. We enrolled 44 children with SCD (mean age, 10.1 years; range, 4-18 years) in an observational study. Standard and tissue Doppler echocardiography, waking oxygen saturation averaged over 5 minutes, and overnight polysomnography were obtained in participants, each within 7 days. Eccentric left ventricular (LV) hypertrophy was present in 46% of our cohort. After multivariable adjustment, LV mass index was inversely related to average asleep and waking oxygen saturation. For every 1% drop in the average asleep oxygen saturation, there was a 2.1 g/m2.7 increase in LV mass index. LV diastolic dysfunction, as measured by the E/E′ ratio, was present in our subjects and was also associated with low oxygen saturation (sleep or waking). Elevated tricuspid regurgitant velocity (≥ 2.5 m/sec), a measure of pulmonary hypertension, was not predicted by either oxygen saturation or sleep variables with multivariable logistic regression analysis. These data provide evidence that low asleep and waking oxygen saturations are associated with LV abnormalities in children with SCD.

BACKGROUNDA survey of overnight oximetry was conducted to estimate the prevalence of nocturnal hypoxaemia in patients with cryptogenic fibrosing alveolitis and to establish whether nocturnal hypoxaemia is related to quality of life.METHODSAll patients with cryptogenic fibrosing alveolitis attending Nottingham City Hospital were invited to enter the study. Spirometric measurements and capillary blood gas tensions were obtained and overnight oxygen saturation was recorded at home. Quality of life was assessed using the Short Form-36, Chronic Respiratory Questionnaire, Hospital Anxiety Depression Scale, and Epworth Sleepiness Score questionnaires.RESULTSSixty seven eligible patients were identified and 50 agreed to enter the study, although two were subsequently excluded because they already used oxygen overnight. In the remaining 48 the mean (SD) overnight oxygen saturation (Sao2) was 92.5 (4.3)% and the median number of dips greater than 4% per hour was 2.3 (interquartile range 1.5–5.3). Daytime oxygen level predicted mean overnight Sao2 (1.94%/kPa, 95% CI 1.22 to 2.66, p<0.001) but percentage predicted forced vital capacity (FVC) did not (0.018%/% predicted FVC, 95% CI –0.04 to 0.08, p=0.5). Nocturnal hypoxaemia was associated with decreased energy levels and impaired daytime social and physical functioning, and these effects were independent of FVC.CONCLUSIONSNocturnal hypoxaemia is common in patients with cryptogenic fibrosing alveolitis and may have an impact on health related quality of life.

Background Earlier detection of chronic obstructive pulmonary disease (COPD) exacerbations may facilitate more rapid treatment with reduced risk of hospitalization. Changes in pulse oximetry may permit early detection of exacerbations. We hypothesized that overnight pulse oximetry would be superior to once-daily monitoring for the early detection of exacerbations. Objective This study aims to evaluate whether measuring changes in heart rate and oxygen saturation overnight is superior to once-daily monitoring of both parameters and to assess symptom changes in facilitating earlier detection of COPD exacerbations. Methods A total of 83 patients with COPD were randomized to once-daily or overnight pulse oximetry. Both groups completed the COPD assessment test questionnaire daily. The baseline mean and SD for each pulse oximetry variable were calculated from 14 days of stable monitoring. Changes in exacerbation were expressed as Z scores from this baseline. Results The mean age of the patients was 70.6 (SD 8.1) years, 52% (43/83) were female, and the mean FEV1 was 53.0% (SD 18.5%) predicted. Of the 83 patients, 27 experienced an exacerbation. Symptoms were significantly elevated above baseline from 5 days before to 12 days after treatment initiation. Day-to-day variation in pulse oximetry during the stable state was significantly less in the overnight group than in the once-daily group. There were greater relative changes at exacerbation in heart rate than oxygen saturation. An overnight composite score of change in heart rate and oxygen saturation changed significantly from 7 days before initiation of treatment for exacerbation and had a positive predictive value for exacerbation of 91.2%. However, this was not statistically better than examining changes in symptoms alone. Conclusions Overnight pulse oximetry permits earlier detection of COPD exacerbations compared with once-daily monitoring. Monitoring physiological variables was not superior to monitoring symptoms, and the latter would be a simpler approach, except where there is a need for objective verification of exacerbations. Trial Registration ClinicalTrials.gov NCT03003702; https://clinicaltrials.gov/ct2/show/NCT03003702

Abstract Abstract 261 Introduction: In children with sickle cell disease (SCD), obstructive sleep apnoea (OSA) is common and the degree of overnight hypoxia is closely correlated with disease severity, particularly frequency of painful crises, risk of stroke and presence of pulmonary hypertension. No studies have examined the prevalence or effects of OSA in adults with SCD. Methods: All adults with SCD attending routine sickle cell out-patient clinics were offered screening for OSA using the Epworth Sleepiness Score (ESS) questionnaire. All of those in whom the score was >10 or in whom there was a high clinical suspicion of OSA were offered overnight domiciliary oximetry. Oximetry traces were both analysed by computer and manually. Computerised analysis was used to quantify night time hypoxic load (mean nocturnal SpO2 and sleep time with SpO2 below 90%) and frequency of desaturation (number of times per hour the SpO2 dropped by >4%, or Overnight Desaturation Index, ODI). Manual analysis of each trace was performed by four independent sleep physicians who assigned a diagnosis of normal, OSA, non-OSA nocturnal hypoxia or inadequate based on the pattern of the oxygen saturation and heart rate traces. These parameters were then correlated with measures of disease severity and presence of complications taken from the patient's medical record. Statistical analysis was performed using the t-test and linear regression. Results: 93 patients completed the ESS, with 34 patients identified for subsequent oximetry (26 ESS>10, 8 clinical suspicion). 22 patients went on to have subsequent oximetry. 17/22 of recordings (77%) were abnormal of which 11 showed OSA (65%) and 6 showed nocturnal hypoxia without OSA (35%). Nocturnal hypoxic load, measured as mean overnight oxygen saturation, was correlated with glomerular filtration rate (r=0.5; p=0.0008) and pulmonary artery systolic pressure estimated by echocardiography (r=0.71; p=0.0001). Furthermore, urine protein level correlated with ODI (r=0.5 p=0.0007) and mean overnight oxygen saturation (r=0.35; p=0.02). In addition, mean overnight oxygen saturation was 87% in male patients that experienced priapism and 94% in those who did not (p=0.004). Mean ODI was 10/hr in patients with priapism and 4 in those without (p=0.008). There were no correlations demonstrated between either hypoxic load or ODI with the frequency of painful crises, frequency of hospital admissions or avascular necrosis. Lung function test parameters, history of chest syndrome, hydroxyurea therapy and Epworth score did not predict either hypoxic load or ODI. However, daytime SpO2 were highly predictive of nocturnal hypoxic load (r=0.69 p=0.0000007) but not ODI. Conclusion: OSA and non-OSA nocturnal hypoxia are common in adults with sickle cell disease. The degree of nocturnal hypoxia is associated with impaired renal function, proteinuria, priapism and pulmonary hypertension. Daytime SpO2 appears to be a better predictor of night time hypoxic load than daytime somnolence. Further work is needed to investigate the effect of interventions such as nocturnal oxygen therapy or continuous positive airway pressure on the associations reported. Disclosures: No relevant conflicts of interest to declare.

ObjectivePulse oximetry is used extensively in hospital and home settings to measure arterial oxygen saturation (SpO2). Interpretation of the trend and range of SpO2values observed in infants is currently limited by a lack of reference ranges using current devices, and may be augmented by development of cumulative frequency (CF) reference-curves. This study aims to provide reference oxygen saturation values from a prospective longitudinal cohort of healthy infants.DesignProspective longitudinal cohort study.SettingSleep-laboratory.Patients34 healthy term infants were enrolled, and studied at 2 weeks, 3, 6, 12 and 24 months of age (N=30, 25, 27, 26, 20, respectively).InterventionsFull overnight polysomnography, including 2 s averaging pulse oximetry (Masimo Radical).Main outcome measurementsSummary SpO2statistics (mean, median, 5th and 10th percentiles) and SpO2CF plots were calculated for each recording. CF reference-curves were then generated for each study age. Analyses were repeated with sleep-state stratifications and inclusion of manual artefact removal.ResultsMedian nocturnal SpO2values ranged between 98% and 99% over the first 2 years of life and the CF reference-curves shift right by 1% between 2 weeks and 3 months. CF reference-curves did not change with manual artefact removal during sleep and did not vary between rapid eye movement (REM) and non-REM sleep. Manual artefact removal did significantly change summary statistics and CF reference-curves during wake.ConclusionsSpO2CF curves provide an intuitive visual tool for evaluating whether an individual's nocturnal SpO2distribution falls within the range of healthy age-matched infants, thereby complementing summary statistics in the interpretation of extended oximetry recordings in infants.

AbstractPrevious research has identified cognitive impairment in children with sickle cell anemia (SCA, Hemoglobin SS) compared with controls, partly accounted for by overt neuropathology after clinical stroke, “covert” (“silent”) infarction, and severity of anemia. However, cognitive deficits have also been identified in children with SCA with no history of stroke and a normal T2-weighted magnetic resonance imaging (MRI) scan. Our aim was to investigate whether nocturnal hemoglobin oxygen desaturation and sleep fragmentation could be associated with cognitive impairment in children with SCA. We assessed 10 children with SCA (9 with normal MRI) using neuropsychological measures of executive function. Cognitive assessment was immediately followed by overnight polysomnography to record nocturnal hemoglobin oxygen saturation and sleep arousals. Decreases in hemoglobin oxygen saturation and/or increased sleep arousals were associated with reduced performance on cognitive assessment. Nocturnal hemoglobin oxygen desaturation and sleep fragmentation may be a contributing factor to executive dysfunction in SCA. (JINS, 2012, 18, 168–173)

Tonsillectomy and adenoidectomy (T&A) is frequently performed in children with sickle cell disease (SCD). Our aim was to evaluate the impact of this surgery on overnight oxygenation and rates of complications in these patients.Children with SCD who underwent T&A between 2008 and 2014 in two tertiary hospitals were retrospectively evaluated. Overnight oximetry and admission rates due to vaso-occlusive pain episodes (VOEs) and acute chest syndrome (ACS) in the year preceding and following the surgery were compared.19 patients (10 males, 53%) with a median age of 6 years (range 3.5–8) were included. A significant increase of mean overnight arterial oxygen saturation measured by pulse oximetry (SpO2) (from 93±3.6% to 95.3±2.8%, p=0.001), nadir SpO2 (from 83.0±7.1% to 88±4.1%, p=0.004) and a reduction of 3% oxygen desaturation index (from a median value of 5.7 to 1.8, p=0.003) were shown. The mean annual rate of ACS decreased from 0.6±1.22 to 0.1±0.2 events per patient-year (p=0.003), while the mean cumulative rate of hospitalisations for all causes and the incidence of VOEs were not affected.T&A improved nocturnal oxygenation and was also associated with a reduction in the incidence of ACS at 1-year follow-up after surgery.

Doctor of Philosphy (PhD)
This thesis describes the work carried out during four treks, each over 10-11 days, from 1400m to 5000m in the Nepal Himalaya and further work performed during several two-night sojourns at the Barcroft Laboratory at 3800m on White Mountain in California, USA. Nineteen volunteers were studied during the treks in Nepal and seven volunteers were studied at White Mountain. All subjects were normal, healthy individuals who had not travelled to altitudes higher than 1000m in the previous twelve months. The aims of this research were to examine the effects on sleep, and the ventilatory patterns during sleep, of incremental increases in altitude by employing portable polysomnography to measure and record physiological signals. A further aim of this research was to examine the relationship between the ventilatory responses to hypoxia and hypercapnia, measured at sea level, and the development of periodic breathing during sleep at high altitude. In the final part of this thesis the possibility of preventing and treating Acute Mountain Sickness with non-invasive positive pressure ventilation while sleeping at high altitude was tested. Chapter 1 describes the background information on sleep, and breathing during sleep, at high altitudes. Most of these studies were performed in hypobaric chambers to simulate various high altitudes. One study measured sleep at high altitude after trekking, but there are no studies which systematically measure sleep and breathing throughout the whole trek. Breathing during sleep at high altitude and the physiological elements of the control of breathing (under normal/sea level conditions and under the hypobaric, hypoxic conditions present at high altitude) are described in this Chapter. The occurrence of Acute Mountain Sickness (AMS) in subjects who travel form near sea level to altitudes above 3000m is common but its pathophysiology not well understood. The background research into AMS and its treatment and prevention are also covered in Chapter 1. Chapter 2 describes the equipment and methods used in this research, including the polysomnographic equipment used to record sleep and breathing at sea level and the high altitude locations, the portable blood gas analyser used in Nepal and the equipment and methodology used to measure each individual’s ventilatory response to hypoxia and hypercapnia at sea level before ascent to the high altitude locations. Chapter 3 reports the findings on the changes to sleep at high altitude, with particular focus on changes in the amounts of total sleep, the duration of each sleep stage and its percentage of total sleep, and the number and causes of arousals from sleep that occurred during sleep at increasing altitudes. The lightest stage of sleep, Stage 1 non-rapid eye movement (NREM) sleep, was increased, as expected with increases in altitude, while the deeper stages of sleep (Stages 3 and 4 NREM sleep, also called slow wave sleep), were decreased. The increase in Stage 1 NREM in this research is in agreement with all previous findings. However, slow wave sleep, although decreased, was present in most of our subjects at all altitudes in Nepal; this finding is in contrast to most previous work, which has found a very marked reduction, even absence, of slow wave sleep at high altitude. Surprisingly, unlike experimental animal studies of chronic hypoxia, REM sleep was well maintained at all altitudes. Stage 2 NREM and REM sleep, total sleep time, sleep efficiency and spontaneous arousals were maintained at near sea level values. The total arousal index was increased with increasing altitude and this was due to the increasing severity of periodic breathing as altitude increased. An interesting finding of this research was that fewer than half the periodic breathing apneas and hypopneas resulted in arousal from sleep. There was a minor degree of upper airway obstruction in some subjects at sea level but this was almost resolved by 3500m. Chapter 4 reports the findings on the effects on breathing during sleep of the progressive increase of altitude, in particular the occurrence of periodic breathing. This Chapter also reports the results of changes to arterial blood gases as subjects ascended to higher altitudes. As expected, arterial blood gases were markedly altered at even the lowest altitude in Nepal (1400m) and this change became more pronounced at each new, higher altitude. Most subjects developed periodic breathing at high altitude but there was a wide variability between subjects as well as variability in the degree of periodic breathing that individual subjects developed at different altitudes. Some subjects developed periodic breathing at even the lowest altitude and this increased with increasing altitude; other subjects developed periodic breathing at one or two altitudes, while four subjects did not develop periodic breathing at any altitude. Ventilatory responses to hypoxia and hypercapnia, measured at sea level before departure to high altitude, was not significantly related to the development of periodic breathing when the group was analysed as a whole. However, when the subjects were grouped according to the steepness of their ventilatory response slopes, there was a pattern of higher amounts of periodic breathing in subjects with steeper ventilatory responses. Chapter 5 reports the findings of an experimental study carried out in the University of California, San Diego, Barcroft Laboratory on White Mountain in California. Seven subjects drove from sea level to 3800m in one day and stayed at this altitude for two nights. On one of the nights the subjects slept using a non-invasive positive pressure device via a face mask and this was found to significantly improve the sleeping oxyhemoglobin saturation. The use of the device was also found to eliminate the symptoms of Acute Mountain Sickness, as measured by the Lake Louise scoring system. This finding appears to confirm the hypothesis that lower oxygen saturation, particularly during sleep, is strongly correlated to the development of Acute Mountain Sickness and may represent a new treatment and prevention strategy for this very common high altitude disorder.