G488 Pulse oximetry is an unreliable measure of haemoglobin oxygen saturation as calculated by earlobe blood gas co-oximetry in ambulatory paediatric sickle cell disease patients

2016 ◽  
Vol 101 (Suppl 1) ◽  
pp. A289-A290 ◽  
Author(s):  
S Zheng ◽  
F Chan ◽  
G Ruiz ◽  
D Rees ◽  
A Gupta
Keyword(s):  
Sickle Cell Disease ◽  
Oxygen Saturation ◽  
Pulse Oximetry ◽  
Sickle Cell ◽  
Blood Gas ◽  
Cell Disease

scholarly journals Comparison of pulse oximetry and earlobe blood gas with CO-oximetry in children with sickle cell disease: a retrospective review

2020 ◽  
Vol 4 (1) ◽  
pp. e000690
Author(s):  
Michele Arigliani ◽  
Sean Zheng ◽  
Gary Ruiz ◽  
Subarna Chakravorty ◽  
Cara J Bossley ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Oxygen Saturation ◽  
Pulse Oximetry ◽  
Sickle Cell ◽  
Blood Gas ◽  
Cell Disease ◽  
Arterial Blood ◽  
Ambulatory Patients ◽  
The Difference ◽  
Age Range

ObjectivesTo investigate the agreement between pulse oximetry (SpO2) and oxygen saturation (SaO2) measured by CO-oximetry on arterialised earlobe blood gas (EBG) in children and adolescents with sickle cell disease (SCD).Design and settingWe retrospectively reviewed 39 simultaneous and paired SaO2 EBG and SpO2 measurements from 33 ambulatory patients with SCD (32 subjects with Haemoglobin SS and one with Haemoglobin Sß+, 52% male, mean±SD age 11.0±3.6, age range 5–18). Measurements were performed between 2012 and 2015 when participants were asymptomatic. Hypoxaemia was defined as SaO2 ≤93%. A Bland-Altman analysis was performed to assess the accuracy of SpO2 as compared with EBG SaO2.ResultsThe mean±SD SpO2 and SaO2 values in the same patients were, respectively, 93.6%±3.7% and 94.3%±2.9%. The bias SpO2–SaO2 was −0.7% (95% limits of agreement from −5.4% to 4.1%) and precision was 2.5%. In 9/39 (23%) cases, the difference in SpO2–SaO2 was greater than the expected error range ±2%, with SaO2 more often underestimated by SpO2 (6/9), especially at SpO2values ≤93%. Thirteen participants (33%) were hypoxaemic. The sensitivity of SpO2 for hypoxaemia was 100%, specificity 85% and positive predictive value 76%.ConclusionsPulse oximetry was inaccurate in almost a quarter of measurements in ambulatory paediatric patients with SCD, especially at SpO2values ≤93%. In these cases, oxygen saturation can be confirmed through EBG CO-oximetry, which is easier to perform and less painful than traditional arterial blood sampling.

Hemoglobin Oxygen Saturation Discrepancy Using Various Methods in Patients with Sickle Cell Disease.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3672-3672
Author(s):  
Shahid Ahmed ◽  
Rabia K. Shahid ◽  
Anita K. Siddiqui ◽  
Cristina P. Sison ◽  
Dilip V. Patel ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Oxygen Saturation ◽  
Pulse Oximetry ◽  
Sickle Cell ◽  
Control Group ◽  
Cell Disease ◽  
Oxyhemoglobin Saturation ◽  
Hemoglobin Oxygen Saturation ◽  
Mcnemar’S Test ◽  
Mcnemar's Test

Abstract Objective: Sickle cell disease (SCD) is characterized by chronic hemolytic anemia and vaso-occlusive painful crises. Recurrent pulmonary microinfarction as well as increased predisposition to lung infection during vaso-occlusive crisis places these patients at high risk for hypoxemia. Furthermore, because hypoxemia is a trigger for sickling and vaso-occlusion, the detection of arterial hypoxemia and its correction are very important during painful episodes. We previously assessed reliability of pulse oximetry in pateints with SCD (Blood2001:98;491 abstr 2049). In present study we evaluated agreement among three available methods for measuring hemoglobin oxygen saturation in a relatively larger group of adult patients with SCD during vaso-occlusive crisis and compared them to a control group. Methods: Eighteen adult hypoxic patients with SCD hospitalized during a painful episode at a tertiary care institution served as the study group, whereas 12 non-SCD hypoxic African-American patients admitted with various cardio-pulmonary diagnoses served the control group. The hemoglobin oxygen saturation was determined simultaneously by pulse oximetry (SpO2), co-oximetry (SO2 [functional oxyhemoglobin saturation] & FO2Hb [oxyhemoglobin fraction]) and by calculation (SaO2) using a normal oxyhemoglobin dissociation curve in the 2 groups.Bland-Altman analysis was carried out to evaluate agreement of various methods in the two groups. Spearman Correlations were calculated for descriptive purposes. As a secondary analysis, McNemar’s Test was used to compare the proportion of ‘critically hypoxic’ patients between two measurement techniques. Results: The two groups were different with respect to age, systolic blood pressure, body temperature, hemoglobin level, serum bilirubin level, blood pH, methemoglobin and carboxyhemoglobin levels. Mean differences between various methods for measuring hemoglobin oxygen saturation in patients with SCD were significantly larger than the control group. Mean bias between SpO2 and SO2, and SpO2 and FO2Hb in patients with SCD were −3.1 ±4.4 (95% CI −11.7 to 5.5) and 2 ±4.1 (95% CI, −6 to 10) respectively compared to −1.4 ±1.4 (95% CI, −4 to 1.4) and 1.2 ±1.5 (95% CI, −1.8 to 4.2) in control group. A bias of −4.5 ±4 (95% CI, −12.3 to 3.8) between SpO2 and SaO2 was noted in patients with SCD compared to −0.08 ±2.1 (95% CI, −4.2 to 4.1) in control. Spearman correlations between various methods in control group were consistently higher (0.82 to 0.99) than patients with SCD (0.59 to 0.89). McNemar’s test for comparing the proportion of "Critically Hypoxic" disposition using a cut-point of 90% oxyhemoglobin saturation showed that there was poor agreement among methods in the sickle cell group whereas acceptable agreement was noted among methods in the control group. Conclusion: Patients with SCD during vaso-occlusive crisis have discrepancies in oxyhemoglobin saturation measurements by various methods. Abnormal pulse oximetry values in these patients should be interpreted cautiously and supplemented by PO2 and co-oximetry.

scholarly journals Variability of pulse oximetry measurement over 1 year in children with sickle cell disease depends on initial oxygen saturation measurement

2010 ◽  
Vol 54 (7) ◽  
pp. 1017-1019 ◽  
Author(s):  
Jonathan E. Mullin ◽  
Ben Cooper ◽  
Sinziana Seicean ◽  
Robert Strunk ◽  
Carol Rosen ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Oxygen Saturation ◽  
Pulse Oximetry ◽  
Sickle Cell ◽  
Cell Disease ◽  
Initial Oxygen ◽  
Saturation Measurement

Accuracy of Pulse Oximetry in Sickle Cell Disease.

1999 ◽  
Vol 10 (2) ◽  
pp. 60
Author(s):  
F O Ortiz ◽  
T K Aldrich ◽  
R L Nagel ◽  
L J. Benjamin
Keyword(s):  
Sickle Cell Disease ◽  
Pulse Oximetry ◽  
Sickle Cell ◽  
Cell Disease

Higher oxygen saturation with hydroxyurea in paediatric sickle cell disease

2019 ◽  
Vol 105 (6) ◽  
pp. 575-579 ◽  
Author(s):  
Lisa van Geyzel ◽  
Michele Arigliani ◽  
Baba Inusa ◽  
Bethany Singh ◽  
Wanda Kozlowska ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Sickle Cell Disease ◽  
Life Expectancy ◽  
Oxygen Saturation ◽  
Sickle Cell ◽  
Randomised Clinical Trial ◽  
Cell Disease ◽  
Respiratory Problems ◽  
Sleep Studies ◽  
Before And After

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.

scholarly journals Variation in fetal hemoglobin parameters and predicted hemoglobin S polymerization in sickle cell children in the first two years of life: Parisian Prospective Study on Sickle Cell Disease

Blood ◽  
1994 ◽  
Vol 84 (9) ◽  
pp. 3182-3188 ◽  
Author(s):  
M Maier-Redelsperger ◽  
CT Noguchi ◽  
M de Montalembert ◽  
GP Rodgers ◽  
AN Schechter ◽  
...  
Keyword(s):  
Sickle Cell Disease ◽  
Oxygen Saturation ◽  
Cell Population ◽  
Sickle Cell ◽  
Clinical Manifestations ◽  
Fetal Hemoglobin ◽  
Cell Disease ◽  
Normal Children ◽  
Hemoglobin S ◽  
F Cells

Abstract Intracellular hemoglobin S (HbS) polymerization is most likely to be the primary determinant of the clinical and biologic manifestations of sickle cell disease (SCD). Fetal hemoglobin (HbF) does not enter the HbS polymer and its intracellular expression in sickle erythrocytes inhibits polymerization. HbF levels, high at birth but decreasing thereafter, protect the newborn from the clinical manifestations of this hemoglobinopathy. We have measured the sequential changes in HbF, F reticulocytes, and F cells in the first 2 years of life in 25 children with SCD and compared the results with those obtained in 30 normal children (AA). We have also calculated HbF per F cell (F/F cell), the preferential survival of F cells versus non-F cells, as measured by the ratio F cells versus F reticulocytes (FC/FR) and polymer tendency at 40% and 70% oxygen saturation. HbF levels decreased from about 80.4% +/- 4.0% at birth to 9.2% +/- 2.9% at 24 months. During this time, we observed a regular decrease of the F reticulocytes and the F cells. The kinetics of the decline of F/F cell was comparable with the decline of HbF, rapid from birth (mean, 27.0 +/- 3.6 pg) to 12 months of age (mean, 8.5 +/- 1.5 pg) and then slower from 12 to 24 months of age (mean, 6.2 +/- 1.0 pg) in the SCD children. In the AA children, the decrease in HbF, due to changes in both numbers of F cells and F/F cell, was more precipitous, reaching steady-state levels by 10 months of age. Calculated values for mean polymer tendency in the F-cell population showed that polymerization should begin to occur at 40% oxygen saturation at about 3 months and increase progressively with age, whereas polymerization at 70% oxygen saturation would not occur until about 24 months. These values correspond to HbF levels of 50.8% +/- 10.8% and 9.2% +/- 2.9%, respectively, and F/F cell levels of 15.6 +/- 4.5 pg and 6.2 +/- 1.0 pg, respectively. In the non--F-cell population, polymerization was expected at birth at both oxygen saturation values. Three individuals had significantly greater predicted polymerization tendency than the remainder of the group because of early decreases in HbF. These individuals in particular, the remainder of the cohort, as well as other recruited newborns, will be studied prospectively to ascertain the relationship among hematologic parameters, which determine polymerization tendency and the various clinical manifestations of SCD.

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