Measurement of hemoglobin saturation by oxygen in children and adolescents with sickle cell disease

Pulse oximetry is a noninvasive method of measuring oxyhemoglobin saturation. The validity of pulse oximetry in sickle cell disease (SCD) has been questioned. We evaluated pulse oximetry, arterial blood gas analysis, and co-oximetry in patients with SCD, and we assessed the effect of dyshemoglobin and altered blood-oxygen affinity on their accuracy. Sixteen patients with SCD aged 7-21 years had arterial and venous blood drawn and transcutaneous pulse oximetry performed. Oxyhemoglobin dissociation curves were plotted from the venous blood of 15 patients. Oxyhemoglobin saturation estimated by arterial blood gas analysis (SaO(2)) and measured by pulse oximetry (SpO(2)) were both higher than the saturation by co-oximetry (FO(2)Hb) (mean +/- SD = 96.3 +/- 1.6%, 94 +/- 3.1%, and 89.1 +/- 3.8%, respectively). There was a significant, positive correlation between SpO(2) and FO(2)Hb (r = 0.7, P = 0.002). The patients had elevated levels of methemoglobin (MetHb) and carboxyhemoglobin (COHb) (2.3 +/- 1.4% and 4.7 +/- 1.3%, respectively). The oxyhemoglobin dissociation curves were frequently shifted to the right with oxygen tensions elevated when hemoglobin was 50% saturated with oxygen (P(50)) (32.5 +/- 4.5 mm Hg). There was a strong correlation between the amounts of dyshemoglobin (MetHb + COHb) and the difference between SaO(2) and FO(2)Hb (r = 0.7, P = 0.002). There was no correlation between the difference between SaO(2) and FO(2)Hb and the P(50) (r = 0.27, P = 0.33) There was also a strong positive correlation between SaO(2)-SpO(2) and dyshemoglobin fraction (r = 0.77, P = 0.001). We conclude that pulse oximetry and arterial blood gas analysis overestimate oxygen saturation when compared to co-oximetry, but that SpO(2) is consistently closer than SaO(2) to FO(2)Hb. SpO(2) is partially affected by MetHb and COHb. The discrepancy between SaO(2) and FO(2)Hb is due to the presence of dyshemoglobin and a shifted oxyhemoglobin dissociation curve, but the effect from dyshemoglobin predominates.     

Daytime steady-state haemoglobin desaturation is a risk factor for overt stroke in children with sickle cell anaemia

Haemoglobin (Hb) desaturation could increase the risk of stroke in sickle cell anaemia (SS) by perturbing endothelial function and limiting oxygen delivery to the brain. We performed a nested case-control study of the Dallas Newborn Cohort to determine whether daytime steady-state Hb desaturation was associated with overt stroke in children with SS. Cases had SS and overt ischaemic strokes. Controls had comparable genotypes but no overt stroke. Cases had lower prestroke steady-state pulse oximetry values (SpO(2)) than controls, and cases' SpO(2) fell even lower as the time to impending stroke decreased. The odds ratio for stroke was 1.32 for each 1% decrease in SpO(2). In conclusion, steady-state Hb desaturation is a risk factor for overt ischaemic stroke in children with SS. Decline in SpO(2) over time further increases this risk. Hb desaturation is easily measured, potentially modifiable, and could be used to identify children with SS at increased risk of stroke.     

Haemoglobin oxygen saturation is a determinant of cerebral artery blood flow velocity in children with sickle cell anaemia

Steady-state haemoglobin (Hb) desaturation is a common finding in sickle cell anaemia (Hb SS) that could predispose to stroke by limiting oxygen delivery to the brain. To determine its association with the risk of overt stroke, we examined the relationship between daytime Hb saturation measured by pulse oximetry (SpO₂) and cerebral artery blood flow velocity measured by transcranial Doppler ultrasonography (TCD), an established risk factor for overt stroke in Hb SS. We studied 181 children using multivariate models to control for known determinants of TCD velocity, including age, haematocrit, and a measure of stenosis. We found that SpO₂ correlated significantly and inversely with TCD velocity in both the right and left middle cerebral arteries. Hb desaturation was associated with increased cerebral artery blood flow velocities and increased odds of abnormal TCD velocities, hence increased risk of stroke. About 5% of the variation in TCD velocity could be ascribed to Hb saturation while controlling for other determinants of TCD velocity. In conclusion, Hb saturation is a determinant of TCD velocity and a risk factor for stroke in children with Hb SS.     

Monitoring carbon dioxide tension and arterial oxygen saturation by a single earlobe sensor in patients with critical illness or sleep apnea

OBJECTIVES: The purpose of the study was to evaluate a novel, combined sensor for transcutaneous monitoring of arterial oxygen saturation and carbon dioxide tension. DESIGN: The new monitoring technique was compared to established reference methods. SETTING: ICU and sleep laboratory of a university hospital. PATIENTS: Eighteen critically ill adult patients with acute respiratory failure or heart failure, and 12 patients with sleep apnea (mean [+/- SD] apnea/hypopnea index, 43 +/- 24 events per hour). MEASUREMENTS: Continuous measurements were performed over several hours by the novel heated (temperature, 42 degrees C) earlobe sensor (TOSCA; Linde Medical Sensors; Basel, Switzerland), incorporating electrochemical and optical elements for carbon dioxide measurement (PtcCO2) and pulse oximetry (SpO2), respectively. The data were compared to the results of repeated arterial blood gas analyses in critically ill patients and to simultaneous nocturnal pulse oximetry performed with different devices with earlobe or finger sensors in sleep apnea patients. RESULTS: In critically ill patients, the mean difference and limits of agreement (bias +/- 2 SDs) of transcutaneous PtcCO2 vs arterial PaCO2 were 3 +/- 7 mm Hg; the corresponding values for changes in PtcCO2 vs PaCO2 were 1 +/- 6 mm Hg. The bias +/- 2 SDs for pulse oximetric SpO2 vs arterial oxygen saturation (SaO2) were 1 +/- 4%. In sleep apnea patients, the combined earlobe sensor identified more transient oxygen desaturations, and the rate of change in oxygen saturation during events was greater compared to those with other tested pulse oximeters, indicating a faster response. CONCLUSIONS: Due to its ability to accurately assess both ventilation and oxygenation by a single transcutaneous sensor, the described noninvasive monitoring technique is a valuable tool for respiratory monitoring with potential applications in critical care and sleep medicine.     

长期无创通气治疗对重叠综合征患者肺功能及夜间血氧的影响

目的 探讨单纯慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者与重叠综合征患者夜间低氧情况及长期呼吸机无创通气治疗对重叠综合征(慢性阻塞性肺疾病患者合并睡眠呼吸暂停低通气综合征)肺功能和血氧的影响.方法 140例稳定期COPD患者均进行夜间氧饱和度监测和肺功能检测,其中重叠综合征患者67例,观察10例重叠综合征患者单纯氧疗和氧疗+呼吸机无创通气治疗前后夜间血氧情况,对5例长期夜间无创通气治疗的重叠综合征患者进行1年动态夜间血氧和肺通气功能监测.结果 10例重叠综合征患者单纯氧疗及氧疗加呼吸机治疗比较,组间在动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、夜间最低氧饱和度(LSaO2)、夜间平均氧饱和度(MSaO2)、血氧饱和度低于90%的时间占总记录时间的百分比(SIT90%)等方面差异有统计学意义(P值均<0.05).长期(1年)无创通气治疗前后肺功能[呼吸峰流量(PEF)、肺活量(FVC)、FVC占预计值%、第1秒用力呼气容积(FEV1)、FEV1占预计值%]及夜间低氧指标(SIT90、MSaO2、LSaO2)明显改善(P值均<0.05).结果 阻塞程度相同的重叠综合征患者夜间低氧比单纯COPD患者严重,长期无创通气治疗可以改善重叠综合征患者肺通气功能及夜间低氧,长期氧疗+无创通气治疗是重叠综合征患者的第一线治疗方案.     

GM-CSF in sickle cell anemia patients with elevated Hb F

We estimated plasma GM-CSF levels in a group of 28 steady-state sickle cell anemia (SS) patients in Kuwait, using an ELISA technique. There were 24 age-matched Hb AA controls, 14 of whom were healthy while 10 were acutely ill at the time of the study. Five SS patients were also studied during 6 episodes of painful crisis. Among the SS patients, 82.1% were homozygous for the Saudi Arabia/India (SAI) haplotype with Hb F ranging from 15 to 35% and total Hb from 8.5 to 11 g/dl. Three patients (siblings) were SAI/Benin compound heterozygotes with Hb F of 9-23% and total Hb >10 g/dl. One patient each was homozygous for the Benin or the Bantu haplotype; they had Hb F <2% and total Hb of 6.6 and 7.2 g/dl, respectively. Four (14. 3%) steady-state SS patients had detectable plasma GM-CSF ranging from 75 to 1,817.6 pg/ml. These included the 2 patients with Hb F <2. 0% and 2 with the SAI/Benin compound heterozygotes with Hb F of 11 and 9%, respectively. Four (66.7%) SS patients in crisis, 6 (42.9%) healthy controls and 6 (60%) acutely ill controls had detectable plasma GM-CSF. A clearcut association of GM-CSF with Hb F level or degree of anemia in steady-state SS patients could not be established. The appearance of GM-CSF in the plasma of patients in crisis and also among control subjects raises the possibility that other factors are involved in the production of this cytokine in the subjects studied.     

Pulse oximetry in sickle cell disease

The place of pulse oximetry in monitoring arterial oxygen saturation in sickle cell disease has been evaluated. In four admissions of patients with sickle cell anaemia with varying degrees of arterial haemoglobin oxygen desaturation, pulse oximetry was compared with a simultaneous assessment of oxygen saturation by arterial blood gas measurement and oxygen dissociation curve (ODC) analysis. Close agreement was found between the oxygen saturation measured by pulse oximetry and that calculated from the measured arterial partial pressure of oxygen (PaO2) with reference to the patient's own ODC. Calculation of oxygen saturation by the blood gas analyser assuming a normal ODC was erroneous. Pulse oximetry is an accurate and effective non-invasive method for monitoring the arterial oxygen saturation in sickle cell disease.     

Clinical correlates of steady-state oxyhaemoglobin desaturation in children who have sickle cell disease

Individuals with sickle cell disease (SCD) may have oxyhaemoglobin desaturation during the steady-state, the causes of which are incompletely known. We studied a cohort of 585 children who have sickle cell anaemia (SS), sickle beta0-thalassaemia (Sbeta0), sickle-haemoglobin C disease (SC), or sickle beta+-thalassaemia (Sbeta+) to determine the relationships between steady-state oxyhaemoglobin saturation (SpO2) and SCD genotype, age, gender, steady-state haemoglobin (Hb) and reticulocyte count, and rate of acute chest syndrome (ACS). The SS/Sbeta0 group (n = 390) had lower mean SpO2 than the SC/Sbeta+ group (n = 195) (96.3% vs. 98.7%, P < 0.001). Among SS/Sbeta0 subjects, a decrease in steady-state SpO2 correlated with a decrease in Hb, an increase in reticulocytes, older age and male gender. These correlations were not found in the SC/Sbeta+ group. Prior ACS did not correlate with steady-state SpO2. A multivariate model explained 45% of the variability in SpO2, but only 5% of the variation in SpO2 was explained by Hb. We conclude that steady-state desaturation is common in individuals with SCD, but it appears to be unrelated to prior episodes of ACS and largely unexplained by chronic anaemia.     

Tumor necrosis factor-alpha is undetectable in the plasma of SS patients with elevated Hb F

Steady-state sickle cell disease (SCD) patients may have increased plasma levels of acute phase reactants and pro-inflammatory cytokines because of subclinical inflammation. We have estimated TNF-alpha levels in the plasma and in supernatants following peripheral blood mononuclear cell (PBMC) activation with phytohemagglutinin (PHA) in a group of Kuwaiti SCD patients using ELISA. The group consisted of 28 SS, 8 Sbeta-thal, and 2 SD patients all in steady state; 5 SS patients were studied during 7 episodes of painful crisis. The subjects were aged 2 to 16 years, with a mean of 7.3 +/- 3.5 years. The beta(S)-globin gene cluster haplotype, alpha-tha1 status, and spleen function were determined in the SS group using standard techniques. Most (82%) were homozygous for the Saudi Arabia/India haplotype and had elevated Hb F levels ranging from 15% to 35%. There were 24 controls (Hb AA or AS), of whom 14 were healthy and 10 were acutely ill at the time of the study. None of the children with SCD (either in steady state or crisis) had detectable plasma TNF-alpha, but four controls (3 acutely ill and one healthy) had levels ranging from 61.7 to 249.8 pg/mL. Following PHA stimulation most subjects responded with high levels of TNF-alpha, with the median level among the steady-state SS patients being significantly higher than that in the controls (both the acutely ill or healthy). It therefore appears that because of the mild disease among our Arab SS children, TNF-alpha is not detectable in their plasma in steady state; these children, however, had a significantly higher response than controls following PBMC activation.     

Pulse oximetry in a cohort study of sickle cell disease

Oxygen saturation was determined by pulse oximetry in a representative sample of Jamaican patients with steady-state sickle cell disease in a cohort study from birth. There were 220 with homozygous sickle cell (SS) disease and 142 with sickle cell-haemoglobin C (SC) disease aged 9–18 years, and 122 with a normal haemoglobin (AA) genotype aged 15–18 years. Pulse oximetry (SpO₂) values were lower in SS disease (mean [95% confidence interval], 92.5 [92.0–93.0]) than in SC disease (96.7 [96.5–96.9]) or AA controls (97.1 [96.8–97.3]). Inhalation of 100% oxygen in SS patients with O₂ saturations below 90% consistently increased saturation to 99–100%. In SS disease, SpO₂ correlated positively with haemoglobin and fetal haemoglobin and negatively with reticulocyte counts but not with MCHC, MCV or bilirubin level. Mean SpO₂ in SS subjects with a normal alpha globin gene complement (mean [SD], 91.7 [3.9]%) was lower than in heterozygotes (93.4 [4.0]%) or homozygotes (96.1 [3.0]%) for α⁺ thalassaemia, the effects of α-thalassaemia not being explained by differences in haemoglobin or MCHC. In SS disease, SpO₂ levels were not associated with age (within this age range), sex, number of sick clinic visits or number of hospital admissions. Higher SpO₂ levels were associated with greater height and weight, more frequent painful crises and less frequent acute chest syndrome, but these associations were not significant after adjustment for haemoglobin level. Desaturation is common in steady-state SS disease and knowledge of the individual’s steady-state value may be important in the interpreting low values during acute complications.     

Arterial oxygen saturation during Nd:YAG laser photoresection of endobronchial tumors under local anesthesia. Use of intermittent supplemental oxygen with pulse oximetry guidance

Although Nd:YAG laser photoresection of endobronchial lung tumor can result in significant arterial oxygen desaturation, oxygen supplementation during procedures is often limited due to fear of intrabronchial combustion. We gave intermittent pulse supplemental oxygen to ten patients during 26 laser procedures performed under local anesthesia using SaO2 measured by a pulse oximeter as a guide. In four procedures (15.4 percent), severe oxygen desaturation contraindicated performing or completing laser phototherapy. In the remaining 22 procedures (84.6 percent), laser photoresection was safely and successfully performed without incident. Thus, pulse oximetry is a valuable tool and intermittent oxygen supplementation with pulse oximeter guidance an effective technique for maintaining adequate oxygenation during laser photoresection.     

Hemoglobin oxygen saturation discrepancy using various methods in patients with sickle cell vaso-occlusive painful crisis

OBJECTIVE: To evaluate agreement among various methods for measuring oxyhemoglobin (O2Hb) saturation in adult hypoxic patients with sickle cell disease (SCD) during painful vaso-occlusive crisis and to compare those results with a control group. PATIENTS AND METHODS: The hemoglobin oxygen saturation was determined simultaneously by pulse oximetry (SpO2), co-oximetry [SO2 (functional oxyhemoglobin saturation) and FO2Hb (oxyhemoglobin fraction)] and by calculation (SaO2) using a normal O2Hb dissociation curve in 18 adult patients with SCD during vaso-occlusive crisis and 12 non-SCD patients with various cardiopulmonary diagnoses. The method proposed by Bland and Altman was used to evaluate agreement of various methods in each of the two groups. RESULTS: Mean differences between various methods in patients with SCD were significantly larger than the control group. Limits of agreement (LOA) were also wider in the SCD group than in the control group. Mean bias between SpO2 and SO2, and SpO2 and FO2Hb in patients with SCD were -3.1 +/- 4.4 (LOA: -11.9 to 5.7) and 2 +/- 4.1 (LOA: -6.2 to 10.2) respectively, compared with -1.4 +/- 1.4 (LOA: -4.2 to 1.4) and 1.2 +/- 1.5 (LOA: -1.9 to 4.3) in the control group. A mean bias of -4.5 +/- 4 (LOA: -12.5 to 3.5) between SpO2 and SaO2 was noted in patients with SCD compared with -0.1 +/- 2.1 (LOA: -4.3 to 4.1) in the control group. The width of LOA for various methods in patients with SCD ranged from 9.8 to 17.6 compared with 1.3 to 8.4 in the control group. CONCLUSION: Patients with SCD during vaso-occlusive crisis have discrepancies in O2Hb saturation measurements by various methods. Abnormal pulse oximetry values in these patients should be interpreted cautiously and supplemented by arterial blood gas analysis and co-oximetry.     

The effect of positional changes on oxygenation in patients with pleural effusions

In unilateral parenchymal pulmonary disease, arterial oxygenation decreases when the patient is positioned such that the abnormal lung is dependent; however, few studies have evaluated the effect of the body position on oxygenation in patients with unilateral or asymmetric pleural effusions. To our knowledge, no previous study has evaluated the possible transient effects of changing position on the level of arterial oxygen saturation (SaO2) in such patients. Accordingly, we studied ten normoxic patients spontaneously breathing room air, who had asymmetric pleural effusions as documented by chest x-ray film and physical examination. We monitored pulse, respiratory rate, and blood pressure every five minutes and SaO2 by ear oximetry continuously while patients were in the following positions: sitting; supine; and left and right lateral decubitus. The mean SaO2 was 95 percent and 94.3 percent in the sitting and supine positions, respectively. Mean SaO2 fell to 93.4 percent when the patients were positioned so that the side with the largest pleural effusion was dependent. When the side with the pleural effusion was down, the mean SaO2 was significantly lower than in either the sitting position or with the side with the pleural effusion up. We could find no significant relationship between the size of the pleural effusion and the amount of arterial oxygen desaturation. We conclude that there is a decrease in SaO2 in normoxic patients when the side with the larger pleural effusion is dependent; however, this decreased SaO2 does not appear to be clinically significant in patients with normal SaO2.     

Clinical events in the first decade in a cohort of infants with sickle cell disease. Cooperative Study of Sickle Cell Disease [see comments]

Within the Cooperative Study of Sickle Cell Disease, 694 infants with confirmed sickle cell disease were enrolled at less than 6 months of age. Information about the nature and frequency of complications was collected prospectively over a 10-year period. Painful crises and acute chest syndrome were the most common sickle cell-related events in homozygous sickle cell anemia (SS), hemoglobin SC disease (SC), and S beta thalassemia patients (overall incidence in SS patients of 32.4 and 24.5 cases per 100 person-years, respectively). Bacteremia occurred most frequently in SS children under 4 years of age and in SC patients less than 2 years of age. The mortality rate was low in this cohort compared with that found in previous reports. Twenty children, all with Hb SS, died (1.1 deaths per 100 person-years among SS patients). Infection, most commonly with Streptococcus pneumoniae and Hemophilus influenzae, caused 11 deaths. Two children died of splenic sequestration, 1 of cerebrovascular accident, and 6 of unclear causes. Two patients underwent cholecystectomies, and 17 underwent splenectomies after one or more splenic sequestration crises. The experience of this cohort should reflect closely the true clinical course of those children with Hb SS and Hb SC disease who are observed in sickle cell centers in the United States.     

Spontaneous desaturations in intubated very low birth weight infants with acute and chronic lung disease.

Patients with chronic lung disease (CLD) have frequent episodes of spontaneous desaturations. Utilizing computerized pulse oximetry (CPO) we quantified the frequency and severity of spontaneous desaturations in very low birth weight (VLBW) infants with CLD. Thirty-four studies by CPO were performed in intubated infants for 4 hours; 17 patients (birth weight, 550-980 g; postnatal age 28-85 days) had CLD, and 17 (birth weight, 520-980 g; postnatal age, 1-7 days) had acute lung disease. Oxygen saturation (SaO2) was measured with the Nellcor N-200 oximeter, its serial output (updated once a second) captured by a computer. Pulse rate, pulse amplitude, and heart rate were also monitored continuously. We measured respiratory system mechanics in 23 patients. Tidal volume (VT), respiratory system compliance (Crs), and resistance (Rrs) were obtained by the PeDS system. Spontaneous desaturation to SaO2 less than 90% occurred for 4.5% of the time in acute patients vs. 27.1% of the time in chronic patients (P less than 0.0001); to SaO2 less than 85%, 0.7% vs. 7.6% of the time in acute vs. chronic patients (P less than 0.002); and to SaO2 less than 80%, 0.4% vs. 2.6% of the time in acute vs. CLD patients (P less than 0.05). Rrs was significantly higher in the ventilated patients with CLD (174 cmH2O/L/s) than in the ventilated patients with acute lung disease (94 cmH2O/L/s, P less than 0.0001). The mean Crs values of the two groups were comparable. Our preliminary data indicate that VLBW infants with CLD receiving assisted ventilation have a greater number of spontaneous desaturation episodes, as compared to patients with acute lung disease.     

Accuracy of two wavelength pulse oximetry in neonates and infants

In 60 neonates (gestational age, 26.5-40 weeks; postnatal age, 1-14 days) and in 11 infants (gestational age, 26-33 weeks; postnatal age, 4.5-38 weeks), the accuracy of two wavelength pulse oximetry was examined. A total of 112 comparisons between transcutaneous pulse oximetry saturation (StcO2, NELLCOR N-100) and arterial oxygen saturation (SaO2, OSM2 RADIOMETER) were obtained. SaO2 ranged from 80 to 100%. Criteria for comparison between StcO2 and SaO2 were standardized: patients in behavioral state 1, StcO2 stable for 2 min, and arterial samples drawn from an indwelling arterial line. StcO2 was significantly related to SaO2 (P less than 0.01), but the difference, StcO2 - SaO2, significantly increased when SaO2 decreased [StcO2 - SaO2(%) = -0.39 SaO2(%) + 37.95; r = -0.64, P less than 0.01]. No significant relationship was found between StcO2 - SaO2 and either bilirubinemia (range, 5-222 mumol/L) or fetal hemoglobin (HbF) (range, 12-95%). We conclude that StcO2 overestimates SaO2 when SaO2 decreases, and this overestimation is not due to high levels of bilirubin or HbF.     

Hematologic and hemorheological determinants of resting and exercise-induced hemoglobin oxygen desaturation in children with sickle cell disease

The aim of the study was to determine the factors associated with resting and exercise-induced hemoglobin oxygen desaturation. The well-established six-minute walk test was conducted in 107 sickle cell children (50 with sickle hemoglobin C disease and 57 with sickle cell anemia) at steady state. Hemoglobin oxygen saturation was measured before and immediately after the six-minute walk test. Blood samples were obtained on the same day to measure hematologic and hemorheological parameters. Exercise-induced hemoglobin oxygen desaturation was defined as a drop in hemoglobin oxygen saturation of 3% or more at the end of the six-minute walk test compared to resting levels. No children with sickle hemoglobin C disease, but approximately 50% of children with sickle cell anemia showed mild or moderate oxygen desaturation at rest, which was independently associated with the percentage of reticulocytes. Exercise-induced hemoglobin oxygen desaturation was observed in 18% of children with sickle hemoglobin C disease and 34% of children with sickle cell anemia, and was independently associated with the six-minute walk test, acute chest syndrome rate and the strength of red blood cell aggregates in children with sickle cell anemia. No association was found in children with sickle hemoglobin C disease between exercise-induced hemoglobin oxygen desaturation and the measured parameters. Hemoglobin oxygen desaturation at rest was common in children with sickle cell anemia but not in children with sickle hemoglobin C disease, and was mainly associated with greater hemolysis. Physiological strain during exercise and red blood cell aggregation properties may predict the occurrence of exercise-induced hemoglobin oxygen desaturation in children with sickle cell anemia.     

Predictors of nocturnal oxygen desaturation in patients with COPD.

The aim of this study was to identify factors which might predict nocturnal desaturation (defined as a fall of > 4% from awake baseline level for > or = 5 min) in normoxic or mildly hypoxic patients with stable COPD [arterial O2 saturation (SaO2) > or = 91%]. The study was prospective in nature, had full ethical approval and was performed in the Respiratory Department of a city teaching hospital. Thirty-three patients [mean (SD) age 67.2 (9) years] with stable COPD [mean (SD) FEV1 36.8 (11.0)% pred.] were recruited via the respiratory outpatient clinics and through the respiratory wards. The following parameters were measured: daytime arterial blood gases; spirometry; lung volumes (helium dilution); single breath CO transfer factor (TLCO and KCO); maximum inspiratory (IMP) and expiratory mouth pressures; pulse oximetry (SpO2) across a 6-min walk test, and SpO2 during sleep. Seventeen patients who experienced nocturnal desaturation had significantly lower mean PaO2 and SaO2, and higher PaCO2 values compared to non-desaturators. There was a positive correlation between mean nocturnal SpO2 and daytime PaO2, SaO2, and minimum exercise SpO2, and a negative correlation between mean nocturnal SpO2 and PaCO2, and FRC. Regression analysis revealed that daytime SaO2 was the only independent predictor of mean nocturnal saturation (accounting for 61% of the variability in the mean nocturnal SpO2). We observed nocturnal desaturation in all patients with a daytime SaO2 < or = 93% but in no patient with SaO2 > or = 95%. We conclude that daytime SaO2 can be used to predict nocturnal desaturation in normoxic or mildly hypoxic patients with stable COPD. Nocturnal desaturation is likely in patients with COPD where daytime SaO2 < or = 93%, and unlikely where daytime SaO2 > or = 95%.     

Is tube feeding associated with altered arterial oxygen saturation in stroke patients?

BACKGROUND: Reduced arterial oxygen saturation (SaO(2)) during swallowing, oral feeding and feeding tube placement has been demonstrated in stroke patients. It is not known if tube feeding causes similar episodes of arterial desaturation and whether there is a case for routine pulse oximetry during tube feeding. OBJECTIVE: To determine if tube feeding in stroke patients is associated with hypoxia. METHODS: We compared ischaemic or haemorrhagic stroke patients who were NG or PEG fed with a control group of age matched non-dysphagic stroke patients who were orally fed. We excluded people already on supplemental oxygen. Pulse oximetry was performed before, during a meal (for 20 min) and for 10 min after and changes from baseline readings determined. RESULTS: Data were collected for 20 controls and 18 tube-fed patients. Mean age was 75 years and median time to assessment 14.5 days. The two groups were reasonably matched for age, sex, type of stroke and time to assessment, but differed significantly in the Oxfordshire Community Stroke Project (OCSP) classification and Rankin score. The mean baseline SaO(2) of controls was 96.5% (SD 1.47) and that of the tube-fed group 96.0% (SD 1.46). Reduction in SaO(2) from baseline during and after feeding ranged from 0.35% to 0.78% with no statistically or clinically significant differences between the two groups. CONCLUSIONS: No clinically significant reduction in SaO(2) was found in our tube-fed patients as compared to controls. Our study suggests that routine pulse oximetry during tube feeding is not necessary.