Non‐invasive measurements of carboxyhemoglobin and methemoglobin in children with sickle cell disease

Abstract

SUMMARY Assessment of oxyhemoglobin saturation in patients with sickle cell disease (SCD) is vital for prompt recognition of hypoxemia. The accuracy of pulse oximeter measurements of blood oxygenation in SCD patients is variable, partially due to carboxyhemoglobin (COHb) and methemoglobin (MetHb), which decrease the oxygen content of blood. This study evaluated the accuracy and reliability of a non-invasive pulse co-oximeter in measuring COHb and MetHb percentages (SpCO and SpMet) in children with SCD. We hypothesized that measurements of COHb and MetHb by non-invasive pulse co-oximetry agree within acceptable clinical accuracy with those made by invasive whole blood co-oximetry. Fifty children with SCD-SS underwent pulse co-oximetry and blood co-oximetry while breathing room air. Non-invasive COHb and MetHb readings were compared to the corresponding blood measurements. The pulse co-oximeter bias was 0.1% for COHb and −0.22% for MetHb. The precision of the measured SpCO was ±2.1% within a COHb range of 0.4–6.1%, and the precision of the measured SpMet was ±0.33% within a MetHb range of 0.1–1.1%. Non-invasive pulse co-oximetry was useful in measuring COHb and MetHb levels in children with SCD. Although the non-invasive technique slightly overestimated the invasive COHb measurements and slightly underestimated the invasive MetHb measurements, there was close agreement between the two methods.

Impairment of neutrophil oxidative burst in children with sickle cell disease is associated with heme oxygenase-1

“…Neutrophil oxidative burst can be determined by flow cytometry relatively easily, but as we have shown it might also be predicted from routine measurement of neutrophil count and carboxyhemoglobin concentration, the latter being measurable non-invasively. 51 HO-1-dependent suppression of neutrophil reactive oxygen species (ROS) may represent an appropriate adaptive response to hemolysis. 18 Increased expression of HO-1 is associated with activation of multiple anti-oxidative response pathways, 48,52 although the exact mechanisms by which HO-1 induction leads to impaired neutrophil oxidative burst remain unknown.…”

Methemoglobinemia and ascorbate deficiency in hemoglobin E β thalassemia: metabolic and clinical implications

“…An early study of a few cases of HbE ␤ thalassemia in northern India suggested that methemoglobin levels might be increased in this condition, 26 and increased levels have been reported in some cases of inherited unstable hemoglobins 27 and sickle cell anemia. 28,29 In the present study, there was a significant increase of methemoglobin in a group of patients with HbE ␤ thalassemia whose mean level of plasma ascorbate was at the lower limit of normal; 10 cases showed subnormal levels. However, no cases were encountered with a reduction to the level found in the propositus in this study and the extent to which ascorbate deficiency may be responsible for the modest increase in methemoglobin in these patients requires further study.…”

Methemoglobin and nitric oxide therapy in Ugandan children hospitalized for febrile illness: results from a prospective cohort study and randomized double-blind placebo-controlled trial

“…It is not clear whether these fluctuations were due to natural variations/regulatory responses in the endogenous reduction systems or were related to MHb measurement using the pulse co-oximeter. However, performance of non-invasive pulse co-oximetry has been previously compared to whole blood co-oximetry in children with sickle cell disease and showed acceptable clinical accuracy (bias of −0.22 % for MHb) [50]. The variations in MHb levels over hospitalization highlight the importance of frequent MHb monitoring during administration of nitric oxide.

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