Jp. Needleman et al., Measurement of hemoglobin saturation by oxygen in children and adolescentswith sickle cell disease, PEDIAT PULM, 28(6), 1999, pp. 423-428
Pulse oximetry is a noninvasive method of measuring oxyhemoglobin saturatio
n. The validity of pulse oximetry in sickle cell disease (SCD) has been que
stioned. We evaluated pulse oximetry, arterial blood gas analysis, and co-o
ximetry in patients with SCD, and we assessed the effect of dyshemoglobin a
nd altered blood-oxygen affinity on their accuracy. Sixteen patients with S
CD aged 7-21 years had arterial and venous blood drawn and transcutaneous p
ulse 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 co
rrelation 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 c
urves were frequently shifted to the right with oxygen tensions elevated wh
en hemoglobin was 50% saturated with oxygen (P-50) (32.5 +/- 4.5 mm Hg). Th
ere 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). T
here was no correlation between the difference between SaO(2) and FO(2)Hb a
nd the P-50 (r = 0.27, P = 0.33) There was also a strong positive correlati
on between SaO(2)-SpO(2) and dyshemoglobin fraction (r = 0.77, P = 0.001).
We conclude that pulse oximetry and arterial blood gas analysis overestimat
e oxygen saturation when compared to co-oximetry, but that SpO(2) is consis
tently 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 presenc
e of dyshemoglobin and a shifted oxyhemoglobin dissociation curve, but the
effect from dyshemoglobin predominates. (C) 1999 Wiley-Liss, Inc.