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

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

“…Steady-state Hb desaturation in SS is largely due to the presence of dyshaemoglobins and a shifted oxyhaemoglobin dissociation curve (Needleman et al, 1999) rather than comorbid conditions. Although our observed 2-3% absolute difference in SpO 2 between cases and controls may seem numerically small, SpO 2 tends to overestimate arterial oxygen saturation by co-oximetry in SS (Needleman et al, 1999). Further, a modest decrease in SpO 2 might be physiologically deleterious to a region of the brain, for example, that is downstream of a critical stenosis in which oxygen extraction is already maximal.…”

“…Finally, although we found no clear associations between co-morbid conditions and Hb desaturation, there was no systematic screening for such causes. However, desaturation is a known complication of SS itself (Rackoff et al, 1993;Homi et al, 1997;Needleman et al, 1999;Setty et al, 2003;Quinn & Ahmad, 2005).…”

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

“…Hemoglobin oxygen desaturation at rest [1][2][3][4][5][6][7] and exerciseinduced hemoglobin oxygen desaturation (EIHOD) 6,7 are common in sickle cell disease (SCD). Cellular activation and abnormal vascular cell adhesion in SCD are caused by resting hemoglobin oxygen desaturation 8 which is associated with an increased risk for vaso-occlusive crises, 9 stroke 10 and elevated tricuspid regurgitation velocity, 6,7 suggesting a role for hemoglobin oxygen desaturation in the occurrence of these complications.…”

Increased von Willebrand factor antigen and high molecular weight multimers in sickle cell disease associated with nocturnal hypoxemia

“…However, oxyhemoglobin desaturation (low SaO2) in SCD patients at steady state could also reflect: (i) a state of chronic increased metabolic demand and oxygen utilization with limited reserve for further increases in oxygen demand and (ii) increased intra-erythrocytic HbS polymer concentration and risk for sickling. Accordingly Needleman et al have shown spectrophotometric measurements of SaO 2 such as pulse oximetry, are accurate in SCD [12]. Therefore we have divided our patients in two groups based on sleeping SaO 2 s. Using data from previous studies in children [13], those with SaO 2 <94% were assigned to the hypoxemic group (n=10); those with sleeping >94% comprised the normoxemic group (n=9).…”