Jp. Needleman et al., Mechanisms of nocturnal oxyhemoglobin desaturation in children and adolescents with sickle cell disease, PEDIAT PULM, 28(6), 1999, pp. 418-422
Oxyhemoglobin desaturation in patients with sickle cell disease has been pr
oposed as a possible mechanism in the initiaton of vasco-occlusive pain cri
ses. Nocturnal oxyhemoglobin desaturation (NOD) has been described with a p
revalence of up to 40% in children and adolescents with sickle cell disease
. The objective of this study was to evaluate the mechanisms of nocturnal o
xyhemoglobin desaturation in sickle cell disease and determine the role of
obstructive sleep apnea. We performed 16-channel polysomnograms and pulmona
ry function testing in 20 patients with sickle cell disease (ages 7-21 year
s) who had documented desaturation on home oximetry studies.
The median saturation awake was 94% (quartile range, 88-95). Median saturat
ion during REM sleep was 93.5% (88-95) and during non-REM sleep 93.5% (87.5
-95). The median respiratory disturbance index was low (1.35 quartile range
, 0.25-2.85). Twelve patients had no obstructive apnea recorded, while 3 pa
tients had a total of 9 or 10 episodes during the entire study. The median
snoring time was 5.65% of total sleep time (quartile range, 1.35-22.65). Th
ere was no correlation between number of obstructive apneas and mean sleepi
ng saturation (r = 0.012, p = 0.95). There was no correlation between pulmo
nary function data and prevalence of NOD. There was a strong, positive corr
elation between sleeping and awake saturation (r = 0.96, p<0.001).
We conclude that while nocturnal oxyhemoglobin desaturation may be common i
n children and adolescents with sickle cell disease, upper airway obstructi
on does not appear to play an important role in its genesis. (C) 1999 Wiley
-Liss, Inc.