Copyright 2016 American Medical Association. All rights reserved.
Cerebral Oximetry in Ugandan Children With Severe Anemia
Clinical Categories and Response to Transfusion
Aggrey Dhabangi, MD; Brenda Ainomugisha, MD; Christine Cserti-Gazdewich, MD; Henry Ddungu, MD;
Dorothy Kyeyune, MD; Ezra Musisi, BS; Robert Opoka, MD; Christopher P. Stowell, MD, PhD; Walter H. Dzik, MD
IMPORTANCE
Severe anemia, defined as a hemoglobin level of less than 5.0 g/dL, affects
millions of children worldwide. The brain has a high basal demand for oxygen and is especially
vulnerable to hypoxemia. Previous studies have documented neurocognitive impairment in
children with severe anemia. Data on cerebral tissue oxygenation in children with severe
anemia and their response to blood transfusion are limited.
OBJECTIVE To measure hemoglobin saturation in cerebral tissue (cerebral tissue oxygen
saturation [tS
O
2
]) before, during, and after blood transfusion in a cohort of children
presenting to hospital with severe anemia.
DESIGN, SETTING, AND PARTICIPANTS This was a prospective, observational cohort study
conducted from February 2013 through May 2015 and analyzed in July 2015 at a university
hospital pediatric acute care facility in Kampala, Uganda, of 128 children, ages 6 to 60 months
who were enrolled in a larger clinical trial, with a presenting hemoglobin level of less than
5.0 g/dL and a blood lactate level greater than 5mM. Most children had either malaria or
sickle cell disease.
EXPOSURES Red blood cell (RBC) transfusion given as 10 mL/kg over 120 minutes.
MAIN OUTCOMES AND MEASURES Clinical and laboratory characteristics of children with
pretransfusion cerebral tS
O
2
levels less than 65%, 65% to 75%, and greater than 75%.
Change in cerebral tS
O
2
as a result of transfusion.
RESULTS Of 128 children included in the study, oximetry results in 8 cases were excluded
owing to motion artifacts; thus, 120 were included in this analysis. Cerebral tS
O
2
values prior
to transfusion ranged from 34% to 87% (median, 72%; interquartile range [IQR], 65%-76%).
Eighty-one children (67%) demonstrated an initial cerebral tS
O
2
level (ⱕ75%) corresponding
to an oxygen extraction ratio greater than 0.36. Patients with sickle cell disease (n = 17) and
malaria (n = 15) contributed in nearly equal numbers to the subgroup with an initial cerebral
tS
O
2
(<65%). The level of consciousness, hemoglobin concentration, blood lactate level, and
thigh muscle tS
O
2
level were poor predictors of cerebral oxygen saturation. Following RBC
transfusion, the median (IQR) cerebral tS
O
2
level increased to 78% (73%-82%) (P < .001), but
21% of children failed to achieve a tS
O
2
level greater than 75%.
CONCLUSIONS AND RELEVANCE Severe anemia in children is frequently associated with low
cerebral oxygenation levels as measured by near-infrared spectroscopy. Hemoglobin level
and lactate concentration did not predict low cerebral tS
O
2
levels. Cerebral tSO
2
levels
increase with RBC transfusion with different patterns of response. More studies are needed
to evaluate the use of noninvasive cerebral tissue oximetry in the care of children with
severe anemia.
JAMA Pediatr. 2016;170(10):995-1002. doi:10.1001/jamapediatrics.2016.1254
Published online August 8, 2016.
Editorial page 936
Supplemental content at
jamapediatrics.com
Author Affiliations: Author
affiliations are listed at the end of this
article.
Corresponding Author: Walter H.
Dzik, MD, Blood Transfusion Service,
Massachusetts General Hospital,
Harvard Medical School, 55 Fruit St,
Room J-224, Boston, MA 02114
(sdzik@mgh.harvard.edu).
Research
JAMA Pediatrics | Original Investigation
(Reprinted) 995
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W
orldwide, millions of children experience substantial
morbidity and mortality from severe anemia each
year.
1
The human brain has both a high resting oxy-
gen extraction ratio and a high blood flow rate that combine to
fulfill a continuous demand for oxygen. Children ages2to6years
have higher cerebral blood flow rates and higher cerebral oxy-
gen consumption rates (mL
O
2
/gm/min) than adults.
2
The aver-
age cerebral metabolic rate in a child (5.25 milliliters of oxygen
per gram per minute) represents more than 50% of total body
oxygen consumption, whereas the average rate in an adult
(3 mL
O
2
/100 g/min) represents 20% of total body oxygen
consumption.
3
The higher oxygen demands of the pediatric brain make
it more vulnerable to cerebral hypoxemia and injury in the set-
ting of severe anemia. Silent cerebral ischemia and progres-
sive neurocognitive deficits are well-recognized conse-
quences of sickle cell disease (SCD),
4
and recent research from
Uganda has demonstrated that severe anemia due to malaria
is also associated with long-term neurocognitive impairment.
5
In sub-Saharan Africa, malaria, human immunodeficiency vi-
rus, nutritional deficiencies, and hemoglobin abnormalities
cause severe pediatric anemia, commonly defined as a hemo-
globin concentration of less than 5.0 g/dL (to convert hemo-
globin to grams per liter, multiply by 10.0).
6
Currently, there
is limited information on the extent to which severe anemia
results in cerebral ischemia in children. Studying the effects
of severe anemia on cerebral oxygenation represents one step
toward a better understanding of the role that severe anemia
may play in subsequent neurologic development and cogni-
tive performance among children worldwide.
Noninvasive assessment of cerebral oxygenation is now
available through severalmeans.Oneapproach uses devices that
emit near-infrared (NIR) light at specific wavelengths ab-
sorbed by oxygenated and deoxygenated hemoglobin.
7
Opti-
cal probes (optodes), placed at a fixed distance from the light
emitters, measure the reflectance by hemoglobin in tissue blood
vessels, and report regional tissue oxygen saturation (tS
O
2
).
Noninvasive measurements of cerebral tS
O
2
have been shown
to correlate with results measured by co-oximetry from samples
obtained from the radial artery and jugular venous bulb of vol-
unteers breathing different concentrations of oxygen.
8
Cere-
bral oximetry has been applied in diverse clinical settings, in-
cluding cardiac surgery,
7,9
neonatal medicine,
7,10
and
neurocritical care.
11
The technology has not been previously
applied to children in sub-Saharan Africa with severe anemia.
Given the frequency and severity of pediatric anemia ob-
served in sub-Saharan Africa
6,12-14
and the importance of the ef-
fective treatment of cerebral hypoxemia, we performed an obser-
vational study in Ugandadesignedtoassess cerebral oxygenation
before, during, and after red blood cell (RBC) transfusion in a co-
hort of children who presented to a pediatric urgent care facility
with severe anemia associated with systemic lactic acidosis.
Methods
We studied tSO
2
as part of a larger randomized clinical trial of
blood transfusion conducted at the pediatric acute care unit
of Mulago Hospital in Kampala, Uganda. The design and pri-
mary outcome of that trial were reported previously.
15
Chil-
dren, ages 6 to 60 months, who presented to hospital with a
hemoglobin level of 5.0 g/dL or less and a blood lactate level
of at least 5mM were screened for enrollment. We excluded
children with severe acute malnutrition, known cardiac dis-
ease, or transfusion within the 48 hours prior to presenta-
tion. Written informed consent was obtained from the parent
or guardian. Patients were enrolled between February 2013 and
May 2015; they were not compensated for their participation.
Patients were monitored for 24 hours after enrollment, and
health status at 30 days was determined by telephone
interview.
15
Data were analyzed in July 2015.
The study was approved by the School of Medicine Re-
search Ethics Committee of Makerere University College of
Health Sciences, the Uganda National Council for Science and
Technology, and the Human Research Committee of the
Massachusetts General Hospital. An independent oversight
committee monitored enrollment and adverse events through-
out the study. The study was registered at clinical trials.gov
(NCT01586923).
Transfusions, Supplemental Oxygen, and Laboratory Assays
All patients received a transfusion of prestorage leuko-
reduced CP2D-AS3 RBCs at a dose of 10 mL/kg by peripheral
vein over 120 minutes using an electromechanical infusion
pump. Some patients received small volumes of additional
intravenous fluid (dextrose, antimalarial medications).
Patients with an arterial oxygen saturation (Sa
O
2
) of less
than 95% (measured with finger oximetry) were given supple-
mental oxygen by nasal prongs. Hemoglobin and lactate
concentrations were measured using point-of-care devices
(Hemocue; Lactate-Pro LT-1710) validated in prior studies of
severe anemia.
15
Hemoglobin and lactate concentrations were
obtained just prior to transfusion (hour 0) and immediately at
the completion of transfusion (hour 2).
15
NIR tSO
2
Monitoring
Patients were monitored using a commercially available de-
vice (EQUANOX 7600, Nonin Medical Inc). All measurements
were done over 120 minutes from the start to the completion
of the RBC transfusion. Pediatric optodes, with an average light
Key Points
Question What are the results of cerebral oximetry obtained in
children with severe anemia and lactic acidosis?
Findings In this cohort study of 120 Ugandan children with severe
anemia, subnormal levels of cerebral oxygen saturation were
commonly seen in children with malaria or sickle cell disease. In
21% of patients, cerebral oximetry did not normalize following a
standard red blood cell transfusion.
Meaning Severe pediatric anemia is associated with abnormalities
in cerebral oximetry, and given the worldwide prevalence of
severe anemia in children, additional study of the extent and
consequences of subnormal cerebral oxygenation in severe
pediatric anemia seems warranted.
Research Original Investigation Cerebral Oximetry in Ugandan Children With Severe Anemia
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penetrance of 12.5 mm, were placed on the left side of the fore-
head above the eyebrow according to the manufacturer’s
directions. Readings were recorded electronically every 4 sec-
onds, and the data transferred to a digital database for analy-
sis. In a subset of 72 children, we placed a second optode on
the left thigh to obtain simultaneous readings from thigh
muscle. The device uses NIR light emitters at 4 different wave-
lengths to measure the reflectance of oxygenated and deoxy-
genated hemoglobin. Data are combined to generate a single
read-out value that estimates the percentage of tS
O
2
. The re-
ported result assumes the hemoglobin saturation in the blood
of cerebral tissue is approximated by
tS
O
2
= 0.3(SaO
2
) + 0.7(Oxygen Saturation).
In healthy individuals, the mean (SD) cerebral tS
O
2
using
4-wavelength NIR spectroscopy is reported as 76% (4.8%).
16,17
For each patient, a graph of tSO
2
over time was prepared by
plotting, at 5-minute intervals, the average reading for 1 min-
ute (average of 15 readings). The graph was prepared from the
device readings by an individual not involved in the care of the
patient and without access to other clinical data. Using the start-
ing value as the baseline, software (Prism 6; Graphpad Inc) was
used to compute the net area under the curve (AUC) of tS
O
2
as
a function of time for 120 minutes during transfusion. The net
AUC represents the overall change in oxygen saturation in re-
sponse to transfusion. Arterial oxygen saturation was directly
measured by finger pulse oximetry. The estimated venous oxy-
gen saturation was directly calculated from the recorded tS
O
2
and the measured SaO
2
using the formula above. The estimated
local tissue oxygen extraction ratio was then calculated from
the measured Sa
O
2
and estimated venous oxygen saturation.
Statistical Analysis
Continuous variables are presented as median and interquar-
tile ranges (IQRs) and compared using the Mann-Whitney test
(2 variables) or the Kruskal-Wallis test (3 variables).
The relationship between hemoglobin level and initial
tS
O
2
level, between lactate level and initial tSO
2
level, and be-
tween initial cerebral tS
O
2
level and thigh tSO
2
level were
examined by linear correlation using GraphPad Prism 6. The
correlation coefficient r
2
was determined by the method of least
squares. The area under the oxygen saturation curve during
transfusion was plotted as a function of the initial tS
O
2
, fitted
to a 1-phase exponential curve using GraphPad Prism 6, and
the goodness of fit (R
2
) determined by the method of least
Table. Clinical Features in All Patients and Features in 3 Subgroups According to Cerebral tSO
2
Values
a
Characteristic
All Patients
(n = 120)
Group
P Value
A: tS
O
2
<65%
(n = 32)
B: tSO
2
65%-75%
(n = 49)
C: tSO
2
>75%
(n = 39)
Cerebral tS
O
2
, median (IQR) 72 (65-76) 59 (49-62) 71 (69-73) 79 (76-81)
Malaria, No. (%) 87 (73) 15 (47) 38 (77) 34 (87) <.001
Sickle cell disease, No. (%) 25 (21) 17 (53) 6 (12) 2 (5) <.001
Female:male 54:66 16:16 20:29 18:21 .71
Age, median (IQR), mo 27.5 (17-42) 27.5 (14-45) 30 (19-39) 27 (22-40) .95
Mean arterial blood pressure,
median (IQR), mm Hg
74 (65-80) 77 (69-81) 73 (68-80) 71 (63-81) .25
Respiratory rate, median (IQR) 58 (50-63) 59 (50-68) 58 (50-62) 58 (49-62) .68
Pulse rate, median (IQR) 162 (152-170) 153 (148-165) 166 (155-175) 162 (152-170) .02
Stupor or coma, No. (%) 44 (37) 9 (28) 16 (32) 19 (49) .15
Coma, No. (%) 11 (9) 1 (0.8) 4 (3) 6 (5) .22
Hemoglobin, level, median (IQR), g/dL 3.2 (2.5-4.1) 2.8 (2.4-3.6) 3.1 (2.7-4.1) 3.4 (2.6-4.5) .15
Systemic lactate, median (IQR), mM 9.3 (6.1-13.0) 9.9 (6.8-13.2) 8.7 (6.0-12.9) 9.4 (6.0-12.9) .61
Sa
O
2
, median, % 99 99 99 98 .71
Estimated cerebral venous oxygen
saturation, median (IQR), %
61 (50-67) 42 (29-47) 61 (55-63) 70 (67-74) NA
Estimated oxygen extraction ratio,
median (IQR)
0.38 (0.30-0.48) 0.57 (0.52-0.68) 0.39 (0.34-0.44) 0.28 (0.22-0.31) NA
Difference between thigh and brain
tSO
2
, median (IQR), %
b
10.8 (8-19) 23 (20-33) 13 (9.7-16) 5.6 (3-9) <.001
Supplemental, No. (%)
Oxygen by nasal prongs 11 (9) 1 (3) 5 (10) 5 (13) .40
Intravenous fluid
c
49 (41) 13 (41) 17 (35) 19 (49) .41
BNP, median (IQR), pg/mL 198 (45.5-696) 326 (97-866) 205 (54-676) 70 (20-390) .13
Need for second transfusion, No. (%) 45 (37) 14 (44) 19 (39) 12 (31) .52
Returned to good health at day 30,
No. (%)
d
87 (88) 22 (88) 33 (80) 32 (97) .08
Died within 30 d, No. (%)
d
8 (8) 2 (8) 5 (12) 1 (3) .41
Abbreviations: BNP, B-type natriuretic peptide, measurements in 30, 38, and 27
patients in groups A, B, and C, respectively; IQR, interquartile range;
NA, comparison not applicable based on definition of groups A, B, and C; Sa
O
2
,
arterial oxygen saturation; tSO
2
, tissue oxygen saturation.
SI conversion: To convert hemoglobin to grams per liter, multiply by 10.0.
a
All data were obtained prior to transfusion.
b
Simultaneous cerebral and thigh measurements in 18, 26, and 28 patients in
groups A , B, and C, respectively.
c
Median (IQR) volume given to those receiving fluid = 50 mL (40-60 mL).
d
Data apply to 25, 41, and 33 patients in groups A, B, and C, respectively.
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squares. A paired test (Wilcoxon signed rank test) was used to
compare oxygen saturation before vs after transfusion within
the same individual. Categorical variables were compared using
the Fisher exact test. The threshold for significance was P < .05.
All comparisons were 2-sided. No corrections were made for
multiple comparisons.
Results
Noninvasive cerebral oximetry was performed in 128 pa-
tients who presented to a pediatric acute care unit in
Kampala, Uganda, and who were enrolled in a larger clinical
trial of blood transfusion.
15
In 8 cases, the readings were con-
sidered unreliable owing to motion artifacts. The remaining
120 cases form the basis for this report.
Baseline Clinical Features
At presentation to hospital, the patients were severely anemic
with a median (IQR) hemoglobin level of 3.2 g/dL (2.5-4.1 g/dL)
and a median (IQR) blood lactate level of 9.3mM (6.1mM-
13.0mM) (Table). The patients had tachycardia and tachypnea
but were not hypotensive. Stupor or coma was initially
present in 37% of children. A minority of children (9%) who
presented with an Sa
O
2
level of less than 95% were given supple-
mental oxygen by nasal prongs and achieved a saturation level
greater than 95%. Patients were not in shock and not given bo-
lus intravenous fluids. Most children (73%) had malaria, and 21%
had SCD. Initial cerebral tS
O
2
values ranged from 34% to 87%
with a median (IQR) value of 72% (65%-76%). These values cor-
respond to a median (IQR) extraction ratio of 0.38 (0.30-0.48).
Eighty-one of 120 children (67%) presented with cerebral tS
O
2
of 75% or less, corresponding to an oxygen extraction ratio
greater than 0.36. The distributions of cerebral tS
O
2
values
before and after RBC transfusion are shown in Figure 1.
We categorized the patients into 3 subgroups based on their
pretransfusion cerebral tS
O
2
values: tSO
2
level of less than 65%
(n=32),tS
O
2
level of 65% to 75% (n = 49), and tSO
2
level greater
than 75% (n = 39). Clinical features for each group are shown in
the Table. The subgroup with cerebral tS
O
2
level of less than 65%
(32 patients) consisted of equal numbers of patients with malaria
and SCD. Sickle cell disease was present in 17 of 32 (53%) of those
with an initial cerebral tS
O
2
level of less than 65%, but only 2 of
39 (5%) of those with an initial cerebral tS
O
2
level greater than
75% (P < .001). The median (IQR) initial tSO
2
level among 25 pa-
tients with SCD was 60% (49%-66%), which was significantly
lower than the median value among 95 patients without SCD,
74% (69%-77%) (P < .001). The lower cerebral tS
O
2
level among
Figure 1. Distribution of Cerebral Tissue Oxygen Saturation (tSO
2
) Values Before and After Red Blood Cell Transfusion in 120 Children
Presenting With Severe Anemia and Lactic Acidosis
40
Patients, No.
25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85-89 90-94 95-100
5
10
15
20
25
30
35
0
Pretransfusion
A
Cerebral t
2
40
Patients, No.
25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65-69 70-74 75-79 80-84 85-89 90-94 95-100
5
10
15
20
25
30
35
0
Posttransfusion
B
Cerebral t
2
A, Pretransfusion. B, Posttransfusion. The white sections of the bars indicate patients with sickle cell anemia. The mean (SD) normal cerebral tSO
2
is 76% (4.8%).
16,17
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patients with SCD occurred despite the fact that their hemoglo-
bin concentration and their SaO
2
level were not significantly dif-
ferent from the patients without SCD: hemoglobin values, 2.9
g/dL (2.3-3.6 g/dL) for patients with SCD vs 3.2 g/dL (2.6-4.3 g/dL)
for patients without SCD (P = .11); Sa
O
2
level, 98% (94%-99%)for
patients with SCD vs 99% (96%-100%) for patients without SCD
(P = .14). The median (IQR) cerebral oxygen extraction ratio for
patientswith SCD was 0.53 (0.46-0.72)compared with 0.34 (0.29-
0.43) for patients without SCD (P < .001).
Predicting Cerebral tSO
2
As shown in the Table, the level of consciousness was not
associated with low cerebral tSO
2
level. All patients had an ini-
tial hemoglobin measurement of less than 5.0 g/dL. While the
lowest cerebral tS
O
2
levels were observed in patients with he-
moglobin values of less than 4.0 g/dL, there was very poor cor-
relation (r
2
= 0.08) between hemoglobin concentration and ce-
rebral tS
O
2
level (see eFigure 1 in the Supplement). All patients
had an initial blood lactate level greater than 45.0 mg/dL (me-
dian, 83.8 mg/dL) with values ranging as high as 186.5 mg/dL.
However, systemic lactate concentrations also did not corre-
late with cerebral tS
O
2
level (r
2
= 0.02) (see eFigure 2 in the
Supplement).
In 72 patients, regional tissue oxygen saturation was
simultaneously measured in the left frontal brain and left thigh
every 4 seconds for 120 minutes during transfusion. In 86%
of cases, thigh tS
O
2
level was higher than cerebral tSO
2
level
throughout the transfusion. Prior to transfusion, the median
(IQR) difference in tS
O
2
between the 2 tissues was 10.8% (8.0%-
19.0%). This difference was maintained following transfu-
sion, 9.3% (6.7%-14.0%) (Figure 2). A low cerebral tS
O
2
level
was not reflected by a corresponding low thigh tS
O
2
level.
Rather, patients with low cerebral tSO
2
level showed a larger
difference between thigh and cerebral readings (Table). Thigh
tS
O
2
level did not correlate with cerebral tSO
2
level (r
2
= 0.12)
and could not be used as a surrogate measurement for the
cerebral saturation (see eFigure 3 in the Supplement).
Response to RBC Transfusion
All 120 patients received transfusion of RBCs as 10 mL/kg over
120 minutes. Transfusion reproducibly increased cerebral tS
O
2
.
The median (IQR) cerebral tSO
2
level before transfusion was 72%
(65%-76%) and rose to 78% (73%-82%) after transfusion (P < .001)
(Figure 2). The overall time-integrated increase in cerebral oxy-
genation was measured as the AUC of the plot of cerebral tS
O
2
level over time during transfusion (Figure 3). A higher AUC re-
flects a greater overall increase in cerebral oxygen saturation. The
median (IQR) AUC during transfusion was 553 (319-1052). As
shown in Figure 3, the magnitude of cerebral tS
O
2
response to
transfusion, as measured by the AUC, was not “fixed” even
though the dose of hemoglobin was the same for all patients
(10 mL/kg). Rather, patients presenting with lower cerebral tS
O
2
obtained greater benefit (higher AUC) from transfusion.
The median (IQR) hemoglobin concentration rose from
3.2 g/dL (2.5-4.1 g/dL) just prior to transfusion to 6.1 g/dL
(5.2-7.2 g/dL) immediately after transfusion, resulting in a
doubling of the oxygen content of blood delivered to the
Figure 2. Regional Tissue Oxygen Saturation (tSO
2
) Levels
Before and After RBC Transfusion
100
90
80
70
60
50
40
30
Regional Tissue
2
Saturation, %
Cerebral (n
=
120)
Before
P<.001 P<.001
After Before After
Thigh (n
=
72)
A, Levels from the brain (n = 120). B, Levels from the thigh (n = 72). The
horizontal bars are the median values, and the error bars are the interquartile
ranges. In both tissues, there was a significant increase in tS
O
2
as a result of
transfusion.
Figure 3. Cerebral Tissue Oxygen Saturation (tSO
2
) in Response
to Red Blood Cell Transfusion
100
45
95
90
85
80
75
70
65
60
55
50
Cerebral S
2
, %
0 10 20 30 40 50 60 70 80 90 100 110 120
Transfusion Time, min
R
2
= 0.55
4000
−2000
2000
0
AUC of tS
2
During Transfusion
30 40 50 60 70 80 90 100
Cerebral
2
Saturation Before Transfusion
Tracing in 30-month-old boy
A
Correlation between response and pretransfusion tS
2
B
A, An individual tracing in a 30-month-old boy with partially treated malaria
who presented to the hospital with a hemoglobin concentration of 3.2 g/dL and
lactate level of 5.9mM. The child was alert, with a blood pressure 104/58
mm Hg, pulse of 163 beats/min, and respiratory rate of 62 breaths/min. The
average cerebral tS
O
2
values are shown every 5 minutes during transfusion with
10 mL/kg of red blood cells. The region shaded in gray is the area under the
curve (AUC) using the initial value as the baseline. B, Correlation between
response to transfusion, measured as AUC, and the pretransfusion cerebral tS
O
2
in the study group of 120 patients.
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