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Original Investigation |

Cerebral Oximetry in Ugandan Children With Severe Anemia Clinical Categories and Response to Transfusion ONLINE FIRST

Aggrey Dhabangi, MD1; Brenda Ainomugisha, MD2; Christine Cserti-Gazdewich, MD3; Henry Ddungu, MD4; Dorothy Kyeyune, MD5; Ezra Musisi, BS5; Robert Opoka, MD6,7; Christopher P. Stowell, MD, PhD8; Walter H. Dzik, MD8
[+] Author Affiliations
1Department of Pediatrics, Child Health and Development Centre, Makerere University, Kampala, Uganda
2Department of Pediatrics, Mulago Hospital, Kampala, Uganda
3University Health Network Laboratory Medicine Program, University of Toronto, Toronto, Ontario, Canada
4Uganda Cancer Institute, Makerere University, Kampala, Uganda
5Uganda National Blood Transfusion Service, Kampala, Uganda
6Department of Pediatrics, Mulago Hospital, Kampala, Uganda
7Makerere University, Kampala, Uganda
8Department of Pathology, Blood Transfusion Service, Massachusetts General Hospital, Harvard Medical School, Boston
JAMA Pediatr. Published online August 08, 2016. doi:10.1001/jamapediatrics.2016.1254
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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 [tSo2]) 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 tSo2 levels less than 65%, 65% to 75%, and greater than 75%. Change in cerebral tSo2 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 tSo2 values prior to transfusion ranged from 34% to 87% (median, 72%; interquartile range [IQR], 65%-76%). Eighty-one children (67%) demonstrated an initial cerebral tSo2 level (≤75%) 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 tSo2 (<65%). The level of consciousness, hemoglobin concentration, blood lactate level, and thigh muscle tSo2 level were poor predictors of cerebral oxygen saturation. Following RBC transfusion, the median (IQR) cerebral tSo2 level increased to 78% (73%-82%) (P < .001), but 21% of children failed to achieve a tSo2 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 tSo2 levels. Cerebral tSo2 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.

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Figure 1.
Distribution of Cerebral Tissue Oxygen Saturation (tSo2) Values Before and After Red Blood Cell Transfusion in 120 Children Presenting With Severe Anemia and Lactic Acidosis

A, Pretransfusion. B, Posttransfusion. The white sections of the bars indicate patients with sickle cell anemia. The mean (SD) normal cerebral tSo2 is 76% (4.8%).16,17

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Figure 2.
Regional Tissue Oxygen Saturation (tSo2) Levels Before and After RBC Transfusion

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 tSo2 as a result of transfusion.

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Figure 3.
Cerebral Tissue Oxygen Saturation (tSo2) in Response to Red Blood Cell Transfusion

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 tSo2 values are shown every 5 minutes during transfusion with 10mL/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 tSo2 in the study group of 120 patients.

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Figure 4.
Representative Examples of the Most Common Patterns of Cerebral Tissue Oxygen Saturation (tSo2) Response to Transfusion

A, Cerebral tSo2 begins at a very low value, improves with transfusion, but does not reach the normal range. B, Cerebral tSo2 rises above 75% during the transfusion. C, Cerebral tSo2 begins above 75% and rises during transfusion. D, Cerebral tSo2 remains relatively unchanged during transfusion. The horizontal dashed lines correspond to an oxygen extraction ratio of approximately 36%.

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