BACKGROUND: Diagnosing brain death in children is challenging. Guidelines recommend using confirmatory testing to provide ancillary information to support the diagnosis. Brain tissue oxygenation (PbtO(2)) is being increasingly used in the adult neurocritical care for continuous monitoring of the adequacy of brain oxygenation; however, data in pediatrics is limited. Evidence from adult studies suggests that persistent PbtO(2) of 0 mmHg is associated with brain death, but this relationship has not yet been demonstrated in children; therefore, we examined our experience with PbtO(2) monitoring and brain death in children with acute neurological pathology. METHODS: We retrospectively reviewed patient records from a prospectively maintained database of 85 children who were ventilated for coma due to acute neurological injury and who received intracerebral monitoring. RESULTS: We identified five children who had suffered brain death while being monitored. PbtO(2) had decreased to 0 mmHg in all five children at the time of brain death diagnosis. In contrast, PbtO(2) in patients, who did not develop brain death, never decreased to 0 mmHg. We review the benefits and drawbacks of using brain tissue oxygenation as ancillary information in diagnosing brain death in children. CONCLUSIONS: Preliminary data from this study suggest that PbtO(2) decreases to 0 mmHg when brain death occurs in children. Further study is needed to determine the limitations, and the sensitivity and specificity of this finding in a larger group of children.
BACKGROUND: Diagnosing brain death in children is challenging. Guidelines recommend using confirmatory testing to provide ancillary information to support the diagnosis. Brain tissue oxygenation (PbtO(2)) is being increasingly used in the adult neurocritical care for continuous monitoring of the adequacy of brain oxygenation; however, data in pediatrics is limited. Evidence from adult studies suggests that persistent PbtO(2) of 0 mmHg is associated with brain death, but this relationship has not yet been demonstrated in children; therefore, we examined our experience with PbtO(2) monitoring and brain death in children with acute neurological pathology. METHODS: We retrospectively reviewed patient records from a prospectively maintained database of 85 children who were ventilated for coma due to acute neurological injury and who received intracerebral monitoring. RESULTS: We identified five children who had suffered brain death while being monitored. PbtO(2) had decreased to 0 mmHg in all five children at the time of brain death diagnosis. In contrast, PbtO(2) in patients, who did not develop brain death, never decreased to 0 mmHg. We review the benefits and drawbacks of using brain tissue oxygenation as ancillary information in diagnosing brain death in children. CONCLUSIONS: Preliminary data from this study suggest that PbtO(2) decreases to 0 mmHg when brain death occurs in children. Further study is needed to determine the limitations, and the sensitivity and specificity of this finding in a larger group of children.
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