Brain tissue oxygenation in children diagnosed with brain death
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Published on: August 19, 2020
Anthony A Figaji1, Samuel J Kent
1University of Cape Town, Cape Town, South Africa.
Insights
Brain tissue oxygenation (PbtO(2)) monitoring may help diagnose brain death in children. In this study, PbtO(2) dropped to 0 mmHg in all children diagnosed with brain death, suggesting its potential as a diagnostic tool.
Area of Science:
- Pediatric Neurocritical Care
- Neurology
- Clinical Monitoring
Background:
- Diagnosing brain death in children presents significant challenges.
- Guidelines advocate for confirmatory testing to support brain death diagnosis.
- Brain tissue oxygenation (PbtO(2)) monitoring is established in adult neurocritical care but limited in pediatrics.
Purpose of the Study:
- To investigate the relationship between PbtO(2) and brain death in pediatric patients.
- To evaluate the utility of PbtO(2) as an ancillary test for diagnosing brain death in children.
Main Methods:
- Retrospective review of 85 children with coma from acute neurological injury requiring ventilation and intracerebral monitoring.
- Analysis of PbtO(2) levels in patients who developed brain death versus those who did not.
Main Results:
- Five children diagnosed with brain death showed a PbtO(2) decrease to 0 mmHg at the time of diagnosis.
- In contrast, PbtO(2) in non-brain-dead patients never reached 0 mmHg.
- The study discusses the advantages and disadvantages of using PbtO(2) in pediatric brain death diagnosis.
Conclusions:
- Preliminary findings suggest PbtO(2) reaching 0 mmHg may indicate brain death in children.
- Further research is necessary to establish the sensitivity and specificity of this PbtO(2) threshold in a larger pediatric cohort.
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.
