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Delayed impairment of cerebral oxygenation after deep hypothermic circulatory arrest in children
E J Pesonen1, K I Peltola, R E Korpela
1Hospital for Children and Adolescents, and Department of Obstetrics and Gynecology, University of Helsinki, Finland. epesonen@helsinki.fi
Insights
Deep hypothermic circulatory arrest (DHCA) can impair cerebral oxygenation for hours after surgery. This study shows reduced oxygen saturation and impaired cerebral energy status up to 6 hours post-DHCA.
Area of Science:
- Cardiovascular Surgery
- Pediatric Cardiology
- Neuroscience
Background:
- Clinical focus on deep hypothermic circulatory arrest (DHCA) has been limited to immediate postoperative outcomes.
- Experimental data suggests potential cerebral oxygenation impairment 2-8 hours post-reperfusion.
Purpose of the Study:
- To investigate cerebral oxygenation and energy status in children following DHCA.
- To assess biochemical markers of reperfusion injury and neutrophil activation post-DHCA.
Main Methods:
- Measured transcerebral differences in hemoglobin oxygen saturation and plasma metabolites (hypoxanthine, xanthine, lactoferrin).
- Analyzed cerebral venous, arterial, and mixed venous samples up to 10 hours postoperatively in 10 pediatric patients.
- Compared measurements to preoperative levels.
Main Results:
- Cerebral venous oxygen saturation significantly decreased 2-6 hours post-DHCA (44-42% vs. preoperative 57%).
- Elevated transcerebral hypoxanthine concentrations observed 30 minutes to 2 hours post-DHCA indicated impaired cerebral energy status.
- Increased lactoferrin levels at 30 minutes post-DHCA suggested neutrophil activation.
Conclusions:
- Cerebral oxygenation and energy status are impaired for up to 6 hours after DHCA.
- Neutrophil activation occurs in the cerebral circulation within 30 minutes of reperfusion post-DHCA.
Background:
Clinical studies of deep hypothermic circulatory arrest (DHCA) have focused only on the immediate postoperative period. However, experimental findings suggest impairment of cerebral oxygenation at 2 to 8 hours after reperfusion.
Methods:
In 10 children who had DHCA for heart operations, transcerebral differences of hemoglobin oxygen saturation and plasma hypoxanthine, xanthine, and lactoferrin concentrations were measured in concurrently obtained cerebral venous, arterial, and mixed venous samples up to 10 hours postoperatively.
Results:
Compared with preoperative levels (57% +/- 7%), cerebral venous oxygen saturation was not significantly reduced until 2 hours (44% +/- 6%) and 6 hours (42% +/- 5%) after DHCA (p < 0.05). A statistically significant transcerebral (ie, cerebral vein versus artery) concentration difference of hypoxanthine was observed at 30 minutes (3.6 +/- 0.9 micromol/L), 1 hour (3.4 +/- 1.1 micromol/L), and 2 hours (3.1 +/- 0.8 micromol/L) after DHCA but not preoperatively (0.4 +/- 0.2 micromol/L). A transcerebral concentration difference of lactoferrin occurred 30 minutes after DHCA (196 +/- 70 microg/mL) but not preoperatively (16 +/- 20 microg/mL).
Conclusions:
Cerebral venous oxygen saturation of hemoglobin decreased as late as 2 to 6 hours after DHCA, in association with impaired cerebral energy status. Neutrophil activation in the cerebral circulation occurred 30 minutes after reperfusion.