Hyperbaric oxygenation is the accepted treatment for cerebral arterial gas embolism. Although earlier start of hyperbaric oxygenation is associated with better outcome, it is unknown how much delay can be tolerated before start of hyperbaric oxygenation. This study investigates the effect of hyperbaric oxygenation on cerebral function in swine when initiated 2 or 4 hours after cerebral arterial gas embolism.
Prospective interventional animal study.
Surgical laboratory and hyperbaric chamber.
Twenty-two Landrace pigs.
Under general anesthesia, probes to measure intracranial pressure, brain oxygen tension (PbtO2), and brain microdialysis, and electrodes for electroencephalography were placed. The electroencephalogram (quantified using temporal brain symmetry index) was suppressed during 1 hour by repeated injection of air boluses through a catheter placed in the right ascending pharyngeal artery. Hyperbaric oxygenation was administered using U.S. Navy Treatment Table 6 after 2- or 4-hour delay. Control animals were maintained on an inspiratory oxygen fraction of 0.4.
Intracranial pressure increased to a mean maximum of 19 mm Hg (SD, 4.5 mm Hg) due to the embolization procedure. Hyperbaric oxygenation significantly increased PbtO2 in both groups treated with hyperbaric oxygenation (mean maximum PbtO2, 390 torr; SD, 177 torr). There were no significant differences between groups with regard to temporal brain symmetry index (control vs 2-hr delay, p = 0.078; control vs 4-hr delay, p = 0.150), intracranial pressure, and microdialysis values.
We did not observe an effect of hyperbaric oxygenation on cerebral function after a delay of 2 or 4 hours. The injury caused in our model could be too severe for a single session of hyperbaric oxygenation to be effective. Our study should not change current hyperbaric oxygenation strategies for cerebral arterial gas embolism, but further research is necessary to elucidate our results. Whether less severe injury benefits from hyperbaric oxygenation should be investigated in models using smaller amounts of air and clinical outcome measures.
1Diving Medical Center, Royal Netherlands Navy, Den Helder, The Netherlands.
2Laboratory of Experimental Intensive Care and Anaesthesiology (L.E.I.C.A.), Department of Anaesthesiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
3Department of Surgery, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
4Department of Radiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
*See also p. 1817.
This work was performed at the Surgical Laboratory, Department of Surgery, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
This research was funded by the Department of Defense of The Netherlands (grant number 009-07-5041-01).
Dr. Hollmann is a board member on the Anesthesia and Analgesia Editorial Board. He is a consultant for HO, Eurocept, and MSD. He has received grant support from IARS, ZonMW, and NHS. He has received payment for lectures from Abbott, MSD, and Pfizer. Dr. Stevens has received payment for lectures and payment for the development of educational presentations from Abbott and AstraZeneca. The remaining authors have disclosed that they do not have conflicts of interest.
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