Intraoperative monitoring of brain tissue oxygen and carbon dioxide pressures reveals low oxygenation in peritumoral brain edema

Brain edema and swelling often complicate surgery for brain tumors. Its pathophysiology is unclear, as is the relationship with brain tissue oxygenation. Our hypothesis was that brain edema around tumor is cytotoxic type caused by impaired local tissue oxygenation due to increased local tissue pressure. Therefore, we monitored brain tissue oxygen pressure (p(ti)O(2)) and carbon dioxide pressure (p(ti)O(2)) in 19 patients undergoing craniotomy for removal of a brain tumor and specifically studied the effect of decompression by dura opening and by tumor removal with respect to the presence of brain swelling. Before craniotomy, multiparameter sensors were inserted into the peri-tumoral brain tissue guided by MRI-based stereotaxy. In eight patients who had severe brain swelling upon opening of the dura mater, p(ti)O(2) immediately rose from 7 +/- 8 mm Hg to 24 +/- 15 mm Hg (P <0.05), whereas in patients who did not have swelling, p(ti)O(2) went from 16 +/- 9 to 18 +/- 10 mm Hg after opening of the dura. The mean p(ti)O(2) of all patients at the start of resection of the tumor was 18 +/- 11 mm Hg, and increased to 30 +/- 15 turn Hg after resection was completed (P <0.05). The effect on p(ti)O(2) of raising the FiO(2) to 1.0 was limited in this group of patients, as an increase greater than 50% was found in only six of twelve patients. Notably, in six patients, sensor malfunctions or associated hardware problems occurred, prohibiting useful data acquisition. We conclude that brain tissue oxygenation is reduced in the peritumoral area and improves after local tissue pressure relief, especially in patients with brain swelling. Thus, ischemic processes may contribute to brain edema around tumors. Intraoperative p(ti)O(2) monitoring may enhance the safety of neuroanesthesia, but the high incidence of failures with this type of sensor remains a matter of concern