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Monitoring brain tissue oxygen tension in brain-injured patients reveals hypoxic episodes in normal-appearing and in peri-focal tissue.
Intensive Care Medicine 2007 December
OBJECTIVE: We compared brain tissue oxygen tension (PtiO2) measured in peri-focal and in normal-appearing brain parenchyma on computerized tomography (CT) in patients following traumatic brain injury (TBI).
DESIGN: Prospective observational study.
SETTING: Neurointensive care unit.
PATIENTS AND PARTICIPANTS: Thirty-two consecutive TBI patients were subjected to PtiO2 monitoring.
INTERVENTIONS: Peri-focal tissue was identified by the presence of a hypodense area of the contusion and/or within 1 cm from the core of the contusion. The position of the tip of the PtiO2 probe was assessed at follow-up CT scan.
MEASUREMENTS AND RESULTS: Mean PtiO2 in the peri-contusional tissue was 19.7+/-2.1 mmHg and was lower than PtiO2 in normal-appearing tissue (25.5+/-1.5 mmHg, p < 0.05), despite a greater cerebral perfusion pressure (CPP) (73.7+/-2.3 mmHg vs. 67.4+/-1.4 mmHg, p < 0.05). We observed both in peri-focal tissue and in normal-appearing tissue episodes of brain hypoxia (PtiO2 < 20 mmHg for at least 10 min), whose median duration was longer in peri-focal tissue than in normal-appearing tissue (51% vs. 34% of monitoring time, p < 0.01). In peri-focal tissue, we observed a progressive PtiO2 increase from pathologic to normal values (p < 0.01).
CONCLUSIONS: Multiple episodes of brain hypoxia occurred over the first 5 days following severe TBI. PtiO2 was lower in peri-contusional tissue than in normal-appearing tissue. In peri-contusional tissue, a progressive increase of PtiO2 from pathologic to normal values was observed over time, suggestive of an improvement at microcirculatory level.
DESIGN: Prospective observational study.
SETTING: Neurointensive care unit.
PATIENTS AND PARTICIPANTS: Thirty-two consecutive TBI patients were subjected to PtiO2 monitoring.
INTERVENTIONS: Peri-focal tissue was identified by the presence of a hypodense area of the contusion and/or within 1 cm from the core of the contusion. The position of the tip of the PtiO2 probe was assessed at follow-up CT scan.
MEASUREMENTS AND RESULTS: Mean PtiO2 in the peri-contusional tissue was 19.7+/-2.1 mmHg and was lower than PtiO2 in normal-appearing tissue (25.5+/-1.5 mmHg, p < 0.05), despite a greater cerebral perfusion pressure (CPP) (73.7+/-2.3 mmHg vs. 67.4+/-1.4 mmHg, p < 0.05). We observed both in peri-focal tissue and in normal-appearing tissue episodes of brain hypoxia (PtiO2 < 20 mmHg for at least 10 min), whose median duration was longer in peri-focal tissue than in normal-appearing tissue (51% vs. 34% of monitoring time, p < 0.01). In peri-focal tissue, we observed a progressive PtiO2 increase from pathologic to normal values (p < 0.01).
CONCLUSIONS: Multiple episodes of brain hypoxia occurred over the first 5 days following severe TBI. PtiO2 was lower in peri-contusional tissue than in normal-appearing tissue. In peri-contusional tissue, a progressive increase of PtiO2 from pathologic to normal values was observed over time, suggestive of an improvement at microcirculatory level.
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