Monitoring brain tissue oxygen tension in brain-injured patients reveals hypoxic episodes in normal-appearing and in peri-focal tissue.

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.

Inaccurate early assessment of neurological severity in head injury.

Intubation, which requires sedation and myorelaxants, may lead to inaccurate neurological evaluation of severely head-injured patients. Aims of this study were to describe the early clinical evolution of traumatic brain injured (TBI) patients admitted to intensive care unit (ICU), to identify cases of over-estimated neurological severity, and to quantify the risk factors for this over-estimation. A total of 753 TBI patients consecutively admitted to ICU of three academic neurosurgical hospitals (NSH) were assessed. Cases whose severity was potentially over-estimated were identified by four criteria and indicated as "mistakenly severe" (MS): (1) no surgical intracranial masses; (2) could not follow commands at neurological assessment; (3) were dismissed from the ICU in < or =3 days to a regular ward; and (4) had regained the ability to obey commands. A total of 675 patients were intubated and/or sedated-paralyzed at the post-stabilization evaluation. In all, 304 patients had surgically treated intracranial masses. Among the 449 non-surgical cases, 58 patients fulfilling the criteria for MS were identified. The main features distinguishing MS from truly severe cases were younger age, higher Glasgow Coma Scale (GCS) score at all time points, Marshall classification of Computerized Tomographic (CT) scan mostly Diffuse Injury I and II, fewer pupillary abnormalities, and a lower frequency of hypoxia, hypotension, and extra-cranial injuries. In a certain proportion of non-surgical TBI patients, mostly intubated and sedated, neurological examination is difficult and severity can be over-estimated. Risk factors for this inaccurate evaluation can be identified, and clinical decisions should be based on further examination.