Patient transport and brain oxygen in comatose patients

Transport of critically ill intensive care unit patients may be hazardous. We examined whether brain oxygen (brain tissue oxygen partial pressure [PbtO2]) is influenced by transport to and from a follow-up head computed tomography (transport head computed tomography [tHCT]) scan.

Forty-five patients (24 men, 21 women; Glasgow Coma Scale score < or =8; mean age, 47.3 +/- 19.0 years) who had a traumatic brain injury (n = 26) or subarachnoid hemorrhage (n = 19) were retrospectively identified from a prospective observational cohort of PbtO2 monitoring in a neurosurgical intensive care unit at a university-based level I trauma center. PbtO2, intracranial pressure, and cerebral perfusion pressure were monitored continuously and compared during the 3 hours before and after 100 tHCT scans.

The mean PbtO2 before and after the tHCT scans for all 100 scans was 37.9 +/- 19.8 mm Hg and 33.9 +/- 17.2 mm Hg, respectively (P = .0001). A decrease in PbtO2 (>5%) occurred after 54 tHCTs (54%) and in 36 patients (80%). In instances in which a decrease occurred, the average decrease in mean, minimum, and maximum PbtO2 was 23.6%, 29%, and 18.1%, respectively. This decrease was greater when PbtO2 was compromised (<25 mm Hg) before tHCT. An episode of brain hypoxia (<15 mm Hg) was identified in the 3 hours before tHCT in 9 and after tHCT in 19 instances. On average, an episode of brain hypoxia was 46.6 +/- 16.0 (standard error) minutes longer after tHCT than before tHCT (P = .008). Multivariate analysis suggests that changes in lung function (PaO2/fraction of inspired oxygen [FiO2] ratio) may account for the reduced PbtO2 after tHCT (parameter estimate 0.45, 95% confidence interval: 0.024-0.871; P = .04).

These data suggest that transport to and from the intensive care unit may adversely affect PbtO2. This deleterious effect is greater when PbtO2 is already compromised and may be associated with lung function.