Brain oxygen tension and outcome in patients with aneurysmal subarachnoid hemorrhage

Poor outcome is common after aneurysmal subarachnoid hemorrhage (SAH). Clinical studies suggest that cerebral hypoxia after traumatic brain injury is associated with poor outcome. In this study we examined the relationship between brain oxygen tension (PbtO(2)) and death after aneurysmal SAH.

Forty-six patients, including 34 women and 12 men (Glasgow Coma Scale Score < or = 8 and median age 58.5 years) who underwent PbtO(2) monitoring were studied prospectively during a 2-year period in a neurosurgical intensive care unit at a University Level I Trauma Center. Brain oxygen tension, intracranial pressure (ICP), mean arterial pressure, cerebral perfusion pressure (CPP), and brain temperature were continuously monitored, and treatment was directed toward ICP, CPP, and PbtO(2) targets. The relationship between PbtO(2) and 1-month survival was examined.

Data were available from 5424 hours of PbtO(2) monitoring. For the entire cohort the mean ICP, CPP, and PbtO(2) were 13.85 +/- 2.40, 84.05 +/- 3.41, and 30.79 +/- 1.91 mm Hg, respectively. Twenty-five patients died (54%). The mean daily PbtO(2) was higher in survivors than nonsurvivors (33.94 +/- 2.74 vs 28.14 +/- 2.59 mm Hg; p = 0.05). In addition, survivors had significantly shorter episodes of compromised PbtO(2) (defined as 15-25 mm Hg) than nonsurvivors (125.85 +/- 15.44 vs 271.14 +/- 55.23 minutes; p < 0.01). Intracranial pressure was similar in survivors and nonsurvivors. In contrast, the average CPP was significantly lower in nonsurvivors than survivors (76.96 +/- 5.50 vs 92.49 +/- 2.75 mm Hg; p = 0.01). When PbtO(2) was stratified according to CPP level, survivors had higher PbtO(2) levels. Following logistic regression, the number of episodes of compromised PbtO(2) (odds ratio 1.1, 95% confidence interval 1.003-1.2) and number of episodes of cerebral hypoxia (< 15 mm Hg; odds ratio 1.3, 95% confidence interval 1.0-1.7) were more frequent in those who died.

Patient deaths after SAH may be associated with a lower mean PbtO(2) and longer periods of compromised cerebral oxygenation than in survivors. This knowledge may be used to help direct therapy.