Brain oxygen tension and outcome in patients with aneurysmal subarachnoid hemorrhage

Author:

Ramakrishna Rohan1,Stiefel Michael1,Udoteuk Joshua1,Spiotta Alejandro1,Levine Joshua M.123,Kofke W. Andrew13,Zager Eric1,Yang Wei4,LeRoux Peter1

Affiliation:

1. Departments of Neurosurgery,

2. Neurology,

3. Anesthesiology and Critical Care, and

4. Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania, Philadelphia

Abstract

Object 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 (PbtO2) and death after aneurysmal SAH. Methods Forty-six patients, including 34 women and 12 men (Glasgow Coma Scale Score ≤ 8 and median age 58.5 years) who underwent PbtO2 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 PbtO2 targets. The relationship between PbtO2 and 1-month survival was examined. Results Data were available from 5424 hours of PbtO2 monitoring. For the entire cohort the mean ICP, CPP, and PbtO2 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 PbtO2 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 PbtO2 (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 PbtO2 was stratified according to CPP level, survivors had higher PbtO2 levels. Following logistic regression, the number of episodes of compromised PbtO2 (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. Conclusions Patient deaths after SAH may be associated with a lower mean PbtO2 and longer periods of compromised cerebral oxygenation than in survivors. This knowledge may be used to help direct therapy.

Publisher

Journal of Neurosurgery Publishing Group (JNSPG)

Subject

Genetics,Animal Science and Zoology

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