Abstract

The purpose of this study was to compare the effect of PbtO2-guided therapy with traditional intracranial pressure- (ICP-) guided treatment on the management of cerebral variables, therapeutic interventions, survival rates, and neurological outcomes of moderate and severe traumatic brain injury (TBI) patients. From 2009 to 2010, TBI patients with a Glasgow coma scale <12 were recruited from 6 collaborative hospitals in northern Taiwan, excluding patients with severe systemic injuries, fixed and dilated pupils, and other major diseases. In total, 23 patients were treated with PbtO2-guided management (PbtO2 > 20 mmHg), and 27 patients were treated with ICP-guided therapy (ICP < 20 mmHg and CPP > 60 mmHg) in the neurosurgical intensive care unit (NICU); demographic characteristics were similar across groups. The survival rate in the PbtO2-guided group was also significantly increased at 3 and 6 months after injury. Moreover, there was a significant correlation between the PbtO2 signal and Glasgow outcome scale-extended in patients from 1 to 6 months after injury. This finding demonstrates that therapy directed by PbtO2 monitoring is valuable for the treatment of patients with moderate and severe TBI and that increasing PaO2 to 150 mmHg may be efficacious for preventing cerebral hypoxic events after brain trauma.

Highlights

  • Survival rates and outcomes for patients suffering from severe traumatic brain injury (TBI) depend on the severity of secondary cerebral insults [1, 2]

  • Twenty-seven TBI patients were treated with traditional intracranial pressure- (ICP-)guided therapy, whereas 23 patients were treated with PbtO2-guided management

  • The average cerebral perfusion pressure (CPP) was significantly higher (P = 0.013) in PbtO2-guided patients compared with intracranial pressure (ICP)-guided patients, these signals were >60 mmHg in both groups

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Summary

Introduction

Survival rates and outcomes for patients suffering from severe traumatic brain injury (TBI) depend on the severity of secondary cerebral insults [1, 2]. Previous studies have shown that cerebral ischemia, which may be caused by systemic hypotension, intracranial hypertension, impaired autoregulation, or hyperventilation, is a common and independent factor associated with neurological deterioration after injury [3,4,5,6,7]. No randomized trial has demonstrated an improved outcome for severe TBI patients provided with intracranial pressure (ICP) signal-guided treatment, current guidelines for severe TBI management recommend ICP monitoring to calculate and maintain cerebral perfusion pressure (CPP) and prevent cerebral ischemia and infarction [8]. Certain studies have confirmed that CPP may not be correlated with cerebral blood flow and oxygen consumption in TBI patients [7, 9,10,11,12]. Certain CPPguided treatments, such as the administration of vasopressor agents or fluid expanders, have been demonstrated to cause adverse effects, including respiratory distress syndrome, and were shown to offset the original benefits of these treatments on the outcome of severe TBI patients [13, 14]

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