Brain Oxygen Monitoring in Traumatic Brain Injury
February 1, 2006 3 minutes read
Brain Oxygen Monitoring in Traumatic Brain Injury
Abstract & Commentary
By Matthew E. Fink, MD, Vice Chairman, Professor of Clinical Neurology, Weill Cornell Medical College, Chief, Division of Stroke and Critical Care Neurology, NewYork-Presbyterian Hospital. Dr. Fink reports no consultant, stockholder, speaker's bureau, research, or other financial relationship with any company related to this field of study.
Synopsis: The addition of brain oxygen monitoring to standard intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring may reduce mortality and improve functional recovery in patients with traumatic brain injury.
Source: Stiefel MF, et al. Reduced Mortality Rate in Patients with Severe Traumatic Brain Injury (TBI) Treated with Brain Tissue Oxygen Monitoring. J Neurosurg. 2005;103:805-811.
Traumatic brain injury is the leading cause of death and disability in young adults in the United States. Among TBI patients with elevated ICP, mortality is common, and current management has focused on reducing elevated ICP. An alternative approach has been to maintain CPP at the expense of ICP by aggressively elevating blood pressure and measuring cerebral blood flow. However, there are serious physiological and technical limitations to this approach, and brain tissue oxygen monitoring may provide additional physiological data that can improve outcome after TBI.
Steifel and colleagues performed a retrospective analysis of 53 consecutive patients with TBI and Glasgow Coma Scale (GCS) less than 8 as part of a prospective observational database. They divided the patients into 2 management groups—Group A (25) patients were managed with ICP monitors alone and Group B (28) patients were managed with ICP monitors plus direct brain tissue PO2 monitors (LICOX; Integra NeuroSciences). Monitors were placed into healthy brain tissue on the side of maximal swelling, according to admission CT scans. Patients with cranial gunshot wounds, those who were medically unstable, or patients with bilateral fixed and dilated pupils, were excluded from analysis.
Standard ICU management in Group A aimed to keep ICP less than 20 mm Hg and CPP greater than 60 mm Hg. Mechanical ventilation was adjusted to keep PCO2 at approximately 35 mm Hg and SaO2 greater than 93%. When ICP rose above 20 mm Hg for more than 5 minutes, intravenous mannitol boluses were administered as needed, to maximum blood osmolarity of 320 mOsm. In Group B patients, in addition to the above therapies, direct brain tissue PO2 monitors were used to maintain brain tissue PO2 > 25 mm Hg. If brain tissue PO2 fell below 25 mm Hg, treatments were instituted to raise blood pressure, increase FiO2, correct respiratory and intravascular volume derangements, provide blood transfusions, and perform decompressive hemicraniectomy. Between the 2 groups, there were no significant differences comparing ICP monitor days, mean daily ICP, mean maximum daily ICP, number of ICP episodes > 20 mm Hg, mean daily CPP, mean minimum daily CPP, or number of CPP episodes < 60 mm Hg.
Eleven (44%) of the 25 patients who had conventional ICP and CPP management died, and 17% of the survivors required additional hospitalization or nursing home placement. In contrast, 7 (25%) of the 28 patients who had brain tissue PO2 monitoring, in addition to ICP and CPP management, died (P < 0.05), and none of the survivors required nursing home placement.
Commentary
Although this study is a nonrandomized series with historical controls, it represents one of the largest studies that systematically evaluated the clinical utility of brain tissue oxygen monitoring in the treatment of patients with severe TBI. The 2 groups were carefully matched for age, admission GCS, and pathological entity and received comparable treatments, except for the use of brain tissue oxygen monitoring. The study suggests that brain tissue oxygen monitoring is a clinically useful technique that may help to improve outcome in acute brain injuries that result in severe vasogenic edema with increased intracranial pressure and secondary brain ischemia, but a randomized clinical trial will be necessary to determine this with certainty.
Continuous monitoring of brain tissue oxygen is an attractive technology, because it reflects the physiological principles that determine brain injury and recovery. One of the primary goals of therapy for TBI, as well as therapy for intracerebral hemorrhage, subarachnoid hemorrhage, acute brain infarction, viral encephalitis, and other acute brain injuries that result in massive brain edema, is to maintain adequate oxygen and glucose delivery to ischemic brain regions that have the potential to survive and recover. Direct measurement of tissue oxygenation should be an excellent indicator of blood flow in the microcirculation, and could be used in a variety of clinical states that result in malignant brain edema.
Traumatic brain injury is the leading cause of death and disability in young adults in the United States.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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