{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T13:48:44Z","timestamp":1791899324635,"version":"4.3.4"},"reference-count":67,"publisher":"Journal of Neurosurgery Publishing Group (JNSPG)","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JNS"],"published-print":{"date-parts":[[2009,10]]},"abstract":"<jats:sec>\n                    <jats:title>Object<\/jats:title>\n                    <jats:p>\n                      Cerebral ischemia is the leading cause of preventable death in cases of major trauma with severe traumatic brain injury (TBI). Intracranial pressure (ICP) control and cerebral perfusion pressure (CPP) manipulation have significantly reduced the mortality but not the morbidity rate in these patients. In this study, the authors describe their 5-year experience with brain tissue oxygen (PbtO\n                      <jats:sub>2<\/jats:sub>\n                      ) monitoring, and the effect of a brain tissue oxygen\u2013directed critical care guide (PbtO\n                      <jats:sub>2<\/jats:sub>\n                      -CCG) on the 6-month clinical outcome (based on the 6-month Glasgow Outcome Scale score) in patients with TBIs.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      One hundred thirty-nine patients admitted to Creighton University Medical Center with major traumatic injuries (Injury Severity Scale [ISS] scores \u2265 16) and TBI underwent prospective evaluation. All patients were treated with a PbtO\n                      <jats:sub>2<\/jats:sub>\n                      -CCG to maintain a brain oxygen level &gt; 20 mm Hg, and control ICP &lt; 20 mm Hg. The role of demographic, clinical, and imaging parameters in the identification of patients at risk for cerebral hypooxygenation and the influence of hypooxygenation on clinical outcome were recorded. Outcomes were compared with those in a historical ICP\/CPP patient cohort. Subgroup analysis of severe TBI was performed and compared to data reported in the Traumatic Coma Data Bank.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The majority of injuries were sustained in motor vehicle crashes (63%), and diffuse brain injury was the most common abnormality (58%). Mechanism of injury, severity of TBI, pathological entity, neuroimaging results, and trauma indices were not predictive of ischemia. Factors affecting death included gunshot injury, poor trauma indices, subarachnoid hemorrhage, and coma. After standard resuscitation, 65% of patients had an initially low PbtO\n                      <jats:sub>2<\/jats:sub>\n                      . Data are presented as means \u00b1 SDs. Treatment with the PbtO\n                      <jats:sub>2<\/jats:sub>\n                      -CCG resulted in a 44% improvement in mean PbtO\n                      <jats:sub>2<\/jats:sub>\n                      (16.21 \u00b1 12.30 vs 23.65 \u00b1 14.40 mm Hg; p &lt; 0.001), control of ICP (mean 12.76 \u00b1 6.42 mm Hg), and the maintenance of CPP (mean 76.13 \u00b1 15.37 mm Hg). Persistently low cerebral oxygenation was seen in 37% of patients at 2 hours, 31% at 24 hours, and 18% at 48 hours of treatment. Thus elevated ICP and a persistent low PbtO\n                      <jats:sub>2<\/jats:sub>\n                      after 2 hours represented increasing odds of death (OR 14.3 at 48 hours). Survivors and patients with good outcomes generally had significantly higher mean daily PbtO\n                      <jats:sub>2<\/jats:sub>\n                      and CPP values compared to nonsurvivors. Polytrauma, associated with higher ISS scores, presented an increased risk of vegetative outcome (OR 9.0). Compared to the ICP\/CPP cohort, the mean Glasgow Outcome Scale score at 6 months in patients treated with PbtO\n                      <jats:sub>2<\/jats:sub>\n                      -CCG was higher (3.55 \u00b1 1.75 vs 2.71 \u00b1 1.65, p &lt; 0.01; OR for good outcome 2.09, 95% CI 1.031\u20134.24) as was the reduction in mortality rate (25.9 vs 41.50%; relative risk reduction 37%), despite higher ISS scores in the PbtO\n                      <jats:sub>2<\/jats:sub>\n                      group (31.6 \u00b1 13.4 vs 27.1 \u00b1 8.9; p &lt; 0.05). Subgroup analysis of severe closed TBI revealed a significant relative risk reduction in mortality rate of 37\u201351% compared with the Traumatic Coma Data Bank data, and an increased OR for good outcome especially in patients with diffuse brain injury without mass lesions (OR 4.9, 95% CI 2.9\u20138.4).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The prevention and aggressive treatment of cerebral hypooxygenation and control of ICP with a PbtO\n                      <jats:sub>2<\/jats:sub>\n                      -directed protocol reduced the mortality rate after TBI in major trauma, but more importantly, resulted in improved 6-month clinical outcomes over the standard ICP\/CPP-directed therapy at the authors' institution.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3171\/2009.4.jns081150","type":"journal-article","created":{"date-parts":[[2009,5,22]],"date-time":"2009-05-22T09:55:26Z","timestamp":1242986126000},"page":"672-682","source":"Crossref","is-referenced-by-count":240,"title":["Brain tissue oxygen monitoring in traumatic brain injury and major trauma: outcome analysis of a brain tissue oxygen\u2013directed therapy"],"prefix":"10.3171","volume":"111","author":[{"given":"Pradeep K.","family":"Narotam","sequence":"first","affiliation":[{"name":"Union Hospital Neuroscience, Terre Haute, Indiana;"},{"name":"Divisions of Neurosurgery and"},{"name":"Trauma, Creighton University Medical Center, Omaha, Nebraska; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John F.","family":"Morrison","sequence":"additional","affiliation":[{"name":"Divisions of Neurosurgery and"},{"name":"Trauma, Creighton University Medical Center, Omaha, Nebraska; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Narendra","family":"Nathoo","sequence":"additional","affiliation":[{"name":"Divisions of Neurosurgery and"},{"name":"Trauma, Creighton University Medical Center, Omaha, Nebraska; and"},{"name":"Alegent Health Neuroscience Specialists, Council Bluffs, Iowa"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1754","reference":[{"key":"b1-1110672","series-title":"Crit Care","first-page":"638","article-title":"Cerebral perfusion pressure and brain ischaemia: can one size fit all?","volume":"9","author":"Andrews","year":"2005"},{"key":"b2-1110672","series-title":"J Trauma","first-page":"1010","article-title":"Prevalence and prognosis of traumatic intraventricular hemorrhage in patients with blunt head trauma","volume":"60","author":"Atzema","year":"2006"},{"key":"b3-1110672","series-title":"Neurocrit Care","first-page":"8","article-title":"Impact of intracranial pressure and cerebral perfusion pressure on severe disability and mortality after head injury","volume":"4","author":"Balestreri","year":"2006"},{"key":"b4-1110672","series-title":"Acta Neurochir Suppl","first-page":"153","article-title":"Monitoring of brain tissue PO2 in traumatic brain injury: effect of cerebral hypoxia on outcome","volume":"71","author":"Bardt","year":"1998"},{"key":"b5-1110672","series-title":"J Neurosurg","first-page":"491","article-title":"The outcome from severe head injury with early diagnosis and intensive management","volume":"47","author":"Becker","year":"1977"},{"key":"b6-1110672","series-title":"Acta Neurochir Suppl","first-page":"111","article-title":"Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury","volume":"71","author":"Bruzzone","year":"1998"},{"key":"b7-1110672","series-title":"Crit Care Med","first-page":"1870","article-title":"Management of severe head injury: institutional variations in care and effect on outcome","volume":"30","author":"Bulger","year":"2002"},{"key":"b8-1110672","series-title":"Minerva Chir","first-page":"1467","article-title":"Severe head trauma. 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