Reduced mortality rate in patients with severe traumatic brain injury treated with brain tissue oxygen monitoring

2005 ◽  
Vol 103 (5) ◽  
pp. 805-811 ◽  
Author(s):  
Michael F. Stiefel ◽  
Alejandro Spiotta ◽  
Vincent H. Gracias ◽  
Alicia M. Garuffe ◽  
Oscar Guillamondegui ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Traumatic Brain Injury ◽  
Mortality Rate ◽  
Brain Tissue ◽  
Tissue Oxygen ◽  
Content Type ◽  
Brain Tissue Oxygen ◽  
Severe Tbi ◽  
Gcs Score ◽  
Fine Print

Object. An intracranial pressure (ICP) monitor, from which cerebral perfusion pressure (CPP) is estimated, is recommended in the care of severe traumatic brain injury (TBI). Nevertheless, optimal ICP and CPP management may not always prevent cerebral ischemia, which adversely influences patient outcome. The authors therefore determined whether the addition of a brain tissue oxygen tension (PO2) monitor in the treatment of TBI was associated with an improved patient outcome. Methods. Patients with severe TBI (Glasgow Coma Scale [GCS] score < 8) who had been admitted to a Level I trauma center were evaluated as part of a prospective observational database. Patients treated with ICP and brain tissue PO2 monitoring were compared with historical controls matched for age, pathological features, admission GCS score, and Injury Severity Score who had undergone ICP monitoring alone. Therapy in both patient groups was aimed at maintaining an ICP less than 20 mm Hg and a CPP greater than 60 mm Hg. Among patients whose brain tissue PO2 was monitored, oxygenation was maintained at levels greater than 25 mm Hg. Twenty-five patients with a mean age of 44 ± 14 years were treated using an ICP monitor alone. Twenty-eight patients with a mean age of 38 ± 18 years underwent brain tissue PO2-directed care. The mean daily ICP and CPP levels were similar in each group. The mortality rate in patients treated using conventional ICP and CPP management was 44%. Patients who also underwent brain tissue PO2 monitoring had a significantly reduced mortality rate of 25% (p < 0.05). Conclusions. The use of both ICP and brain tissue PO2 monitors and therapy directed at brain tissue PO2 is associated with reduced patient death following severe TBI.

Brain tissue oxygen–directed management and outcome in patients with severe traumatic brain injury

2010 ◽  
Vol 113 (3) ◽  
pp. 571-580 ◽  
Author(s):  
Alejandro M. Spiotta ◽  
Michael F. Stiefel ◽  
Vicente H. Gracias ◽  
Alicia M. Garuffe ◽  
W. Andrew Kofke ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Severe Traumatic Brain Injury ◽  
Tertiary Care ◽  
Care Hospital ◽  
Tissue Oxygen ◽  
Brain Tissue Oxygen ◽  
Severe Tbi

Object The object of this study was to determine whether brain tissue oxygen (PbtO2)–based therapy or intracranial pressure (ICP)/cerebral perfusion pressure (CPP)–based therapy is associated with improved patient outcome after severe traumatic brain injury (TBI). Methods Seventy patients with severe TBI (postresuscitation GCS score ≤ 8), admitted to a neurosurgical intensive care unit at a university-based Level I trauma center and tertiary care hospital and managed with an ICP and PbtO2 monitor (mean age 40 ± 19 years [SD]) were compared with 53 historical controls who received only an ICP monitor (mean age 43 ± 18 years). Therapy for both patient groups was aimed to maintain ICP < 20 mm Hg and CPP > 60 mm Hg. Patients with PbtO2 monitors also had therapy to maintain PbtO2 > 20 mm Hg. Results Data were obtained from 12,148 hours of continuous ICP monitoring and 6,816 hours of continuous PbtO2 monitoring. The mean daily ICP and CPP and the frequency of elevated ICP (> 20 mm Hg) or suboptimal CPP (< 60 mm Hg) episodes were similar in each group. The mortality rate was significantly lower in patients who received PbtO2-directed care (25.7%) than in those who received conventional ICP and CPP–based therapy (45.3%, p < 0.05). Overall, 40% of patients receiving ICP/CPP–guided management and 64.3% of those receiving PbtO2–guided management had a favorable short-term outcome (p = 0.01). Among patients who received PbtO2-directed therapy, mortality was associated with lower mean daily PbtO2 (p < 0.05), longer durations of compromised brain oxygen (PbtO2 < 20 mm Hg, p = 0.013) and brain hypoxia (PbtO2 < 15 mm Hg, p = 0.001), more episodes and a longer cumulative duration of compromised PbtO2 (p < 0.001), and less successful treatment of compromised PbtO2 (p = 0.03). Conclusions These results suggest that PbtO2-based therapy, particularly when compromised PbtO2 can be corrected, may be associated with reduced patient mortality and improved patient outcome after severe TBI.

Regional cerebrovascular and metabolic effects of hyperventilation after severe traumatic brain injury

2002 ◽  
Vol 96 (1) ◽  
pp. 103-108 ◽  
Author(s):  
Michael N. Diringer ◽  
Tom O. Videen ◽  
Kent Yundt ◽  
Allyson R. Zazulia ◽  
Venkatesh Aiyagari ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Metabolic Rate ◽  
Severe Traumatic Brain Injury ◽  
Content Type ◽  
Severe Tbi ◽  
The Mean ◽  
Gcs Score ◽  
Energy Failure ◽  
Fine Print

Object. Recently, concern has been raised that hyperventilation following severe traumatic brain injury (TBI) could lead to cerebral ischemia. In acute ischemic stroke, in which the baseline metabolic rate is normal, reduction in cerebral blood flow (CBF) below a threshold of 18 to 20 ml/100 g/min is associated with energy failure. In severe TBI, however, the metabolic rate of cerebral oxygen (CMRO2) is low. The authors previously reported that moderate hyperventilation lowered global hemispheric CBF to 25 ml/100 g/min but did not alter CMRO2. In the present study they sought to determine if hyperventilation lowers CBF below the ischemic threshold of 18 to 20 ml/100 g/min in any brain region and if those reductions cause energy failure (defined as a fall in CMRO2). Methods. Two groups of patients were studied. The moderate hyperventilation group (nine patients) underwent hyperventilation to PaCO2 of 30 ± 2 mm Hg early after TBI, regardless of intracranial pressure (ICP). The severe hyperventilation group (four patients) underwent hyperventilation to PaCO2 of 25 ± 2 mm Hg 1 to 5 days postinjury while ICP was elevated (20–30 mm Hg). The ICP, mean arterial blood pressure, and jugular venous O2 content were monitored, and cerebral perfusion pressure was maintained at 70 mm Hg or higher by using vasopressors when needed. All data are given as the mean ± standard deviation unless specified otherwise. The moderate hyperventilation group was studied 11.2 ± 1.6 hours (range 8–14 hours) postinjury, the admission Glasgow Coma Scale (GCS) score was 5.6 ± 1.8, the mean age was 27 ± 9 years, and eight of the nine patients were men. In the severe hyperventilation group, the admission GCS score was 4.3 ± 1.5, the mean age was 31 ± 6 years, and all patients were men. Positron emission tomography measurements of regional CBF, cerebral blood volume, CMRO2, and oxygen extraction fraction (OEF) were obtained before and during hyperventilation. In all 13 patients an automated search routine was used to identify 2.1-cm spherical nonoverlapping regions with CBF values below thresholds of 20, 15, and 10 ml/100 g/min during hyperventilation, and the change in CMRO2 in those regions was determined. In the regions in which CBF was less than 20 ml/100 g/min during hyperventilation, it fell from 26 ± 6.2 to 13.7 ± 1 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.59 (p < 0.0001), and CMRO2 was unchanged (1.12 ± 0.29 compared with 1.14 ± 0.03 ml/100 g/min; p = 0.8). In the regions in which CBF was less than 15 ml/100 g/min during hyperventilation, it fell from 23.3 ± 6.6 to 11.1 ± 1.2 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.63 (p < 0.0001), and CMRO2 was unchanged (0.98 ± 0.19 compared with 0.97 ± 0.23 ml/100 g/min; p = 0.92). In the regions in which CBF was less than 10 ml/100 g/min during hyperventilation, it fell from 18.2 ± 4.5 to 8.1 ± 0 ml/100 g/min (p < 0.0001), OEF rose from 0.3 to 0.71 (p < 0.0001), and CMRO2 was unchanged (0.78 ± 0.26 compared with 0.84 ± 0.32 ml/100 g/min; p = 0.64). Conclusions. After severe TBI, brief hyperventilation produced large reductions in CBF but not energy failure, even in regions in which CBF fell below the threshold for energy failure defined in acute ischemia. Oxygen metabolism was preserved due to the low baseline metabolic rate and compensatory increases in OEF; thus, these reductions in CBF are unlikely to cause further brain injury.

Management guided by brain tissue oxygen monitoring and outcome following severe traumatic brain injury

2009 ◽  
Vol 111 (4) ◽  
pp. 644-649 ◽  
Author(s):  
Ross P. Martini ◽  
Steven Deem ◽  
N. David Yanez ◽  
Randall M. Chesnut ◽  
Noel S. Weiss ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mortality Rate ◽  
Hospital Mortality ◽  
Brain Tissue ◽  
Resource Utilization ◽  
Hospital Length Of Stay ◽  
Icp Monitoring ◽  
Tissue Oxygen ◽  
Brain Tissue Oxygen

Object The authors sought to describe changes in clinical management associated with brain tissue oxygen (PbO2) monitoring and how these changes affected outcomes and resource utilization. Methods The cohort study comprised 629 patients admitted to a Level I trauma center with a diagnosis of severe traumatic brain injury over a period of 3 years. Hospital mortality rate, neurological outcome, and resource utilization of 123 patients who underwent both PbO2 and intracranial pressure (ICP) monitoring were compared with the same measures in 506 patients who underwent ICP monitoring only. The main outcomes were hospital mortality rate, functional independence at hospital discharge, duration of mechanical ventilation, hospital length of stay, and hospital cost. Multivariable regression with robust variance was used to estimate the adjusted differences in the main outcome measures between patient groups. The models were adjusted for patient age, severity of injury, and pathological features seen on head CT scan at admission. Results On average, patients who underwent ICP/PbO2 monitoring were younger and had more severe injuries than patients who received ICP monitoring alone. Relatively more patients treated with PbO2 monitoring received osmotic therapy, vasopressors, and prolonged sedation. After adjustment for baseline characteristics, the hospital mortality rate was, if anything, slightly higher in patients undergoing PbO2-guided management than in patients monitored with ICP only (adjusted mortality difference 4.4%, 95% CI −3.9 to 13%). Patients who underwent PbO2-guided management also had lower adjusted functional independence scores at hospital discharge (adjusted score difference −0.75, 95% CI −1.41 to −0.09). There was a 27% relative increase (95% CI 6–53%) in the median hospital length of stay when the PbO2 group was compared with the ICP-only group. Conclusions The mortality rate in patients with traumatic brain injury whose clinical management was guided by PbO2 monitoring was not reduced in comparison with that in patients who received ICP monitoring alone. Brain tissue oxygen monitoring was associated with worse neurological outcome and increased hospital resource utilization.

The predictive value of catecholamines in assessing outcome in traumatic brain injury

1987 ◽  
Vol 66 (6) ◽  
pp. 875-882 ◽  
Author(s):  
Paul D. Woolf ◽  
Robert W. Hamill ◽  
Louyse A. Lee ◽  
Christopher Cox ◽  
Joseph V. McDonald
Keyword(s):  
Patient Outcome ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Plasma Norepinephrine ◽  
Content Type ◽  
Ventilatory Assistance ◽  
Traumatically Brain Injured ◽  
Gcs Score ◽  
Length Of Hospitalization ◽  
Fine Print

✓ Because of the central role of the sympathetic nervous system in mediating the stress response, plasma norepinephrine (NE), epinephrine (E), and dopamine (DA) levels were measured in 61 traumatically brain-injured patients to determine whether catecholamine (CA) levels obtained within 48 hours after injury provide reliable prognostic markers of outcome. Patient outcome was determined at 1 week using the Glasgow Coma Scale (GCS) and at the time of discharge using the Glasgow Outcome Scale (GOS). Levels of NE, E, and DA correlated highly with the admission GCS score (NE: r = 0.58, p < 0.0001; E: r = 0.46, p < 0.0025; DA: r = 0.27, p < 0.04). Moreover, in the 21 patients with GCS scores of 3 or 4 on admission, NE levels predicted outcome at 1 week. All six patients with NE levels less than 900 pg/ml (normal level less than 447 pg/ml) improved to GCS scores of greater than 11, while 12 of 15 with NE values greater than 900 pg/ml remained with GCS scores of 3 to 6 or died. Levels of E and DA were not as useful. Catecholamine levels also increased significantly as the GOS score worsened. Levels of NE and E were significantly higher in patients who died or remained persistently vegetative than in those with better outcomes. In the 54 patients who survived beyond 1 week, significant correlations were present between the length of hospitalization and NE (r = 0.71, p < 0.0001) and E (r = 0.61, p < 0.0001) levels. Concentrations of NE (r = 0.61, p < 0.0004) and E (r = 0.48, p < 0.01) were also highly correlated with the duration of ventilatory assistance. Analysis of the interactions of CA levels and GCS scores, duration of ventilatory assistance, and length of hospitalization revealed that the CA's either enhanced the reliability of the GCS score or were independent predictors of outcome. Thus, these findings indicate that alterations in circulating CA levels reflect the severity of the neurological insult and provide support for the use of CA measurements as a physiological marker of patient outcome in both the acute and chronic phases of traumatic brain injury.

The outcome of severe closed head injury

1991 ◽  
Vol 75 (Supplement) ◽  
pp. S28-S36 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Theresa Gautille ◽  
Melville R. Klauber ◽  
Howard M. Eisenberg ◽  
John A. Jane ◽  
...  
Keyword(s):  
Head Injury ◽  
Mortality Rate ◽  
Severe Head Injury ◽  
Closed Head Injury ◽  
Data Bank ◽  
Content Type ◽  
Severity Of Injury ◽  
Gcs Score ◽  
Fine Print ◽  
Overall Mortality

✓ The outcome of severe head injury was prospectively studied in patients enrolled in the Traumatic Coma Data Bank (TCDB) during the 45-month period from January 1, 1984, through September 30, 1987. Data were collected on 1030 consecutive patients admitted with severe head injury (defined as a Glasgow Coma Scale (GCS) score of 8 or less following nonsurgical resuscitation). Of these, 284 either were brain-dead on admission or had a gunshot wound to the brain. Patients in these two groups were excluded, leaving 746 patients available for this analysis. The overall mortality rate for the 746 patients was 36%, determined at 6 months postinjury. As expected, the mortality rate progressively decreased from 76% in patients with a postresuscitation GCS score of 3 to approximately 18% for patients with a GCS score of 6, 7, or 8. Among the patients with nonsurgical lesions (overall mortality rate, 31%), the mortality rate was higher in those having an increased likelihood of elevated intracranial pressure as assessed by a new classification of head injury based on the computerized tomography findings. In the 276 patients undergoing craniotomy, the mortality rate was 39%. Half of the patients with acute subdural hematomas died — a substantial improvement over results in previous reports. Outcome differences between the four TCDB centers were small and were, in part, explicable by differences in patient age and the type and severity of injury. This study describes head injury outcome in four selected head-injury centers. It indicates that a mortality rate of approximately 35% is to be expected in such patients admitted to experienced neurosurgical units.

Sign in / Sign up

Export Citation Format

Share Document