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The goals of this study were to determine the incidence and duration of hypotension and hypoxia in the prehospital setting in patients with potentially survivable brain injuries, and to prospectively examine the association of these secondary insults with mortality and disability at hospital discharge.Trauma patients with suspected brain injuries underwent continuous blood pressure and pulse oximetry monitoring during helicopter transport. Postadmission inclusion criteria were (1) diagnosis of acute traumatic brain injury (TBI) confirmed by computed tomography (CT) scan, operative findings, or autopsy findings; and (2) Head Abbreviated Injury Scale (AIS) score ofor = 3 or Glasgow Coma Scale (GCS) score ofor = 12 within the first 24 hours of admission. Patients were excluded with (1) no abnormal intracranial findings on the patient's CT scan; (2) determination of a nonsurvivable injury (based on an AIS score of 6 for any body region; or, (3) death in less than 12 hours after injury. Primary outcome measures included mortality and Disability Rating Scale score at discharge.We enrolled 150 patients into the study. Fifty-seven patients had at least one secondary insult; 37 had only hypoxic episodes, 14 had only hypotensive episodes, and 6 patients had both. Demographics and injury characteristics did not differ between those with and those without secondary insults. The mortality for patients without secondary insults was 20%, compared with 37% for patients with hypoxic episodes, 8% for patients with hypotensive episodes, and 24% for patients with both. The Disability Rating Scale score at discharge was significantly higher in patients with secondary insults. Using multivariate analysis, the calculated odds ratio of mortality caused by prehospital hypoxia after head injury was 2.66 (p0.05).Secondary insults after TBI are common, and these insults are associated with disability. Hypoxia in the prehospital setting significantly increases the odds of mortality after brain injury controlled for multiple variables.

Background: Age has been shown to be a primary determinant of survival following isolated traumatic brain injury (TBI). We have previously reported that patients ≥65 years who survived mild TBI have decreased functional outcome at 6 months compared with younger patients. The purpose of this study was to further investigate the effect of age on outcome at 1 year in all patients surviving isolated TBI. Methods: The Western Trauma Association multicenter prospective study included all patients sustaining isolated TBI defined as Abbreviated Injury Scale score for Head ≥ 3 with an Abbreviated Injury Scale score in any other body area £ 1. Outcome data included discharge disposition, Glasgow Outcome Scale score (1 = dead to 5 = full recovery) and modified Functional Independence Measure (FIM) score measuring feeding, expression, and locomotion (1 = total dependence to 4 = total independence) for each component at discharge and 1 year. Results: In all, 295 patients were enrolled with a follow-up of 82%, resulting in 241 study patients. An additional five patients died from non-TBI causes and were excluded. The mean and median times for the last follow-up in the 236 remaining patients were 307 and 357 days, respectively. Patients were divided into four age ranges: 18 to 29 years (n = 66), 30 to 44 years (n = 54), 45 to 59 years (n = 50), and ≥60 years (n = 65). More severe THIS, as measured by admitting Glasgow Coma Scale (GCS), were observed in the youngest group compared with all others but there were no differences in mean GCS between the remaining three groups. There were no differences in neurosurgical intervention between the groups. Age was a major determinant in the outcome at discharge and last follow-up. Patients over 60 years discharged with a GOS ≤4 were less likely to improve at 1 year than all other groups (37% versus 63 to 85%; p ≤ 0.05). Patients between 18 and 29 years of age had the lowest mean Glasgow Outcome Scale and discharge FIM scores, which correlated with the low admission GCS. Despite the increased severity of TBI, this group had the best FIM score at 1 year. In contrast, patients older than 60 years had the least improvement and had a significantly lower final FEM score at 1 year compared with all other groups. Conclusion: Older patients following isolated TBI have poorer functional status at discharge and make less improvement at 1 year compared with all other patients. These worse outcomes occur despite what appears to be less severe TBI as measured by a higher GCS upon admission. Differences in outcome begin to appear even in patients between 45 and 59 years. Further investigations with more detailed outcome instruments are required to better understand the qualitative limitations of a patient's recovery and to devise strategies to maximize functional improvement following TBL Age is an exceedingly important parameter affecting recovery from isolated TBI.

Elderly patients (aged 60 years and older) have been demonstrated to have an increased mortality after isolated traumatic brain injury (TBI); however, the prognosis of those patients surviving their hospitalization is unknown. We hypothesized that surviving elderly patients would also have decreased functional outcome, and this study examined the functional outcome of patients with isolated TBI at discharge and at 6 months posthospitalization.This was a multicenter prospective study of all patients with isolated moderate to severe TBI defined as Head Abbreviated Injury Scale score of 3 with an Abbreviated Injury Scale score in any other body area of 1. Patients surviving to discharge gave their consent and were enrolled. Data collected included demographics, Glasgow Coma Scale (GCS) score at admission, and neurosurgical interventions. Outcome data included discharge disposition and Glasgow Outcome Scale score and modified Functional Independence Measure (FIM) score at discharge and at 6 months.Two hundred thirty-five patients were enrolled, with 44 (19%) aged greater than or equal to 65 years. Mechanisms of injury were falls (34%), assaults (28%), motor vehicle collisions (14%), pedestrian (11%), and other (12%). Falls were more common in the older patients and assaults in the younger group. The mean admitting GCS score was 12.8 (95% confidence interval [CI], 12.4-13.3), with older patients having a higher mean GCS score, 14.1 (95% CI, 13.6-14.6) versus 12.5 (95% CI, 12.0-13.1; p = 0.03). There were no differences in the percentage of patients admitted to the intensive care unit or requiring neurosurgical intervention between younger and older patients. Because there were few elderly patients with low GCS scores who survived to discharge, outcome measures focused on those patients with GCS scores of 13 to 15. A greater percentage of elderly were discharged to rehabilitation (28% vs. 16%, p =0.08). The mean discharge FIM score was 10.4 (95% CI, 9.8-11.0) for the elderly versus 11.4 (95% CI, 11.1-11.7) for the young (p =0.001), with 68% elderly and 89% young discharged with total independent scores of 11 to 12. At 6 months, the difference narrowed, but the mean FIM score was still greater for the young group, 11.7 (95% CI, 11.6-11.9) versus 11.0 (95% CI, 10.6-11.4; p0.001).Functional outcome after isolated mild TBI as measured by the Glasgow Outcome Scale and modified FIM is generally good to excellent for both elderly and younger patients. Older patients required more inpatient rehabilitation and lagged behind their younger counterparts but continued to recover and improve after discharge. Although there were statistically significant differences in the FIM score at both discharge and 6 months, the clinical importance of these small differences in the mean FIM score to the patient's quality of life is less clear. Measurable improvement in functional status during the first 6 months after injury is observed in both groups. Aggressive management and care of older patients with TBI is warranted, and efforts should be made to decrease inpatient mortality. Continued follow-up is ongoing to determine whether these outcomes persist at 12 months.

Background: The ideal resuscitation fluid for the trauma patient would be readily available to prehospital personnel, universally compatible, effective when given in small volumes, and capable of reversing tissue hypoxia in critical organ beds. Recently developed hemoglobin-based oxygen-carrying solutions possess many of these properties, but their ability to restore tissue oxygen after hemorrhagic shock has not been established. We postulated that a small-volume resuscitation with HBOC-201 (Biopure) would be more effective than either lactated Ringer's (LR) solution or hypertonic saline dextran (HSD) in restoring baseline tissue oxygen tension levels in selected tissue beds after hemorrhagic shock. We further hypothesized that changes in tissue oxygen tension measurements in the deltoid muscle would reflect the changes seen in the liver and could thus be used as a monitor of splanchnic resuscitation. Methods: This study was a prospective, blinded, randomized resuscitation protocol using anesthetized swine (n = 30), and was modeled to approximate an urban prehospital clinical time course. After instrumentation and splenectomy, polarographic tissue oxygen probes were placed into the liver (liver Po 2 ) and deltoid muscle (muscle Po 2 ) for continuous tissue oxygen monitoring. Swine were hemorrhaged to a mean arterial pressure (MAP) of 40 mm Hg over 20 minutes, shock was maintained for another 20 minutes, and then 100% oxygen was administered. Animals were then randomized to receive one of three solutions: LR (12 mL/kg), HSD (4 mL/kg), or HBOC-201 (6 mL/kg). Physiologic variables were monitored continuously during all phases of the experiment and for 2 hours postresuscitation. Results: At a MAP of 40 mm Hg, tissue Po 2 was 20 mm Hg or less in both the liver and muscle beds. There were no significant differences in measured liver or muscle Po 2 values after resuscitation with any of the three solutions in this model of hemorrhagic shock. When comparing the hemodynamic effects of resuscitation, the cardiac output was increased from shock values in all three animal groups with resuscitation, but was significantly higher in the animals resuscitated with HSD. Similarly, MAP was increased by all solutions during resuscitation, but remained significantly below baseline except in the group of animals receiving HBOC-201 (p < 0.01). HBOC-201 was most effective in both restoring and sustaining MAP and systolic blood pressure. There was excellent correlation between liver and deltoid muscle tissue oxygen values (r = 0.8, p < 0.0001). Conclusion: HBOC-201 can be administered safely in small doses and compared favorably to resuscitation with HSD and LR solution in this prehospital model of hemorrhagic shock. HBOC-201 is significantly more effective than HSD and LR solution in restoring MAP and systolic blood pressure to normal values. Deltoid muscle Po 2 reflects liver Po 2 and thus may serve as an index of the adequacy of resuscitation in critical tissue beds.

Objectives: Prophylactic hyperventilation of patients with head injuries worsens outcome, presumably by exacerbating tissue hypoxia. Oxygen tension in brain tissue (P br O 2 ) provides a direct measurement of cerebral metabolic substrate delivery and varies with changing end-tidal carbon dioxide tension (ETCO 2 ) and mean arterial pressure. However, the effects of hyperventilation and hypoventilation on P br O 2 during hemorrhagic shock are not known. The aim of this study was to examine the effects of alteration in ventilation on P br O 2 in hemorrhaged swine. Methods: Clark-type polarographic probes were inserted into the brain tissue of seven swine to measure P br O 2 directly. To examine the effects of alterations in ventilation on hemorrhage-induced hypotension, swine were hemorrhaged to 50% estimated blood volume and P br O 2 was monitored during hyperventilation (RR = 30) and hypoventilation (RR = 4). Results: After the 50% hemorrhage, P br O 2 declined rapidly from 39.8 ± 4.6 mm Hg to 11.4 ± 2.2 mm Hg. Hyperventilation resulted in a further 56% mean decrease in P br O 2 . Hypoventilation produced a 166% mean increase in P br O 2 . These changes were significant (p = 0.001) for absolute and percentage differences from baseline. Conclusion: During hemorrhage, alterations in ventilation significantly changed P br O 2 : hyperventilation increased brain-tissue hypoxia whereas hypoventilation alleviated it. This finding suggests that hyperventilation has deleterious effects on brain oxygenation in patients with hemorrhagic shock and those with head trauma. Conversely, hypoventilation with resultant hypercapnia may actually help resolve hemorrhagic shock-induced cerebral hypoxia.

Objectives: Recently developed polarographic microelectrodes permit continuous, reliable monitoring of oxygen tension in brain tissue (Pbro 2 ), The aim of this study was to investigate the feasibility and utility of directly monitoring Pbro 2 in cerebral tissue during changes in oxygenation or ventilation and during hemorrhagic shock and resuscitation. We also sought to develop a model in which treatment protocols could be evaluated using Pbro 2 as an end point. Methods: Licox Clark-type polarographic probes were inserted in the brain tissue of 16 swine to monitor Pbro 2 . In eight swine, changes in Pbro 2 were observed over a range of fractional concentrations of inspired O 2 (Fio 2 ) as well as during periods of hyperventilation and hypoventilation. In eight other swine, Pbro 2 was monitored during a graded hemorrhage of up to 70% estimated blood volume and during the resuscitation period. Results: When Fio 2 was elevated to 100%, Pbro 2 increased from a baseline of 15 ± 2 mm Hg to 36 ± 11 mm Hg. Hyperventilation while breathing 100% oxygen resulted in a 40% decrease in Pbro 2 (p < 0.05), whereas hypoventilation increased Pbro 2 to 88 mm Hg (p < 0.01). A graded hemorrhage to 50% estimated blood volume significantly reduced Pbro 2 , mean arterial pressure, and intracranial pressure (p < 0.01). Continued hemorrhage to 70% estimated blood volume resulted in a Pbro 2 of 2.9 ± 1.5 mm Hg. After resuscitation, Pbro 2 was significantly elevated, reaching 65 ± 13 mm Hg (p < 0.01), whereas mean arterial pressure and cerebral perfusion pressure simply returned to baseline. Conclusion: Directly measured Pbro 2 was highly responsive to changes in Fio 2 , ventilatory rate, and blood volume in this experimental model. In particular, hypoventilation significantly increased Pbro 2 , whereas hyperventilation had the opposite effect. The postresuscitation increase in Pbro 2 may reflect changes in both O 2 delivery and O 2 metabolism. These experiments set the stage for future investigations of a variety of resuscitation protocols in both normal and injured brain.