Brain Resuscitation Research Articles

Cooling strategies and transport theories for brain hypothermia resuscitation

The brain is one of the most important organs in a biological body whose normal function depends heavily on an uninterrupted delivery of oxygen. Unlike skeletal muscles that can survive for hours without oxygen, neuron cells in the brain are easily subjected to an irreversible damage within minutes from the onset of oxygen deficiency. With the interruption of cardiopulmonary circulation in many cardiac surgical procedures or accidental events leading to cerebral circulation arrest, an imbalance between energy production and consumption will occur which causes a rapid depletion of oxygen due to the interrupted blood-flow to the brain. Meanwhile, the cooling function of the blood flow on the hot tissue will be stopped, while metabolic heat generation in the tissues still keeps running for awhile. Under such adverse situations, the potential for cerebral protection through hypothermia has been intensively investigated in clinics by lowering brain temperature to restrain the cerebral oxygen demands. The reason can be attributed to the decreased metabolic requirements of the cold brain tissues, which allows a longer duration for the brain to endure reduced oxygen delivery. It is now clear that hypothermia would serve as the principal way for neurologic protection in a wide variety of emergency medicines, especially in cerebral damage, anoxia, circulatory arrest, respiratory occlusion, etc. However, although brain cooling has been found uniquely significant in clinical practices, the serious lack of knowledge on the mechanisms involved prevents its further advancement in brain resuscitation. Compared with the expanded trials in clinics, only very limited efforts were made to probe the engineering issues involved, which turns out to be a major obstacle for the successful operation of brain hypothermia resuscitation. From the viewpoint of biothermal medical engineering, the major theories and strategies for administering brain cooling can generally be classified into three categories: heat transfer, oxygen transport and cooling strategy. Aiming to provide a complete overview of the brain hypothermia resuscitation, this article comprehensively summarizes the recent progresses made in theoretical, practical and experimental techniques in the area. Particularly, attention is paid to the mathematical models to quantify the heat and oxygen transport inside the cerebral tissues. Typical cooling strategies to effectively lower brain temperature and thus decrease oxygen consumption rate in the cerebral tissues are analyzed. Approaches to deliver oxygen directly to the target tissues are discussed. Meanwhile, some future efforts worth pursuing within the area of brain cooling are suggested.

Conventional neurocritical care and cerebral oxygenation after traumatic brain injury

Control of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is the foundation of traumatic brain injury (TBI) management. In this study, the authors examined whether conventional ICP- and CPP-guided neurocritical care ensures adequate brain tissue O2 in the first 6 hours after resuscitation. Resuscitated patients with severe TBI (Glasgow Coma Scale score < or = 8 and Injury Severity Scale score > or = 16) who were admitted to a Level I trauma center and who underwent brain tissue O2 monitoring within 6 hours of injury were evaluated as part of a prospective observational database. Therapy was directed to maintain an ICP of 25 mm Hg or less and a CPP of 60 mm Hg or higher. Data from a group of 25 patients that included 19 men and six women (mean age 39 +/- 20 years) were examined. After resuscitation, ICP was 25 mm Hg or less in 84% and CPP was 60 mm Hg or greater in 88% of the patients. Brain O2 probes were allowed to stabilize; the initial brain tissue O2 level was 25 mm Hg or less in 68% of the patients, 20 mm Hg or less in 56%, and 10 mm Hg or less in 36%. Nearly one third (29%) of patients with ICP readings of 25 mm Hg or less and 27% with CPP levels of 60 mm Hg or greater had severe cerebral hypoxia (brain tissue O2 < or = 10 mm Hg). Nineteen patients had both optimal ICP (< 25 mm Hg) and CPP (> 60 mm Hg); brain tissue O2 was 20 mm Hg or less in 47% and 10 mm Hg or less in 21% of these patients. The mortality rate was higher in patients with reduced brain tissue O2. Brain resuscitation based on current neurocritical care standards (that is, control of ICP and CPP) does not prevent cerebral hypoxia in some patients. This finding may help explain why secondary neuronal injury occurs in some patients with adequate CPP and suggests that the definition of adequate brain resuscitation after TBI may need to be reconsidered.

Manual Chest Compression vs Use of an Automated Chest Compression Device During Resuscitation Following Out-of-Hospital Cardiac Arrest

High-quality cardiopulmonary resuscitation (CPR) may improve both cardiac and brain resuscitation following cardiac arrest. Compared with manual chest compression, an automated load-distributing band (LDB) chest compression device produces greater blood flow to vital organs and may improve resuscitation outcomes. To compare resuscitation outcomes following out-of-hospital cardiac arrest when an automated LDB-CPR device was added to standard emergency medical services (EMS) care with manual CPR. Multicenter, randomized trial of patients experiencing out-of-hospital cardiac arrest in the United States and Canada. The a priori primary population was patients with cardiac arrest that was presumed to be of cardiac origin and that had occurred prior to the arrival of EMS personnel. Initial study enrollment varied by site, ranging from late July to mid November 2004; all sites halted study enrollment on March 31, 2005. Standard EMS care for cardiac arrest with an LDB-CPR device (n = 554) or manual CPR (n = 517). The primary end point was survival to 4 hours after the 911 call. Secondary end points were survival to hospital discharge and neurological status among survivors. Following the first planned interim monitoring conducted by an independent data and safety monitoring board, study enrollment was terminated. No difference existed in the primary end point of survival to 4 hours between the manual CPR group and the LDB-CPR group overall (N = 1071; 29.5% vs 28.5%; P = .74) or among the primary study population (n = 767; 24.7% vs 26.4%, respectively; P = .62). However, among the primary population, survival to hospital discharge was 9.9% in the manual CPR group and 5.8% in the LDB-CPR group (P = .06, adjusted for covariates and clustering). A cerebral performance category of 1 or 2 at hospital discharge was recorded in 7.5% of patients in the manual CPR group and in 3.1% of the LDB-CPR group (P = .006). Use of an automated LDB-CPR device as implemented in this study was associated with worse neurological outcomes and a trend toward worse survival than manual CPR. Device design or implementation strategies require further evaluation. clinicaltrials.gov Identifier: NCT00120965.

Dose-dependent neuroprotection by 17β-estradiol after cardiac arrest and cardiopulmonary resuscitation

Despite recent advances in the treatment of cardiac arrest, neurologic outcome remains poor. 17beta-Estradiol (E2) has been widely shown to reduce damage after experimental brain injury. The present study determined whether E2 also improves neuronal survival after experimental cardiac arrest and cardiopulmonary resuscitation and if any protection is dose-dependent. A randomized trial. A research laboratory. Male C57Bl/6 mice weighing 20-25 g. Mice were randomized into one of six groups, receiving treatment with 0.5, 2.5, 12.5, 25, or 50 mug of E2 or vehicle 1.5 mins after return of spontaneous circulation. Ten minutes after induction of cardiac arrest (by KCl injection), cardiopulmonary resuscitation was initiated (with chest compressions, intravenous epinephrine, and ventilation with 100% O2). Additional animals of each E2-treated group were used for plasma estradiol-level analysis. Brains were removed for quantification of injury in the hippocampus and caudoputamen on day 3. The E2 0.5 group had physiologic estrogen levels 60 min after injection (mean +/- se, 28 +/- 5 pg/mL), whereas the E2 50 group still showed supraphysiologic levels 360 min after administration (245 +/- 32 pg/mL). Hippocampal damage was not altered with E2 treatment. Only posttreatment with the lowest E2 dose (E2 0.5) resulted in attenuated neuronal injury in the rostral and caudal caudoputamen (34 +/- 11% and 27 +/- 11%), in comparison with vehicle (68 +/- 5, p < .05; 63 +/- 4%, p < .001). Higher E2 doses did not affect brain injury. We conclude that E2 has a critical dosing effect on neuronal survival, physiologic levels of E2 are neuroprotective after cardiac arrest/cardiopulmonary resuscitation, and acute exposure is sufficient for brain resuscitation.

Does Blood Ammonia Level at Time of Initial Treatment Predict the Outcome of Patients in Cardiopulmonary Arrest on Arrival?

Recently, comprehensive medical care is being promoted for when resuscitation is performed on patients in cardiopulmonary arrest on arrival (CPAOA), with an emphasis on not only cardiac resuscitation but also on brain resuscitation. When a patient in CPAOA is transported to hospital, how the arrest occurred and how much time has elapsed from the onset of arrest are frequently unknown. Even in witnessed CPA cases, the time elapsed since CPA is often incorrect, and this information is especially important. In this study, we examined an objective index to enable estimation of the time elapsed from the onset of CPA to the arrival at hospital where emergency management was performed. We studied 225 patients with witnessed intrinsic cardiogenic out-of-hospital CPA (128 male and 97 female) who were transported to our hospital during the period from April 1996 to March 2003. We statistically analyzed the correlation between the blood ammonia level at the time of the initial management and the time elapsed from confirmation of CPA to arrival at the hospital (CPA-arrival time). There was a positive correlation between the blood ammonia level at the time of initial management and the CPA-arrival time. Patients who made a full recovery showed a significantly lower blood ammonia level at the time of initial management than those who did not make a full recovery. Also, many patients whose blood ammonia level was less than 180μg/dl at the time of initial management were able to make a full recovery. Based on these results, we conclude that the blood ammonia level can potentially be used as a useful index for estimating the time elapsed since CPA and the neurological prognosis including brain resuscitation.

Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate during cardiopulmonary resuscitation

The use of sodium bicarbonate (SB) in cardiopulmonary resuscitation (CPR) is controversial. This study analyzes the effects of SB use on CPR outcome in the Brain Resuscitation Clinical Trial III (BRCT III), which was a multicenter randomized trial comparing high-dose to standard-dose epinephrine during CPR. Sodium bicarbonate use in BRCT III was optional. The entire BRCT III database was reviewed. Analysis included only patients who arrested out of the hospital and whose time from collapse to initiation of ACLS was no longer than 30 min (total n = 2122 patients). Sodium bicarbonate use by the 16 participating study sites was analyzed. The study sites were divided according to their SB usage profile: 'low SB user' sites administered SB in less than 50% of CPRs and their first epinephrine to SB time exceeded 10 min; and 'high SB user' sites used SB in over 50% of CPRs and their first epinephrine to SB time was <10 min. Sites' SB usage rates ranged between 3.1% and 98.2% of CPRs. Sodium bicarbonate usage rates correlated inversely with the sites' intervals from collapse (r = - 0.579 P = 0.018) from initiation of ACLS (r = - 0.685 P = 0.003) and from first epinephrine (r = - 0.611 P = 0.012) to SB administration. Mean ROSC rate in the 'high SB user' sites was 33.5% (CI = 30.0-37.0) compared to 25.7% (CI = 23.1-28.4) in the 'low SB user' sites. In the 'high SB user' sites, hospital discharge rate was 5.3% (CI = 3.6-7.0) compared to 3% (CI = 2.0-4.0) in the 'low SB user' sites, and 5.3% (CI = 3.6-7.0) had a favorable neurological outcome compared to 2.1% (CI = 1.2-3.0) in the 'low SB user' sites. Collapse to ACLS interval was 8.5 min (CI = 8.1-9.0) in the 'high SB user' sites compared to 10.2 min (CI = 9.8-10.6) in the 'low SB user' sites, and their ACLS to first epinephrine interval was 7.0 min (CI = 6.5-7.5) compared to 9.7 min (CI = 9.3-10.2). Multivariate regression analysis found that belonging to 'high SB user' sites independently increased the chances for ROSC (OR 1.36, CI 1.08-1.7) and for achieving a good neurological outcome (OR 2.18, CI 1.23-3.86). Earlier and more frequent use of SB was associated with higher early resuscitability rates and with better long-term outcome. Sodium bicarbonate may be beneficial during CPR, and it should be subjected to a randomized clinical trial.

Hypertonic saline solutions in brain injury.

Hypertonic saline solutions have received renewed attention as effective agents for the treatment of cerebral edema and in brain resuscitation in a variety of brain injury paradigms. Although evidence of the beneficial action of hypertonic saline solutions in traumatic brain injury is robust, data supporting use in other conditions are only now mounting. Osmotic properties of hypertonic saline solutions have been well studied in laboratory-based studies in animal models and in patients with acute brain injury. There are, in addition, emerging data on the extraosmotic actions on brain pathophysiology. This review cites baseline literature and provides new evidence of actions of hypertonic saline solutions: (a). in augmenting cerebral blood flow after subarachnoid hemorrhage, (b). as an antiinflammatory adjunct, and (c). utility in chemonucleolysis for intervertebral disc disease and treatment of seizures associated with severe hyponatremia. Brain injury from diverse etiologies including trauma, ischemic stroke, global cerebral ischemia from cardiac arrest, intraparenchymal or subarachnoid hemorrhage, infection, or toxic-metabolic derangements are commonly encountered in the clinical setting. Many of these conditions are associated with cerebral edema with or without elevated intracranial pressure. Osmotherapy constitutes the cornerstone of medical therapy for such patients. Hypertonic saline solutions have received renewed attention in clinical practice as osmotic agents for cerebral resuscitation. This article reviews experimental and clinical evidence of the efficacy of hypertonic saline solutions and elaborates on their use in patients with acute neurologic injury. Important areas for current and future research are highlighted before the use of hypertonic saline solutions can be accepted for widespread use.

Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest

Longstreth WT Jr, Fahrenbruch CE, Olsufka M, et al (University of Washington, Seattle, WA; Seattle Fire Department, Seattle, WA) Cardiopulmonary resuscitation (CPR) can be lifesaving for patients with life-threatening cardiac arrhythmias, but many will survive with poor neurologic outcomes. Magnesium and diazepam have been studied as possible treatments to enhance neurologic outcomes after cardiac arrest. Both treatments have shown encouraging results in animals, perhaps by protecting the brain from excitotoxicity. The effects of magnesium and diazepam, alone or in combination, on neurologic outcomes after out-of-hospital cardiac arrest were evaluated. The randomized controlled trial included 300 patients with out-of-hospital cardiac arrest evaluated by Seattle paramedics. All patients had regained a systolic blood pressure of 90 mm Hg or higher and had not yet awakened. Immediately after resuscitation, the patients received intravenous injections of magnesium 2 g or placebo, then 10 mg of intravenous diazepam or placebo. The 4 groups were compared for the percentage of patients awakening, defined as following commands or speaking comprehensibly. Three-month outcomes were assessed by record review and telephone interviews. A federal waiver of informed consent was obtained for the study. Despite randomization procedures, there were significant differences among groups, with patients receiving diazepam being more severely ill than those receiving placebo. Overall, 36% of the patients awakened at any time during the 3-month follow-up period after cardiac arrest. After adjustment for baseline characteristics, this outcome was not significantly different between groups. Adjusted rates of independent functioning were also similar between groups. There were no significant interactions, and no apparent adverse effects of treatment. For patients with out-of-hospital arrest, treatment with magnesium, diazepam, or both after resuscitation does not appear to improve neurologic outcomes. Rates of awakening or functional independence are not significantly different among patients receiving these treatments, after adjustment for baseline characteristics. Further studies are needed to identify effective approaches to “brain resuscitation.”

Reanimación cerebro-cardio-pulmonar del paciente adulto en el servicio de urgencias: Protocolo de atención en un hospital de tercer nivel, E.S.E.

La presente investigación se realizó para determinar las actividades que ejecuta el equipo interdisciplinario del servicio de urgencias de un hospital de tercer nivel durante el proceso de reanimación de un paciente adulto. Se recolectó información de una muestra de 38 personas por medio de la aplicación de una encuesta y lista de chequeo. Los resultados obtenidos con la aplicación de los instrumentos informan que en dicho servicio existe una sala exclusiva para reanimación cerebro cardio-pulmonar, que los medicamentos y elementos para llevar a cabo el proceso de reanimación son suficientes y que participan de dos a cuatro personas lideradas por el médico. Es importante resaltar que durante la recolección de los datos se detectó que en esta institución no se realiza educación continuada ni entrenamiento sobre el proceso de reanimación, por lo cual fue necesario diseñar y socializar un protocolo que sirva como modelo de organización y funcionamiento para llevar a cabo el proceso de reanimación cerebro cardio-pulmonar y así fortalecer los conocimientos previos, experiencia y habilidades del equipo interdisciplinario. El protocolo de reanimación cerebro cardio-pulmonar contiene bases teóricas sobre paro cardio-respiratorio, los tipos de reanimación, la fisiopatología del paro cardio-respiratorio, los pasos a seguir en el proceso de reanimación básica y avanzada, con la asignación de actividades que debe realizar cada uno de los integrantes del equipo interdisciplinario, para llevar a cabo una reanimación exitosa.

Numerical studies on the effect of lowering temperature on the oxygen transport during brain hypothermia resuscitation

There have been arguments about the advantage and shortcoming of hypothermia on the brain resuscitation during circulation arrest. People usually accepted that hypothermia may decrease the cerebral oxygen demands, which is beneficial for the patient to sustain longer time when subjected to a hypoxia. However, there are also quite a few disputes claiming that the blood viscosity would increase with the reduction of temperature, which may lead to an increase of cerebral vascular resistance and thus worsen the hypoxia state. To resolve this critical issue, a heat transfer model was established to characterize the thermal response of brain tissue during hypothermia resuscitation. Combined with this model, a compartmental model taking account of the temperature effect was further developed to analyze the transient oxygen partial pressure ( PO 2) distribution over the successive branches of the vascular network during circulation arrest. Using the morphological and physiological data of a sheep brain, effects of lowering temperature on the oxygen consumption dynamics were studied. Calculations indicated that the lower the temperature, the slower the decreasing rate for the PO 2. Although immediately lowering the brain temperature may induce an evident increase in blood viscosity and subsequently a decrease in blood flow rate, which is responsible for oxygen delivery, it seems to always result in a monotonic increase of PO 2. The results show a good qualitative accord with the experimental data. They also present better understanding on the transient oxygen transport in brain hypothermia during circulation arrest.

Clinical use of sodium bicarbonate during cardiopulmonary resuscitation—is it used sensibly?

This study retrospectively analyzed the pattern of sodium bicarbonate (SB) use during cardiopulmonary resuscitation (CPR) in the Brain Resuscitation Clinical Trial III (BRCT III). BRCT III was a prospective clinical trial, which compared high-dose to standard-dose epinephrine during CPR. SB use was left optional in the study protocol. Records of 2915 patients were reviewed. Percentage, timing and dosage of SB administration were correlated with demographic and cardiac arrest variables and with times from collapse to Basic Life Support, to Advanced Cardiac Life Support (ACLS) and to the major interventions performed during CPR. SB was administered in 54.5% of the resuscitations. The rate of SB use decreased with increasing patient age—primarily reflecting shorter CPR attempts. Mean time intervals from arrest, from start of ACLS and from first epinephrine to administration of the first SB were 29±16, 19±13, and 10.8±11.1 min, respectively. No correlation was found between the rate of SB use and the pre-ACLS hypoxia times. On the other hand, a direct linear correlation was found between the rate of SB use and the duration of ACLS. We conclude that when SB was used, the time from initiation of ACLS to administration of its first dose was long and severe metabolic acidosis probably already existed at this point. Therefore, if SB is used, earlier administration may be considered. Contrary to physiological rationale, clinical decisions regarding SB use did not seem to take into consideration the duration of pre-ACLS hypoxia times. We suggest that guidelines for SB use during CPR should emphasize the importance of pre-ACLS hypoxia time in contributing to metabolic acidosis and should be more specific in defining the duration of ‘protracted CPR or long resuscitative efforts’, the most frequent indication for SB administration.

Role of calcineurin and immunophilin on ischemic brain damage and new approach for the brain resuscitation

Role of calcineurin and immunophilin on ischemic brain damage and new approach for the brain resuscitation

A limited interval of delayed modest hypothermia for ischemic brain resuscitation is not beneficial in neonatal swine.

This investigation determined if a short interval of modest hypothermia (1 h) initiated 30 min after brain ischemia provided neuroprotection. The rationale for the time and duration of brain cooling reflects the likelihood that the implementation of neuroprotective strategies will occur at an interval shortly after ischemia, and that long-term maintenance of normothermia is a cornerstone of neonatal stabilization. Studies were performed in 22 ventilated neonatal mini-swine in a superconducting magnet to obtain 31P magnetic resonance spectra. After a control period all animals underwent 15 min of global brain ischemia and were maintained normothermic for the first 30 min post-ischemia. In one group of 11 swine normothermia was continued. In the other group of 11 swine, modest hypothermia was initiated at 30 min post-ischemia, continued for 1 h and followed by resumption of normothermia. Animals were subsequently weaned from ventiltor support, removed from the magnet, and underwent neurobehavioral and histologic assessment at 72 h post-ischemia. Both groups had similar severity of ischemia, as indicated by identical changes in arterial blood pressure and pH, alterations in brain beta-nucleotide triphosphate (% of control where control = 100%, 32 +/- 28 vs 27 +/- 26% for normothermic and hypothermic groups, respectively), and the extent of intraischemic brain acidosis (6.13 +/- 0.19 vs 6.14 +/- 0.14 for normothermic and hypothermic groups, respectively). In both groups the distribution of stages of encephalopathy were the same: 1 normal and 10 abnormal (4 mild, 2 moderate, and 4 severe) normothermic, and, 3 normal and 8 abnormal (4 mild, 2 moderate, and 2 severe) hypothermic animals. There was no difference in the extent of neuronal injury between groups. We conclude that a 1-h interval of modest hypothermia initiated at 30 min post-ischemia does not confer neuroprotection.

Acute stroke units

In December of 1996, the National Institute of Neurological Disorders and Stroke (NINDS) sponsored a national symposium on Rapid Identification and Treatment of Acute Stroke. 1 One of the basic messages taken from this meeting was that every hospital that cares for patients with acute stroke needs a stroke plan. This plan should cover stroke care from prehospital recognition through rehabilitation and recovery and should also address secondary prevention issues. During the acute phase of stroke, an acute stroke unit (ASU) provides the necessary infrastructure for optimal care of stroke patients delivered by a multidisciplinar y team. An ASU serves as a critical link in the continuum of care by providing the necessary setting in which to continue the emergency brain resuscitation efforts 2 begun in the emergency department (ED). In an ASU, stroke critical pathways facilitate an efficient diagnostic evaluation for stroke patients and help execute timely decisions regarding management issues and disposition plans. Generally, standard hospital delivery systems for acute stroke care are inadequate compared with systems for state-of~the-art emergency cardiac care. The ASU was initially developed in the 1960s to try to replicate the success of coronary care units. 3 The mission of ASU care has changed over the past three decades. The initial goal of reduction in mortality was deemphasized because there was no proven effective treatment for this complicated and often devastating disorder. Instead, ASU care evolved into a multidisciplinar y team approach to stroke diagnosis, aggressive management of the neurological and medical complications of stroke, secondary prevention of stroke, patient and family education, and early involvement of rehabilitation specialists and services.

International Trauma Anesthesia and Critical Care Society (ITACCS)

International Trauma Anesthesia and Critical Care Society (ITACCS)

脳蘇生の進歩

脳蘇生の進歩

Research Connections

The purpose of this research utilization article is to familiarize cardiovascular nurses with the Brain Resuscitation Clinical Trials (BRCTs) I and II and discuss the application of these trials to nursing practice. The BRCTs are a series of studies that examine the effects of selected interventions on neurologic outcome after cardiac arrest.

P-78 Brain resuscitation by Osmo-/Onkotherapy: Effects on systemic and cerebral blood-flow in patients with increased intracranial pressure

P-78 Brain resuscitation by Osmo-/Onkotherapy: Effects on systemic and cerebral blood-flow in patients with increased intracranial pressure

Head trauma and brain resuscitation

Traumatic brain injury causes death or prolonged disability in an unacceptably high number of patients. Although primary brain injury, that is, neurologic tissue structurally damaged by trauma, cannot be improved therapeutically at present, secondary brain injury, that is, injury produced by subsequent hypotension, hypoxia, or intracranial hypertension, can potentially be improved or avoided. Effective systemic resuscitation, currently achievable, is one key to reducing secondary injury.

Hypertonic saline improves brain resuscitation in a pediatric model of head injury and hemorrhagic shock

Introduction: Brain injury accompanied by hypovolemic shock is a frequent cause of death in multiply injured children. Hypertonic saline (HTS) has been shown to return hemodynamics to normal in adult models, without increasing intracranial pressure (ICP) as seen with crystalloids. To assess fluid resuscitation, the authors evaluated HTS versus lactated Ringer's solution (LR) with respect to hemodynamics and cerebrovascular hemoglobin oxygen saturation (Sco 2 in anesthetized, head-injured, 1-month-old piglets. Methods: Group 1 (n =6) was studied for 3.5 hours after a cryogenic brain injury and no shock. Groups 2 and 3 had cryogenic brain injury followed by hemorrhagic shock, in which mean arterial pressure (MAP) was reduced to 40 to 50 mm Hg and maintained for 30 minutes. Group 2 (n = 5) was then resuscitated with 1 mL of 7.5% HTS per 1 mL of blood loss. Group 3 (n = 6) was resuscitated with 3 mL of LR per 1 mL of blood loss. Sco 2 was determined by near-infrared spectroscopy in the injured region of the brain. All data were analyzed using analysis of variance with repeated measures. Results: MAP, ICP, temperature, serum sodium, and cardiac output (CO) were similar in all groups during baseline and between groups 2 and 3 during shock. After resuscitation, MAP, CO, and core temperature were similar in all three groups, and serum sodium was increased in the HTS group (by 29%). Sco 2 increased transiently after cryogenic injury in all groups, then gradually decreased to below baseline. After shock, Sco 2 decreased precipitously in groups 2 and 3. After resuscitation, Sco 2 was different in the two resuscitation groups, increasing in the HTS group, above baseline values, but remaining below baseline values in the LR group ( P < .002). ICP was lowered by HTS resuscitation and increased by LR resuscitation ( P < .002). Conclusion: In our model of head injury and shock, resuscitation with either HTS or LR restored MAP and CO to control levels. However, during shock, the injured brain was severely deoxygenated, and administration of HTS restored cerebral oxygenation whereas LR did not, reflecting improved cerebral resuscitation by HTS without elevating ICP. The data suggest that HTS is a better resuscitation fluid than LR in head-injured children with hemorrhagic shock.