Hypothermia and injury

PURPOSE OF REVIEW: Recent studies demonstrating that mild therapeutic hypothermia can improve the outcome from several ischemic and traumatic insults have led to increased interest in the potential benefits of hypothermia after injury. Previous clinical studies, however, have suggested that hypothermia is detrimental to trauma patients. This most likely is a result of differences in the physiologic effects between uncontrolled exposure hypothermia and controlled therapeutic hypothermia. The laboratory and clinical data regarding traumatic hemorrhagic shock and hypothermia are presented, as well as a novel approach to the patient with exsanguinating trauma: suspended animation. Therapeutic hypothermia for traumatic brain injury is discussed. RECENT FINDINGS: Laboratory studies of hemorrhagic shock demonstrate improved survival with mild hypothermia. For the first time, this was shown in a study in a large animal outcome model of hemorrhagic shock with trauma and intensive care. Because clinical studies continue to suggest an association between the development of hypothermia and worse outcomes in trauma patients, clinicians are continuing efforts to prevent and treat hypothermia. For exsanguination cardiac arrest, laboratory studies have demonstrated the feasibility of inducing hypothermic preservation via a rapid aortic flush (suspended animation). For traumatic brain injury, the most recent clinical trial did not show an overall benefit, but it seems that patients who arrive mildly hypothermic have better outcomes if hypothermia is maintained. SUMMARY: The dichotomy between laboratory findings that show a benefit of hypothermia and clinical findings that suggest detrimental effects remains difficult to explain. For now, preventing hypothermia remains prudent. Suspended animation seems promising for patients with exsanguinating trauma. Clinical trials of mild hypothermia during hemorrhagic shock and suspended animation for exsanguination are indicated. Clinical trials of hypothermia for traumatic brain injury are in progress.     

Induced hypothermia in critical care medicine: a review

BACKGROUND: Clinical trials of induced hypothermia have suggested that this treatment may be beneficial in selected patients with neurologic injury. OBJECTIVES: To review the topic of induced hypothermia as a treatment of patients with neurologic and other disorders. DESIGN: Review article. INTERVENTIONS: None. MAIN RESULTS: Improved outcome was demonstrated in two prospective, randomized, controlled trials in which induced hypothermia (33 degrees C for 12-24 hrs) was used in patients with anoxic brain injury following resuscitation from prehospital cardiac arrest. In addition, prospective, randomized, controlled trials have been conducted in patients with severe head injury, with variable results. There also have been preliminary clinical studies of induced hypothermia in patients with severe stroke, newborn hypoxic-ischemic encephalopathy, neurologic infection, and hepatic encephalopathy, with promising results. Finally, animal models have suggested that hypothermia that is induced rapidly following traumatic cardiac arrest provides significant neurologic protection and improved survival. CONCLUSIONS: Induced hypothermia has a role in selected patients in the intensive care unit. Critical care physicians should be familiar with the physiologic effects, current indications, techniques, and complications of induced hyperthermia.     

The effectiveness of early prophylactic hypothermia in adult patients with traumatic brain injury: A systematic review and meta-analysis

ObjectivesPreviously published systematic reviews have explored the effects of therapeutic hypothermia on adult patients with traumatic brain injury (TBI). However, none explored the effect of early prophylactic hypothermia (within 6 h from injury to hypothermia induction). Animal studies indicated that early prophylactic hypothermia may reduce secondary injury and improve neurological outcomes. This systematic review aimed to investigate the effects of early prophylactic hypothermia on adult TBI regarding mortality, favourable outcomes, and complications.Data sourceWe searched electronic databases including Cochrane CENTRAL, PubMed, MEDLINE, CINAHL, EMBASE, Web of Science, OpenGrey, and ClinicalTrials.gov from inception to June 12, 2019. Manual search was conducted for additional information.Review methodsOnly randomised controlled trials were included. The Cochrane Collaboration Risk of Bias Tool was used to assess the quality of included studies. We extracted general demographic characteristics, the initiation timing, methods of cooling, duration, target temperature, rewarming rate, mortality, neurological outcomes, and complications.ResultsSix studies with a total of 1207 participants were included. Meta-analyses showed no significant difference in mortality and favourable outcomes (risk ratio = 1.11, 95% confidence interval = 0.90–1.37, P = 0.32; risk ratio = 1.03, 95% confidence interval = 0.91–1.16, P = 0.65, respectively). Similar results were found regarding different durations of hypothermia and different rewarming rates. Various complications were reported in the included studies. No statistical difference was found in three studies, while complications were reported to be significantly higher in the hypothermia group in the other three studies.ConclusionsThis review does not support the use of early prophylactic hypothermia (within 6 h after injury) as a neurological protection strategy in adult patients with TBI, irrespective of the short term or long term. No significant benefits were found regarding hypothermia with different rewarming rates. Owing to the limited number of studies, more randomised controlled trials with higher quality are required to establish true effects of early hypothermia in adult TBI.     

Therapeutic hypothermia in traumatic brain injury

Traumatic brain injury is a leading cause of death by trauma in adults in the United States and a major contributor to permanent physical, emotional, and psychological disabilities. Therapeutic hypothermia, defined as cooling of the body to less than 36 degrees C, has been shown to decrease mortality and morbidity and improve long-term outcomes by protecting the brain from secondary brain injury. The most commonly seen benefits of hypothermic temperatures of 32 degrees C to 33 degrees C are a significant reduction in intracranial hypertension and improved cerebral perfusion and oxygenation. Although evidence to date is insufficient to recommend the routine use of therapeutic hypothermia outside of the research setting, therapeutic hypothermia is used in multiple healthcare facilities in the world. The following article will define hypothermia and provide critical information necessary to provide care for the critically ill patient under therapeutic hypothermia. It will define the processes of brain injury and how hypothermia is thought to counteract those to protect the brain. Also included is a review of 2 major randomized, controlled trials of hypothermia for traumatic brain injury that have been instrumental in establishing guidelines and directing further research.     

Induced hyperthermia exacerbates neurologic neuronal histologic damage after asphyxial cardiac arrest in rats

BACKGROUND: Temperature is an important modulator of the evolution of ischemic brain injury--with hypothermia lessening and hyperthermia exacerbating damage. We recently reported that children resuscitated from predominantly asphyxial arrest often develop an initial spontaneous hypothermia followed by delayed hyperthermia. The initial hypothermia observed in these children was frequently treated with warming lights which, despite careful monitoring, often resulted in overshoot hyperthermia. We have previously reported in a rat model of asphyxial cardiac arrest that active warming, to prevent spontaneous hypothermia, worsens brain injury. OBJECTIVE: We sought to determine whether delayed induction of hyperthermia would worsen brain injury after asphyxial arrest in rats. DESIGN: Male Sprague-Dawley rats were asphyxiated for 8 mins and resuscitated. An implantable temperature probe was placed into the peritoneum before asphyxia. The probe is a component of a computer-based, radiofrequency, telemetry system (Minimitter, Sunriver, OR) that allowed continuous acquisition and manipulation (via heating and cooling devices) of core (intraperitoneal) body temperature. Body temperature was monitored but not manipulated for the first 24 hrs of recovery. Rats were assigned to: no temperature manipulation (n = 21), induced hyperthermia (40 +/- 0.5 degrees C) for 3 hrs beginning at 24 hrs (n = 21), or induced hyperthermia at 48 hrs (n = 10). Control groups included sham rats (all surgical procedures except asphyxia) treated with induced hyperthermia at 24 hrs (n = 4) or 48 hrs (n = 4) and na?ve rats (n = 4). Rats were killed at 7 days and injured neurons in hematoxylin and eosin stained coronal brain sections through dorsal hippocampus were scored in a semiquantitative manner on a scale of 0 to 10 (0 = normal; 1 = up to 10% neurons with ischemic neuronal changes; 10 = 90-100% neurons with ischemic neuronal changes). Normal-appearing neurons were also counted in CA1. The number of normal-appearing neurons in a 20x field in CA1 were also counted. MAIN RESULTS: All na?ve and sham hyperthermia control rats survived the protocol. There was a trend toward a larger mortality rate in asphyxiated rats treated with induced hyperthermia at 24 hrs (9 of 21 died) vs. asphyxiated rats without induced hyperthermia (3 of 21) or with hyperthermia induced at 48 hrs (3 of 10) (Kaplan-Meier p=.0595). Asphyxiated rats with hyperthermia induced at 24 hrs had larger (worse) histopathology damage scores than rats subjected to asphyxia without induced hyperthermia (9.3 +/- 1.5 vs. 6.2 +/- 2.6; p=.001). Histopathology damage scores in asphyxiated rats with hyperthermia induced at 48 hrs did not differ from those in rats asphyxiated without induced hyperthermia (6.4 +/- 3.0 vs. 6.2 +/- 2.6; p=.907). There were fewer normal-appearing CA1 neurons in asphyxiated rats with hyperthermia induced at 24 hrs vs. rats subjected to asphyxia without induced hyperthermia (33 +/- 13 vs. 67 +/- 36; p=.002). The number of normal-appearing CA1 neurons in asphyxiated rats with hyperthermia induced at 48 hrs did not differ from that in rats asphyxiated without induced hyperthermia (59 +/- 21 vs. 67 +/- 36; p=.885). CONCLUSIONS: Induced hyperthermia when administered at 24 hrs, but not 48 hrs, worsens ischemic brain injury in rats resuscitated from asphyxial cardiac arrest. This may have implications for postresuscitative management of children and adults resuscitated from cardiac arrest. The common clinical practice of actively warming patients with spontaneous hypothermia might result in iatrogenic injury if warming results in hyperthermic overshoot. Avoidance of hyperthermia induced by active warming at critical time periods after cardiac arrest may be important.     

Dopaminergic and serotonergic mechanisms of thermoregulation: mediation of thermal effects of apomorphine and dopamine

The effects of dopaminergic and serotonergic antagonists on apomorphine- and dopamine-induced changes in body temperature were studied in the rat. Intraperitoneal administration of apomorphine produced dose-dependent hypothermia. At a dose of 0.1 mg/kg, apomorphine caused either no significant effect or a slight decrease in body temperature. However, it caused hyperthermia in rats pretreated with the DA antagonist, haloperidol, and hypothermia in rats pretreated with the serotonin depletor, p-chlorophenylalanine or serotonin antagonists, cyproheptadine, metergoline or cinanserin. Intracerebroventricular injection of 100 micrograms/2 microliter of DA transiently decreased body temperature. Pretreatment with cyproheptadine potentiated and prolonged the responses. However, the same injection of DA produced hyperthermia in haloperidol-pretreated animals. These data suggest that both dopaminergic and serotonergic mechanisms in the brain mediate the effects of apomorphine on body temperature. We propose that apomorphine can simultaneously activate two opposing DA-related thermoregulatory mechanisms with different sensitivities to haloperidol: a haloperidol-sensitive hypothermia and a haloperidol-nonsensitive hyperthermia mechanisms. Furthermore, the action of the latter mechanism is mediated by a secondary activation of serotonergic mechanisms.     

The impact of brain temperature and core temperature on intracranial pressure and cerebral perfusion pressure.

Hyperthermia has been demonstrated to increase neuronal injury when present during or after an acute brain injury. The assumption that core temperature equals brain temperature exists. If the temperature of an injured brain is higher than core temperature, episodes of neural hyperthermia may go undetected. The objectives of this study were to (1) determine if differences exist between brain temperature and core temperature in subjects with acute neurological injuries in both normothermic and febrile states and (2) investigate the impact of brain and core temperatures on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). The study was conducted through a retrospective chart audit of patients age 18 years or older admitted to a level I trauma center with a diagnosis of brain injury whose condition warranted placement of a pulmonary artery catheter (which measured core temperature) and an intraventricular catheter (which measured brain temperature). Thirty-one charts contained complete data; nine charts provided partial data. Mean brain temperature (100.8 degrees F, SD = 0.69) was found to be significantly higher than mean core temperature (100.2 degrees F, SD = 0.74; p = .00). Brain temperature means were hyperthermic (> or = 100.9 degrees F), while matching core temperatures were normothermic in almost one-third of the subjects. There was no significant difference found between hyperthermic ICP or CPP and normothermic ICP or CPP determined by brain or core temperature. No significant correlation was found between temperature and intracranial dynamics. Future research is needed with prospectively collected data of adequate sample size to continue to investigate the impact of core and brain temperature on the intracranial dynamics of ICP and CPP.     

Current status of cerebral protection with mild-to-moderate hypothermia after traumatic brain injury

PURPOSE OF REVIEW: The aim of this article is to review the current status of protective effects of mild-to-moderate hypothermia on traumatic brain injury. RECENT FINDINGS: More than 30 clinical studies have reported effects of therapeutic hypothermia on outcome of traumatic brain injury and cerebral ischemia. Only one clinical trial of short-term mild hypothermia did not show any effect in patients with severe traumatic brain injury. Long-term mild hypothermia may be useful for severe traumatic brain-injured patients. SUMMARY: Mild-to-moderate hypothermia plays a significant role in cerebral protection after traumatic brain injury.     

Inducing hypothermia to decrease neurological deficit: literature review

AIM: This paper reports a literature review to examine the effectiveness of inducing hypothermia to decrease neurological deficit after out-of-hospital cardiac arrest. BACKGROUND: After cardiac arrest, severe neurological impairment is a major problem. Outcome after anoxic brain injury following cardiac arrest varies from normal function to brain death. However, a large proportion of these patients are left with severe disability and completely dependent on others for basic needs. Since the 1950s, several studies have shown how hypothermia can be neuroprotective. Recently, these studies have been taken to human trials in populations experiencing out-of-hospital cardiac arrest. METHODS: A literature search was conducted using the Ovid and MDConsult databases for the years 1966-2004 and the keywords included hypothermia, therapeutic hypothermia, and cardiac arrest. Only English language papers were retrieved. Six human trials were found. RESULTS: All six studies showed improved neurological outcomes and four of these showed a decrease in mortality. Minimal complications exist from inducing mild hypothermia after cardiac arrest, and include decreased heart rate, increased systemic vascular resistance, transient electrolyte abnormalities (increased serum potassium and glucose), possible increase in pneumonia or other infectious processes, possible rebound hyperthermia, possible hypotension, and possible arrhythmias. CONCLUSIONS: Based on the review of these studies and the recommendations from the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation, advanced practice nurses should promote this practice, but look for further research on specific treatment recommendations.     

Posttraumatic hypothermia is neuroprotective in a model of traumatic brain injury complicated by a secondary hypoxic insult.

OBJECTIVE: Human traumatic brain injury frequently results in secondary complications, including hypoxia. In previous studies, we have reported that posttraumatic hypothermia is neuroprotective and that secondary hypoxia exacerbates histopathologic outcome after fluid-percussion brain injury. The purpose of this study was to assess the therapeutic effects of mild (33 degrees C) hypothermia after fluid-percussion injury combined with secondary hypoxia. In addition, the importance of the rewarming period on histopathologic outcome was investigated. DESIGN: Prospective experimental study in rats. SETTING: Experimental laboratory in a university teaching hospital. INTERVENTION: Intubated, anesthetized rats underwent normothermic parasagittal fluid-percussion brain injury (1.8-2.1 atmospheres) followed by either 30 mins of normoxia (n = 6) or hypoxic (n = 6) gas levels and by 4 hrs of normothermia (37 degrees C). In hypothermic rats, brain temperature was reduced immediately after the 30-min hypoxic insult and maintained for 4 hrs. After hypothermia, brain temperature was either rapidly (n = 6) or slowly (n = 5) increased to normothermic levels. Rats were killed 3 days after traumatic brain injury, and contusion volumes were quantitatively assessed. MEASUREMENTS AND MAIN RESULTS: As previously shown, posttraumatic hypoxia significantly increased contusion volume compared with traumatic brain injury-normoxic animals (p <.02). Importantly, although posttraumatic hypothermia followed by rapid rewarming (15 mins) failed to decrease contusion volume, those animals undergoing a slow rewarming period (120 mins) demonstrated significantly (p <.03) reduced contusion volumes, compared with hypoxic normothermic rats. CONCLUSIONS: These data emphasize the beneficial effects of posttraumatic hypothermia in a traumatic brain injury model complicated by secondary hypoxia and stress the importance of the rewarming period in this therapeutic intervention.     

Moderate hypothermia may be detrimental after traumatic brain injury in fentanyl-anesthetized rats

OBJECTIVES: To determine whether transient, moderate hypothermia is beneficial after traumatic brain injury in fentanyl-anesthetized rats. DESIGN: Prospective, randomized study. SETTING: University-based animal research facility. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: All rats were intubated, mechanically ventilated, and anesthetized with fentanyl (10 microg/kg intravenous bolus and then 50 microg.kg(-1).hr(-1) infusion). Controlled cortical impact was performed to the left parietal cortex, followed immediately by 1 hr of either normothermia (brain temperature 37 +/- 0.5 degrees C) or hypothermia (brain temperature 32 +/- 0.5 degrees C). Hypothermic rats were rewarmed gradually over 1 hr. Fentanyl anesthesia and mechanical ventilation were continued in both groups until the end of rewarming (2 hrs after traumatic brain injury). MEASUREMENTS AND MAIN RESULTS: Histologic assessment performed 72 hrs after traumatic brain injury was the primary outcome variable. Secondary outcome variables were physiologic variables monitored during the first 2 hrs after traumatic brain injury and plasma catecholamine and serum fentanyl concentrations measured at the end of both hypothermia and rewarming (1 and 2 hrs after traumatic brain injury). Contusion volume was larger in hypothermic vs. normothermic rats (44.3 +/- 4.2 vs. 28.6 +/- 4.0 mm, p <.05), but hippocampal neuronal survival did not differ between groups. Physiologic variables did not differ between groups. Plasma dopamine and norepinephrine concentrations were increased at the end of hypothermia in hypothermic (vs. normothermic) rats (p <.05), indicating that hypothermia augmented the systemic stress response. Similarly, serum fentanyl concentrations were higher in hypothermic (vs. normothermic) rats at the end of both hypothermia and rewarming (p <.05), demonstrating that hypothermia reduced the clearance and/or metabolism of fentanyl. CONCLUSIONS: Moderate hypothermia was detrimental after experimental traumatic brain injury in fentanyl-anesthetized rats. Since treatment with hypothermia has provided reliable benefit in experimental traumatic brain injury with inhalational anesthetics, these results indicate that the choice of anesthesia/analgesia after traumatic brain injury may dramatically influence response to other therapeutic interventions, such as hypothermia. Given that narcotics commonly are administered to patients after severe traumatic brain injury, this study may have clinical implications.     

Clinical review: Neuromonitoring - an update

Critically ill patients are frequently at risk of neurological dysfunction as a result of primary neurological conditions or secondary insults. Determining which aspects of brain function are affected and how best to manage the neurological dysfunction can often be difficult and is complicated by the limited information that can be gained from clinical examination in such patients and the effects of therapies, notably sedation, on neurological function. Methods to measure and monitor brain function have evolved considerably in recent years and now play an important role in the evaluation and management of patients with brain injury. Importantly, no single technique is ideal for all patients and different variables will need to be monitored in different patients; in many patients, a combination of monitoring techniques will be needed. Although clinical studies support the physiologic feasibility and biologic plausibility of management based on information from various monitors, data supporting this concept from randomized trials are still required.     

Is keeping cool still hot? An update on hypothermia in brain injury

PURPOSE OF REVIEW: The purpose of this review is to examine recent research results for hypothermia as a treatment for brain injury. RECENT FINDINGS: One potential application for hypothermia is as a means of control of elevated intracranial pressure in which hypothermia is induced when intracranial pressure becomes uncontrollable by conventional means. A second application is as a neuroprotectant in which hypothermia is induced very early and maintained for a specified period as a means of diminishing the biochemical cascade that produces secondary brain injury. The clinical data indicate that hypothermia reduces elevated intracranial pressure, but no conclusion can be drawn as to whether this improves outcome over existing techniques (eg, mannitol and barbiturates). There is little evidence that hypothermia acts as a neuroprotectant in trials, all of which used treatment windows of over 4 hours. SUMMARY: Hypothermia is a useful adjunct to barbiturates and mannitol to control elevated intracranial pressure. The results of trials that have tested systemic hypothermia as a neuroprotectant have been negative or equivocal, and cooling may have been induced outside the treatment window.     

Microsensor and microdialysis technology. Advanced techniques in the management of severe head injury

Neuroscientists continue the search for the "magic bullet" that will prevent the deleterious effects of primary and secondary brain injury. Indirect measurement of the effects of primary and secondary brain injury through the study of ICP- or CPP-directed management, CBF monitoring, Sjo2 monitoring, and TCD monitoring has led to improved care of persons with brain injury. Although the findings from brain injury research using microsensor and microdialysis technology are only preliminary and extensive research is still needed, these technologies have dramatically expanded knowledge about brain injury at the cellular level. Extended neuromonitoring is poised to enter a new and exciting phase because of the growth in knowledge regarding the cellular events associated with brain injury. The recent approval of NeuroTrend by the FDA will further promote this growth. Applications of the technology have already expanded to include uses beyond the management of traumatic brain injury. Microsensor and microdialysis technology is being used intraoperatively to determine "safe" temporary clipping times for aneurysm surgery and is also being used within the critical care setting to improve the monitoring and management of subarachnoid hemorrhage patients who are experiencing vasospasm. The ultimate application of this new technology is to improve long-term outcomes for patients with brain injury through the reduction of secondary brain injury. If that goal is to be accomplished, then it will be important for nurses caring for patients with brain injury to become immersed in this exciting new phase in brain injury monitoring. Nurses must obtain a comprehensive knowledge base of brain injury pathophysiology and how extended neuromonitoring can lead to improved outcomes. Technical proficiency will also be important to ensure that treatment and research conclusions are based on accurate data. Finally and perhaps most importantly, it will be critical for nurses to participate in and develop research studies that explore the impact of interventions, especially nursing care activities, on the injured brain if these exciting new advances are to be translated into tangible benefits for brain-injured patients.     

Unexpected fatal neurological deterioration after successful cardio-pulmonary resuscitation and therapeutic hypothermia

A 77-year-old woman was admitted to the intensive care unit after successful cardiopulmonary resuscitation for out-of-hospital cardiac arrest due to pulseless electrical activity. She was treated with mild therapeutic hypothermia to minimise secondary anoxic brain damage. After a 24 h period of therapeutic hypothermia with a temperature of 32.5 degrees C, the patient was rewarmed and sedation discontinued. Neurological evaluation after 24 h revealed a maximum Glasgow Coma Score of E4M4Vt with spontaneous breathing. However the patient developed a fever reaching 39 degrees C for several hours that was unresponsive to conventional cooling methods. In the subsequent 24 h patient developed apnoea, hypotension and bradycardia with deterioration of the coma score. Diabetes insipidus was confirmed. Cerebral CT was performed which showed diffuse brain oedema with herniation and brainstem compression. The patient died within hours. Autopsy showed massive brain swelling and tentorial herniation. Hyperthermia possibly played a pivotal role in the development of this fatal insult to this vulnerable brain after cardiac arrest and therapeutic hypothermia treatment. The acute histopathological alterations in the brain, possibly caused by the deleterious effects of fever after cardiac arrest in human brain, may be considered a new observation.     

Exercise to Enhance Neurocognitive Function After Traumatic Brain Injury

Vigorous exercise has long been associated with improved health in many domains. Results of clinical observation have suggested that neurocognitive performance also is improved by vigorous exercise. Data derived from animal model–based research have been emerging that show molecular and neuroanatomic mechanisms that may explain how exercise improves cognition, particularly after traumatic brain injury. This article will summarize the current state of the basic science and clinical literature regarding exercise as an intervention, both independently and in conjunction with other modalities, for brain injury rehabilitation. A key principle is the factor of timing of the initiation of exercise after mild traumatic brain injury, balancing potentially favorable and detrimental effects on recovery.     

Revisiting therapeutic hypothermia for severe traumatic brain injury… again

Improved understanding of the molecular mechanisms of secondary brain injury has informed the optimum depth and duration of cooling and led to increased clinical interest in the therapeutic moderate hypothermia for severe traumatic brain injury over the past two decades. Although several large multi-center clinical trials have not found a treatment effect, multiple single-center trials have, and a recent meta-analysis by Crossley and colleagues now finds that the cumulative findings of those single-center trials dilute the multi-center trial results and show an overall reduction in mortality and poor outcomes associated with cooling. The need for consistent support of key physiologic parameters during cooling is emphasized by this finding.     

Cardiac arrest caused by accidental severe hypothermia and myocardial infarction during general anesthesia

Therapeutic hypothermia is often used for traumatic brain injury because of its neuroprotective effect and decreased secondary brain injury. However, this procedure lacks clinical evidence supporting its efficacy, and adverse outcomes have been reported during general anesthesia. A 61-year-old man with a history of percutaneous coronary intervention (PCI) was admitted with traumatic brain injury. Immediately after admission, he underwent mild therapeutic hypothermia with a target temperature of 33.0°C for neuroprotection. During general anesthesia for emergency surgery because he developed a mass effect, hypothermic cardiac arrest occurred following an additional decrease in the core body temperature. Moreover, myocardial infarction caused by restenosis of the previous PCI lesion also contributed to the cardiac arrest. Although the patient recovered spontaneous circulation after an hour-long cardiopulmonary resuscitation with rewarming, he eventually died of subsequent repetitive cardiac arrests. When anesthetizing patients undergoing therapeutic hypothermia, caution is required to prevent adverse outcomes that can be caused by unintentional severe hypothermia and exacerbation of underlying heart disease.     

脑温变化对大鼠局灶性脑缺血影响的病理研究

目的通过光镜、电镜观察,对比研究缺血前预高温和缺血后轻度高温、亚低温对局灶脑缺血早期脑组织病理形态演变的影响。方法64只Wistar大鼠按随机数字表法分为:轻度高温、常温假手术组,预高温、轻度高温、常温、亚低温缺血2h再灌注4h(O2R4)组及常温、亚低温缺血6h无灌注(O6R0)组(共8组,n=8),采用改良的Nagasawa局灶脑缺血模型,分别观察了脑缺血组织损伤的病理变化。结果与常温缺血组比较,轻度高温组脑缺血组织局部损伤加重,损伤范围最大;缺血前预高温和亚低温有改善脑缺血组织损伤的作用,该作用以亚低温O2R4组更明显,亚低温对O6R0组作用有限。结论轻度高温对缺血神经细胞向不可逆损伤和坏死演化、对损伤范围扩展均有促进作用;缺血前预高温和亚低温对暂时性脑缺血有明显保护作用,亚低温对持续性脑缺血无明显保护作用。     

Admission hypothermia and outcome after major trauma

OBJECTIVE: Uncontrolled exposure hypothermia is believed to be deleterious in the setting of major trauma. Prevention of hypothermia in the injured patient is currently practiced in both prehospital and in-hospital settings. However, this standard is based on studies of limited patient series that were not designed to identify the independent relationship between hypothermia and mortality. Recent studies suggest that therapeutically applied hypothermia may benefit selected patient subsets. The goal of this study was to evaluate the independent association between admission hypothermia and mortality after major trauma, with adjustment for clinical confounders. DESIGN: Retrospective analysis of a statewide trauma registry. The primary outcome was death at hospital discharge. The key exposure was hypothermia, defined as body temperature /=16 yrs of age for the years 2000-2002. Transferred patients were excluded. Patients were excluded if temperature or route of temperature measurement was not known. Both the full cohort and a subset with isolated severe head injury were evaluated. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Of 38,520 patients, 1,921 (5.0%) were hypothermic at admission. Admission hypothermia was independently associated with increased odds of death in both the full cohort (odds ratio, 3.03; 95% confidence interval, 2.62-3.51) and the subset with isolated severe head injury (2.21; 1.62-3.03), with adjustment for age, severity and mechanism of injury, and route of temperature measurement. CONCLUSIONS: Admission hypothermia is independently associated with increased adjusted odds of death after major trauma. The increase in mortality is not completely attributable to physiologic presentation or injury pattern or severity.