对大面积脑梗死中枢性高热病人头部低温降温时间的研究

[目的]探讨头部低温对大面积脑梗死（LCI）中枢性高热降温最佳治疗时间。[方法]将136例LCI高热病人随机分为4组，A组30例，为体温恢复后（≤37．5℃）即停止头部低温治疗；B组34例，为体温恢复后继续头部低温治疗1d～2d；C组41例．为体温恢复后头部低温继续治疗3d～4d；D组31例，为体温恢复后头部低温继续治疗5d～6d。4组头部低温方法相同。[结果]4组比较，头部低温起始时间无统计学意义（P〉0．05），体温恢复时间厦3d体温恢复率无统计学意义（P〉0．05），再发热率以A组、B组较高（P〈0．05）；治疗后神经功能缺损程度评分、日常生活能力评定以C组、D组效果较佳（P〈0．05）。[结论]LCI高热病人体温恢复后，适当延长头部低温治疗时间，可起到降温与治疗双重作用。继续低温治疗3d～4d为最佳。     

头部低温治疗高血压性脑出血高热的最佳疗程的研究

目的探讨头部低温对高血压性脑出血(HIH)高热降温最佳治疗时间.方法 176例HIH高热病人随机分为四组,A组43例,为体温恢复后(≤37.5℃)即停止头部低温治疗者;B组44例,为体温恢复后头部低温继续治疗1～2 d者;C组51例,为3～4 d者;D组38例,为5～6 d者.结果四组比较,头部低温启始时间、体温恢复时间及3天体温恢复率均无显著性差异(P＞0.05);体温再发率以A、B两组最高(P＜0.05);治疗前后神经功能缺损评分(NDS)、日常生活质量评分(ADL)比较,以C、D组效果最佳(P＜0.05).结论头部低温降温治疗时间为体温恢复后继续治疗3～4 d者最佳.     

不同启始时间头部低温对大面积脑梗死并中枢性高热降温效果比较

目的观察不同启始时间头部低温对大面积脑梗死(LCI)合并中枢性高热的降温效果。方法将154例中枢性高热LCI病人按入院时间顺序分为4组,A组34例,为高热后≤3 h行头部低温降温;B组35例,为高热后4-6 h行头部低温降温;C组45例,为7-9 h行头部低温降温;D组40例,为10-12 h行头部低温降温。结果 4组比较,头部低温治疗时间无显著性差异(均P>0．05),3 d体温恢复率无显著性差异(均P>0．05),体温再发率以A、B两组最低(均P<0．05),生存者治疗前后神经功能缺损程度评分(NDS)、日常生活能力评定(ADL)以A、B两组效果最佳(均P<0．05),肺部感染以 C、D发生率为高(均P<0．05)。结论 LCI中枢高热者6 h内应用头部低温治疗可达到治疗及降温双重作用。     

不同启始时间头部低温对高血压性脑出血高热降温效果比较

目的观察不同启始时间头部低温对高血压性脑出血(HypertensiveIntracerebralHemor-rhage,HIH)高热降温效果。方法203例HIH病人,分为4组。A组58例,为高热后≤3h行头部低温降温者;B组55例,为高热后4~6h行头部低温降温者;C组47例,为高热后7~9h行头部低温降温者;D组43例,为高热后10~12h行头部低温降温者。4组均应用颅脑降温治疗仪行头部低温。结果4组比较,3d体温恢复率无显著性差异(P>0.05),高热再发率以A、B两组最低(P<0.05),生存者治疗前后神经功能缺损程度评分(NDS)、日常生活能力评分(ADL)比较以A、B两组效果最佳(P<0.05,P<0.01),A、B两组肺部感染率明显低于C、D两组(P<0.05),C、D两组病死率高(P<0.05)。结论对HIH高热病人行头部低温降温最佳启始时间为高热发生6h内,大于6h则效果不显著。     

头部低温对高血压脑出血患者血清炎性细胞因子含量的影响

目的观察高血压脑出血（HIH）患者白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF—α）含量的变化及头部低温对其的影响。方法124例HIH患者根据是否加用头部低温治疗分为头部低温组（63例）和对照组（61例）。采用酶联免疫吸附法（ELISA）和放射免疫法测定两组患者治疗前及治疗后8d血清IL-6、TNF—α含量。并与正常组（40例）进行比较。同时，对两组患者中存活者生活质量进行比较。结果头部低温组和对照组治疗前IL-6、TNF—α明显升高，与正常组比较差异均有显著性（P均〈0．01）；治疗前头部低温组和对照组间IL-6和TNF—α差异均无显著性（P均〉0．05）；治疗后8d，头部低温组IL-6、TNF—α较治疗前明显降低（P均〈0．05），对照组降低不明显（P均〉0．05），头部低温组与对照组比较差异均有显著性（P均〈0．01）。头部低温组较对照组存活者预后的生活质量明显提高（P〈0．05）。结论HIH早期血清IL-6、TNF—α含量明显升高，头部低温可有效降低其含量，提高存活者预后生活质量。     

不同方法对大面积脑梗死高热降温的效果比较

目的：探讨3种不同方法对大面积脑梗死高热病人的降温效果。方法：将105例大面积脑梗死高热病人随机分为颅脑降温治疗仪组、冰袋组和酒精擦浴组，以3组病人30min内体温恢复率、体温反复率、3天以内体温恢复率、病死率、生存者治疗前后神经功能缺损评分与日常生活质量评分等指标进行对照观察。结果：30min内体温恢复率以酒精擦浴为佳（P〈0．01）；体温反复者以颅脑降温治疗仪最低（P〈0．01）；3天以内体温恢复率以颅脑降温治疗仪最高（P〈0．05）；生存者治疗前后神经功能缺损评分、日常生活质量评分比较以颅脑降温治疗仪组效果最佳（P〈0．05，P〈0．01）；病死率颅脑降温治疗仪组最低（P〈0．05）。结论：颅脑降温治疗仪不但降温效果较佳，而且对减少病死率及提高病人愈后生活质量起到积极的作用。     

不同方法对高血压性脑出血脑疝高热降温效果比较

目的：探讨三种不同方法对高血压性脑出血脑疝（HCHCH）高热病人的降温效果。方法：将96例HCHCH高热病人，随机分为颅脑降温治疗仪（HTI）组，冰袋组和酒精擦浴组，以三组病人30min内体温恢复率，体温反复率，3天以内体温恢复率，病死率，生存者治疗前后神经功能缺损评分（NDS）与日常生活质量（ADL）等指标进行对照观察，结果：三组比较30min内体温恢复率以酒精擦浴为佳（P＜0．01），体温反复者以HTI最低（P＜0．01），3天以内体温恢复率以HTI最高（P＜0．05），生存者治疗前后NDS，ADL比较以HTI组效果最佳（P＜0．05，P＜0．01）；病死率HTI组最低（P＜0．05），结论：HTI不但降温效果较佳，而且对减少病死率及提高病人愈后生活质量起到积极的作用。     

早期头部低温对高血压脑出血患者高热降温及护理

目的 观察早期头部低温对高血压脑出血患者高热降温效果,探讨其护理措施.方法 将204例患者分为四组:A组51例,出现高热4 h内采用颅脑降温仪进行头部降温;B组51例,在高热后4～8 h采用颅脑降温仪行头部降温;C组51例,在高热后4 h内用冰帽进行头部降温;D组51例,在高热后4～8 h用冰帽进行头部降温.结果 四组比较,3 d内体温恢复率A组最高,C组次之,B及D组较差;高热再发率A组最低,C组次之,D组最高.生存者治疗前后神经功能缺损程度评分、日常生活能力评分比较,A组最佳,C组次之,D组最差;病死率比较以B、D两组为高.结论 对高血压脑出血患者早期头部降温能够改善患者预后,降温方法以颅脑降温仪进行头部降温为佳.     

早期头部低温对高血压脑出血患者高热降温及护理

目的 观察早期头部低温对高血压脑出血患者高热降温效果,探讨其护理措施.方法 将204例患者分为四组:A组51例,出现高热4 h内采用颅脑降温仪进行头部降温;B组51例,在高热后4～8 h采用颅脑降温仪行头部降温;C组51例,在高热后4 h内用冰帽进行头部降温;D组51例,在高热后4～8 h用冰帽进行头部降温.结果 四组比较,3 d内体温恢复率A组最高,C组次之,B及D组较差;高热再发率A组最低,C组次之,D组最高.生存者治疗前后神经功能缺损程度评分、日常生活能力评分比较,A组最佳,C组次之,D组最差;病死率比较以B、D两组为高.结论 对高血压脑出血患者早期头部降温能够改善患者预后,降温方法以颅脑降温仪进行头部降温为佳.     

大面积脑梗死并高热老年患者的亚低温治疗疗效观察

目的 观察亚低温治疗对大面积脑梗死并高热老年患者生命体征的影响及其临床疗效。方法 46例发病2。1h内入院的老年大面积脑梗死并高热患者随机分为亚低温组和对照组各23例。亚低温组给予33℃～35℃的低温治疗，对照组给予常规降温治疗，10d后评定两组患者的体温、心率等，并根据死亡率及神经功能缺损评分评估患者的预后。结果 10d后。亚低温组患者的体温、心率均低于对照组。死亡率亦低于对照组，神经功能改善（P〈0．05），预后较好。结论 亚低温治疗老年大面积脑梗死并高热患者安全有效。     

Is there a self-preserving hypothermic mechanism in shock?

Hypoxia-induced hypothermia (HIH) is regarded as an adaptive response to hypoxia in a variety of creatures, but no details of the mechanism have yet been elucidated in the clinical setting. This study was designed to analyze alteration of core body temperature with hemorrhagic shock and to clarify HIH in the clinical setting. Patients were categorized in the hemorrhage shock (S, n = 15) or cardiopulmonary arrest (C, n = 88) group. The tympanic membrane temperature (TMT) was measured, and the length of the interval of call-to-arrival (CTA) at a hospital was set as the time-course parameter. There was a significant negative linear relationship between CTA interval and TMT (S group: TMT = -0.055 degrees C, CTA = +36.1 min, r = -0.833, P < 0.001; C group: TMT = -0.046 degrees C, CTA = +36.3 min, r = -0.548, P < 0.001). Analysis of variance revealed no significant difference in the slope of the regression lines of both groups. However, when the CTA interval was used as a covariate, there was a significant difference in the TMT (P = 0.014), which means that the regression line of the S group was significantly lower than that of the C group with time. Furthermore, in the S group, all patients were hypothermic (<35 degrees C) when their CTA interval was more than 20 min; on the other hand, in the C group, only 64 (75%) of 85 were hypothermic. Patients in S group were more likely to become hypothermic (P < 0.05). In humans with cellular hypoxia, HIH takes place, as seen in other animals. This result emphasizes the necessity for studies of analysis of the mechanisms of temperature control and determination of optimal body temperature during acute critical care.     

体温对豚鼠耳蜗电图-脑干听觉诱发电位综合波的影响

背景脑干听觉诱发电位(brainstem auditory evoked potentials,BAEP)和耳蜗电图(electrocochleogram,ECochG)两者综合波的新记录方法具有特殊临床意义,探讨体温升高和体温降低对其的影响对进一步明确ECochG-BAEP综合波的生理特性和指导其临床应用有重要意义.目的观察体温升高和体温降低对ECochG-BAEP综合波的影响效应.设计随机区组设计.单位暨南大学医学院生理教研室.对象实验于2002-07/09在暨南大学医学院生理学教研室进行,选择成年豚鼠(300～350 g),雌雄不拘,由第一军医大学动物实验中心提供,随机分为体温降低组(20只)和体温升高组(20只).干预体温降低组,体表物理降温法逐步降低豚鼠体温;体温升高组,体表物理升温法逐步升高豚鼠体温.主要观察指标ECochG-BAEP综合波的波形、波峰潜伏期(PL)、波峰间潜伏期(IPL)和波幅随体温发生的变化.结果随体温降低(36～25℃)和体温升高(36～42℃),ECochG-BAEP综合波波形始终兼具BAEP和ECochG两者的特点,有十分明显突出的1波;各波PL和IPL随体温降低而逐步延长,但随体温升高而逐渐缩短;1,2,3波波幅在体温降低至30～29℃时开始出现显著降低,1,2波波幅也在体温升高至40℃后开始出现显著降低.结论体温降低和体温升高对ECochG-BAEP SW的PL,IPL和波幅均有显著影响,但其波形始终兼具BAEP和ECochG两者的特点.     

Predictive values of triage temperature and pulse for antibiotic administration and hospital admission in elderly patients with potential infection

To determine how well triage temperature and pulse abnormalities in elderly patients with potential infections predict antibiotic administration and hospital admission. Data from the National Hospital Ambulatory Care Survey (2001-2002), a sample of US emergency departments, were used. Patients (>or=65 years) with a reason for visit suggesting potential infection were included. Of 10,586 patients 65 years or older, 32% had reasons for visit suggesting potential infection. The negative predictive value for predicting intensive care unit admission (n = 154) for triage hyperthermia (temperature >or=38 degrees C) was 96% (95% confidence interval, 95%-96%); hypothermia (temperature 相似文献   

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.     

犬多发伤合并海水浸泡的早期综合救治

目的：观察犬多发伤合并海水浸泡救治前后水、电解质变化，探讨犬多发伤早期综合救治方案。方法：成年杂种犬20只，制作多发伤动物模型。随机分为多发伤救治组(n=10)：海水浸泡1h后打捞出水救治；对照组(n=10)；海水浸泡1h打捞出水后不予救治。救治组在补液、复温同时行破裂小肠一期切除吻合术和右下肢软组织爆炸伤清创术，观察救治前后水、电解质、酸碱平衡的改善情况，体温变化和术后吻合口并发症及犬存活情况。结果：多发伤合并海水浸泡犬水、电解质、酸碱平衡紊乱和体温过低于救治后4--6h得以纠正，小肠吻合口并发症低，1周存活率为80％；对照组水、电解质、酸碱平衡紊乱和体温过低在打捞出水后继续加重，全部于6h内死亡，死亡率为100％。结论：对多发伤合并海水浸泡应实施早期综合救治，可同时行破裂小肠一期切除吻合术和软组织爆炸伤清创术。     

温度干预护理对全麻术后低体温患者的影响

目的探讨全麻恢复期低体温的护理措施，以避免低体温导致的不良反应。方法选择54例择期腹部手术后发生低体温的患者，随机分为对照组和试验组，每组27例。分别监测术前和人麻醉复苏室（PACU）时的体温，记录患者在PACU的复温时间和停留时间。结果温度干预护理后低体温患者复温时间和在PACU停留时间明显缩短。结论加强对PACU患者的体温护理，可缩短患者在PACU的复温时间、停留时间，减少低体温造成的并发症，减轻患者的经济负担。     

Mild hypothermia prolongs the survival time during uncontrolled hemorrhagic shock in rats

OBJECTIVE: To test our hypothesis that during lethal uncontrolled hemorrhagic shock (UHS) in rats, mild hypothermia of either 36 or 34 degrees C would prolong the survival time in comparison with normotherma of 38 degrees C. METHODS: Twenty-four rats were lightly anesthetized with halothane and maintained spontaneous breathing. UHS was induced by blood withdrawal of 2.5 ml/100 g over 15 min, followed by 75% tail amputation. Immediately after the tail cut, the rats were randomly divided into three groups (eight rats for each); normothermic Group 1 (control, rectal temperature 38 degrees C), and mild hypothermic Groups 2 (36 degrees C) and 3 (34 degrees C). Hypothermia was induced and maintained by body surface cooling. The rats were then observed without fluid resuscitation until their death (apnea and no pulse) or for a period of 240 min maximum. RESULTS: The rectal temperature was cooled down to 36 and 34 degrees C in 5 and 10 min, respectively. The mean survival time, which was 76+/-26 min in the control group (38 degrees C), was nearly doubled by mild hypothermia, 178+/-65 min for Group 2 (36 degrees C) (P<0.01 vs. control) and 144+/-54 min for Group 3 (34 degrees C) (P<0.05 vs. control) (no significant difference between Group 2 and 3). Additional blood losses from tail stumps were not significantly different among the three groups. CONCLUSION: Mild hypothermia of either 36 or 34 degrees C prolongs the survival time during lethal UHS in rats.     

Hypothermia attenuates the severity of oxidative stress development in asphyxiated newborns

Purpose

This retrospective case-control study aimed to examine the development of oxidative stress in asphyxiated infants delivered at more than 37 weeks of gestation.

Material and Methods

Thirty-seven neonates were stratified into 3 groups: the first group experienced hypothermia (n = 6); the second received hypothermia cooling cup treatment for 3 days, normothermia (n = 16); and the third was the control group (n = 15).Serum total hydroperoxide (TH), biological antioxidant potential, and oxidative stress index (OSI) (calculated as TH/biological antioxidant potential) were measured within 3 hours after birth.

Results

Serum TH and OSI levels gradually increased after birth in hypothermia and normothermia cases. At all time points, serum TH and OSI levels were higher in hypothermia and normothermia cases than in control cases. Serum TH and OSI levels were higher in normothermia cases than in hypothermia cases at days 3, 5, and 7.

Conclusion

This study demonstrated that hypothermia attenuated the development of systemic oxidative stress in asphyxiated newborns.