长时程亚低温疗法对重型颅脑损伤患者术后凝血功能、氧化应激损伤和炎性因子水平的影响

目的长时程亚低温疗法对重型颅脑损伤患者术后凝血功能、氧化应激损伤和炎性因子水平的影响。方法随机将128例重型颅脑损伤患者分为2组,各64例。对照组实施常规救治,观察组在对照组基础上联合亚低温治疗。比较2组患者治疗前后GCS评分、凝血系统、氧化应激损伤及炎性因子水平和并发症发生率。结果治疗前,2组患者的GCS评分、凝血功能、氧化应激损伤及炎性因子等指标差异无统计学意义(P0.05)。治疗后,2组患者的上述指标均有改善,但观察组改善幅度优于对照组,总有效率(71.88%)高于对照组(53.13%)。观察组迟发颅内血肿、纤溶亢进发生率低于对照组,低血压发生率高于对照组,差异均有统计学意义(P0.05)。2组肺炎发生率无统计学意义(P0.05)。结论长时程亚低温疗法能改善重型颅脑损伤患者凝血功能、氧化应激损伤及炎性因子水平。     

亚低温治疗重型颅脑损伤的临床体会

亚低温治疗能显著降低重型颅脑损伤病人的死亡率，改善颅脑损伤病人的神经功能，目前，国内外有条件的医院已将亚低温治疗方法列为重型颅脑损伤病人的治疗常规。我院自2003年始对重型颅脑损伤病人进行亚低温治疗。本文对2003年6月-2005年2月应用亚低温和常规治疗两种方法对51例重型颅脑损伤病人（GCS≤8分），进行分组治疗列项对照，并对其结果加以分析讨论。     

亚低温治疗重型颅脑损伤临床研究

目的观察亚低温治疗重型颅脑损伤的疗效。方法将43例重型颅脑损伤(格拉斯哥昏迷评分<8分)病人分为两组:亚低温组(22例)采用全身冰毯降温,使体温降至32~35℃5d,同时使用冬眠合剂;对照组(21例)给予常规治疗。结果亚低温组病人预后良好率60%(13/22),病死率26%(5/22);对照组预后良好率29%(6/22),病死率48%(10/21),两组病人疗效比较差异有统计学意义(P均<0.05)。结论亚低温治疗重型颅脑损伤疗效明显优于常温治疗重型颅脑损伤的疗效。     

亚低温对重症脑外伤免疫功能与获得性肺炎的影响及与预后关系的研究

目的研究亚低温对重型颅脑损伤患者免疫功能的影响，及院内获得性肺炎的发生与细菌分布，与预后的关系。方法将85例重型颅脑损伤患者（GCS评分≤8分）随机分为亚低温治疗组和常温治疗组。亚低温组45例．伤后24小时内采用亚低温治疗，使直肠温度控制在33℃～35℃，维持5～7天；常温治疗组40例，其它治疗两组基本相同。分别在入院后第1、3、5、7及14天检测两组患者血清免疫球蛋白与补体水平和外周血T-淋巴细胞转化率的动态变化，并分析两组患者院内获得性肺炎的发生情况。感染细菌的分布，两组患者之间预后的比较。结果亚低温治疗组与常温治疗组两组患者的免疫球蛋白水平和T-淋巴细胞转化率在第1、3、14天均无显著差异（P〉0．05），而在第5、7天有统计学上意义（P〈0．05）。而在院内获得性肺炎的发生上与细菌类型上无显著差异。两者之间的预后亚低温治疗组明显好于非亚低温治疗组。结论亚低温治疗能明显改善重型颅脑损伤患者的预后，但在长时程的治疗过程中。会明显抑制重型颅脑损伤患者的免疫功能，而在亚低温治疗期间患者院内获得性肺炎的发生率并没有明显增加。     

亚低温治疗重型颅脑损伤临床分析

目的研究亚低温对重型颅脑损伤患者颅内压（ICP）及并发症的影响。方法重型颅脑损伤患者68例,随机分为亚低温组（n=38）及常温常规治疗组（n=30）。亚低温组接受32℃～35℃低温治疗,常温常规治疗组除亚低温治疗外,其余治疗同亚低温组。比较两组的ICP、预后和并发症的差异。结果亚低温治疗组伤后ICP显著低于常温常规治疗组（P（0.01）。预后显著好于常温常规治疗组（P〈0.05）。应激性溃疡、肝肾功能异常和外伤性癫痫的发生率显著低于常温常规治疗组（P〈0.01）。结论亚低温对重型颅脑损伤患者ICP升高有明显的治疗作用,可以改善重型颅脑损伤患者的预后,减少全身并发症。     

亚低温治疗重型颅脑损伤效果观察

将78例重型颅脑损伤病人随机分为亚低温组和对照组,各39例.两组病人均采用脱水、抗炎等治疗,亚低温组在此基础上施行亚低温治疗,即使肛温降至33～34 ℃,持续5～7 d.结果亚低温组血糖和血乳酸较对照组明显降低(P＜0.05);亚低温组在治疗后1 d颅内压即较对照组明显降低(P＜0.05),7 d基本降至正常.提示亚低温治疗能有效降低重型颅脑损伤病人的颅内压、血糖和血乳酸水平,改善预后.护理中应注意加强对皮肤、体温和生命体征的监护,采用自然复温法逐步复温效果较好.     

亚低温治疗重型颅脑损伤患者体液免疫功能变化的研究

本院于2002年7月至2005年12月。应用亚低温治疗救治重型颅脑损伤患51例。并与同期常温对照组的46例进行对比观察，旨在进一步探讨亚低温治疗对重型颅脑损伤患体液免疫功能和预后的影响。     

亚低温治疗重型颅脑损伤的临床体会

目的 探讨亚低温脑保护疗法对救治重型颅脑损伤的疗效。方法 将132例重型颅脑损伤随机平均分为治疗组与对照组，进行对比分析，并且前瞻性分析两组疗效。结果 治疗组66例患者，存活率为77．3％，恢复良好率54．5％（36／66），病死率18．2％（12／66）。疗效明显优于对照组，未发生相关的并发症。结论 亚低温治疗能显著降低重型颅脑损伤患者的死亡率，改善颅脑损伤患者神经功能预后，并具有安全、显著降低病死率及癫痫发生率等优点。     

亚低温治疗重型颅脑损伤的观察及护理

亚低温是轻度低温（３３℃～３５℃）和中度低温（２９℃～３２℃）的合称。国内临床研究大都选择３３℃～３５℃轻度低温治疗重型颅脑损伤，疗效显著犤１犦。本院颅脑外科在１９９９年１０月至２００２年２月，对４８例重型颅脑损伤患者施行亚低温疗法，取得一定疗效。现将观察方法及护理体会报告如下。临床资料１．一般资料：本组４８例，男３８例，女１０例；年龄１９～６８岁，平均４１岁。病人均经CT扫描和临床表现诊断为重型颅脑损伤，GCS评分３～８分。２．方法：本组病人均于入院４～６小时内开始亚低温治疗。降温采用Medi－Ther…     

亚低温治疗重型颅脑损伤患者临床分析

我院于1999年10月～2000年8月共收治重型颅脑损伤患48例(GCS≤8分)，随机分成常规治疗组及常规治疗加亚低温治疗组，结果表明，亚低温组治疗重型颅脑损伤患取得明显效果。     

Study of the effects of mild hypothermia on cerebral PO2, PCO2 and pH and body temperature in patients with acute severe head injury

I nrecent20yearsmostanimalexperimentsandclinicalstudieshavedemonstratedthatmildhypothermia(32℃ 35℃)hasaffirmatoryeffectonbrainprotection.Butthereareafewresearchreportsthatdenythebrainprotectioneffectofmildhypothermia.Wetreated38patientswithacuteseverehe…     

Study on changes of partial pressure of brain tissue oxygen and brain temperature in acute phase of severe head injury during mild hypothermia therapy

Ahighdeathrateofseverebraininjurieshasattractedmuchattention .Mildhypothermiatherapyandmonitoringbrainoxygenmetabolismandcerebralbloodflowhavebeendoneinmanyhospitals.Wimaretal1elucidatedthevalueofmonitoringbrainoxygeninseverebraininjuries.Butthemechanismofmildhypothermiaremainsunclear .Zhang2 reportedthatmildhypothermiatherapycouldrecoverthebrainoxygentonormal.Gupta3 usedanesthesiacoolingandobservedduringmildhypothermiathebrainoxygenwasdecreased .Wehavetreated 116patientswithseverebraininjuri…     

Study on therapeutic mechanism and clinical effect of mild hypothermia in patients with severe head injury

BACKGROUND: The therapeutic mechanism and clinical effect of mild hypothermia in patients with severe head injury were studied. METHODS: All 396 patients with severe head injury [Glasgow Coma Scale score (GCS) equal to or less than 8 on admission] were randomly divided into the hypothermic group (198 cases) and the control group (198 cases). Hypothermia was induced within 24 hours of injury. Rewarming began 1 to 7 days (average 62.4 +/- 27.6 h) after the rectal temperature (RT) reached 32.0 to 35.0 degrees C. Meanwhile, the vital signs, intracranial pressure (ICP), blood gas values, blood electrolytes, brain tissue oxygen pressure (P(bt)O2), brain tissue temperature (BT), cerebral blood flow (CBF), and jugular venous oxygen saturation (S(jv)O2) were measured. The rectal temperature of control patients was induced to 36.5 to 37.0 degrees C. According to GOS, the prognosis of the patients was evaluated. RESULTS: In comparison with control group, during mild hypothermia the high level of ICP, hyperglycemia and blood lactic acid significantly decreased (p < 0.05) and cerebral flow improved dominantly. The vital signs, blood gas values, and blood electrolytes did not change significantly. Decreased mortality and good recovery were also found in hypothermia group. CONCLUSIONS: Mild hypothermia is safe and effective for preventing brain damage on patients with severe head injury, as well as reducing mortality and improving the prognosis. It is important to monitor P(bt)O2, BT, CBF, and S(jv)O2 in hypothermic therapy.     

Changes of evoked potentials and evaluation of mild hypothermia for treatment of severe brain injury

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Effect of mild hypothermia on partial pressure of oxygen in brain tissue and brain temperature in patients with severe head injury

OBJECTIVE: To study the changes of partial pressure of oxygen in brain tissue (P(bt)O(2)) and brain temperature (BT) in patient s in acute phase of severe head injury, and to study the effect of mild hypothermia on P(bt)O(2) and BT. METHODS: The P(bt)O(2) and the BT of 18 patients with severe head injury were monitored, and the patients were treated with mild hypothermia within 20 hours after injury. The rectal temperature (RT) of the patients was kept on 31.5-34.9 degrees C for 1-7 days (57.7 hours+/-28.4 hours averagely), simultaneously, the indexes of P(bt)O(2) and BT were monitored for 1-5 days (with an average of 54.8 hours+/-27.0 hours). According to Glasgow Outcome Scale (GOS), the prognosis of the patients was evaluated at 6 months after injury. RESULTS: Within 24 hours after severe head injury, the P(bt)O(2) was significantly lower (9.6 mm Hg+/-6.8 mm Hg, 1 mm Hg=0.133 kPa) than the normal value (16-40 mm Hg). After treatment of mild hypothermia, the mean P(bt)O(2) increased to 28.7 mm Hg+/-8.8 mm Hg during the first 24 hours, and the P(bt)O(2) was still maintained within the range of normal value at 3 days after injury. The BT was higher than the RT in the patients in acute phase of severe head injury, and the difference between the BT and the RT significantly increased after treatment of mild hypothermia. Hyperventilation (the partial pressure of carbon dioxide in artery (P(a)CO(2)) approximately 25 mm Hg) decreased the high intracranial pressure (ICP) and significantly decreased the P(bt)O(2). CONCLUSIONS: This study demonstrates that P(pt)O(2) and BT monitoring is a safe, reliable and sensitive diagnostic method to follow cerebral oxygenation. It might become an important tool in our treatment regime for patients in the acute phase of severe head injury requiring hypothermia and hyperventilation.     

从神经电生理角度探讨亚低温对特重型颅脑伤的疗效

目的　通过诱发电位(EP)监测,探讨亚低温对特重型颅脑伤的疗效。　方法　选择受伤后10h内入院的特重型颅脑伤患者(GCS≤5)24例,患者随机分为亚低温组和常温组。亚低温组体温降至32～34℃,于降温前、降温过程中及复温后监测正中神经短潜伏期体感诱发电位(SLSEP)和脑干听觉诱发电位(BAEP);常温组在同样的时间段监测上述指标。统计分析亚低温组与常温组诱发电位的变化情况。　结果　亚低温组在治疗前后SLSEP的N20波幅变化值为(0.67±0.41)μV,常温组为(0.61±0.39)μV,两者差异无显著性意义(P＞0.05);BAEP的V/I波幅比值,差异也无显著性意义（P＞0.05）。　结论　从神经电生理角度来看,亚低温对GCS为3～5分的特重型颅脑伤无明显疗效。     

Traumatic panhypopituitarism: case report

We describe a case of traumatic panhypopituitarism following head injury. Generally considered, posttraumatic hypopituitarism occurs in patients who have suffered from severe head injury. However there were a few case reports of panhypopituitarism due to mild and moderate head injury. A 51-year-old male presented with a history of blunt head injury caused by a concrete block hitting his head directly during work. On admission, initial Glasgow Coma Scale was 14. Open depressed skull fracture was suspected. Emergency craniectomy and debridement were performed. Ten days after surgery, hypothermia, lethargy and appetite loss were manifested. Endocrinological examination showed panhypopituitarism with diabetes insipidus. MRI revealed ruptured pituitary stalk and pituitary gland hemorrhage. Coronal and sagittal MRI was helpful for the diagnosis of traumatic panhypopituitarism. General condition was recovered by hormone replacement therapy. It is important for medical staff carefully to observe vital signs and clinical symptoms, even if mild brain injury. Pituitary function test should also be undergone, if panhypopituitarism was suspected from clinical condition.     

Effect of long-term mild hypothermia therapy in patients with severe traumatic brain injury: 1-year follow-up review of 87 cases

OBJECT: The goal of this study was to investigate the protective effects of long-term (3-14 days) mild hypothermia therapy (33-35 degrees C) on outcome in 87 patients with severe traumatic brain injury (TBI) (Glasgow Coma Scale score < or = 8). METHODS: In 43 patients assigned to a mild hypothermia group, body temperatures were cooled to 33 to 35 degrees C a mean of 15 hours after injury and kept at 33 to 35 degrees C for 3 to 14 days. Rewarming commenced when the individual patient's intracranial pressure (ICP) returned to the normal level. Body temperatures in 44 patients assigned to a normothermia group were maintained at 37 to 38 degrees C. Each patient's outcome was evaluated 1 year later by using the Glasgow Outcome Scale. One year after TBI, the mortality rate was 25.58% (11 of 43 patients) and the rate of favorable outcome (good recovery or moderate disability) was 46.51% (20 of 43 patients) in the mild hypothermia group. In the normothermia group, the mortality rate was 45.45% (20 of 44 patients) and the rate of favorable outcome was 27.27% (12 of 44 patients) (p < 0.05). Induced mild hypothermia also markedly reduced ICP (p < 0.01) and inhibited hyperglycemia (p < 0.05). The rates of complication were not significantly different between the two groups. CONCLUSIONS: The data produced by this study demonstrate that long-term mild hypothermia therapy significantly improves outcomes in patients with severe TBI.     

Significance of consecutive bilateral surgeries for patients with acute subdural hematoma who develop contralateral acute epi- or subdural hematoma

BACKGROUND: Although rare, patients with acute subdural hematoma (ASDH) because of severe head injury can develop contralateral acute epi- or subdural hematoma, requiring consecutive surgical procedures. The choice of treatment strategies for such patients is clinically important. METHODS: Among 88 patients with ASDH who were surgically treated over 13 years, we encountered and studied 5 patients who developed contralateral acute epi- or subdural hematoma (5.7%). RESULTS: All 5 patients were male, ranging in age from 17 to 40. According to the Glasgow Coma Scale on admission, 1 patient was rated 3, 1 was 4, 1 was 5, and 2 were 6. All patients underwent consecutive surgical procedures for ASDH and contralateral ASDH and/or acute epidural hematoma, and were given postoperative supportive therapy with barbiturates and mild hypothermia. Patients' outcomes according to the Glasgow Outcome Scale were as follows: 1 patient, good recovery (20.0%); 1, mild disability (20.0%); 2, severe disability (40.0%), and 1, persistent vegetative state (20.0%). No patients died. Although decompressive craniectomy and evacuation of hematoma may lead to contralateral acute epi- or subdural hematoma in patients with ASDH, this therapy is justified because hematoma irrigation with trephination therapy has a poor outcome for comatose patients. CONCLUSION: Awareness of intraoperative brain swelling is important, as it suggests the development of contralateral hematoma. Immediate computed tomography and a rapid return to the operating room are therefore critical.     

The importance of brain temperature in patients after severe head injury: relationship to intracranial pressure,cerebral perfusion pressure,cerebral blood flow,and outcome

Brain temperature was continuously measured in 58 patients after severe head injury and compared to rectal temperature, intracranial pressure, cerebral blood flow, and outcome after 3 months. The temperature difference between brain and rectal temperature was also calculated. Mild hypothermia (34-36 degrees C) was also used to treat uncontrollable intracranial pressure (ICP) above 20 mm Hg when other methods failed. Brain and rectal temperature were strongly correlated (r = 0.866; p < 0.001). Four groups were identified. The mean brain temperature ranged from 36.9 +/- 0.4 degrees C in the normothermic group to 38.2 +/- 0.5 degrees C in the hyperthermic group, 35.3 +/- 0.5 degrees C in the mild therapeutic hypothermia group, and 34.3 +/- 1.5 degrees C in the hypothermia group without active cooling. The mean DeltaT(br-rect) was positive for patients with a T(br) above 36.0 degrees C (0.0 +/- 0.5 degrees C) and negative for patients during mild therapeutic hypothermia (-0.2 +/- 0.6 degrees C) and also in those with a brain temperature below 36 degrees C without active cooling (0.8 +/- -1.4 degrees C) - the spontaneous hypothermic group. The cerebral perfusion pressure (CPP) was increased significantly by active cooling compared to the normothermic and hyperthermic groups. The mean cerebral blood flow (CBF) in patients with a brain temperature between 36.0 degrees C and 37.5 degrees C was 37.8 +/- 14.0 mL/100 g/min. The lowest CBF was measured in patients with a brain temperature <36.0 degrees C and a negative brain-rectal temperature difference (17.1 +/- 14.0 mL/100 g/min). A positive trend for improved outcome was seen in patients with mild hypothermia. Simultaneous monitoring of brain and rectal temperature provides important diagnostic and prognostic information to guide the treatment of patients after severe head injury (SHI) and the wide differentials that can develop between the brain and core temperature, especially during rapid cooling, strongly supports the use of brain temperature measurement if therapeutic hypothermia is considered for head injury care.