优质护理在颅脑创伤性水肿患者甘露醇治疗中的应用价值

目的:分析优质护理在颅脑创伤性水肿患者甘露醇治疗中的应用价值。方法:选取我院2015年1月—2016年12月收取的50例应用甘露醇治疗的颅脑创伤性水肿患者,将这50例患者随机分为对照组和观察组各25例,对照组患者进行常规护理,观察组患者进行优质护理,比较两组患者治疗后的效果、神经功能评分、生活能力评分以及护理满意度。结果:观察组患者在经过优质护理后治疗效果明显优于对照组(P<0.05);两组患者的神经功能评分都有明显的降低,但是观察组患者降低程度更为明显(P<0.05);两组患者的生活能力评分也都有所提高,但观察组患者生活能力评分提高更明显(P<0.05);观察组患者的护理满意度也明显高于对照组,两组患者比较差异具有统计学意义(P<0.05)。结论:对使用甘露醇治疗颅脑创伤性水肿的患者实施优质护理可以有效地提高患者的治疗效果,降低患者的精神功能评分,提高患者的生活能力评分,并且能够提高患者的护理满意度,具有很高的应用价值,值得临床推广应用。

对颅脑创伤性脑水肿患者应用托拉塞米联合甘露醇治疗的效果分析

目的：探讨托拉塞米联合甘露醇治疗颅脑创伤性脑水肿的疗效。方法：本院对42例颅脑创伤性脑水肿患者进行托拉塞米联合甘露醇治疗,随机分成两组,对照组20例,观察组22例。对照组采用单纯的甘露醇治疗,而观察组则采取托拉塞米联合甘露醇治疗,疗程为2周,在2012年6月∽2013年6月随访的一年中,比较治疗效果及其神经功能和生活功能的改善情况。结果：对照组的总体治疗有效率为71.42%,观察组的总体治疗有效率为90.04%,两组比较差异有统计学意义（P〈0.05）。在治疗两周的时间内,对照组的神经功能评分由（21.5±8.9）分减少至（16.4±8.5）分,生活能力评分由（41.5±5.8）分升高至（58.7±7.9）分;观察组神经功能评分由（21.2±9.5）分减少至（8.9±7.5）分,生活能力评分由（42.2±5.2）分升高至（67.4±8.2）分,从结果显示可以看出,治疗后观察组的神经功能恢复情况明显小于对照组,而生活能力评分却高于对照组,具有差异性的统计学意义（P〈0.05）。结论：托拉塞米和甘露醇都是很好的利尿剂,在临床运用中配合治疗是治疗颅脑创伤性脑水肿的一种有效手段,通过临床治疗方法的肯定,明显可以改善患者的神经功能和生活能力,临床具有很强的安全性。

Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury

Objective: To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI). Methods: In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain. Results: Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP. Conclusions: In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.