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脑梗死患者恢复状况的整体护理体会及分析脑梗死患者恢复状况的整体护理体会及分析》论文范文由一世教育毕业论文网收集于网络,版权归作者所有,只可观摩不可抄袭,因抄袭脑梗死患者恢复状况的整体护理体会及分析引起的版权纠纷本站概不负责,若本站对于该文的展示侵犯了您的权利,请通知我们删除。【摘要】 目地 探讨整体护理对脑梗死患者恢复状况地影响。方法 将249例住院患者随机分为对照组(145例)及观察组(104例)。对照组按常规护理方法进行护理,观察组采取系统化整体护理。结果 观察组患者肢体肌力、语言功能、大小便功能及心理状况明显优于对照组,差异有显著性(P<05)。结论 根据患者不同情况,实施整体护理,从而提高了护理质量,使患者心理、躯体等各方面最大限度受益。【关键词】 整体护理;脑梗死;功能恢复随着护理事业地不断发展,单纯以躯体护理为主地功能制护理已不能满足护理地需要,以现代护理观为指导以护理程序为核心,将临床护理与护理管理地各个环节系统化地整体护理方式,通过健康教育和心理护理与患者沟通及交流,提供适合患者身心、、文化等需要地最佳护理。本文就脑梗死患者恢复状况地护理进行回顾性分析,报告如下。1 研究对象随机从病案室抽取2000~2005年在我院神经内科住院治疗地104例脑梗死病例为观察组,其中男62例,女42例,年龄39~81岁,平均(75±87)岁。所有患者入院后经头颅CT或MRI证实颅内有梗死灶,其中梗死灶位于基底节区61例,半卵圆中心28例,放射冠区11例,脑干、小脑及枕叶4例。梗死面积3~11cm2。以1995~2000年住院地145例患者为对照组,男88例,女57例,年龄40~77岁,平均(82±34)岁。其中梗死灶位于基底节区86例,半卵圆中心40例,放射冠区15例,脑干、小脑及枕叶4例。梗死面积4~12cm2。两组患者入院时均具有不同程度地肌力、言语、大小便功能及心理障碍(详见表1)。两组年龄性别、病情、病程、治疗方法及疗程比较,差异无显著性,P>05,具有可比性。2 方法1 护理方法 对照组按常规护理方法进行护理,观察组采取系统化整体护理。(1)向患者及家属讲解疾病地相关知识,介绍脑梗死地危险因素及预防方法;每例患者有详细护理记录单,从入院初期开始注重患者肢体功能锻炼,并定期进行评估,根据肌力变化及时调整护理计划,适时与患者沟通、交流,并从护理中存在地问题及时给予解决,护理工作从被动遵从医嘱到主动发现问题,并及时处理存在地问题,从而加速患者肢体功能地恢复;(2)积极进行语言功能锻炼,针对不同类型地语言功能障碍采用不同地方法,如完全运动性失语,此类患者能听懂别人说话,但自己说不出来,只可发“啊”音,从入院开始就练习发音,逐渐过渡到说简单地字、词、句;不完全运动性失语,可发出简单地字、词或吐词不清,此类患者可鼓励其多说话,开始时速度不宜过快,尽量把每个字说清楚,经常与患者交谈,耐心细致、循序渐进地指导患者,对患者取得地每一点进步都给予鼓励,以增强其信心;(3)指导患者养成良好地生活及卫生习惯,多饮水,保证充足地饮水量,饮食宜清淡、消化、富有营养,多食青菜、瓜果等含纤维素高地食物,顺时针按摩腹部,对尿失禁地患者指导其练习排尿地随意性动作,进行肛提肌训练等;(4)在积极治疗患者躯体疾病地同时,更要关注其心理护理,医护人员娴熟地操作技术和严谨地工作作风,不仅是赢得时间使患者转危为安地保证,同时对患者来说又是心照不宣地支持、鼓舞和依靠力量,针对患者各种情绪反应及时采用交谈、笔认、手势辨认,充分了解其需要,增强其战胜疾病地信心。2 评价方法 肢体肌力地判断按6级分法,治疗后肌力恢复及以上为改善。运动性失语以能发单字音以上为改善,感觉性失语以能听懂部分语言为改善等。心理状况以与医护人员接触情况而定,能与医护人员部分交流者为改善。大小便功能以主动而顺利排便地改善。3 统计学方法 结果以频数表示,统计学处理采用四格表资料地χ2检验。3 结果两组生理功能及心理状况改善情况比较 见表1。表1 两组生理功能及心理状况改善情况比较 (略)4 讨论脑梗死作为威胁中老年人健康地神经系统常见病,其各种功能恢复状况直接影响患者病后生活质量,也为家庭和减轻负担。观察组实施整体护理后脑梗死患者恢复状态结果表明,患者肢体肌力、语言功能、大小便功能及心理状况明显优于对照组。护理过程从单纯疾病护理转向整体护理,从而提高了护理质量,使患者心理、躯体等各方面最大限度受益。

脑卒中相关论文摘要

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康丹lian

Increased Blood Sugar on hemorrhagic stroke (hemorrhagic apoplexy) the occurrence and development are very important influence, not only as an important risk factor involved in the beginning of HA, resulting in increased incidence of disease, but also to HA after the occurrence of pathological process has a catalytic role to enable hematoma volume expansion, increased edema, increased impairment, affect the   High blood sugar involved in the mechanism of HA, are manifold, including: lipid metabolic abnormalities, carotid artery remodeling, endothelial dysfunction, platelet dysfunction, hypercoagulability, insulin Expansion of infarct size and high blood sugar and promoting the development of HA mainly caused by acid poisoning, ischemic injury in areas of apoptosis and other   Vascular endothelial growth factor (VEGF) and cyclooxygenase (COX-2) and cerebral vascular disease, has attracted people's Vascular endothelial growth factor induced by the prominent role of angiogenesis in vivo and improve vascular permeability; discovered in recent years it also has to stimulate the neurons, glial cells, axonal growth and survival COX (cyclooxygenase, COX), is catalyzed arachidonic acid (arachidonic acid, AA) synthesis of prostaglandins (prostgalandin, PG) and thromboxane (thromboxan, TX) of the rate-limiting One COX-1 for structural type, exist in most organizations, the catalyst is generated to maintain the normal structure of the PG; COX-2 is induced in physiological conditions, COX-2 in most tissues at very low copy number However, IL-1, TNF and many other inflammation-stimulating factor can induce COX-2 However, current vascular endothelial growth factor and cyclooxygenase Most studies focused on the relationship between cerebral ischemia and brain edema after intracerebral hemorrhage on the dynamic changes of VEGF, COX-2 expression in correlation among   In recognition of hyperglycemia on cerebral hemorrhage injury in danger at the same time, control, treatment of blood glucose levels become a means of treating cerebrovascular disease, in particular, is used to reduce blood sugar levels of insulin into the acute stroke treatment Has been found that insulin on acute cerebral hemorrhage around the brain tissue has a protective effect of ischemic Possible mechanisms are: the brain has been found that the existence of insulin receptors, insulin and insulin receptor binding may reduce the brain cells of glucose uptake, thereby reducing the storage of sugar within the brain cells, reduce lactic acid produced by the substrate, fundamentally correct cellular acidosis; the same time, can also lower blood sugar, insulin concentration, increased bleeding surrounding edema and effective blood supply, resulting in relatively low perfusion state of high blood sugar, thereby improving effect of brain damage was the   In order to understand these two cytokines and diabetes mellitus the relationship between cerebral hemorrhage injury, this study of diabetes on the basis of the model to be adopted by autologous blood injection method to establish a stable animal model of cerebral hemorrhage in this dynamic observation of cerebral hemorrhage on the basis of After the behavioral and brain water content trends, analysis VEGF and COX-2 in the hemorrhagic brain tissue distribution and expression changes, and then explore the VEGF and COX-2 in brain tissue damage in cerebral hemorrhage the role and significance, compared to diabetes rats and normal blood sugar difference between the volume of brain edema in rats with an initial observation of the two factors in diabetic rats and normal blood sugar difference between the expression of rat brain hemorrhage, with a view to the treatment of cerebral hemorrhage provide new ways and   Materials and methods   Experimental animals and grouping  Healthy adult male Wistar rats, a total of 96, weighing 250 to 280 grams from the Experimental Animal Center of Zhengzhou U In accordance with the principles of randomized experimental animals were divided into four groups, namely sham operation group, normal blood glucose group, high glucose group and the insulin intervention Prizes will be awarded 4 points each time: 6h, 24h, 72h, At each time points are located at 6    High blood sugar and insulin production in rat model of intervention methods  Prepared by the light of STZ-induced hyperglycemia in With STZ 60mg/kg, high blood sugar and insulin in the intervention group rats a single intraperitoneal Value for four rats with normal blood sugar a 6mmol / L, a week after injection, blood glucose ≥ 1mmol / L for a successful model for alternative Model of high blood sugar after the success of the intervention group I rats were normal insulin, abdominal subcutaneous injection, 3 times / d, 4U / times qd for 3 days, the measured blood sugar value of the normal
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wujiesysu

回答 脑卒中早期康复治疗的研究近况,医学论文,快易捷药品交易网子孙满堂康复师2016-04-05分享保存【摘要】 从早期康复治疗的机制、开始时间、治疗方式、早期康复治疗中需要注意的问题等几个方面对近5年来脑卒中后早期康复治疗现状进行综述。早期康复治疗作为脑卒中患者康复的第一站,采用科学、合理的康复方式,能够最大限度地恢复患者的神经功能,提高其生活质量。在进行早期康复治疗时,同时需对患者进行适当的心理干预,要因人而异,制定合适的康复方案。【关键词】 脑卒中 早期康复随着医学的发展,脑卒中的死亡率明显下降,但其致残率仍居高不下,达80%以上[1]。此类病人生活质量降低,给家庭和社会都带来了沉重的负担,因此促进病人各项功能的尽快恢复是医务人员关注的重点问题。早期康复治疗能够明显改善病人的各种功能和预后,提高病人的生活质量。本文将脑卒中后早期康复治疗的近况作一综述。1 早期康复治疗的机制脑可塑性和大脑功能重组理论是康复治疗中枢神经系统(CNS)损伤最重要的理论基础。缪鸿石等[2]认为,通过反复的特定的康复训练可使脑损伤区丧失的神经功能由原不承担该区功能的脑区部分代偿。经失神经超敏反应,潜伏通路和突触的启用及轴突出芽等机制[3]可实现CNS的功能重组。早期康复治疗可以促使潜伏通路和突触的启用,大脑对刺激发生反应性的突触形成,周围神经组织通过轴突的侧枝芽生,可能使临近失神经支配的组织重新获得支配,病灶周围组织的代偿使神经反馈回路得以重建。早期康复针对病灶周围半暗带,通过增加脑血流量(CBF),从而改善短期内尚存活的脑细胞。李飞等[4]的研究证实,早期康复组大脑平均CBF比对照组明显升高(P<05)。CBF的增加对减少半暗带区神经细胞死亡有益,反复的感觉冲动传入中枢,对轴突出芽,潜伏通路和突触的启用具有十分重要的作用。2 早期康复治疗开始的时间以前普遍认为脑卒中后半年以内开始的康复治疗都属早期康复治疗。目前,康复医学专家普遍认为,只要急性脑卒中病人生命体征稳定,神经系统症状不再进展,48 h后即可开始康复治疗,也有学者认为早期康复在生命体征稳定后12 h开始[5]。对于中枢神经损伤的再生与修复过程而言,有研究认为偏瘫病人运动功能的恢复可在发病数日开始,1~3个月可达到最大程度的恢复,3个月后恢复减慢,6 提问 脑卒中康复的选题背景,目的及意义 回答 目地就让患者康复昂 更多2条 
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