低血糖颅脑损伤.ppt_第1页
低血糖颅脑损伤.ppt_第2页
低血糖颅脑损伤.ppt_第3页
低血糖颅脑损伤.ppt_第4页
低血糖颅脑损伤.ppt_第5页
免费预览已结束,剩余44页可下载查看

下载本文档

版权说明:本文档由用户提供并上传,收益归属内容提供方,若内容存在侵权,请进行举报或认领

文档简介

1、低血糖症相关的神经系统损害 酒钢医院神经内、外科,Hypoglycemia in diabetesCryer PE et al. Diabetes Care.2003 June;26(6):1902-1912.,一次严重的医源性低血糖 或由此诱发的心血管事件可能会抵消 一生维持血糖在正常范围所带来的益处,高血糖,低血糖,高,低,低血糖诊断标准,对具体患者来说,个体的低血糖标准可能有较大差异,症状与血糖值可以不同步 当血糖小于2.8mmol/L,可诊断为低血糖症 一般患者发生低血糖时出现低血糖(Whipple)三联征,即:低血糖症状和体征;血糖浓度低;血糖浓度升高至正常水平时症状消失或显著减轻,

2、引起低血糖的原因,最常见的是降糖药物使用不当所致。 对胰岛素过度敏感。 胰岛素过多:胰岛素瘤,异位胰岛素分泌瘤。 反应性低血糖症:早期糖尿病,功能性低血糖,营养性低血糖 肝脏疾病 中毒:药物中毒,酒精中毒,大量食荔枝 糖原累积病 胃大部分切除术后 肾上腺皮质或垂体前叶疾病,急性低血糖时的生理反应,增加拮抗激素的分泌,以拮抗胰岛素的作用,升高血糖 使心血管系统发生相应变化,以利于葡萄糖在体内各种组织间的转运 产生一系列预警症状,如饥饿,以迅速纠正低血糖,血糖水平及生理应答反应(1),血糖水平降低至 4.6 mmol/l时,胰岛素分泌受抑制 血糖水平在 3.8mmol/l时,胰高血糖素、肾上腺素开

3、始释放 血糖水平在 3.0mmol/l时,开始出现低血糖症状 血糖水平低于2.8mmol/l时,患者出现进行性认知能力下降 血糖低于1.0mmol/l时,患者出现昏迷,血糖水平及生理应答反应(2),低血糖的表现,肾上腺交感神经症状 中枢神经症状,肾上腺交感神经症状,低血糖的症状:交感神经和肾上腺髓质兴奋的表现: 焦急不安 情绪激动 手足颤抖、软弱 饥饿感 心慌 出汗 面色苍白 当血糖降至60ml/dl(3.3mmol/L)以下时就要注意是否出现上述症状。,中枢神经症状,如果血糖低于40mg/dl(2.2mmol/L),就可能出现下述症状: 头痛 躁动 疲倦,可有幻觉 意识丧失 视物不清 语言迟

4、钝 神经过敏 癫痫发作 是由于脑细胞葡萄糖供应不足所致。( 通常低血糖发展很快),中枢神经受抑的表现,血糖下降而持久所致。表现为中枢缺氧缺糖症群,越高级的中枢受抑制越早,恢复越迟。 大脑皮层:意志朦胧,头痛头晕,嗜睡,精神失常。 皮层下中枢:神志不清,躁动惊厥,瞳孔散大。 延脑:昏迷,反射消失,呼吸浅弱,血压下降,瞳孔缩小,历时较久者,不易恢复。 混合性:兼有上二种表现,多见。,低血糖的不典型表现,意识障碍合并抽搐,易误诊为癫痫 精神症状,烦躁不安,易激惹,情绪激动,语无伦次,有骂人、打人,幻视有时可误诊为脑病及酒精中毒 神志清楚,出现肢体,言语障碍,容易误诊为脑血管病 昏迷,瞳孔不等大,对光

5、反射迟钝,易误诊为脑疝,低血糖的危害,1型糖尿病患者中至少4%是死于低血糖 心血管系统功能 神经系统 其它:眼睛、肾脏 社会活动(学习、就业等),低血糖影响心血管系统功能,心率增加 脉压增加 静息期心肌缺血 心绞痛 心梗,低血糖相关的神经系统损害,低血糖的神经系统损害在有关著作和论文中被作为“神经低血糖”、“低血糖脑病”“低血糖偏瘫”,“低血糖昏迷”,“低血糖危象”,“缺糖性脑病”等等。 有人认为为了便于对本病综合征 的研究,称做“低血糖的神经系统损害”较为合适,低血糖性脑病可能发病机制,低血糖引起交感神经兴奋而导致脑血管痉挛 原有脑动脉硬化的动脉狭窄所引起神经功能损伤 低血糖引起神经系统的选

6、择受损,低血糖影响大脑功能,脑干脊髓,Rostrocaudal sensitivity to neuroglycopenia,脑皮质 海马,基底神经节 前部丘脑,低血糖对脑损害的Himwich分期,分期 症状体征 动静脉氧压差 EEG,I期:大脑皮质损害 II 期:脑皮质下间脑损害 III 期:中脑损害 IV 期:神经元损害 V 期:神经元损害及生命中枢损害,定向力下降,吐词不清,嗜睡 感觉分辨力丧失,对刺激无反应,但有自主性运动行为,心率快,瞳孔扩大 张力性肌强直,眼非同向偏斜,跖反射异常 转动头部可诱发四肢的伸肌痉挛 昏迷、呼吸弱、心动过缓,眼球固定,瞳孔缩小,无对光反射,体温下降,6.8

7、 2.6 1.8,慢波活动增加,节律(814cps) 带慢波活动 节律(14cps ) 节律极慢或无脑电波,Himwich HE.In: Brain Metabolism and Cerebral Disorders.Baltimore,William blood volume was in fact increased by 20%25%, a finding that is also suggestive of maximal vasodilatation (see text). (d) Graph of single-oxel MR spectroscopic data in affec

8、ted right cerebral cortex shows decreased N-acetylaspartate (NAA) level, preserved choline (Cho) and creatine (Cr) levels, and no evidence of abnormal lactate level (arrow1.3 ppm).,大脑皮质损害,丘脑未累及,Diffusion-weighted magnetic resonance (MR) imaging (A) and T2-weighted MR imaging (B) showed a diffuse cor

9、tical high signal. The brainstem,cerebellum, and thalamus were spared as were the dorsofrontal cortex and occipital poles. The signal change in the hippocampus was relatively small on diffusion-weighted MR imaging. On T2-weighted MR imaging, a focal high-signal lesion was seen in the thalamus bilate

10、rally (more prominent on the left side) and in the centrum semiovale. Diffuse white matter lesions were seen on the T2-weighted MR image,新生儿低血糖MR表现,病例1MR I 生后34 h出现低血糖表现, 58 h入院, 血糖为1. 7mm ol/L。A D 为生后3 d所见。A, B分别为矢状面T1W I和横断面T2W I, 可见顶枕叶T1W I低信号, 而T2W I改变不明显; C为DW I, 可见顶枕叶皮层高信号, 提示明显的细胞毒性水肿; D F为生后

11、13 d T1W I( D) , T2W I( E )和DW I( F)图像, 枕部可见明显的T1W I低信号, T2W I高信号, 而DW I顶枕部转为低信号, 提示皮层发生水肿坏死。,皮质、基底节、脑室旁白质损害,Fig. 1 ad (Patient 5) A 57-year-old diabetic man was found in a coma 6 h after he was last seen. Glucose level was 16 mg/dL at presentation. Fluid-attenuated inversion recovery image (a) on t

12、he day of admission shows slightly increased signal intensity in the cerebral cortex and basal ganglia. Diffusion-weighted images (b, c) clearly show bilaterally symmetrical hyperintense lesions in the cerebral cortex, basal ganglia, and periventricular white matter (arrows). ADC map (d) obtained at

13、 the same level as c shows corresponding reduced ADC,内囊、放射冠损害,Figure 1. Diffusion-weighted MRI on admission showing the hyperintensity lesions within the bilateral internal capsule, corona radiata, and frontoparietal cortex. Note that bilateral hippocampi do not disclose any hyperintensity lesions.,

14、Figure 2. Diffusion-weighted MRI 10 days after glucose infusion showing regression of the hyperintensity lesions.,半卵圆中心非对称损害,Fig. 5 a, b (Patient 17) A 91-year-old diabetic man admitted for drowsiness for 10 h. Glucose level was 24 mg/dL at presentation .Diffusion-weighted image (a) on the day of ad

15、mission shows focal area of unilateral hyperintense lesion in the left centrum semiovale (arrows) with reduced ADC value (b),放射冠、胼胝体损害,Figure 1. A, Initial DWI (repetition time/echo time/ 4100/96/90; 1000 s/mm2; field of view 230 mm; matrix: 128128) with increased signal intensities in bilateral cor

16、ona radiata and splenium. B, Initial ADC maps with signal reduction also in bilateral corona radiata and splenium corresponding to DWI images.,内囊、胼胝体损害,Figure 1 (A) Diffusion-weighted imaging (DWI) on admission showing hyperintense lesions in the splenium of the corpus callosum and the bilateral pos

17、terior limbs of the internal capsules. (B) DWI obtained 2 h after glucose infusion showing almost full recovery except for a small part of the spleniumof the corpus callosum. (C) DWI obtained 2 days after glucose infusion showing complete regression of the hyperintense lesions.,海马、皮质、胼胝体损害,Figure 2:

18、 Images in 51-year-old man (patient 2) found unconscious, with a Glasgow Coma Scale score of 7 and withdrawal to pain. (a) Fluid-attenuated inversion recovery and (b)DWMRimages show increased signal intensity in the head, body, and tail of the hippocampus bilaterally (arrowheads) and in the cerebral

19、cortex (arrow). (c) T2-weightedMRimage shows bilateral patchy hyperintense lesions in the cerebral cortex ,including the insula (arrow). There is also involvement of the splenium of the corpus callosum (arrowheads) .On (d) corresponding DW MR image, the hyperintense lesions are more prominent than t

20、hey are on c.,胼胝体、脑干损害,Figure 4: Images in 61-year-old man (patient 8) admitted for drowsiness, confusion, left hemiparesis, and slurred speech. (a, b) DW MR images show hyperintense lesions in the left hemipons and the splenium of the corpus callosum. (c, d) Repeat DW MR images obtained 36 hours la

21、ter show no change in the pontine lesion,but reversal of the callosal abnormality.,胼胝体、白质弥漫损害,Fig. 3 ad (Patient 14) A 32-year-old woman was found in a coma 2 days after she was last seen. Glucose level was 33 mg/dL at presentation. Diffusion-weighted images(a, b) on the day of admission show bilate

22、rally symmetrical confluent hyperintense lesions in the periventricular and subcortical white matters. There are also involvements of the corpus callosum and internal capsule. ADC maps (c, d) at the same levels as a and b show decreased ADC in these lesions ;the lesions spared the cortical and deep gray matter,低血糖对眼的影响,低血糖可显著减少玻璃

温馨提示

  • 1. 本站所有资源如无特殊说明,都需要本地电脑安装OFFICE2007和PDF阅读器。图纸软件为CAD,CAXA,PROE,UG,SolidWorks等.压缩文件请下载最新的WinRAR软件解压。
  • 2. 本站的文档不包含任何第三方提供的附件图纸等,如果需要附件,请联系上传者。文件的所有权益归上传用户所有。
  • 3. 本站RAR压缩包中若带图纸,网页内容里面会有图纸预览,若没有图纸预览就没有图纸。
  • 4. 未经权益所有人同意不得将文件中的内容挪作商业或盈利用途。
  • 5. 人人文库网仅提供信息存储空间,仅对用户上传内容的表现方式做保护处理,对用户上传分享的文档内容本身不做任何修改或编辑,并不能对任何下载内容负责。
  • 6. 下载文件中如有侵权或不适当内容,请与我们联系,我们立即纠正。
  • 7. 本站不保证下载资源的准确性、安全性和完整性, 同时也不承担用户因使用这些下载资源对自己和他人造成任何形式的伤害或损失。

评论

0/150

提交评论