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糖尿病患者出现手麻就是糖尿病神经病变?症结其实出在患者的睡姿上

2022-08-13 呼吸科的故事 呼吸科的故事

我们对于很多概念认识过于模糊,有些医生是凭感觉做事,而不是通过一个个具体病例去学习和掌握知识,错过了成长的机会。

每天查房都有一个小故事,故事虽小,却有一定的教育意义。今天给大家带来的故事是一个由于没有仔细询问病史闹出的笑话。

韩老爷子今年88岁,但平时身体状态不错,既往在12年前曾因胃癌行胃大部切除术,还有多年的高血压病史,目前服用氨氯地平降压药,血压控制尚可。除此之外没有其他疾病史。

老爷子这一次因为发热、咳嗽前来住院,胸部CT显示有双肺散在斑片状渗出影,诊断”肺炎“住院,入院后体温很快恢复正常,精神状态也不错。可是老爷子说自己的手麻、脚麻,生化检查发现血糖增高(空腹7.5~11.55mmol/L),糖化血红蛋白7.3%,主管医生考虑会不会有糖尿病神经病变,于是一方面联系内分泌科,另一方面直接给病人服用甲钴胺。

今天查房时,管床医生汇报完病史,我向患者进一步了解情况,患者告诉我们--他只有右手中间几根手指麻木,右手大拇指和小指均没有异常,左手和双下肢也没有麻木感。

我一听就明白这根本不可能是什么糖尿病周围神经病变,因为患者是单手中的中间三指麻木,而糖尿病周围神经病变通常是双侧同时发生的。我推测患者的症状可能是神经压迫的表现,其中导致正中神经压迫的腕管综合征可能性最大。

腕管综合征(Carpal Tunnel Syndrome)是最常见的周围神经卡压性疾患,也是手外科医生最常进行手术治疗的疾患。腕管综合征发生的原因,是腕管内压力增高导致正中神经受卡压。腕管是一个由腕骨和屈肌支持带组成的骨纤维管道。前者构成腕管的桡、尺及背侧壁,后者构成掌侧壁。腕管顶部是横跨于尺侧的钩骨、三角骨和桡侧的舟骨、大多角骨之间的屈肌支持带。正中神经和屈肌腱由腕管内通过(屈拇长肌腱,4条屈指浅肌腱,4条屈指深肌腱)。 

尽管腕管两端是开放的入口和出口,但其内组织液压力却是稳定的。腕管内最狭窄处距离腕管边缘约50px,这种解剖特点与腕管综合症患者切开手术时正中神经形态学表现相符。正中神经走行在屈肌支持带下方,紧贴屈肌支持带。在屈肌支持带远端,正中神经发出返支,支配拇短展肌,拇短屈肌浅头,和拇对掌肌。其终支是指神经,支配拇、示、中指和环指桡侧半皮肤   。

无论是腕管内的内容物增加,还是腕管容积减小,都可导致腕管内压力增高。最常见的导致腕管内压力增高的原因,是特发性腕管内腱周滑膜增生和纤维化,其发生的机理尚不明了。有时也可见到其他一些少见病因,如屈肌肌腹过低,类风湿等滑膜炎症,创伤或退行性变导致腕管内骨性结构异常卡压神经。

常见症状包括正中神经支配区(拇指,示指,中指和环指桡侧半)感觉异常和/或麻木。夜间手指麻木很多时候是腕管综合征的首发症状,许多患者均有夜间手指麻醒的经历。很多患者手指麻木的不适可通过改变上肢的姿势或甩手而得到一定程度的缓解。

正中神经也存在变异,但是不论怎么变异,大拇指都是会受累的。但是韩大爷大拇指却没有症状,这让我很是不解。

就在我和规培生们分析病情的时候,韩大爷插了一句话:“我平时睡觉喜欢往右边躺,我的右手就垫在我的身体之下。”接着他做了一个示范动作,如下:

我们看到后,恍然大悟到--原来韩大爷的的所谓手麻是因为他的手掌及右手中间三指长期受身体压迫所导致的,根本不是什么糖尿病导致的周围神经病变,因此也不需要用甲钴胺治疗,只要睡觉时改变体位--仰卧位就好了。

感悟:

1.询问病史一定要认真,不要一听到患者说手麻连鉴别分析都不做,直接给患者就戴上某个诊断,给予某种治疗。这种工作习惯和态度不仅不能让我们的诊断水平提高,反而培养了一种懒惰的思维模式,也不可能真正解决病人的问题。

2.我们对于很多概念认识过于模糊,有些医生是凭感觉做事,而不是通过一个个具体病例去学习和掌握知识,错过了成长的机会。其实,糖尿病周围神经病变最常见是脚麻,而不是手麻,它的特点有:(1)从远端开始;(2)有对称性;(3)逐渐向上发展;(4)除了麻,还会有袜套样感觉、踩棉花感、蚁走感等。本患者的临床表现与此相差十万八千里。

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    2022-08-06 ZGMFX29A

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目前认为糖尿病同痴呆有一定的联系,虽然并没有完全阐明这两者之间具体的联系,但是通过多年来临床大量病人的研究,从现象推断,很多糖尿病患者相比于一般人群而言更容易发生痴呆

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全世界每6秒钟就有一个人因糖尿病死亡,中国的糖尿病患者人数已经位居全球第一。

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JAMA子刊:高频(10khz)脊髓刺激对疼痛性糖尿病神经病变患者的影响

循证治疗指南应考虑10 kHz SCS在连续护理中的定位。在实践中,对常规治疗反应不足的PDN患者应考虑使用10khz SCS。

Radiology:糖尿病多发性神经病变患者的3T MR神经成像

尽管一些临床和血清学危险因素,如高血糖、血脂异常和肾功能下降已经在体内和体外研究中被确定,但糖尿病多发性神经病变(DPN)的确切代谢过程仍不明确。

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