老奶奶突发昏迷诊治后考虑脑血管意外 最后却被证实为一常见病

2019-02-22 刘鲁沂 李小丽 田行瀚 危重症病例剖析

65岁女性,因昏迷2小时,伴四肢间断性抽搐、小便失禁且发热入院。经过相关检查及治疗,考虑脑血管意外的可能性较大,但最终被证实为高血糖高渗状态所并发的神经系统症状,连发热也是高血糖脱水导致的脱水热,这到底是怎么回事呢?

65岁女性,因昏迷2小时,伴四肢间断性抽搐、小便失禁且发热入院。经过相关检查及治疗,考虑脑血管意外的可能性较大,但最终被证实为高血糖高渗状态所并发的神经系统症状,连发热也是高血糖脱水导致的脱水热,这到底是怎么回事呢?

一、病例简介

(一)基本资料

患者,女,65岁,退休工人。

(二)主诉、现病史

因“昏迷2小时”入院。入院前2小时,家人发现患者昏迷于床上,呼之不应,伴四肢间断性抽搐、小便失禁,且发热,无大便失禁、呕吐,为求诊治急拨打120,以“昏迷原因待查”收入院。

(三)入院查体

T 38.5℃,P 110次/分,R 20次/分,BP 100/60mmHg,浅昏迷,偶有躁动,双侧瞳孔等大等圆,直径约2.0mm,光反射迟钝,右侧压眶有反应,左侧压眶反应差,唇无发绀,右侧鼻唇沟略浅,双肺呼吸音粗,未闻及干湿啰音。心界不大,心率110次/分,律齐,无杂音。腹软,肝脾肋下未及,肠鸣音正常。双下肢无水肿。神经系统:颈稍强,布鲁津斯基征弱阳性,克尼格阴性;肌力查体不配合,肌张力减弱,双侧巴宾斯基征弱阳性。

(四)辅助检查

入院急查头颅CT双侧颞顶叶少量硬膜下血肿;血糖示:33.6mmol/L;尿酮体:1+,电解质肝肾功能正常,血常规示:白细胞计数11.6×109/L,中性粒细胞百分比80%,血红蛋白78g/L,血小板计数236×109/L。

(五)入院诊断

昏迷原因待查:①脑梗死?②高血糖高渗状态?③病毒性脑炎?

(六)治疗经过

入院后给予控制血糖[0.1U/(kg·h)]、补液、降颅压、镇静止抽、改善脑细胞代谢等药物应用。入院第2天:患者血糖降至12mmol/L左右,但仍间断抽搐,昏迷程度较前减轻,处于昏睡状态,心率呼吸平稳,余查体无明显变化,给予复查头颅CT未见异常(硬膜下血肿消失)。考虑老年女性,既往无明显病史(但亦无相关检查),本次昏迷、发热、血糖高伴抽搐为主要症状,但入院第2天未再发热,余症状仍存在,查体处于昏睡状态,双侧瞳孔等大等圆,直径约2mm,光反射迟钝,右侧压眶有反应,左侧压眶反应差,唇无发绀,右侧口角松弛,右侧鼻唇沟略浅,双肺呼吸音稍粗糙,未闻及干湿啰音。心界不大,心率110次/分,律齐,无杂音。腹软,肝脾肋下未及,肠鸣音正常。双下肢无水肿。神经系统:颈稍强,布鲁津斯基征弱阳性,克尼格阴性;肌力查不配合,肌张力减弱,双侧巴宾斯基征弱阳性。复查头颅CT(已发病后24小时)未见异常(硬膜下血肿消失)。入院后6小时左右,血糖一直维持在10mmol/L左右,若是糖尿病高渗性昏迷应该已经清醒,因而不支持糖尿病高渗性昏迷;患者无脑膜刺激征弱阳性,但入院后未应用退热、抗感染的情况下今日未再发热,且无头痛、呕吐等颅高压症症状,因此不支持脑炎的诊断,因存在神志不清、口角歪斜、一侧肌力偏差、双侧巴氏征弱阳性,因此还是考虑脑血管意外的可能性较大,且患者为交叉性瘫痪、瞳孔偏小,多提示发病部位在脑干,头颅CT未见异常,可能是患者还未形成梗死。另外,患者入院时有明显发热,查体脑膜刺激征弱阳性,尽管未再发热,但不能排除中枢神经系统感染,故加用抗病毒药物。入院第3天:患者未发热,血糖控制11mmol/L左右,意识障碍较前减轻,处于意识模糊,查体能部分配合,精神差,言语稍不清,右侧口略松弛,颈稍强,左侧上肢肌力Ⅳ级,余肢体肌力正常,余查体同入院第2天,查头颅MRI仍无亦常,随行腰椎穿刺,但多人、多次、多腰椎间隙穿刺成功后均无脑脊液流出,负压抽吸才见清晰透明的脑积液,抽6ml送检,常规回示:细胞数为0,黏蛋白试验阴性。生化示:糖7mmol/L,余正常。中枢神经感染可排除,3天查头颅MRI仍无异常,也排除脑血管意外,主要考虑高血糖高渗状态所并发的神经系统症状,停用一切降颅压及抗病毒药物,继续控制血糖、补液,患者神志渐转清,追述病史,患者近半年来就烦渴多饮多尿,未治疗,因此推测其原来就有糖尿病,只是未检查及治疗。治疗2周:该患者症状完全消失,痊愈出院。

二、病例剖析

高血糖高渗状态(hyperglycemic hyperosmolar status,HHS),是糖尿病急性代谢紊乱的另一临床类型,以严重高血糖、高血浆渗透压、脱水为特点,无明显酮症酸中毒,患者常有不同程度的意识障碍或昏迷。“高血糖高渗状态”与以前所称“高渗性非酮症性糖尿病昏迷”略有不同,因为部分患者并无昏迷,部分患者可伴有酮症。多见于老年糖尿病患者,原来无糖尿病病史,或仅有轻度症状,用饮食控制或口服降糖药治疗。

本病诱因为引起血糖增高和脱水的因素:急性感染、外伤、手术、脑血管意外等应激状态,使用糖皮质激素、免疫抑制剂、利尿剂、甘露醇等药物,水摄入不足或失水,透析治疗,静脉高营养疗法等。有时在病程早期因误诊而输入大量葡萄糖液或因口渴而摄入大量含糖饮料可诱发本病或使病情恶化。本病起病缓慢,最初表现为多尿、多饮,但多食不明显或反而食欲减退,以致常被忽视。渐出现严重脱水和神经精神症状,患者反应迟钝、烦躁或淡漠、嗜睡,逐渐陷入昏迷、抽搐,晚期尿少甚至尿闭。就诊时呈严重脱水、休克,可有神经系统损害的定位体征,但无酸中毒样大呼吸。与DKA相比,失水更为严重、神经精神症状更为突出。

因此,该患者的前因后果就一清二楚了,患者原有糖尿病,未检查与治疗,长时间的高血糖,使其脱水渐加重,以致出现昏迷伴抽搐,其发热也是脱水导致的脱水热,入院后补液量不足,并应用甘露醇等脱水药,使在血糖得到控制的情况下病情缓解较慢,在严重脱水的情况下,致使其脑积液明显减少,而不能自动流出,出现了罕见的需抽吸方可见的脑积液,其神经系统症状均为高血糖高渗状态所引起,因此用一元论完全可以解释本患者。

通过这个病例,可以得到如下经验教训:①一部分糖尿病患者及家属是不知道患其病的,所以其诉无糖尿病病史,不一定可靠;②高血糖高渗状态可以出现发热、神经系统体征,不要误认为一定是脑血管意外,但它与脑血管意外的体征有一定的区别,就是定位不太明确,且颅脑影像检查无异常;③高血糖高渗状态可出现轻度的脑膜刺激征;④行腰椎穿刺时,若感觉进针很顺利,但不出脑积液,可以试抽一下,以防遇到脑脊液压而不能自行流出的情况。

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    2019-07-27 huirong
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    2019-02-25 jyzxjiangqin

    脑血管意外的治疗。

    0

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    2019-02-24 wgx307

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