Wijnia Jan W
Slingedael Center of Expertise for Korsakoff Syndrome, Slinge 901, 3086 EZ Rotterdam, The Netherlands.
J Clin Med. 2022 Nov 15;11(22):6755. doi: 10.3390/jcm11226755.
The purpose of this article is to improve recognition and treatment of Wernicke-Korsakoff syndrome. It is well known that Korsakoff syndrome is a chronic amnesia resulting from unrecognized or undertreated Wernicke encephalopathy and is caused by thiamine (vitamin B1) deficiency. The clinical presentation of thiamine deficiency includes loss of appetite, dizziness, tachycardia, and urinary bladder retention. These symptoms can be attributed to anticholinergic autonomic dysfunction, as well as confusion or delirium, which is part of the classic triad of Wernicke encephalopathy. Severe concomitant infections including sepsis of unknown origin are common during the Wernicke phase. These infections can be prodromal signs of severe thiamine deficiency, as has been shown in select case descriptions which present infections and lactic acidosis. The clinical symptoms of Wernicke delirium commonly arise within a few days before or during hospitalization and may occur as part of a refeeding syndrome. Wernicke encephalopathy is mostly related to alcohol addiction, but can also occur in other conditions, such as bariatric surgery, hyperemesis gravidarum, and anorexia nervosa. Alcohol related Wernicke encephalopathy may be identified by the presence of a delirium in malnourished alcoholic patients who have trouble walking. The onset of non-alcohol-related Wernicke encephalopathy is often characterized by vomiting, weight loss, and symptoms such as visual complaints due to optic neuropathy in thiamine deficiency. Regarding thiamine therapy, patients with hypomagnesemia may fail to respond to thiamine. This may especially be the case in the context of alcohol withdrawal or in adverse side effects of proton pump inhibitors combined with diuretics. Clinician awareness of the clinical significance of Wernicke delirium, urinary bladder retention, comorbid infections, refeeding syndrome, and hypomagnesemia may contribute to the recognition and treatment of the Wernicke-Korsakoff syndrome.
本文旨在提高对韦尼克-科尔萨科夫综合征的认识及治疗水平。众所周知,科尔萨科夫综合征是一种因未被识别或治疗不充分的韦尼克脑病导致的慢性失忆症,由硫胺素(维生素B1)缺乏引起。硫胺素缺乏的临床表现包括食欲不振、头晕、心动过速和膀胱潴留。这些症状可归因于抗胆碱能自主神经功能障碍,以及意识模糊或谵妄,这是韦尼克脑病经典三联征的一部分。在韦尼克阶段,严重的合并感染(包括不明原因的败血症)很常见。这些感染可能是严重硫胺素缺乏的前驱症状,如在一些描述感染和乳酸酸中毒的病例中所示。韦尼克谵妄的临床症状通常在住院前几天内或住院期间出现,也可能作为再喂养综合征的一部分出现。韦尼克脑病主要与酒精成瘾有关,但也可发生于其他情况,如减肥手术、妊娠剧吐和神经性厌食症。酒精相关的韦尼克脑病可通过在行走困难的营养不良酒精患者中出现谵妄来识别。非酒精相关的韦尼克脑病的发病通常以呕吐、体重减轻以及硫胺素缺乏导致的视神经病变引起的视觉症状等为特征。关于硫胺素治疗,低镁血症患者可能对硫胺素无反应。在酒精戒断的情况下或质子泵抑制剂与利尿剂联合使用的不良反应中尤其如此。临床医生对韦尼克谵妄、膀胱潴留、合并感染、再喂养综合征和低镁血症的临床意义的认识可能有助于韦尼克-科尔萨科夫综合征的识别和治疗。