Busani Stefano, Bonvecchio Cinzia, Gaspari Arianna, Malagoli Marcella, Todeschini Alessandra, Cautero Nicola, Girardis Massimo
Cattedra di Anestesia e Rianimazione, Policlinico di Modena, Università di Modena e Reggio Emilia, Modena, Italy.
BMC Res Notes. 2014 Oct 14;7:718. doi: 10.1186/1756-0500-7-718.
Wernicke's encephalopathy is an acute neurological disorder resulting from thiamine deficiency mainly related to alcohol abuse. Severe thiamine deficiency is an emerging problem in non-alcoholic patients and it may develop in postoperative surgical patients with risk factors.
We reported a case of a 46 years old woman who underwent, one year before, to cephalic duodenopancreatectomy complicated with prolonged recurrent vomiting. She underwent to a second surgical operation for intestinal sub-occlusion and postoperatively she developed septic shock and hemorrhagic Wernicke's disease. After ICU admission, because of neurological deterioration, she underwent CT scan and MRI that highlighted a strong suspicion for Wernicke's disease. We treated her with an initially wrong low dose of thiamine, then after MRI we increased the dosage with a neurological status improvement. Despite therapeutic efforts used to control septic shock and thrombocytopenia, she died on the 21st day after surgery because of massive cerebral bleeding and unresponsive cerebral edema.
Early detection of subclinical thiamine deficiency is a difficult task, as symptoms may be nonspecific. Wernicke's disease remains a clinical diagnosis because there are no specific diagnostic abnormalities revealed in cerebrospinal fluid, electroencephalogram or evoked potentials. About this, the best aid for a correct diagnosis is the clinical suspicion and clinicians should consider the disorder in any patients with unbalanced nutrition, increased metabolism or impaired food absorption. A hallmark of our case was the brain hemorrhage in the typical areas of the Wernicke's disease, maybe triggered by the thrombocytopenia secondary to sepsis. It might be a good clinical practice administer thiamine to all patients presenting with coma or stupor and risk factors related with thiamine deficiency. Any therapeutic delay may result in permanent neurological damage or death.
韦尼克脑病是一种急性神经障碍,由主要与酒精滥用相关的硫胺素缺乏引起。严重硫胺素缺乏在非酒精性患者中是一个新出现的问题,并且可能在有风险因素的术后外科患者中发生。
我们报告了一例46岁女性病例,该患者一年前接受了胰十二指肠切除术,术后出现长期反复呕吐。她因肠梗阻接受了第二次手术,术后发生感染性休克和出血性韦尼克病。入住重症监护病房后,由于神经功能恶化,她接受了CT扫描和MRI检查,结果高度怀疑为韦尼克病。我们最初用错误的低剂量硫胺素对她进行治疗,然后在MRI检查后增加了剂量,她的神经状态有所改善。尽管采取了治疗措施来控制感染性休克和血小板减少症,但她在术后第21天因大量脑出血和无反应性脑水肿死亡。
亚临床硫胺素缺乏的早期检测是一项艰巨的任务,因为症状可能不具有特异性。韦尼克病仍然是一种临床诊断,因为脑脊液、脑电图或诱发电位中没有显示出特异性的诊断异常。关于这一点,正确诊断的最佳辅助手段是临床怀疑,临床医生应在任何营养不均衡、代谢增加或食物吸收受损的患者中考虑这种疾病。我们病例的一个特点是在韦尼克病的典型区域出现脑出血,可能是由败血症继发的血小板减少症引发的。对所有出现昏迷或昏睡且有硫胺素缺乏相关风险因素的患者给予硫胺素可能是一种良好的临床实践。任何治疗延迟都可能导致永久性神经损伤或死亡。