scholarly journals Don’t seek, don’t find: The diagnostic challenge of Wernicke’s encephalopathy

Author(s):  
Sara Kohnke ◽  
Claire L Meek

Wernicke’s encephalopathy is caused by thiamine deficiency and has a range of presenting features, including gait disturbance, altered cognitive state, nystagmus and other eye movement disorders. In the past, Wernicke’s encephalopathy was described almost exclusively in the alcohol-dependent population. However, in current times, Wernicke’s encephalopathy is also well recognized in many other patient groups, including patients following bariatric surgery, gastrointestinal surgery, cancer and pancreatitis. Early recognition of Wernicke’s encephalopathy is vital, as prompt treatment can restore cognitive or ocular function and can prevent permanent disability. Unfortunately, Wernicke’s encephalopathy is often undiagnosed – presumably because it is relatively uncommon and has a variable clinical presentation. Clinical biochemists have a unique role in advising clinicians about potential nutritional or metabolic causes of unexplained neurological symptoms and to prompt consideration of thiamine deficiency as a potential cause in high-risk patient groups. The aim of this review is to summarize the clinical features, diagnosis and treatment of Wernicke’s encephalopathy and to highlight some non-traditional causes, such as after bariatric surgery.

2011 ◽  
Vol 2011 ◽  
pp. 1-3 ◽  
Author(s):  
Akinori Uruha ◽  
Toshio Shimizu ◽  
Tomoji Katoh ◽  
Yasushi Yamasaki ◽  
Shiro Matsubara

We report a 74-year-old man with Wernicke's encephalopathy (WE) whose only prior illness was peptic ulcer disease. Upper gastrointestinal endoscopy demonstrated gastric ulcer scars accompanied by marked deformity, without pathologic evidence of malignancy. WE due to peptic ulcer disease in previous reports was substantially associated with thiamine deficiency due to recurrent vomiting or surgical procedures. In our case, however, there was no history of vomiting or gastrointestinal surgery. Besides, we thoroughly ruled out other known clinical settings related to WE. There is the possibility that peptic ulcer disease itself provoked thiamine deficiency due to malabsorption.


2017 ◽  
Vol 16 (1) ◽  
pp. 54-56 ◽  
Author(s):  
Tahera Begum ◽  
Shafiul Hasan ◽  
M Nazimuddin

Wernicke’s encephalopathy is a common and preventable acute neurological symptom due to deficiency of thiamine. Alcoholism also causes Thiamine deficiency. It can occur in non-alcoholic conditions such as prolonged starvation, hyperemesis graviderum, bariatric surgery, HIV, AIDS. The characteristics clinical triad of disease is ophthalmoplagia,ataxia & global confusion. Here a patient was studied who was diagnosed on M.R.I as Wernicke’s encephalopathy.Chatt Maa Shi Hosp Med Coll J; Vol.16 (1); Jan 2017; Page 54-56


2015 ◽  
Vol 24 (1) ◽  
pp. 77-82 ◽  
Author(s):  
Angelo Restivo ◽  
Mauro Giovanni Carta ◽  
Anna Maria Giulia Farci ◽  
Laura Saiu ◽  
Gian Luigi Gessa ◽  
...  

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 709-713
Author(s):  
Piergiorgio Fedeli ◽  
Richard Justin Davies ◽  
Roberto Cirocchi ◽  
Georgi Popivanov ◽  
Paolo Bruzzone ◽  
...  

AbstractCarl Wernicke described the disease bearing his name in 1881 and reported three cases characterized by the presence of mental confusion, ataxia, and ophthalmoplegia. Wernicke’s disease is mainly observed in alcoholic patients, due to decreased vitamin intake as a consequence of an unbalanced diet, and a reduction of absorption due to the effects of alcohol. Likewise, inadequate vitamin intake is prevalent in older patients. Wernicke’s encephalopathy due to inappropriate total parenteral nutrition (TPN) occurs infrequently; recently, there is an increase in the literature concerning Wernicke’s encephalopathy in patients after general and bariatric surgeries. We present two cases of Wernicke’s encephalopathy after oncologic gastrointestinal surgery by failure to administer vitamin B1 during TPN; to our knowledge, these are the first two cases of Wernicke’s encephalopathy after colorectal surgery for cancer. In our opinion, timely diagnosis and treatment are mandatory to avoid nonfunctional recovery and consequent malpractice legal actions as well as an increase in the health-care costs correlated with the prolonged hospital stay and with the nonfunctional recovery.


2021 ◽  
Vol 14 (3) ◽  
pp. e239977
Author(s):  
Kaushiki Kirty ◽  
Yashendu Sarda ◽  
Annu Jacob ◽  
Delanthabettu Venugopala

We report a case of a 26-year-old pregnant woman, who presented with subacute limb weakness. This was initially suspected to be Guillain-Barre syndrome but subsequently found to be the motor neuropathy of dry beriberi (vitamin B1, thiamine deficiency) along with associated Wernicke’s encephalopathy (WE). The underlying cause was revealed as hyperemesis gravidarum (HG). HG complicates up to 3% of pregnancies and if severe, without nutritional supplements, may lead to electrolyte disturbances, calorie loss and vitamin deficiency. Although the association of HG and WE was first reported in 1939, it remains an under diagnosed condition with potential for serious and permanent neurological deficits, and some mortality, in both mother and baby. Early recognition of the problem, with timely and careful fluid, electrolyte, glucose and vitamin replacement is needed to avoid complications. We highlight current best practice in the treatment of WE. An open mind to the possibility of HG complications in any pregnant woman presenting with neurological symptoms is probably the most important lesson to learn from the front line.


2019 ◽  
Vol 12 (1) ◽  
pp. e227412 ◽  
Author(s):  
Timothy Xin Zhong Tan ◽  
Kheng Choon Lim ◽  
Charles Chan Chung ◽  
Than Aung

A 56-year-old teetotaller man with hypertension and gout presented with a week duration of painless worsening diplopia on a background of loss of weight and appetite, generalised lethargy and weakness for 1 year. On examination, he was noted to be hypothermic and tachycardic with generalised muscle wasting. Proximal myopathy, lower limb fasciculations and areflexia, restricted bilateral eye abduction and nystagmus were observed. Blood investigations demonstrated compensated lactic acidosis, acute kidney injury and leucocytosis. A nerve conduction study showed severe length-dependent axonal sensorimotor polyneuropathy. This was a diagnostic dilemma until an MRI brain revealed symmetrical signal abnormality and enhancement in the periaqueductal area indicative of Wernicke’s encephalopathy, caused by thiamine deficiency from poor nutrition. Beriberi, also caused by thiamine deficiency, accounted for his tachycardia, polyneuropathy, areflexia, hypothermia and biochemical abnormalities. Both beriberi and Wernicke’s encephalopathy are medical emergencies, which were treated with intravenous thiamine to good effect.


1993 ◽  
Vol 27 (4) ◽  
pp. 638-652 ◽  
Author(s):  
Bruce Spittle ◽  
Josie Parker

Wernicke's encephalopathy producing an altered mental state may occur in malnourished psychiatric patients even in the absence of alcohol abuse. A case is reported of a woman, aged 61 years, with schizophrenia who refused her medication for four months, had the delusion she was dying from a tumour, and withdrew to her bed with a neglect of her nutrition. She was committed to hospital in a mute unresponsive state and after taking some food and fluids for four days lapsed into coma. She responded within three hours to the administration of thiamine. Clinicians need to remain vigilant to the possibility that an altered mental state in malnourished patients may be due to thiamine deficiency rather than to the primary psychiatric disorder. If doubt exists as to the presence of Wernicke's encephalopathy, then parenteral thiamine should be administered.


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