scholarly journals Starvation-induced diplopia and weakness: a case of beriberi and Wernicke’s encephalopathy

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.


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.


2014 ◽  
Vol 155 (12) ◽  
pp. 469-474
Author(s):  
Adrián Tóth ◽  
Gabriella Aradi ◽  
György Várallyay ◽  
Zsuzsanna Arányi ◽  
Dániel Bereczki ◽  
...  

Wernicke’s encephalopathy is an acute, potentially life-threatening, neurological syndrome resulting from thiamine deficiency. The disorder is still greatly underdiagnosed and, without prompt treatment, the condition can lead to the chronic form of the disease, Korsakoff’s syndrome or even death. In developed countries Wernicke’s encephalopathy has been associated with alcoholism, but in recent years there has been an increasing number of non-alcoholic cases. Authors report the case of a 23-year-old woman who developed oculomotor dysfunction, encephalopathy and ataxia as a result of an extreme diet and use of diet pills. The diagnosis of Wernicke’s encephalopathy was supported by the resolution of neurological signs after parenteral thiamine replacement. This case is presented because of the rare etiology and diagnostic difficulty, and the latest diagnostic and therapic guidelines are also highlighted. Orv. Hetil., 2014, 155(12), 469–474.


Author(s):  
R. O. Kantariya ◽  
O. N. Vetchinnikova ◽  
A. V. Vatazin ◽  
L. A. Sherman

Background. Non-alcoholic Wernicke’s encephalopathy occurs in various somatic conditions with thiamine deficiency, excessive excretion of thiamine, or impaired thiamine metabolism. Very few cases of this pathology have been described in chronic kidney disease (CKD). We present a unique case of non-alcoholic Wernicke’s encephalopathy in a patient with a kidney transplant is presented.Past medical history. The patient underwent kidney transplantation in 2008. Outpatient follow-up by a nephrologist was irregular. Renal graft function remained relatively stable: blood creatinine 200–240 μmol/L, estimated glomerular filtration rate 40–30 mL/min, tacrolimus plasma concentrations tended to increase (5.7–7.6–8.4–10.4 ng/mL); repeated graft biopsy (in 2015 and in 2017) determined the chronic toxicity of calcineurin inhibitors. The patient’s condition worsened in late January 2020: body temperature increased to 38°C, nausea, vomiting, loose, watery stools for up to 5 times per day, 8 kg weight loss, decreased diuresis. A few days later, double vision, shaky gait and then immobility appeared. Biochemical examination results: potassium 3.8 mmol/L, sodium 139 mmol/L, alpha-amylase 159 units/L (norm 0–100 units/L), creatinine 242 mmol/L, urea 13.2 mmol/L; ultrasound signs of pancreatitis. Magnetic resonance imaging (MRI) of the brain: bilateral diffuse lesions of the midbrain, thalamus, and cerebellum. Based on the clinical picture and on brain MRI results, Wernicke’s encephalopathy was diagnosed. Parenteral administration of thiamine had a good effect.Conclusion. Possible mechanisms of the development of Wernicke’s encephalopathy in a patient were discussed. Vigilance is required regarding this disease when metabolic disorders occur in patients with CKD.


2019 ◽  
Vol 2 (1-3) ◽  
pp. 1-7 ◽  
Author(s):  
Kazuteru Monden ◽  
Hiroshi Sadamori ◽  
Masayoshi Hioki ◽  
Satoshi Ohno ◽  
Mitsue Rikimaru ◽  
...  

Background: Wernicke’s encephalopathy (WE) is caused by thiamine deficiency and classically appears as changes in mental status, oculomotor manifestations, and gait ataxia. WE is mostly found in patients with chronic alcoholism and malnutrition, and has rarely been reported following pancreaticoduodenectomy. Case Presentation: A 77-year-old woman was admitted to our hospital complaining of loss of appetite and weakness of the lower extremities. No abnormalities were found on blood examination. One year earlier, she had undergone pancreaticoduodenectomy for bile duct cancer, and pancreatic fistula developed as a postoperative complication. On hospital day 8, her level of consciousness deteriorated, and she experienced difficulty bending the lower limbs and walking. Computed tomography and upper gastrointestinal series showed dilatation of the residual stomach and stenosis of the gastrojejunostomy. Laboratory test results were normal except for blood gas analysis, which revealed severe lactic acidosis. A diagnosis of WE was suspected due to lactic acidosis secondary to thiamine deficiency. Definitive diagnosis was confirmed by magnetic resonance imaging of the brain. Intravenous infusion of high-dose thiamine (1,200 mg/day) was commenced, leading to improvement of her neurological condition. Conclusions: Physicians should recognize that pancreaticoduodenectomy, when complicated by gastrojejunostomy stenosis resulting in pancreatic fistula, can lead to WE. In this case, blood gas analysis was helpful in arriving at the correct diagnosis. A high degree of suspicion should be maintained if any of the classical features of WE are observed following pancreaticoduodenectomy.


2021 ◽  
Vol 14 (8) ◽  
pp. e244082
Author(s):  
Esther Shan Lin Hor ◽  
Gurpreet Pal Singh ◽  
Nurul Akhmar Omar ◽  
Vincent Russell

We report the case of a middle-aged woman with a history of bipolar disorder, in the absence of alcohol or substance misuse. The patient had been maintained on fluphenazine decanoate depot and now presented acutely with cognitive dysfunction and rigidity. Laboratory tests revealed elevated creatine kinase, acute kidney injury with metabolic acidosis and transaminitis, leading to a provisional diagnosis of neuroleptic malignant syndrome (NMS). Neuroleptics were withheld; dialysis was commenced; and blood biochemistry parameters improved in tandem. However, mental status changes persisted, and re-evaluation revealed multidirectional nystagmus with bilateral past-pointing. MRI confirmed the diagnosis of Wernicke’s encephalopathy (WE). Prompt recovery followed treatment with high-dose intravenous thiamine. We discuss the co-occurrence of NMS and non-alcoholic WE—highlighting the need for a high index of suspicion for these relatively rare neuropsychiatric diagnoses which are often missed in those with atypical presentations.


2006 ◽  
Vol 10 (4) ◽  
pp. 290-293 ◽  
Author(s):  
Kae Ueda ◽  
Daisuke Takada ◽  
Akiko Mii ◽  
Yuko Tsuzuku ◽  
Sabine Kyoko Saito ◽  
...  

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.


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