PARENTERAL THIAMINE AND WERNICKE'S ENCEPHALOPATHY: THE BALANCE OF RISKS AND PERCEPTION OF CONCERN (original) (raw)
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Parenteral thiamine use in the prevention and treatment of Wernicke-Korsakoff syndrome
Psychiatric Bulletin, 2005
A pre-/post-intervention audit of 163 case notes was conducted to assess the efficacy of printing information about the identification and treatment of the Wernicke-Korsakoff syndrome on the hospital alcohol detoxification sheet. RESULTS Parenteral thiamine was indicated in 42 of 163 patients; 26 had symptoms suggestive of Wernicke's encephalopathy and 16 were at risk. The intervention increased the chance of appropriate parenteral treatment by an odds ratio of 5.9 (95% CI 1.3-27.8). Admission to a specialist alcohol unit increased the chance of appropriate treatment by an odds ratio of 7.0 (95% CI 1.52-32.25). The mean number of doses rose from 3.08 to 4.62. CLINICAL IMPLICATIONS A simple intervention may lead to improved treatment of patients with Wernicke-Korsakoff syndrome.
Wernicke's encephalopathy in a child with high dose thiamine therapy
Korean journal of pediatrics, 2014
Wernicke's encephalopathy is an acute neurological disorder characterized by mental confusion, oculomotor dysfunction, and ataxia. It has been reported in individuals with alcohol dependence, hyperemesis gravidarum, and prolonged parenteral nutrition without vitamin supplementation. Here we present the case of a 13-year-old male patient with neuroblastoma and a history of poor oral intake and nausea for 3 months. After admission, he showed gait disturbances, nystagmus, and excessive dizziness; his mental state, however, indicated he was alert, which did not fit the classical triad of Wernicke's encephalopathy. A diagnosis of Wernicke's encephalopathy was made only after brain magnetic resonance imaging and serum thiamine level analyses were performed. The patient's symptoms remained after 5 days of treatment with 100-mg thiamine once daily; thus, we increased the dosage to 500 mg 3 times daily, 1,500 mg per day. His symptoms then improved after 20 days of replacement...
Topics in Clinical Nutrition, 2012
Wernicke-Korsakoff syndrome (WKS) is a disorder of the brain caused by deficiency of thiamine that is common in patients with alcoholism. Thiamine supplementation is a usual treatment in the management of WKS but no standard recommendations have been established. This article discusses the link between supplementation of thiamine and the treatment of WKS in patients with alcoholism, whether thiamine supplementation can improve symptoms of WKS and the current recommendations for thiamine supplementation in managing WKS. Evidence-based research is needed to determine the best thiamine supplementation regimen for patient with WKS.
Psychosomatics, 2018
Background-Wernicke's encephalopathy (WE) is a common neuropsychiatric syndrome due to thiamine deficiency. There is no consensus regarding thiamine dosing when WE is suspected. A longstanding dosing strategy for WE is 100 mg daily, yet updated clinical guidelines suggest using high dose intravenous thiamine (HDIV). Objective-To describe thiamine prescribing practices at a large, public academic hospital and investigate clinical characteristics and outcomes associated with HDIV thiamine in patients with encephalopathy who received IV thiamine. Methods-Electronic medical records of hospitalized patients who received thiamine between 4/4/2014 and 11/1/2015 were reviewed. Chi-square tests, Wilcoxon Rank Sum tests, and logistic regression were used to compare clinical variables in patients with encephalopathy who received HDIV thiamine (≥200 mg twice daily) vs. lower doses of IV thiamine. Results-Among the total 5,236 thiamine orders, 29% (n=1,531) were IV; 10% (n=150) of IV orders met HDIV criteria. In patients with encephalopathy who received IV thiamine (n=432), HDIV thiamine was administered to 20% (n=86) and only 2.1% (n=9) received dosing consistent with Royal College of Physicians guidelines. In bivariable analyses, HDIV thiamine was associated with surgical services (p=0.001), psychiatric consultation (p<0.001), and decreased mortality (p=0.004). In multivariable models, the association between HDIV thiamine and decreased inhospital mortality did not meet statistical significance (p=0.061).
EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy
European Journal of Neurology, 2010
Background: Although Wernicke encephalopathy (WE) is a preventable and treatable disease it still often remains undiagnosed during life. Objectives: To create practical guidelines for diagnosis, management and prevention of the disease. Methods: We searched MEDLINE, EMBASE, LILACS, Cochrane Library. Conclusions and recommendations: 1 The clinical diagnosis of WE should take into account the different presentations of clinical signs between alcoholics and non alcoholics (Recommendation Level C); although prevalence is higher in alcoholics, WE should be suspected in all clinical conditions which could lead to thiamine deficiency (good practice point-GPP). 2 The clinical diagnosis of WE in alcoholics requires two of the following four signs; (i) dietary deficiencies (ii) eye signs, (iii) cerebellar dysfunction, and (iv) either an altered mental state or mild memory impairment (Level B). 3 Total thiamine in blood sample should be measured immediately before its administration (GPP). 4 MRI should be used to support the diagnosis of acute WE both in alcoholics and non alcoholics (Level B). 5 Thiamine is indicated for the treatment of suspected or manifest WE. It should be given, before any carbohydrate, 200 mg thrice daily, preferably intravenously (Level C). 6 The overall safety of thiamine is very good (Level B). 7 After bariatric surgery we recommend follow-up of thiamine status for at least 6 months (Level B) and parenteral thiamine supplementation (GPP). 8 Parenteral thiamine should be given to all at-risk subjects admitted to the Emergency Room (GPP). 9 Patients dying from symptoms suggesting WE should have an autopsy (GPP).
Encephalopathy despite thiamine repletion during alcohol withdrawal
Cleveland Clinic journal of medicine, 2014
The Clinical Picture Encephalopathy despite thiamine repletion during alcohol withdrawal M anaging a patient with chronic alcohol abuse who is beginning to withdraw is a situation in which to expect the unexpected. A 61-year-old man with a 40-year history of alcohol abuse was admitted to the hospital after presenting with a 6-month history of weakness and increasing frequency of falls, as well as a 2-day history of myalgias and fatigue. He had anorexia and chronic diarrhea, and he reported an unintentional 100-lb weight loss over the past year. He consumed at least three to five alcoholic drinks daily, including a daily "eye-opener," and his diet was essentially devoid of meat, bread, fruits, and vegetables. His last drink had been on the morning of admission. On physical examination, his vital signs were notable for marked orthostatic hypotension. He had angular cheilitis, an erythematous, scaly facial rash, and poorly healing severe sunburn on the dorsal surface of the left forearm, acquired 1 month earlier after minimal sun exposure while driving his car (FIGURE 1). The neurologic examination noted decreased sensation in a stocking distribution, reduced proprioception in both great toes, and an intention tremor. His upper extremities were slightly hyperreflexic, he had down-going toes, he did not have clonus, and his gait was wide-based. Laboratory results were notable for mild anemia, with an elevated mean corpuscular volume of 109.2 fL and a normal thyrotropin level. Urinalysis and urine culture were normal. Stool testing for Clostridium difficile toxin was negative. Computed tomography of the head was unremarkable. He was placed on the Clinical Institute Withdrawal Assessment for Alcohol revised protocol, 1 and he was started on careful fluid, electrolyte, and nutritional management, including intravenous supplementation with thiamine 100 mg daily, folic acid 1 mg twice daily, THE CLINICAL PICTURE
Haemorrhagic thiamine deficient encephalopathy following prolonged parenteral nutrition
Journal of Neurology, Neurosurgery & Psychiatry, 1992
Neuropathological examination of three patients who were maintained on parenteral nutrition without substitution of thiamine demonstrated an acute haemorrhagic encephalopathy. The lesions differed substantially from the classic features of thiamine deficient encephalopathy regarding the histopathological alterations and the topographical distribution. The extreme rapidity of thiamine deprivation may have been responsible for the abrupt clinical onset of the disease and the intensity of the morphological alterations.