Summary. An Orphanet summary for this disease is currently under development. However, other data related to the disease are accessible from the Additional. Pittella JE, de Castro LP. Wernicke’s encephalopathy manifested as Korsakoff’s syndrome in a patient with promyelocytic leukemia. South Med. Wernicke encephalopathy (WE) is an acute neurological condition characterized by a clinical Diekfuss JA, De Larwelle J, McFadden SH.
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Wernicke’s encephalopathy induced by total parental nutrition. Sequeira Lopes da Silva 1R. Almaraz Velarde 2F. Olgado Ferrero 1M.
Robles Marcos 2D. Wernicke’s encephalopathy is an acute neurological syndrome due to thiamine deficiency, which is characterized by a typical triad of mental status changes, oculomotor dysfunction and ataxia. Despite the fact that Wernicke’s encephalopathy, in developed countries, is frequently associated with chronic alcoholism, there have been a number of published cases associating this encephalopathy with parenteral feeding without vitamin supplementation. Thiamine supplementation, along with other vitamins, is recommended for patients in risk of developing this syndrome.
Wernicke’s encephalopathy WE is an acute neuropsychiatric syndrome that results from thiamine vitamin B1 deficiency and that is characterized by a triad of mental-status changes, oculomotor dysfunction and ataxia.
Orphanet: Encefalopatia de Wernicke
Due to its high morbi-mortality, diagnosis and treatment should be made as soon as possible. The authors report the case of a year-old man that during prolonged total parenteral nutrition TPNdue to a bleeding ulcer which required surgery in different occasions, developed a WE, with substantial improvement when intravenous thiamine was administered.
A year-old man without any relevant medical history was admitted in our Intensive Care Unit with the diagnosis of hemorrhagic shock due to a bleeding ulcer in the first duodenal curve. He had required a bilateral vagotomy and pyloroplasty after failure of endoscopic treatment. During his stay, the patient presented a new episode of upper digestive hemorrhage requiring surgical intervention, in which a partial gastrectomy and Roux-en-Y Gastric Bypass was made.
Antibiotics were prescribed due to Escherichia coli peritonitis. At the twentieth day, he had a new episode of severe hematochezia with hypotension and tachycardia, requiring urgent surgery, diagnosing pancreatic and biliary fistula; the gastroduodenal artery was sutured and a Whipple procedure was performed.
After withdrawing the sedatives and extubating the patient, a confusional state with important mental sluggish was noticed, accompanied also by horizontal nystagmus to both sides and paralysis of the left arm.
Treatment with mg intravenous thiamine, three times per day, was started, with remission of the nystagmus and significant improvement of his confusional state in the three following days. Thiamine is a water-soluble B-complex vitamin that participates as a coenzyme in the oxidative decarboxylation of pyruvate and alfa-ketoglutarate and also in the pentose phosphate pathway. Absorption occurs in the duodenum by a rate-limited process.
The recommended dose of thiamine for a healthy adult is 1,4 mg of per day or 0,5 mg per Kcal of consumed, increasing its demands in subjects with high metabolic rate e. WE is an acute syndrome that requires an emergent treatment due to its high morbi-mortality and that is characterized by the typical triad of mental confusion, oculomotor dysfunction and gait ataxia.
The prevalence of this encephalopathy in men is higher than in women 1,7: In developed countries, most cases of WE are associated with chronic alcoholism, which due to their inadequate dietary intake, reduced gastrointestinal absorption, decreased hepatic storage and impaired utilization, seem to be more susceptible in developing this encephalopathy. Other predisposition factors and clinical settings associated to WE and that are commonly encountered in our clinical practice are the hyperemesis gravidarum, gastrointestinal surgery 5 including bariatric surgerysystemic diseases such as cancer and related conditions malignancy is the most common disorder that precipitates a WE in childrensevere infections AIDS, for exampleendocrinological disorders as thyrotoxicosis and also hemo and peritoneal dialysis.
In his two years study, Francini-Pesenti observed a high prevalence of WE in this type of patients, 3 a conclusion similar to that of Hahn, that reported an increase of this syndrome in patients with TPN, that due to a shortage of multivitamin infusions, were not receiving thiamine. Only one-third of patients will have all three of the typical symptoms, being the confusional state the most frequent one, followed by ataxia and ocular dysfunction.
Wernicke Encephalopathy – StatPearls – NCBI Bookshelf
Mental changes range from apathy, profound indifference and enecfalopatia sluggishness to, when left untreated, stupor and coma. Nystagmus is the most common oculomotor dysfunction, and usually is evoked by horizontal gaze to both sides. As the WE progresses, one can encounter bilateral lateral rectus palsy and, in advanced cases, complete ophthalmoplegia with nonreactive, miotic pupils. Other less frequent symptoms are hypothermia, tachycardia, hearing loss and epileptic seizures.
Overt of a “wet beriberi” and a WE is rare. Diagnosis is primarily a clinical one, and the high rate of undiagnosed WE cases can be explained by the non-specific clinical presentation in many patients. MRI is currently considered the most valuable imaging study available.
A typical finding is the bilateral symmetrical T2 abnormal hyperintense signal affecting the periacqueductal gray matter, around the third ventricle and the medial thalamus and the mamillary bodies, 8 which encefapopatia be found atrophic in a WE that has evolved for more than a week.
WE is a medical emergency and treatment should be started as soon as one considers this diagnosis. Diagnostic testing should not delay treatment. Though no randomized study wernkcke to support a particular dosing regimen, it is recommended that patients should be treated with a minimum of mg thiamine intravenously dissolved in ml of normal saline and infused over 30 minutesthree times daily for two to three days, followed by mg intravenously for three to five more days, or until the end of the clinical improvement 1.
Magnesium and other vitamins should be replaced as well. Daily oral administration of mg thiamine should be continued after completion sernicke parenteral treatment until patients are considered no longer at risk of developing a WE.
The authors would like to point out the absolute necessity of thiamine and other multivitamin supplementation in patients with TPN, in order to prevent a WE, and to remark the importance of its clinical suspicion in undernourished patients that present any of the typical symptoms. Since the infusion of intravenous glucose solutions can precipitate a WE, these should be preceded or encetalopatia by the administration of thiamine.
Sechi G, Serra A. Lancet Neurol ; 6: Rev Esp Anestesiol Reanim ; Wernicke’s syndrome during parenteral feeding: Singh S, Kumar A. Wernicke encephalopathy after obesity surgery: Wernicke encephalopathy and beriberi during total parenteral nutrition attributable to multivitamin infusion shortage.
Wernicke’s encephalopathy during parenteral nutrition. Journal of Parenteral and Enteral Nutrition ; Introduction Wernicke’s encephalopathy WE is an acute neuropsychiatric syndrome that results from thiamine vitamin B1 deficiency and that is characterized by a triad of mental-status changes, oculomotor dysfunction and ataxia. Case report A year-old man without any relevant medical history was admitted in our Intensive Care Unit with the diagnosis of hemorrhagic shock due to a bleeding ulcer in the first duodenal curve.
Discussion Thiamine is a water-soluble B-complex encefakopatia that participates as a coenzyme in the oxidative decarboxylation of pyruvate and alfa-ketoglutarate and also in the pentose phosphate pathway.