Haemorrhagic thiamine deficient encephalopathy following prolonged parenteral nutrition (original) (raw)
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Thiamine-Responsive Lactic Acidosis, Encephalopathy, and Shock
Journal of Pharmacy Technology, 1998
Objective: To report a case of severe lactic acidosis, encephalopathy, and hypotension in a patient receiving total parenteral nutrition without multivitamin supplementation and the dramatic response to intravenous administration of thiamine. Case Summary: A 15-year-old African-American girl undergoing treatment for chronic myelogenous leukemia with allogenic bone marrow transplantation and requiring total parenteral nutrition was admitted to our intensive care unit for management of life-threatening lactic acidosis, encephalopathy, and hemodynamic instability. Because of the manufacturing shortage of parenteral multivitamin preparations, oral multivitamins were prescribed; however, the patient was unable to swallow the oral multivitamins because of oral mucositis. Intravenous administration of thiamine promptly reversed the profound metabolic, neurologic, and hemodynamic abnormalities. Discussion: Carbohydrate loading associated with inadequate thiamine intake may result in potenti...
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...
PARENTERAL THIAMINE AND WERNICKE'S ENCEPHALOPATHY: THE BALANCE OF RISKS AND PERCEPTION OF CONCERN
Alcohol and Alcoholism, 1997
Wernicke's encephalopathy, a disorder with significant mortality and high morbidity, is common amongst alcohol-dependent patients. Thiamine deficiency appears to play a key role in its aetiology, and parenteral high-dose thiamine is effective in prophylaxis and treatment. Unfortunately, reports of rare anaphylactoid reactions have led to a dramatic reduction in the use of parenteral thiamine, and it is possible that this change in treatment has led, or will lead, to an increase in morbidity and mortality. There is a need for education of doctors who treat alcohol-dependent patients, in order to ensure appropriate use of parenteral thiamine in prophylaxis and treatment of this disorder.
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).
Metabolic and Histological Reversibility of Thiamine Deficiency
Journal of Cerebral Blood Flow & Metabolism, 1983
The rapid improvement in the clinical manifestations of thiamine deficiency with thiamine supplementation is well known. To study this process in more detail, we rendered rats thiamine deficient either by dietary deprivation alone (DD) or, in addition, by daily pyrithiamine administration (DD + PT). We observed the cerebral metabolic and histological responses of these rats after 1 or 7 days of thiamine supplementation both prior to and at the onset of clinical sequelae. The cerebral metabolic response to thiamine deficiency and replenishment was determined with the [14C]deoxyglucose technique for measurement of local cerebral glucose utilization (LCGU). Our results indicate that thiamine replenishment reverses the LCGU changes resulting from thiamine deprivation of short duration. However, prolonged thiamine deprivation may result in LCGU changes that are not completely reversible by thiamine replenishment, before the appearance of the clinical or histological consequences of thiam...
Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults
Frontiers in Psychiatry, 2019
Thiamine (vitamin B1) is an essential nutrient that serves as a cofactor for a number of enzymes, mostly with mitochondrial localization. Some thiamine-dependent enzymes are involved in energy metabolism and biosynthesis of nucleic acids whereas others are part of the antioxidant machinery. The brain is highly vulnerable to thiamine deficiency due to its heavy reliance on mitochondrial ATP production. This is more evident during rapid growth (i.e., perinatal periods and children) in which thiamine deficiency is commonly associated with either malnutrition or genetic defects. Thiamine deficiency contributes to a number of conditions spanning from mild neurological and psychiatric symptoms (confusion, reduced memory, and sleep disturbances) to severe encephalopathy, ataxia, congestive heart failure, muscle atrophy, and even death. This review discusses the current knowledge on thiamine deficiency and associated morbidity of neurological and psychiatric disorders, with special emphasis on the pediatric population, as well as the putative beneficial effect of thiamine supplementation in autism spectrum disorder (ASD) and other neurological conditions.
Thiamine deficiency and delirium
Innovations in clinical neuroscience, 2013
Thiamine is an essential vitamin that plays an important role in cellular production of energy from ingested food and enhances normal neuronal actives. Deficiency of this vitamin leads to a very serious clinical condition known as delirium. Studies performed in the United States and other parts of the world have established the link between thiamine deficiency and delirium. This literature review examines the physiology, pathophysiology, predisposing factors, clinical manifestations (e.g., Wernicke's encephalopathy, Wernicke-Korsakoff syndrome, structural and functional brain injuries) and diagnosis of thiamine deficiency and delirium. Current treatment practices are also discussed that may improve patient outcome, which ultimately may result in a reduction in healthcare costs.
Computed tomography findings in thiamine deficiency-induced coma
Neurocritical Care, 2006
Although brain magnetic resonance imaging is a more sensitive diagnostic tool in the evaluation of coma, noncontrast head computed tomography (CT) may demonstrate highly specific findings in some cases of coma. We present a case of thiamine deficiency-induced coma associated with acute necrosis of fornices documented on CT and review cardinal neuroimaging features of Wernicke encephalopathy. Acute fornices necrosis is a novel finding on head CT suggestive of thiamine deficiency.
Increased cerebral free radical production during thiamine deficiency
Metabolic Brain Disease, 1997
Concentration of reactive oxygen species (ROS) and the antioxidant glutathione (GSH) was measured in thalamus and cortex after 13 and 14 days of pyrithiamine-induced thiamine deficiency (PTO) in the rat. The concentration of ROS was significantly elevated in thalamus and cortex on day 14 when righting reflexes were absent and spontaneous seizures occured. No significant changes in GSH concentration were observed in thalamus or cortex on either day of treatment. These findings suggest that increased formation of free radicals occurs during the more acute symptomatic stage of thiamine deficiency and may contribute to the structural damage described in this model of Wernicke's encephalopathy.
JPEN. Journal of parenteral and enteral nutrition, 2015
Thiamine is a water-soluble vitamin implicated in several metabolic processes. Its deficiency, due to prolonged parenteral nutrition without adequate vitamin supplementation, can lead to multiorgan failure characterized by cardiovascular impairment and metabolic acidosis refractory to bicarbonate administration. Only thiamine administration allows the remission of symptoms. We report 2 preterm infants with acute thiamine deficiency due to prolonged parenteral nutrition without adequate vitamin supplementation.