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Wernicke's Encephalopathy: Role of Thiamine

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Wernicke's Encephalopathy: Role of Thiamine NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #75 Carol Rees Parrish, R.D., M.S., Series Editor Wernicke’s Encephalopathy: Role of Thiamine Allan D. Thomson Irene Guerrini E. Jane Marshall Wernicke’s encephalopathy, a neuropsychiatric disorder which arises as a result of thiamine deficiency, is a condition frequently associated with alcohol misuse, and has a high morbidity and mortality. In 80% of cases, the diagnosis is not made clinically prior to autopsy and inadequate treatment can leave the patient with permanent brain damage: the Korsakoff syndrome. Recommendations are provided for the prophylac- tic treatment of Wernicke’s encephalopathy as well as the treatment of the suspected or diagnosed case. INTRODUCTION the brain. It can occur in the context of inadequate ernicke’s encephalopathy (WE) is an acute dietary intake, and is also seen in a number of medical neuropsychiatric disorder which arises as the conditions associated with excessive loss of thiamine Wresult of an inadequate supply of thiamine to from the body, or impaired absorption of thiamine from the intestinal tract (1) (Table 1). In the developed world, WE is most commonly Allan D. Thomson, National Addiction Centre, Institute associated with alcohol misuse. Early and adequate of Psychiatry, King’s College, London, UK and Molecu- treatment with thiamine, by the appropriate route, can lar Psychiatry Laboratory, Windeyer Institute of Medical reverse the induced biochemical changes in the brain Sciences, Research Department of Mental Health and prevent the development of structural lesions; fail- Sciences, University College London, London Medical ure to treat results in permanent brain damage called School, London, UK. Irene Guerrini, Molecular Psychia- the Korsakoff Syndrome (KS) (1). WE that is not asso- try Laboratory, Windeyer Institute of Medical Sciences, Research Department of Mental Health Sciences, Uni- ciated with alcohol misuse can usually be treated with versity College London, London Medical School, Lon- smaller oral doses of thiamine. These patients rarely don, UK and Bexley Substance Misuse Service, South develop KS, indicating that the combined effect of thi- London and Maudsley NHS Foundation Trust, London, amine deficiency and alcohol misuse produces a syner- UK. E. Jane Marshall, National Addiction Centre, Insti- gistic effect which is much more detrimental than either tute of Psychiatry, King’s College, London, UK. alone (2,3). PRACTICAL GASTROENTEROLOGY • JUNE 2009 21 Wernicke’s Encephalopathy NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #75 lesions were present in 1.4% of general medical Table 1 Some clinical conditions which may co-exist with alcohol patients, increasing to 12.5% in known “alcoholics” use disorders, causing patients to be at additional risk and to 35% in “alcoholics” with cerebellar damage of developing Wernicke’s Encephalopathy (1,5). The reduction in the number of autopsies being carried out worldwide has denied us this gold standard • Protein-calorie malnutrition from malabsorption by which to judge the incidence of WE, but it is • Anorexia nervosa unlikely to have declined (2). • Intravenous infusions including total parenteral nutrition without adequate thiamine • Refeeding syndrome • Patients with protracted vomiting including pregnancy, FAILURE TO TREAT toxemia WERNICKE’S ENCEPHALOPATHY • Teenage pregnancy with poor nutrition/drug misuse while Wernicke’s encephalopathy is a medical emergency. mother still growing Untreated, it leads to death in up to 20% of cases (5), • Carbohydrate loading IV/oral when thiamine stores are minimal • Diabetic ketoacidosis or, in 85% of the survivors, to the chronic form of the • Chronic renal failure, dialysis condition, the Korsakoff syndrome. Some 25% of the • AIDS, drug misuse Korsakoff group will require long-term institutional- • Patients on diuretics for ascites ization (6,7). • Partial gastrectomy, gastrectomy or gastric stapling, gastric The characteristic neuropathology of WE involves bypass, gastric or esophageal carcinoma, widespread neuronal loss, micro-hemorrhages, and gliosis in the carcinomas paraventricular peri-aqueductal grey matter and in the • Severe obesity, ulcerative colitis, pernicious anemia • Prisoners admitted to police cells, prison; individuals who mammillary bodies (8). The amnesia of KS is probably are homeless or living in hostels due to the interruption of diencephalic-hippocampal • Patients with Alzheimer’s disease or neglect in old age, circuits involving the thalamic nuclei and the mammil- especially if living alone lary bodies (9). • Chronic schizophrenia Clinically, “KS” is characterized by a memory dis- • Widespread tuberculosis order, occurring in clear consciousness, such that the • Thyrotoxicosis (very high thyroid hormone levels) patients appear to be entirely in possession of their fac- • Increased requirements caused by fever, pregnancy and adolescent growth ulties. However, they show a severe impairment of cur- • Thiaminases are enzymes that break down thiamine in food rent and recent memory, repeatedly asking the same (found in raw freshwater fish, raw shellfish, etc.—e.g. Japan) questions over and over again, and failing to recognize • Genetic abnormality of transketolase enzyme people they had met since the onset of the illness. The ill- ness seems to affect mainly the consolidation of recent memory traces more than remote memories, but the In this paper we concentrate on the management of impairment may involve memories from up to 30 years patients with alcohol misuse who present with WE. We before. Sometimes, affected individuals fill the memory discuss clinical presentation, appropriate treatment and gaps creating “false memories” (confabulations); these how to prevent the development of permanent brain false recollections often represent real memories jum- damage from KS. bled up and recalled out of temporal sequence. HOW COMMON IS THE DEVELOPMENT OF WERNICKE’S ENCEPHALOPATHY? WERNICKE’S ENCEPHALOPATHY WE is not diagnosed prior to autopsy in 80% of cases. The thiamine requirement for healthy individuals is Clinicians fail to diagnose the syndrome, perhaps in related to their carbohydrate intake and is between 1–2 the belief that it occurs less commonly than it does mg per day: this requirement increases with alcohol (1,4). Autopsy studies have shown that Wernicke (continued on page 24) 22 PRACTICAL GASTROENTEROLOGY • JUNE 2009 Wernicke’s Encephalopathy NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #75 (continued from page 22) Figure 1. Mechanisms of nutritional deficiency in alcohol misuse Reproduced from Thomson (2000) reference (10) by kind permission of Oxford University Press. misuse. The body can only store between 30–50 mg of state may be further exacerbated by diarrhea, steator- thiamine, thus body stores of individuals on a thiamine rhea and vomiting (10) (Figure 1). deficient diet are likely to be depleted in four-to-six As these changes continue, oral thiamine becomes weeks. Further thiamine deprivation causes a signifi- less effective as a therapeutic agent. Finally, oral thi- cant decrease in the activity of many enzymes which amine taken as medication or as food, is inadequate, as play a key role in metabolism (9). both continuing heavy alcohol use and malnutrition However, diets are rarely totally devoid of thi- interfere with absorption of thiamine from the GI tract amine and the time it takes for significant thiamine (10,11). depletion to develop will vary. During the initial In order for dietary thiamine to become active in phases of deprivation, the thiamine deficit can be cor- brain cells, it must undergo at least four transport rected by oral supplementation. Individuals with alco- steps. It is first taken up by the brush border of the hol misuse problems are, however, at particular risk of intestine and then exported by the enterocyte into the developing thiamine deficiency. As their drinking pro- blood. In man this requires an active, saturable, stereo- gresses, so alcohol, often high in carbohydrate and specific and sodium-dependent transport mechanism. with low or absent amounts of thiamine, is substituted This mechanism limits thiamine absorption in health to for food. With the onset of alcohol-related liver dam- no more than 4.5 mg–5.6 mg per oral dose greater than age the ability to store thiamine in the liver is progres- 15 mg. Absorption can decrease to less than 1.5 mg per sively reduced. An already compromised nutritional oral dose in the abstinent, but malnourished alcoholic, 24 PRACTICAL GASTROENTEROLOGY • JUNE 2009 Wernicke’s Encephalopathy NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #75 Figure 2. Patient with (a) Ophthalmoplegia due to Wernicke’s encephalopathy (left); (b) six hours after IV thiamine hydrochloride (right). or less if he is also intoxicated (1). Thiamine must then physician must rely upon clinical information to recog- cross the blood-brain barrier to reach the neurons and nize patients at risk of developing WE or to make a pre- finally it must be transported into the mitochondria and sumptive or definitive diagnosis of WE (2). nuclei of the neurons. See Guerrini, et al for further discussion about thiamine transporters (12). CLINICAL SIGNS AND SYMPTOMS OF THIAMINE DEFICIENCY MAKING THE DIAGNOSIS In 1881 Wernicke drew attention to what has come to be called the “classic triad” of signs and symptoms of Studies have reported that circulating levels of thi- WE: oculomotor abnormalities, cerebellar dysfunction amine are reduced in 30%–80% of alcohol misusers. and confusion (2,16)
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