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Wernicke Encephalopathy—Clinical Pearls
by
Thusius, Nuria
, Loukianova, Larissa L.
, Sinha, Shirshendu
, Kataria, Archish
, Kolla, Bhanu Prakash
in
Alcoholism
/ Apraxia
/ Ataxia
/ Brain research
/ Cognition
/ Cognitive ability
/ Coma
/ Death
/ Dehydrogenases
/ Diagnosis
/ Drug abuse
/ Eating disorders
/ Encephalopathy
/ Enzymes
/ Evidence-based medicine
/ Gait
/ Gait Apraxia
/ Gastrointestinal diseases
/ Gastrointestinal surgery
/ Heart failure
/ Humans
/ Hyperemesis gravidarum
/ Hypotension
/ Hypothermia
/ Intestinal obstruction
/ Laboratories
/ Malignancy
/ Malnutrition
/ Memory
/ Memory Disorders
/ Metabolism
/ Nutrient deficiency
/ Patients
/ Pearls
/ Phosphate esters
/ Psychiatry
/ Pyrimidines
/ Risk factors
/ Thiamine
/ Thiamine - administration & dosage
/ Thiamine - pharmacology
/ Vitamin B
/ Vitamin deficiency
/ Wernicke Encephalopathy - diagnosis
/ Wernicke Encephalopathy - drug therapy
/ Wernicke Encephalopathy - physiopathology
/ Wernicke's encephalopathy
/ Wernicke, Carl
2019
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Wernicke Encephalopathy—Clinical Pearls
by
Thusius, Nuria
, Loukianova, Larissa L.
, Sinha, Shirshendu
, Kataria, Archish
, Kolla, Bhanu Prakash
in
Alcoholism
/ Apraxia
/ Ataxia
/ Brain research
/ Cognition
/ Cognitive ability
/ Coma
/ Death
/ Dehydrogenases
/ Diagnosis
/ Drug abuse
/ Eating disorders
/ Encephalopathy
/ Enzymes
/ Evidence-based medicine
/ Gait
/ Gait Apraxia
/ Gastrointestinal diseases
/ Gastrointestinal surgery
/ Heart failure
/ Humans
/ Hyperemesis gravidarum
/ Hypotension
/ Hypothermia
/ Intestinal obstruction
/ Laboratories
/ Malignancy
/ Malnutrition
/ Memory
/ Memory Disorders
/ Metabolism
/ Nutrient deficiency
/ Patients
/ Pearls
/ Phosphate esters
/ Psychiatry
/ Pyrimidines
/ Risk factors
/ Thiamine
/ Thiamine - administration & dosage
/ Thiamine - pharmacology
/ Vitamin B
/ Vitamin deficiency
/ Wernicke Encephalopathy - diagnosis
/ Wernicke Encephalopathy - drug therapy
/ Wernicke Encephalopathy - physiopathology
/ Wernicke's encephalopathy
/ Wernicke, Carl
2019
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Wernicke Encephalopathy—Clinical Pearls
by
Thusius, Nuria
, Loukianova, Larissa L.
, Sinha, Shirshendu
, Kataria, Archish
, Kolla, Bhanu Prakash
in
Alcoholism
/ Apraxia
/ Ataxia
/ Brain research
/ Cognition
/ Cognitive ability
/ Coma
/ Death
/ Dehydrogenases
/ Diagnosis
/ Drug abuse
/ Eating disorders
/ Encephalopathy
/ Enzymes
/ Evidence-based medicine
/ Gait
/ Gait Apraxia
/ Gastrointestinal diseases
/ Gastrointestinal surgery
/ Heart failure
/ Humans
/ Hyperemesis gravidarum
/ Hypotension
/ Hypothermia
/ Intestinal obstruction
/ Laboratories
/ Malignancy
/ Malnutrition
/ Memory
/ Memory Disorders
/ Metabolism
/ Nutrient deficiency
/ Patients
/ Pearls
/ Phosphate esters
/ Psychiatry
/ Pyrimidines
/ Risk factors
/ Thiamine
/ Thiamine - administration & dosage
/ Thiamine - pharmacology
/ Vitamin B
/ Vitamin deficiency
/ Wernicke Encephalopathy - diagnosis
/ Wernicke Encephalopathy - drug therapy
/ Wernicke Encephalopathy - physiopathology
/ Wernicke's encephalopathy
/ Wernicke, Carl
2019
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Journal Article
Wernicke Encephalopathy—Clinical Pearls
2019
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Overview
Wernicke encephalopathy (WE) was first described by Carl Wernicke in 1881. WE is caused by thiamine deficiency. Alcoholism is the most common etiologic factor associated with WE in the United States, but it can occur in any patient with a nutritional deficiency state such as hyperemesis gravidarum, intestinal obstruction, and malignancy. WE is a clinical diagnosis. The common findings include mental status changes, ocular dysfunction, and a gait apraxia, present in only 10% of cases. Only a few cases of WE are diagnosed before death. Approximately 80% of patients with untreated WE have development of Korsakoff syndrome, which is characterized by memory impairment associated with confabulation. The initial clinical diagnosis of WE is critical, keeping in mind that the classic triad of symptoms is often absent. Recognition of nutritional deficiency and any portion of the classic triad should prompt treatment. Additionally, hypothermia, hypotension, and coma should raise clinical suspicion for the disease. Primary treatment includes timely administration of thiamine, for which the route and dosage remain controversial. Clinical judgment should be exercised in diagnosis and treatment (dosage, frequency, route of administration and duration) in all cases of WE. Overdiagnosis and overtreatment may be preferred to prevent prolonged or persistent neurocognitive impairments given the excellent safety profile of thiamine. Further prospective research is warranted to better understand the disease biology, risk factors, and treatment recommendations.
Publisher
Elsevier Inc,Frontline Medical Communications Inc,Elsevier Limited
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