Abstract
Wernicke’s encephalopathy is caused by thiamine deficiency and has a range of presenting features, including gait disturbance, altered cognitive state, nystagmus and other eye movement disorders. In the past, Wernicke’s encephalopathy was described almost exclusively in the alcohol-dependent population. However, in current times, Wernicke’s encephalopathy is also well recognized in many other patient groups, including patients following bariatric surgery, gastrointestinal surgery, cancer and pancreatitis. Early recognition of Wernicke’s encephalopathy is vital, as prompt treatment can restore cognitive or ocular function and can prevent permanent disability. Unfortunately, Wernicke’s encephalopathy is often undiagnosed – presumably because it is relatively uncommon and has a variable clinical presentation. Clinical biochemists have a unique role in advising clinicians about potential nutritional or metabolic causes of unexplained neurological symptoms and to prompt consideration of thiamine deficiency as a potential cause in high-risk patient groups. The aim of this review is to summarize the clinical features, diagnosis and treatment of Wernicke’s encephalopathy and to highlight some non-traditional causes, such as after bariatric surgery.
Highlights
Wernicke’s encephalopathy (WE), an acute neurological disorder caused by thiamine deficiency, WE can be challenging to diagnose clinically or biochemically
Wernicke’s encephalopathy (WE), an acute neurological disorder caused by thiamine deficiency, Corresponding author: Claire L Meek, Institute of Metabolic Science, Metabolic Research Laboratories, University of Cambridge, Addenbrooke’s Hospital, Box 289, Hills Road, Cambridge CB2 0QQ, UK
WE should be considered in patients with other conditions affecting nutrition, including hyperemesis gravidarum and following bariatric surgery
Summary
WE can be challenging to diagnose clinically or biochemically. Presentation of one or more of the classic triad of symptoms (described in Box 1) is highly suggestive of the condition, but these features are not always present. These tests are not available in most clinical laboratories and treatment cannot be delayed to wait for the result. Many countries fortify food with thiamine.[71] Many hospitals use thiamine administration prophylactically for high-risk groups, including patients with malnutrition, hypoglycaemia or alcohol dependence.[10,60,72] Recent studies have questioned this practice, providing evidence that there was no difference between administering thiamine before or after short-term glucose treatment.[72,73] Patients with a history of bariatric surgery are advised to take prophylaxis indefinitely due to decreased ability to absorb thiamine. The prognosis in WE is often poor, with around 50% of patients having long-term consequences, including memory impairment or Korsakoff’s syndrome.[2,3] In patients with WE due to alcohol dependence, around 80% will develop Korsakoff’s syndrome, and around 40% could die as a complication of Wernicke–Korsakoff syndrome.[2,12] even among patients with a non-alcohol-related cause, only around 20% of patients make a complete recovery while a further 20% may die due to complications of the disease
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