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Wernicke-Korsakoff Syndrome Workup

  • Author: Glen L Xiong, MD; Chief Editor: David Bienenfeld, MD  more...
 
Updated: Apr 18, 2016
 

Approach Considerations

The primary focus should not necessarily be an accurate diagnosis, but to prevent harm from worsening Wernicke-Korsakoff syndrome in vulnerable patients. If there is clinical uncertainty, patients should be empirically treated while additional evaluations are undertaken.

Initial laboratory studies are directed at the differential diagnostic possibilities that can be identified and corrected rapidly.

Maintain a high level of suspicion for thiamine deficiency to avoid iatrogenic precipitation of Wernicke-Korsakoff syndrome. Heightened awareness should lead to prophylactic supplementation in at-risk patients.

This syndrome is most commonly observed in patients with alcoholism. Consequently, when these patients present to an emergency department, they are routinely administered thiamine prior to glucose infusion.

Several other categories of patients are at increased risk for thiamine deficiency, including inpatients receiving total parental nutrition, which necessitates vigilant monitoring for indicative signs and symptoms to ensure prompt treatment.

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Laboratory Tests

Laboratory studies to detect various morbidities in the diagnosis of Wernicke-Korsakoff syndrome include the following:

  • Electrolytes - To rule out an acute metabolic derangement causing mental confusion
  • Lactic acidosis may occur as a result of thiamine deficiency and is often under-recognized. Supplementation with thiamine often leads to resolution of lactic acidosis [38, 39]
  • Magnesium level as it may explain impaired thiamine utilization [40]
  • Complete blood count (CBC) - To rule out an acute infectious process, thrombocytosis, or erythrocytosis predisposing to thrombosis and infarction
  • Coagulation panel - To evaluate for a potential bleeding diathesis
  • Arterial blood gas - To evaluate for hypoxemia, hypercarbia, acidosis, or alkalosis
  • Serum/urine toxic drug screen - To rule out acute toxic ingestion; this is most helpful if results are available rapidly
  • Liver-associated enzymes - May provide evidence of alcohol abuse or liver dysfunction

Serum thiamine levels

Serum thiamine levels have been used in case reports to confirm Wernicke-Korsakoff syndrome. However, studies have not directly examined the correlation between a critical serum thiamine level and the development of neurologic symptoms and Wernicke-Korsakoff syndrome itself. One small study did show that the serum thiamine level correlated well with cerebellar vermal atrophy.[41] For now, the role of serum thiamine levels remains uncertain, although it may eventually play a part in confirming the diagnosis of Wernicke-Korsakoff syndrome and/or monitoring adequacy of treatment.

Lumbar puncture/CSF analysis

Seriously consider this procedure for any confused patient with fever and/or headache, particularly elderly patients, to rule out an infectious etiology. Patients with Wernicke-Korsakoff syndrome have a protein content that is within the reference range or mildly elevated without pleocytosis on CSF analysis.

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Imaging Studies

CT brain scan (noncontrast)

Computed tomography (CT) scanning can help in the rapid assessment for hemorrhage, mass effect, edema, and large, subacute stroke.

MRI of the brain with contrast

MRI can be a useful confirmatory in cases in which there is a clinical suspicion or a diagnostic procedure in patients presenting with a suggestive history and stupor or coma, in whom ataxia and ophthalmoplegia are not detectable. The possible diagnosis of Wernicke-Korsakoff syndrome should be communicated to the radiologists prior to ordering the scan to confirm that protocols suitable for the highest-yield imaging of the mammillary bodies, hippocampus, medial thalami, periaqueductal region, and the tectum of the midbrain are used. While specificity of MRI findings is high, the sensitivity is not; one study reported 53%.[42] Nevertheless, early diagnosis of WKS using MRI (T2 and FLAIR hyperintensities) in typical locations (thalami, mammillary bodies, tectal plate, and peraqueductal area) and atypical locations (cerebellum, cranial nerve nuclei, and cerebral cortex) has been proposed.[43]

As opposed to structural lesions and necrosis of the mammillary bodies, another study compared 9 patients with chronic Wernicke encephalopathy to 7 patients with Alzheimer disease and 37 controls. They found that 78% (7) of the chronic Wernicke patients had smaller mammillary bodies than 36 of 37 controls and 7 of 7 Alzheimer patients. The decrease was not related to age or ventricular size and is consistent with previous reports of autopsy findings.[44]

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Contributor Information and Disclosures
Author

Glen L Xiong, MD Associate Clinical Professor, Department of Psychiatry and Behavioral Sciences, Department of Internal Medicine, University of California, Davis, School of Medicine; Medical Director, Sacramento County Mental Health Treatment Center

Glen L Xiong, MD is a member of the following medical societies: AMDA - The Society for Post-Acute and Long-Term Care Medicine, American College of Physicians, American Psychiatric Association, Central California Psychiatric Society

Disclosure: Received royalty from Lippincott Williams & Wilkins for book editor; Received grant/research funds from National Alliance for Research in Schizophrenia and Depression for independent contractor; Received consulting fee from Blue Cross Blue Shield Association for consulting. for: Received book royalty from American Psychiatric Publishing Inc.

Coauthor(s)

Christopher A Kenedi, MD, MPH, FACP, FRACP Honorary Senior Lecturer, Auckland University School of Medicine; Consultant Physician and Psychiatrist, Liaison Psychiatry Division, Auckland City Hospital, New Zealand; Adjunct Faculty of Medicine, Adjunct Faculty of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, North Carolina

Christopher A Kenedi, MD, MPH, FACP, FRACP is a member of the following medical societies: Academy of Psychosomatic Medicine, American College of Physicians, American Psychiatric Association, American Academy of HIV Medicine, Royal Australian and New Zealand College of Psychiatrists

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

David Bienenfeld, MD Professor, Departments of Psychiatry and Geriatric Medicine, Wright State University, Boonshoft School of Medicine

David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, Association for Academic Psychiatry

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Alan DeAngelo, MD; Alan Halliday, MD; and G Patrick Daubert, MD, to the development and writing of the source article.

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