1. Identification and Management of Wernicke’s Encephalopathy
Case Review of Patient K
Julie Hughett RN, MSN, CNL, CCRN

2. Objectives
Utilize EBP to recognize patient’s with increased risk for WE.
Utilize EBP to differentially diagnose WE and successfully treat WE.
Understand the interprofessional care required to decrease risk of permanent irreversible Korsakoff’s Syndrome.

3. Background 52 y/o AAM with cc of chest pain and leg swelling.
PMH: COPD, CAD, AICD, Anxiety, HTN, Polysubstance abuse, and Chronic ETOH.

4. Admission Labs Albumin: 1.8 Magnesium: 1.4 Potassium: 2.3 BAL: 0.29
INR: 1.5

5. Hospital Course
July 17th: Admitted to telemetry floor with CIWA protocol.
July 19th: Transferred to SICU for severe alcohol withdrawal.
July19th: Intubated and sedated for patient and staff safety due to severe AWS.
July 26th: Extubated.
July 29th: Reintubated for respiratory distress aspiration pneumonia.
August 19th: Tracheostomy and Peg tube
August 19th: Discharged to LTAC

6. Patient K Outcome
Patient K was discharged to an LTAC on August 19th, ventilator dependent, alert to self only, able to follow simple, one step commands with inconsistency, and NPO except tube feeds

7. What is Wernicke’s Encephalopathy?
Wernicke encephalopathy is an acute neuropsychiatric emergency due to brain thiamine deficiency. The brain uses glucose as its main source of energy and is susceptible to injury due to acute thiamine deficiency (Day et al., 2015, p. 246). Thiamine is a cofactor for enzymes required for aerobic glucose metabolism in the brain. Without thiamine, glucose is metabolized by an anaerobic pathway producing lactic acid as a by-product resulting in focal acidosis and cell death (Day et al., 2015).

8. Identifying Patients at risk for WE
Get a detailed history of alcohol use from every patient.
Alcohol Dependence

9. Identifying Patients at risk for WE
Alcohol Withdrawal Syndrome
(AWS)
Alcohol withdrawal syndrome (AWS) is a common problem in the hospital setting and many AWS patients present with multiple issues including electrolyte imbalances, liver disease, polysubstance abuse, seizures, depression, withdrawal symptoms, delirium tremens, and Wernicke-Korsakoff syndrome (McKeon, Frye, & Delanty, 2008, p. 854).

10. Identifying Patients at risk for WE
The greater the degree of malnutrition that a patient exhibits correlates with the greater likelihood for severe AWS as well as the likelihood to develop Wernicke’s encephalopathy (WE) (McKeon et al., 2008, p. 859).
Malnutrition

11. Diagnosing WE
Clinical diagnosis of Wernicke’s encephalopathy (WE) is missed in 75-80% of cases and will co-exist with other disorders that cause confusion; alcohol withdrawal syndrome (AWS), sepsis, hypoxia, head injury, and hepatic encephalopathy (Latt & Dore, 2014, p. 911).

12. Signs and Symptoms of WE
WE signs and symptoms include mental status changes, ataxia, and oculomotor abnormalities (Roffman & Stern, 2006, p. 172).

13. When to Consider WE
WE is a clinical diagnosis and should be considered in patients with evidence of alcohol misuse and any one of the following; acute confusion, decreased consciousness, ataxia, ophthalmoplegia, memory disturbances, and/or dietary deficiencies (Day et al., 2015).
Clinical signs and symptoms such as nausea, vomiting, loss of appetite, and emotional changes are often present before the later “classical triad” of WE becomes evident (Wijnia, Wan de Wetering, Zwart, Nieuwenhuis, & Goossensen, 2012, p. 104).

14. Treatment of WE
Parenteral thiamine, 500 mg three times a day, is recommended for alcohol dependent individuals with poor nutrition and other comorbidities such as severe withdrawal symptoms or induced coma (McKeon et al., 2008, p. 859). Patient’s with low magnesium levels are unresponsive to thiamine replacement (Salen & O’Connor, 2015, para. 7).

15. Korsakoff’s Syndrome
Failure to institute adequate thiamine replacement therapy in suspected WE patients has an associated mortality of 20%, with 75% of those patients developing Korsakoff’s syndrome, a permanent irreversible psychosis (McKeon et al., 2008, p. 859).

16. Conclusion Screen patients thoroughly for alcohol dependence
Get baseline labs including protein and magnesium
Presume WE in medical cases where it can not be ruled out.

17. References
Day, MD, MSc, FRCPC, G. S., Ladak, BScPhm, S., Curley, MSc, BScPhm, K., Farb, PhD, N. A., Masiowski, MD, FRCPC, P., Pringsheim, MD, FRCPC, T., ... Ferland, MSc, BPharm, A. (2015, April). Thiamine prescribing practices within university-affiliated hospitals: A multicenter retrospective review. Journal of hospital medicine, 10,
Latt, N., & Dore, G. (2014, June 17). Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Internal Medicine Journal, 44,
McKeon, A., Frye, M. A., & Delanty, N. (2008). The alcohol withdrawal syndrome. J Neurol Neurosurg Psychiatry, 79,
Roffman, M.D., J. L., & Stern, M.D., T. A. (2006). Alcohol withdrawal in the setting of elevated blood alcohol levels. Primary Care Companion Journal of Clinical Psychiatry, 8, Retrieved from
Ross, Ph.D, L. J., Wilson, B.Sc., M., Banks, Ph.D., M., Rezannah, B.Nurt.Diet, F., & Daglish, M.D., M. (2012). Prevalence of malnutrition and nutritional risk factors in patients undergoing alcohol and drug treatment. Nutrition, 28,
Salen, MD, P. N., & O’Connor, MD, MPH, R. E. (2015). Wernicke encephalopathy treatment and management. Emedicine. Retrieved from
Strain, PharmD, J., & Kling, PharmD, C. (2010, September). Thiamine dosing for Wernicke’s Encephalopathy in alcoholics: Is traditional dosing inadequate? Pharmacology Focus,
Wijnia, MD, J. W., Van de Wetering, MD, PhD, B. J., Zwart, MSc, E., Nieuwenhuis, MD, K. A., & Goossensen, MSc, PhD, M. (2012). Evolution of Wernicke-Korsakoff syndrome in self-neglecting alcoholics: Preliminary results of relation with wernicke-delirium and diabetes mellitus. The American Journal on Addictions, 21,