Wernicke Encephalopathy Staff Awareness: A Retrospective Descriptive Study

Saturday, 27 July 2019

Michael Vargas Chavez, MSN, RN, EMT-I
Surgical Intensive Care Unit, Covenant Medical Center, LUBBOCK, TX, USA

Abstract: Background: The purpose of the this study is to inform bedside nurses, physicians, dieticians, students, and researchers of the current literature based on Evidence-Base Practice with the awareness and treatment of Wernicke’s. Wernicke Encephalopathy (WE) is a neuropsychiatric disorder that is clinically misdiagnosed in 75-80% in the clinical setting. Wernicke encephalopathy is a neuropsychiatric emergency with a high morbidity (84%) and mortality (up to 20%) (Flynn, Macaluso, D’Emparie, & Toutman, 2015). Wernicke is a result of thiamine deficiency and is readily reversible if treated with adequate doses of parenteral thiamine, preferably with the first 48-72 hours of the onset of symptoms (Latt & Dore, 2014). Wernicke encephalopathy can result in permanent brain damage, Wernicke Karsakoff’s, long-term placement such as nursing homes, or death. Patients, who survive, 80 to 85%, develop a chronic disorder of severe memory deficits with amnestic states that include learning deficits and short-term memory loss (Nishimoto, Usery, Winton, & Twilla, 2017). Wernicke encephalopathy is difficult to differentiate from drunkenness, but can mimic other diseases such as alcohol withdrawal, benzodiazepine withdrawals, sepsis, hypoxia, hepatic encephalopathy, and head injuries. There is no simple blood test or screening tool to detect WE. Diagnosis of WE is based on symptoms presented: ataxia, nystagmus, and delirium. Thomson, Marshell, & Bell (2012) noted in study that 18.6% showed no signs, 37.1% show one sign, 27.8% showed two signs, and 16.5% showed three signs also known as the classic triad. It is essential to consider the diagnosis of Wernicke Encephalopathy in any confused dependent patient attending the acute care setting (Stewart and Swain, 2012). Different case studies involving high doses of parenteral thiamine have been performed on client that presented with symptoms of WE. Isenber-Grzeda (2015), presented a case involving patients with three different cancers that were at high risk of WE. Each client was given 500 milligrams (mg) intravenous (IV) three times a day (T.I.D.) with a rapid reversals of alter mental status. Based of the literature and findings, this project was divided into three phases. Phase one involved an integrative research review (IRR). The IRR focused on “Treatment with Thiamine to reduce Neuropsychiatric Syndrome.” The findings of this IRR revealed multiple studies suggest the dosing regimen is 500 mg intravenous three times daily for two to three days with a further 250 mg intravenous thiamine for the next two to three days. The intravenous regimen is then followed by oral thiamine supplementation indefinitely. Phase two involved a second IRR that focused on, “Can alcohol assessment screening tools be modified to more accurately identify patients with Thiamine deficiency to reduce Wernicke Encephalopathy?” In conclusion of the second IRR, a review of the use of the most common symptom-triggered treatment tool, the CIWA, revealed that it was used inappropriately in >50% of cases (McPherson, Benson, & Forrest, 2012). Phase three, involved a descriptive retrospective chart review with the approval of Institutional Review Board (IRB). 1,515 charts were received from Covenant Health Lubbock. Charts dated from January 2017 to May 2018, with ICD-10 codes G92, G93.40, G93.41, G93.43, and G93.49. IRB approved the ICD10 code G92. 222 charts codes G92, 35 out of the 222 charts met criteria for the retrospective chart review. Factors that were assess was age, ethnicity, gender, alcohol use, alcohol of choice, thiamine order, alcohol screening completion in the electronic medical record, screening tool and protocol used, days in the hospital, days in the intensive care unit, WE symptoms, and diagnosis of WE.