Wernicke Encephalopathy: Nursing Implications in Diagnosis and Neurological Recovery-An Updated Review

Abstract

Background: Wernicke Encephalopathy (WE) is an acute neurological disorder primarily caused by thiamine deficiency. It commonly manifests in patients with chronic alcohol use but can also occur in other contexts such as malnutrition, hyperemesis gravidarum, and prolonged parenteral nutrition. WE is life-threatening, affecting both the central and peripheral nervous systems, and is often misdiagnosed or underdiagnosed due to its nonspecific presentation. Timely diagnosis and intervention are essential to preventing irreversible neurological damage.

Aim: This updated review aims to explore the nursing implications for the diagnosis and neurological recovery of patients with Wernicke Encephalopathy. It highlights the clinical features, underlying causes, and treatment strategies for effective management.

Methods: A comprehensive review of current literature was conducted, focusing on the clinical presentation, pathophysiology, risk factors, assessment methods, and treatment options for WE. Studies related to thiamine deficiency, diagnostic criteria, nursing management, and medical interventions were analyzed.

Results: The review confirms that thiamine deficiency remains the primary cause of WE, most commonly linked to chronic alcohol use. Diagnosis relies on the clinical triad of confusion, ataxia, and ophthalmoplegia, although these symptoms may not always present together. Thiamine supplementation, particularly through parenteral administration, is crucial for the management of WE. However, persistent neurological deficits may develop, transitioning to chronic Korsakoff syndrome if not addressed promptly.

Conclusion: Early identification and intervention are crucial in managing Wernicke Encephalopathy. Nurses play a pivotal role in monitoring symptoms, administering treatments, and providing education to patients and caregivers. Timely thiamine therapy, along with management of associated deficiencies, is essential to optimize recovery and prevent long-term neurological damage.