Case Presentation: Introductions: Wernicke encephalopathy (WE) is an acute syndrome requiring emergent treatment to prevent death and neurologic morbidity. Although WE is most often associated with chronic alcoholism, it also occurs in other settings such as poor nutrition caused by malabsorption, poor dietary intake, and ESRD pts on dialysis. Autopsy studies have consistently revealed a higher incidence of Wernicke lesions in the general population than is predicted by clinical studies, suggesting that it is clinically under-recognized. WE produces petechial hemorrhagic necrosis in midline brain structures and corresponding deficits in mentation, oculomotor function, and gait ataxia. Only 1/3 of these pts have all 3 symptoms. Absence of one or more of the classic symptoms may lead to under-diagnosis. Thiamine replacement is mandatory early in disease.
Discussion: Case Description: The patient is a 32-year-old non-alcoholic female who had an elective abortion due to severe hyperemesis gravidarum 3 weeks prior to presentation. Prior to the abortion, pt had anorexia, and weight loss. One week prior to presentation, she became minimally verbal with decreased eye contact, and developed short term memory loss. Psychiatry was consulted and diagnosis of major depressive disorder with catatonic features was made and olanzapine initiated for mood stabilization. Two days later, neurology consulted due to persistent symptoms. Nystagmus and intermittent myoclonic type jerks were noted on examination, and EEG was obtained which was normal. Neurologist agreed that the presentation was likely psychiatric in origin. Myoclonic jerks and nystagmus worsened and MRI was obtained five days after admission which revealed hyperintense T2/FLAIR signal abnormality involving the medial border of the thalami along the third ventricle extending to the mammillary bodies and to the periaqueductal gray regions consistent with Wernicke Encephalopathy. She was placed on high-dose thiamine and her signs and symptoms including oral intake, eye contact and verbal communication improved. She remained weak, unsteady and continued to have short term memory impairment. Patient was discharged home on oral thiamine. On return one month later, weakness, nystagmus, and ataxia had resolved. Three months after hospital discharge, EEG was repeated, with normal result. MRI was repeated and showed nearly complete resolution of lesions. Short term memory remained limited.
Conclusions: Discussion: The main barrier to diagnosis of WE is a low index of suspicion in the non-alcoholic patient, especially when the classic triad of clinical symptoms is not present and the patient is not a known alcoholic. Physician should have high index of suspicion for Wernicke encephalopathy for all at-risk patients with undiagnosed altered mental status, oculomotor disorders, or ataxia. Diagnostic testing should not delay treatment, which should immediately follow consideration of the diagnosis. Intravenous administration of thiamine is safe, simple, inexpensive, and effective in treating this condition.
To cite this abstract:Raissi, A; Doering, T. NON-ALCOHOLIC WERNICKE ENCEPHALOPATHY IN THE SETTING OF HYPEREMESIS GRAVIDARUM AND POOR DIETARY INTAKE. Abstract published at Hospital Medicine 2019, March 24-27, National Harbor, Md. Abstract 924. https://www.shmabstracts.com/abstract/non-alcoholic-wernicke-encephalopathy-in-the-setting-of-hyperemesis-gravidarum-and-poor-dietary-intake/. Accessed December 6, 2019.