Wernicke Encephalopathy in a Non Alcoholic Patient

Archana Pareek, MD*, KU Medical center, Kansas City, KS and Dr. Padma Poddutoori, KU medical center, Kansas City, KS

Meeting: Hospital Medicine 2016, March 6-9, San Diego, Calif.

Abstract number: 725

Categories: Adult, Clinical Vignettes Abstracts

Keywords: , , ,

Case Presentation:

51 y.o. female with history of Gastric bypass surgery 10 years ago presented with abdominal pain, nausea, vomiting and diplopia. Reported nausea, vomiting on and off since her surgery but worse in the 6 weeks prior to admission. Work up showed mildly elevated LFT’s and biliary sludge. She underwent Laparoscopic cholecystectomy for symptomatic cholelithiasis and biliary dyskinesia. 2 days post-op developed mental status changes, became disoriented. CT Head was unremarkable. Initially, her symptoms were attributed to delirium, but it did not improve. MRI Head showed signal abnormality and enhancement in the mamillary bodies and peri-aqueductal gray matter as well as in region of area postrema compatible with Wernicke Encephalopathy. Ophthalmology evaluation revealed symmetric deficits in upward gaze, abduction and adduction suggestive of bilateral 6th nerve palsy, partial 3rd nerve palsy and papilledema concerning for increased intracranial pressure. LP showed normal opening pressure. Thiamine levels were low. She was placed on high dose thiamine IV. She had some improvement but did not have complete resolution of symptoms and thiamine was continued at the time of discharge from the hospital. 

Discussion:

Wernicke encephalopathy (WE) is the acute phase of a potentially fatal disorder resulting from Thiamine deficiency with  inadequate supply of thiamine to the brain. Commonly seen with chronic alcohol use. Malnutrition unrelated to alcohol misuse is another important cause of WE. Thiamine diphosphate acts as a cofactor for a number of thiamine-dependent enzymes. Thiamine deficiency reduces the activity of these enzymes and this leads to alterations in mitochondrial activity, impairment of oxidative metabolism and decreased energy status eventually leading to selective neuronal death. Initially, the changes are reversible with administration of thiamine but once necrosis occurs, the changes become irreversible, leading to permanent neurological sequelae-Korsakoff psychosis (KP) or death. KP is characterized by amnesia, disorientation and confabulation. Owing to the close relationship between WE and KP, the disorder is often referred to as the Wernicke–Korsakoff syndrome (WKS). The ‘classic triad’ of WE, Oculomotor abnormalities, Cerebellar dysfunction (ataxia) and Confusion is seen only in 16.5% of patients. It is therefore likely that WE has been under-diagnosed. The consequences of inadequate treatment of WE are significant and it may be fatal in up to 20% of patients. It is, therefore, essential to have a high index of suspicion for WE particularly in the population with malnutrition unrelated to alcohol misuse.

Conclusions:

In our patient, the Thiamine deficiency was related to protracted emesis with underlying history of gastric bypass surgery. Also our patient had papilledema which is rare in WE, the mechanism of production of papilledema in WE is unclear. Prompt Thiamine supplementation is required in WE or suspected WE and delaying treatment may increase the likelihood of morbidity and mortality.

To cite this abstract:

Pareek A, Poddutoori P. Wernicke Encephalopathy in a Non Alcoholic Patient. Abstract published at Hospital Medicine 2016, March 6-9, San Diego, Calif. Abstract 725. Journal of Hospital Medicine. 2016; 11 (suppl 1). https://www.shmabstracts.com/abstract/wernicke-encephalopathy-in-a-non-alcoholic-patient/. Accessed July 24, 2019.

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