47 Case report: Wernicke encephalopathy, not always caused by alcohol!
Boer, S.M. de, Buren, M. van
Locatie(s): Auditorium 2
Categorie(ën): Parallelsessie
Introduction: In confused patients known with alcohol abuse, the diagnosis of Wernicke encephalopathy (WE) should be considered. Moreover when patients also show neurological symptoms. This case illustrates that WE must be considered even in the absence of alcohol abuse.
Case: A 53-year old women, with a history of Hashimoto hypothyroidism and Morbus Crohn for which a 80 cm resection of the ileum was performed twenty years ago, was admitted to our hospital because of recently developed confusion.
She had no specific complaints and there was no history of alcohol abuse. According to the general practitioner she had an appropriate dietary intake, until she developed confusion three weeks ago. On physical examination she appeared to have ataxia, nystagmus and inversion position of hands and feet. Laboratory results showed TSH 11 mU/l, free T4 26 pmol/l, leukocytes 10.7 109/l and CRP 20. The urine sediment was full of leukocytes.
We treated her for an UTI with complementary delirium with antibiotics and Haloperidol, on which she didn’t improve clinically.
CT brain and liquor examination (including virus diagnostics) showed no abnormalities. MRI showed large atrophy of the frontal and parietal convexity.
EEG showed diffuse encephalopathy. Because of the combination of confusion, ataxia and nystagmus the possibility of WE was raised.
Additional laboratory results indeed showed a vitamine B1 deficiency of 45 nmol/l, with no other deficiency. For exclusion of alcohol abuse as a cause for the thiamine deficiency, a C-DTECT was analysed, which showed to be low. Although her M. Crohn appeared to be in remission, we presumed that malabsorption due to her former resection of the ileum was the cause of the deficiency.
Treatment with thiamine iv 500 mg t.i.d., vitamine B complex t.i.d. and vitamine C 500 mg od was started during three days. After these days we switched to thiamine 100 mg oral od for maintenance; vitamine B complex and C are continued.
In a few days her eye movements and ataxia improved. However, her confusion remained unchanged.
Conclusion: WE is an acute neurological disorder, characterized by a classical triade of encephalopathy, oculomotor dysfunction and ataxia. It is the most known neurological complication of thiamine deficiency. In 77% of the cases the deficiency is due to alcohol. This case illustrates that a former intestinal resection of the ileum can also be a cause of WE.
A quick start of Thiamine treatment on clinical suspicion is important, even when there is no history of alcohol abuse.