Hyperemesis gravidarum induced Wernicke’s encephalopathy
Wernicke’s encephalopathy is an acute neuropsychiatric disorder caused by thiamin deficiency. It is most often observed decreased with alcohol abuse and poor nutrition, gastric carcinoma, pyloric obstruction, prolonged parenteral feeding, hunger strike, chronic kidney disease, malignancy , anorexia nervosa and hyperemesis gravidarum.
Wernicke’s encephalopathy is recognized if there are two of the following four signs; a) dietary deficiencies, (b) oculomotor abnormalities, (c) cerebellar dysfunction, and (d) either an altered mental state or mild memory impairment.
Wernicke’s encephalopathy is diagnosed based on the clinical presentation and rapid reversal of symptoms with thiamine. Thiamine status in the body determined by the blood transketolase activity and thiamine pyrophosphate but this test is very costly; hence MRI plays an important role in the diagnosis of W.E. The periventricular regions of the diencephalon, mesencephalon, brainstem and superior vermis of cerebellum are sensitive to thiamine deficiency due to cellular dependence on oxidative metabolism that causes T2W hyperintensities in these regions. The MRI of brain has high (93%) specificity and moderate (53%) sensitivity.
Thiamine is an important cofactor for several enzymes including transketolase, pyruvate dehydrogenase and α-ketoglutarate dehydrogenase in the Kreb’s and pentose phosphate cycle. Deficiency of these enzymes results in focal acidosis, depolarization of neurons due to n-methyl-D- aspartate receptor mediated excitotoxity which ultimately result in alteration ob blood brain barrier, generation of free radical scavengers and cell death due to necrosis and apoptosis.
Thiamine requirements are increased during pregnancy and its deficiency by the impaired absorption due to hyperemesis gravidarum. Body stores of thiamin last for only 18-20 days. Depletion of thiamin due to reduced intake due to any cause or prolonged vomiting, results in thiamine deficiency and W.E.
Thiamine dependence is increased with high metabolic rate or high glucose intake and forms the basis of recommending thiamin before intravenous glucose therapy.
W.E is managed with high doses of thiamine, 500 mg/ day 8 hourly for 2 days followed by 250 mg /day until the patient tolerates oral thiamine( 100mg/day at lest three months) during treatment ocular signs improve first followed by ataxia and confusion subsequently.
Reference: Journal of the Neurological Sciences, Volume 284, Issues 1-2, 15 September 2009, Pages 214-216.
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