Wernicke’s Encephalopathy With Hyperemesis and Ketoacidosis

Selitsky, Tamila; Chandra, Pradeep; Schiavello, Henry

doi:10.1097/01.aog.0000172373.41828.8a

Cited by 37 publications

(24 citation statements)

References 25 publications

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“…Apart from these factors, the literature reports that nonalcoholic WE could occur after most gastrointestinal surgical procedures, including gastric bypass surgery, 7-9 gastrojejunostomy, 10 gastrectomy, 11 colectomy, 12 and even therapy with an intragastric balloon. 13 In addition, hyperemesis gravidarum, [14][15][16] chemical therapy, 17 anorexia nervosa, 18 AIDS, 19 and even wrong formula feeding 20 were also reported as predisposing factors (Table 1). 6,[21][22][23][24][25][26][27] Because the healthy body's reserves of thiamine are sufficient for up to 18 days, any condition that induces thiamine deficiency lasting 2 to 3 weeks may lead to WE.…”

Section: Discussionmentioning

confidence: 99%

Clinical Characteristics and MR Imaging Features of Nonalcoholic Wernicke Encephalopathy

Fei¹,

Zhong²,

Jin³

et al. 2008

AJNR Am J Neuroradiol

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Section: Discussionmentioning

confidence: 99%

Clinical Characteristics and MR Imaging Features of Nonalcoholic Wernicke Encephalopathy

Fei¹,

Zhong²,

Jin³

et al. 2008

AJNR Am J Neuroradiol

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“…While death associated with hyperemesis is rare, deaths that have occurred are typically associated with Wernicke's encephalopathy. The severity of the complications of this condition, highlight the necessity for early diagnosis and treatment [19]. Most patients with severe disease continued to manifest subsequent impairments, with complete remission of symptoms occurring in only a minority of patients.…”

Section: Maternal Complicationsmentioning

confidence: 99%

Hyperemesis Gravidarum: A Review of Recent Literature

et al. 2017

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Background: In the United States, hyperemesis gravidarum is the most common cause of hospitalization during the first half of pregnancy and is second only to preterm labor for hospitalizations in pregnancy overall. In approximately 0.3-3% of pregnancies, hyperemesis gravidarum is prevalent and this percentage varies on account of different diagnostic criteria and ethnic variation in study populations. Despite extensive research in this field, the mechanism of the disease is largely unknown. Although cases of mortality are rare, hyperemesis gravidarum has been associated with both maternal and fetal morbidity. The current mainstay of treatment relies heavily on supportive measures until improvement of symptoms as part of the natural course of hyperemesis gravidarum, which occurs with progression of gestational age. However, studies have reported that severe, refractory disease manifestations have led to serious adverse outcomes and to termination of pregnancies. Summary: Despite extensive research in the field, the pathogenesis of hyperemesis gravidarum remains unknown. Recent literature points to a genetic predisposition in addition to previously studied factors such as infectious, psychiatric, and hormonal contributions. Maternal morbidity is common and includes psychological effects, financial burden, clinical complications from nutritional deficiencies, gastrointestinal trauma, and in rare cases, neurological damage. The effect of hyperemesis gravidarum on neonatal health is still debated in literature with conflicting results regarding outcomes of birth weight and prematurity. Available therapy options remain largely unchanged in the past several decades and focus on parenteral antiemetic medications, electrolyte repletion, and nutritional support. Most studies of therapeutic options do not consist of randomized control studies and cross-study analysis is difficult due to considerable variation of diagnostic criteria. Key Messages: Hyperemesis gravidarum carries a significant burden on maternal health and US health care. Most published research on pathogenesis is observational and suggests multifactorial associations with hyperemesis gravidarum. Precise, strictly defined criteria for clinical diagnosis are likely to benefit meta-analyses of further research studies regarding pathogenesis as well as therapeutic options.

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“…6 Hyperemesis gravidarum and diabetic ketoacidosis with administration of intravenous glucose has also been associated with the development of Wernicke's encephalopathy. 7 Our patient presented with a history of only 2 weeks of vomiting and weight loss, followed by a 21-day hospital stay with minimal oral intake leading to depletion of his thiamine stores. At the time of hospitalization, he likely had subclinical hyperthyroidism, which developed into thyrotoxicosis during hospitalization as a result of iodinated intravenous contrast, referred to as the Jod-Basedow phenomenon.…”

Section: Discussionmentioning

confidence: 90%