Gestational Thyrotoxicosis with Acute Wernicke Encephalopathy: A Case Report.

Ohmori, Nariko; Tushima, Toshio; Sekine, Y.; Sato, Kanji; Shibagaki, Yasuro; Ijuchi, Shinichirou; Takano, Kazue

doi:10.1507/endocrj.46.787

Cited by 19 publications

(9 citation statements)

References 15 publications

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“…Thiamine depletion was aggravated by hyperthyroidism or gestational thyrotoxicosis in six cases (60,61,65,69,73,79) and required the administration of propanolol (61,65,69,73) or other beta-blockers (60) and propylthiouracil (61,65,69,73). Some patients exhibited unexpected signs such as epileptic seizures (69,70a, 70b), flapping tremor (73) (ie, hypodense areas around the aqueduct and caudate nuclei) only in the case described by Ohkoshi et al (78).…”

Section: Review Of the Literaturementioning

confidence: 98%

Hyperemesis Gravidarum Complicated by Wernicke Encephalopathy: Background, Case Report, and Review of the Literature

Chiossi¹,

Neri²,

Cavazzuti³

et al. 2006

Obstetrical & Gynecological Survey

190

143

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Wernicke encephalopathy (WE) is a rare but known complication of severe hyperemesis gravidarum caused by thiamine deficiency. This article presents an unusual case that occurred at our institution and reviews the 48 previously published cases of WE in pregnancy. Considering all the 49 cases, the mean (+/-standard deviation) patients' age was 26.7 +/- 4.9 years, the mean gestational age when WE manifested was 14.3 +/- 3.4 weeks, and the mean duration of vomiting and feeding difficulties was 7.7 +/- 2.8 weeks. Wernicke's classic triad (confusion, ocular abnormalities, and ataxia) manifested in only 46.9% (23 of 49) of the patients. Confusion affected 63.3% (31 of 49) of the patients, ocular signs 95.9% (47 of 49) and symptoms 57.1% (28 of 49), and ataxia 81.6% (40 of 49). Deterioration of consciousness affected 53.1% (26 of 49) of the subjects and memory impairment 61.2% (30 of 49). Complete remission of the disease occurred in only 14 of 49 cases. Symptom resolution required months and permanent impairments were common. The overall pregnancy loss rate, directly (spontaneous fetal loss) and indirectly (planned abortion) attributable to WE, was 47.9% (23 of 49). The diagnosis of WE is clinical and can be rapidly confirmed by magnetic resonance imaging. We emphasize the importance of thiamine supplementation to women with prolonged vomiting in pregnancy, especially before intravenous or parenteral nutrition. We also underline the necessity to promptly replace vitamin B1 when neurologic symptoms and/or signs develop in a patient with hyperemesis gravidarum.

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Section: Review Of the Literaturementioning

confidence: 98%

Hyperemesis Gravidarum Complicated by Wernicke Encephalopathy: Background, Case Report, and Review of the Literature

Chiossi¹,

Neri²,

Cavazzuti³

et al. 2006

Obstetrical & Gynecological Survey

190

143

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“…1,2 Early manifestations encompass a wide range of nonspecific symptoms, such as fatigue, emotional lability, memory loss, sleep disorders, angina, anorexia, and abdominal pain. 9 Secondary deficiency develops from conditions in which thiamine requirements increase, such as pregnancy and lactation, hyperthyroidism and febrile disorders, 12,13 impaired absorption, or defective use of thiamine from liver disease. 3,4 The cerebral variety, called Wernicke-Korsakoff syndrome or Wernicke's encephalopathy, is characterized by confusion, nystagmus, and ophthalmoplegia, progressing to coma and death if untreated.…”

Section: Commentmentioning

confidence: 99%

Conservative Management of a Bleeding Renal Angiomyolipoma in Pregnancy

Storm

Mowad²

2006

Obstetrics & Gynecology

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“…This has been reported 4 previous times in the published literature. [8][9][10][11] Neither malnourishment nor thyrotoxicosis alone should cause Wernicke's encephalopathy; however, together, they augmented the depletion of thiamine.…”

Section: Discussionmentioning

confidence: 99%