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CASE REPORT
Year : 2013  |  Volume : 3  |  Issue : 2  |  Page : 142-145

Wernicke's encephalopathy and Hyperemesis gravidarum


1 Department of Obstetrics and Gynecology/ Northern Area Hospital, Hamad Medical Corporation; Doha, Qatar
2 Department of Internal Medicine/NAH, Hamad Medical Corporation; Doha, Qatar

Date of Submission13-Apr-2012
Date of Acceptance26-May-2012
Date of Web Publication3-Jun-2013

Correspondence Address:
Ummunissa Firdous
Department of OBGY/NAH, Hamad Medical Corporation, Doha
Qatar
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2231-0738.112841

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   Abstract 

Recent research is concentrated around micronutrients and antioxidant's role in degenerative neurological disorders; but still the vitamin deficiency in special situations can lead to life threatening medical emergencies. Hyperemesis gravidarum rarely leads to Wernicke's encephalopathy. It is a medical metabolic neurological emergency. Wernicke's encephalopathy is manifested by triad of confusion, opthalmoplegia and ataxia. Early detection and proper supplementation of thiamine is essential for treatment. Clinical manifestations of Wernicke's encephalopathy are due to the involvement of specific area of the brain where thiamine content and turnover is maximized. We report a case of Wernicke's encephalopathy in a pregnant woman known to have thyroid disorder, hyperemesis gravidarum; she was managed with intravenous dextrose infusion. The condition was diagnosed early by clinical manifestations and improved dramatically with thiamine supplementation. Wernicke's encephalopathy occurring due to hyperemesis gravidarum and hyperthyroidism is rare. High index of suspicion is essential for early diagnosis and proper supplementation of thiamine.

Keywords: Wernicke′s encephalopathy, hyperemesis gravidarum, thiamine


How to cite this article:
Firdous U, Sharara HA, Nahia FA, Al Saqqa M, Musaed S. Wernicke's encephalopathy and Hyperemesis gravidarum. Int J Nutr Pharmacol Neurol Dis 2013;3:142-5

How to cite this URL:
Firdous U, Sharara HA, Nahia FA, Al Saqqa M, Musaed S. Wernicke's encephalopathy and Hyperemesis gravidarum. Int J Nutr Pharmacol Neurol Dis [serial online] 2013 [cited 2020 Jun 6];3:142-5. Available from: http://www.ijnpnd.com/text.asp?2013/3/2/142/112841


   Introduction Top


Vitamin and mineral deficiency in pregnancy can lead to life threatening clinical conditions. Recent studies are looking at the roles of micronutrients such as antioxidants, vitamins E and C, omega-3 fatty acid and the large range of other phytochemical-rich whole foods; which led to the generation of a new era for human health, especially for the neurodegenerative diseases [1] and neurodevelopmental disorders. [2] Even folates and vitamin deficiency proved to cause carcinoma. [3] But the nutritional, vitamin and mineral deficiency in special circumstances can lead to life-threatening clinical emergencies.

Wernicke's encephalopathy is a rare life threatening metaboli emergency; caused by deficiency of thiamine (vitamin B1). If not detected early it can be potentially fatal; it commonly occurs in chronic alcoholism. It was first described by Wernicke's in 1881. Wernicke's encephalopathy is manifested by triad of confusion, opthalmoplegia and ataxia. [3] Wernicke's encephalopathy is rarer to occur during pregnancy, in medical literature, till date only 50 cases are reported. [4] We report a case of Wernicke's encephalopathy due to hyperemesis gravidarum and hyperthyroidism.


   Illustrated Case Top


Presentation

A 30 year gravida 7; Para 4 women: presented at 7 weeks of gestation with hyperemesis and ketonuria. She had Hypothyroidism for 9 years, and was treated with Thyroxin 100 mcg once daily; thyroid function tests showed hyperthyroidism, she responded to reduced dose of thyroxin, intravenous (IV) fluid and discharged home. But readmitted after two weeks with hyperemesis, ketonuria and raised liver functions. Thyroid functions were within normal limits. She was admitted and started on dextrose intravenous fluids. She was discharged against medical advice.

She represented 2 weeks later with hyperemesis, weight loss of 10 kg, anorexia; abnormal liver function [Figure 1], ketonuria, hypokalemia and hypomagnesaemia [Figure 2]. She was admitted and started on intravenous dextrose 5%, potassium chloride and magnesium infusions. On day 15 she developed abnormal eye movements, nystagmus and confusion. By day 16, she was unable to walk because of ataxia. Magnetic resonance imaging (MRI) brain was planned; from clinical triad and risk factors, she was diagnosed as a case of Wernicke's encephalopathy due to hyperemesis gravidarum and hyperthyroidism, and started on thiamine.
Figure 1: MRI fi ndings in Wernicke's encephalopathy

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Figure 2: Serum electrolytes and admission days

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Past medical history

She had 9 years history of hypothyroidism, treated with thyroxin, but no regular follow-up; No history of gastritis/diabetes mellitus or hypertension. No history of alcohol intake or smoking.


   Background Top


As our patient had hyperemesis; malnourished, significant weight loss, receiving Intravenous (IV) dextrose water for longer duration, developed typical neurological manifestations; all these factors helped us in diagnosing Wernicke's encephalopathy.

Differential diagnosis

Initial neurological manifestations thought to be related to antiemetic medication; but in spite of stopping the antiemetic, patient deteriorated neurologically; this differentiate that manifestation were not due to medications. Cerebral venous sinus thrombosis was not possible, as patient was not having headache and coagulation parameters were normal. Patient was afebrile, no leucocytosis and neck rigidity; this ruled out the central nervous system infections. Our patient was not having diplopia and no other endocrinal abnormality; no question of having pituitary apoplexy.

Hospital course

She was started on thiamine 100 mgs IV once daily and initial IV fluid changed to normal saline. She had a dramatic improvement in two days of therapy; by day 22 her ataxia was much better and by day 26 she was able to walk. She was tolerating oral feeds, shifted to oral thiamine and discharged home on day 31. Her pregnancy was continued, followed in out patients' clinic regularly, with a small for date fetus; she delivered baby boy at 38 th weeks of gestation normally without any surgical assistant.


   Discussion Top


Wernicke's encephalopathy is a medical metabolic neurological emergency. Overall incidence of Wernicke's encephalopathy is 0.04-0.13%. Common to occur with chronic alcohol misuse but the prevalence is increasing in non-alcoholic patients. [5]

Hyperemesis gravidarum rarely leads to Wernicke's encephalopathy; first described by Sheehan in 1938 and to the date only 50 cases are reported in the literature. [6] After reviewing these patients; their mean age was 26 years, gestational age 14 weeks, vomiting/feeding difficulty for 8 weeks, confusion occurred in 64%, ocular sign in 96%, ataxia 82% and complete remission of disease in 28% of these patients [Table 1]. [7]
Table 1: Summary of reported cases of Wernicke's encephalopathy and Hyperemesis gravidarum

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In addition to hyperemesis gravidrum; our patient initially had hyperthyroidism which also increases the thiamine demand and then for hyperemesis gravidarum on dextrose intravenous fluids, these factors in combination with the poor oral intake must have led to Wernicke's encephalopathy. On an average human body has thiamine storage for three weeks. Pathophysiology of Wernicke's encephalopathy is the deficiency of thiamine (vitamin B1). Thiamine acts as coenzyme in various stages of carbohydrate metabolism. Thiamine deficiency causes specific changes in periaqueductal grey matter, mammillary bodies and medial thalamus of the brain, as these areas have maximum thiamine content and turnover. These give peculiar clinical manifestations as well as typical magnetic resonance image findings [Figure 3].
Figure 3: Liver functions and admission days

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Ninety percent of these patients will have ocular signs. Caine et al. has proposed clinical criteria for diagnosis of Wernicke's encephalopathy; if two of the following four signs are present (i) dietary deficiency (ii) oculomotor abnormalities (iii) cerebellar dysfunction (iv) either an altered mental state or mild memory loss [Table 2]. [8]
Table 2: Clinical Criteria for diagnosis of Wernicke's encephalopathy

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Treatment of Wernicke's encephalopathy is essentially supplementation of IV thiamine 100 mgs once or twice daily; in addition to thiamine other electrolyte abnormality and vitamin deficiency should be corrected. Once patient is able to tolerate oral feeds; they can be shifted to the oral thiamine or multivitamins.

As for as the morbidity and mortality of patients with hyperemesis gravidarum leading to Wernicke's encephalopathy is concerned majority of them will have minimal residual neurological impairment and 28% will have full recovery. Fetal effects could be neurobehavioral disorders in the adult age. [9] If deficiency is not detected early and treated properly can lead to fatal outcome.


   Conclusion Top


Wernicke's encephalopathy occurring due to hyperemesis gravidarum and hyperthyroidism is rare. High index of suspicion is essential for early diagnosis and proper supplementation of thiamine for better clinical outcome.

 
   References Top

1.Guillemin GJ. Editorial for the first issue of the International Journal of Nutrition, Pharmacology, Neurological Diseases. Int J Nutr Pharmacol Neurol Dis 2012;1:2.  Back to cited text no. 1
    
2.Essa MM, Guillemin GJ, Waly MI, Al-Sharbati MM, Al-Farsi YM, Hakkim FL, et al. Reduced levels of antioxidant proteins in children with autism in Oman. Int J Nutr Pharmacol Neurol Dis 2012;2:53-6.  Back to cited text no. 2
  Medknow Journal  
3.Waly MI, Arafa MA, Jriesat SB, Sallam SA, Al-Kafajei A. Folate and vitamin B12 deficiency is associated with colorectal cancer in Jordan. Int J Nutr Pharmacol Neurol Dis 2012;2:57-60.  Back to cited text no. 3
  Medknow Journal  
4.So YT, Simon RP. Deficiency diseases of the nervous system. In: Neurology in Clinical Practice. 2 nd ed. Philadelphia: El Sevier-Inc; 2004. p. 1701-4.  Back to cited text no. 4
    
5.Sechi G, Serra A. Wernicke's encephalopathy: New clinical settings and recent advances in diagnosis and management. Lancet Neurol 2007;6:442-55.  Back to cited text no. 5
    
6.Shalchian S, de Noordhout AM, Fumal A, Tebache M. A rare complication of hyperemesis during pregnancy: Wernicke's encephalopathy. Acta Neurol Belg 2010;110:209-11.  Back to cited text no. 6
    
7.Chiossi G, Neri I, Cavazzuti M, Basso G, Facchinetti F. Hyperemesis gravidrum complicated by Wernicke encephalopathy: Background, case report and review of the literature. Obstet Gynecol Surv 2006;61:255-68.  Back to cited text no. 7
    
8.Caine D, Halliday GM, Kril JJ, Harper CG. Operational criteria for the classification of chronic alcoholics: identification of Wernicke's encephalopathy. J Neurol Neurosurg Psychiatry 1997;62:51-60.  Back to cited text no. 8
    
9.Mullin PM, Bray A, Schoenberg F, Mac gibbon KW, Romero R, Goodwin TM, et al. Prenatal exposure to Hyperemesis gravidrum linked to increased risk of psychological and behavioral disorders in adulthood. J Develop Origins Health and disease 2011;2:200-4.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2]


This article has been cited by
1 Wernicke’s encephalopathy in hyperemesis gravidarum: A systematic review
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European Journal of Obstetrics & Gynecology and Reproductive Biology. 2019; 236: 84
[Pubmed] | [DOI]



 

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