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A rare complication of vomiting in pregnancy: Wernicke encephalopathy
NEUROL-1771; No. of Pages 4 revue neurologique xxx (2017) xxx–xxx
Available online at
ScienceDirect www.sciencedirect.com
Letter to the Editor
A rare complication of vomiting in pregnancy: Wernicke encephalopathy Introduction Wernicke encephalopathy (WE) is a rare, serious and acute neurological disorder resulting from vitamin B1 deficiency [1]. The mortality rate is estimated to be 30% [2]. It is mainly associated with excessive alcohol intakes, although several cases have been found in the context of hyperemesis gravidarum [3], a state of severe nausea and vomiting during pregnancy that leads to dehydration, electrolyte and acid–base disorders, malnutrition and weight loss [4]. The association of the two conditions was first described in 1939, and its incidence seems to be underestimated [2]. Traditionally, the clinical diagnosis of WE rests on a classic triad of ocular signs, altered consciousness and ataxia, as described by Wernicke in his original article [5]. In the present report, we describe four cases of WE revealed in the context of hyperemesis gravidarum (Table 1). The aim of this report is to demonstrate that this is a serious complication that can readily arise in the absence of adequate prevention, and also to describe our experience in terms of its clinical management and outcomes.
Case reports Case 1 A 21-year-old woman, who had already had one pregnancy and one delivery (G1P1), presented at 12 weeks of gestation with an altered mental state and intractable vomiting lasting for 6 weeks. The patient had received symptomatic treatment (rehydration with isotonic glucose solution, antiemetic treatment), but 3 days after admission, she presented with an altered mental state (disorientation). Physical examination revealed an ataxic gait, but neither diplopia nor nystagmus. She had no fever and no impairment of either her circulatory or respiratory function. Laboratory tests showed mild hypokalemia, cholestasis with cytolysis, a mild increase of pancreatic enzymes and collapsed levels of thyroid-stimulating hormone (TSH). Renal assessments were normal. Ultrasonography showed a normal singleton pregnancy in
accordance with gestational age. Six months after the onset of symptoms, she still had some memory disorder and ataxia. After intravenous (IV) thiamine supplementation, the pregnancy was uneventful, with vaginal delivery of a eutrophic baby at week 38. One year later, no neurological abnormalities were observed.
Case 2 A 28-year-old primigravida woman was hospitalized in our gynecology department at week 18 of gestation for intractable vomiting lasting 5 weeks, with clinical effects (asthenia, dehydration and poor general condition) and severe electrolyte disorders. The patient was managed with antiemetic treatment (metoclopramide) and proton pump inhibitors (PPIs) together with rehydration using isotonic glucose solution and polyionic infusion. Despite these measures, the symptoms and electrolyte disturbances persisted, prompting the patient to be transferred to the intensive care unit. Neurological examination revealed a static and kinetic cerebellar syndrome in association with a pyramidal syndrome (all tendon reflexes were hyperactive). Brain computed tomography (CT) was normal although, a few days later, the patient developed diplopia and nystagmus. Metabolic encephalopathy was suspected, but her brain magnetic resonance imaging (MRI) was normal. Vitamin B1 therapy was started. The pregnancy was carried to term and the patient gave birth, by vaginal delivery, to a eutrophic and healthy baby. By 6 months after delivery, the patient’s symptoms had completely disappeared. Confusion and ataxia had disappeared within the first week of treatment whereas nystagmus was the last to go.
Case 3 This 22-year-old primigravida woman was hospitalized at 15 weeks of gestation after 5 weeks of uncontrollable vomiting. She was admitted to our gynecology department and treated in the usual way (rehydration, glucose saline infusion, antiemetic, gastric protection with PPIs). She presented with a confusional state, cerebellar ataxia, diplopia and nystagmus.
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022
NEUROL-1771; No. of Pages 4
2
revue neurologique xxx (2017) xxx–xxx
Table 1 – Summary of four cases of Wernicke encephalopathy. Case
Weeks of gestation
1
12
2
18
3
15
4
16
Clinical triad Confusion Nystagmus Ataxia Confusion Nystagmus Ataxia Confusion Nystagmus Ataxia Confusion Nystagmus Ataxia
Radiological signs + + + + + + + +
Outcome
No magnetic resonance imaging (MRI)
Favorable
Normal cerebral MRI
Favorable
Bilateral T2 and FLAIR hyperintensities in mammillary bodies
Favorable
Normal cerebral MRI
Spontaneous abortion
+ +
Physiologically, the patient developed mild hepatic cytolysis, increased pancreatic enzymes and electrolyte disorders. Metabolic encephalopathy was suspected, and MRI showed bilateral and symmetrical signals on T2-weighted sequences and fluid-attenuated inversion recovery (FLAIR) hyperintensities in mammillary bodies (Fig. 1). Vitamin B1 supplementation was started. After 2 weeks of treatment, the patient had only lateral nystagmus, as the ataxia and diplopia had disappeared. She gave birth to healthy baby boy at 39 weeks of gestation, but with cesarean section because of acute fetal distress.
Case 4 A 23-year-old multiparous woman presented at gestational week 16 of a twin pregnancy with intractable vomiting lasting 8 weeks. The initial examination revealed an asthenic and dehydrated patient, with polypnea and sinus tachycardia, but no signs of low peripheral perfusion. Her physiological assessments showed severe hypokalemia (with electrical signs) and collapsed levels of TSH. Rehydration with isotonic saline glucose, potassium supplementation, antiemetic and gastro-protective PPIs were started to correct these disorders. However, after 10 days, the patient developed vertical nystagmus, ataxia without delirium and complete loss of deep tendon reflexes. Further assessments revealed hepatic cytolysis and cholestasis, and increased pancreatic enzymes. WE was suspected. Her brain MRI was normal, but vitamin B1 blood levels were low, so vitamin B1 supplementation was started. The outcome was marked by a spontaneous abortion at week 20 of gestation; her symptoms finally disappeared 1 year later.
Discussion WE is an acute neurological syndrome resulting from a deficiency of thiamine, a cofactor in several biochemical pathways in the brain [6]. Thiamine deficiency can arise under a number of circumstances, but typically with excessive alcohol intakes and after gastrectomy. However, it is also seen with prolonged fasting causing malnutrition, prolonged vomiting, gastrointestinal neoplasia, anorexia nervosa, malabsorption syndrome, bariatric surgery for morbid obesity, hemodialysis and peritoneal dialysis [2].
In cases of thiamine deficiency, the disorder is made acutely worse by the introduction of sweet foods and/or parenteral nutrition without vitamin supplementation, a complication due to the sweet solutes and subsequent brutal consumption of body reserves of thiamine via glucose metabolism [3]. This explains the aggravation of the secondary neurological status after infusions of IV glucose without thiamine supplementation in our present cases. Nevertheless, early detection of subclinical thiamine deficiency is a difficult task, as symptoms may be non-specific with, for example, headaches, fatigue, irritability and abdominal discomfort [7]. Definite thiamine deficiency presents with WE with an acute onset, and is characterized by changes in mental status, ocular abnormalities and ataxia. In spite of significant advances in imaging and laboratory assessments, the diagnosis remains clinical, with the classic triad, found in 66% of cases, of ophthalmological disorders (93%), confusion with temporospatial disorientation (80%) and ataxia (76%). More rarely, diminished deep tendon reflexes, peripheral polyneuropathy and decreased tone or dysarthria are also observed [8]. Brain CT has low sensitivity for detection of WE lesions, but can at least exclude any other possible pathologies responsible for symptoms [9]. Brain MRI offers better sensitivity and, while it cannot rule out WE, it is still probably the best way to confirm the diagnosis. Its specificity is estimated to be as high as 93%. Bilateral and symmetrical hyperintense lesions on T2-weighted and FLAIR sequences are mainly observed in periaqueductal gray matter, thalamus, mammillary bodies and around the third ventricle [9]. According to the European Federation of Neurological Societies (EFNS) guidelines [10], brain imaging investigations and measurement of total blood thiamine levels should be included in the paraclinical workup of all patients suspected to have WE, although it is important not to delay thiamine treatment while awaiting the results of investigations. According to many case reports, treatment with either 100 or 200 mg of IV thiamine may be curative in non-alcoholic patients (Table 2) [11]. Administration of thiamine improves the patient’s condition. However, neurological dysfunction may still persist [12]. A confusional state, ataxia and ophthalmoplegia usually resolve within hours of thiamine repletion if administered early in the disease course, whereas impaired memory and learning responds more slowly and often incompletely [13]. Also, WE can evolve into a chronic form of thiamine deficiency
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022
NEUROL-1771; No. of Pages 4 revue neurologique xxx (2017) xxx–xxx
3
Fig. 1 – Brain MRI shows hyperintense signals on (A) T2-weighted and (B) fluid-attenuated inversion recovery (FLAIR) sequences in mammillary bodies (arrows).
Table 2 – Recommended thiamine regimens for hospital inpatients with Wernicke encephalopathy (WE). Treatment of patients with definitive WE diagnosis Prophylactic treatment of patients with suspected or at risk of WE
At least 200–500 mg t.d.s. IV for 5–7 days, followed by oral thiamine, 100 mg t.d.s. for 1–2 weeks and 100 mg/day thereafter At least 100–200 mg t.d.s. IM or IV for 3–5 days, followed by oral thiamine 100 mg t.d.s. for 1–2 weeks and 100 mg/day thereafter
Source: Latt and Dore, 2014 [11]; IV: intravenous; IM: intramuscular.
known as Korsakoff’s psychosis, characterized by memory loss (global amnesia) and confabulation. Patients with Korsakoff’s psychosis often have permanent neurological disability and require long-term institutionalization. According to Spruill and Kuller [14], fetal outcome was favorable in various published cases when treatment was started within
24 h of the onset of neurological disorders. The treatment may also reduce the chances of spontaneous abortion [14]. The largest cohort in the literature, published in 2001 by TogayIsikay et al. [15], confirms our approach and recommends systematic thiamine supplementation as early as possible to prevent WE.
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022
NEUROL-1771; No. of Pages 4
4
revue neurologique xxx (2017) xxx–xxx
Conclusion Hyperemesis gravidarum can induce serious neurological complications. Thus, providing women with information about the condition, and the appropriate management of vomiting and thiamine supplementation in patients who have acute neurological symptoms, may preclude both maternal and fetal morbidity.
Disclosure of interest The authors declare that they have no competing interest.
references
[1] Adioui T, Nejjari F, Tamzaourte M, Basr H, Rouibaa F, Aourarh A. [Gayet–Wernicke encephalopathy: a rare complication of prolonged parenteral nutrition]. Presse Med 2015;44(5):561–4. [2] Kleinert-Altamirano AP, Juarez-Jimenez H. [Wernicke’s encephalopathy and Caine criteria. Report of six cases]. Rev Med Inst Mex Seguro Soc 2014;52(1):104–7. [3] Yahia M, Najeh H, Zied H, Khalaf M, Salah AM, Sofienne BM, et al. Wernicke’s encephalopathy: a rare complication of hyperemesis gravidarum. Anaesth Crit Care Pain Med 2015;34(3):173–7. [4] Jarraya A, Elleuch S, Zouari J, Trigui K, Sofiene A, Smaoui M, et al. [Hyperemesis gravidarum with severe electrolyte disorders: report of a case]. Pan Afr Med J 2015;20:264. [5] Behura SS, Swain SP. Neuropsychological functioning in Wernicke’s encephalopathy. Ind Psychiatry J 2015;24(1): 99–103. [6] Nardone R, Holler Y, Storti M, Christova M, Tezzon F, Golaszewski S, et al. Thiamine deficiency induced neurochemical, neuroanatomical, and neuropsychological alterations: a reappraisal. Sci World J 2013;2013:309143. [7] Kopelman MD, Thomson AD, Guerrini I, Marshall EJ. The Korsakoff syndrome: clinical aspects, psychology and treatment. Alcohol Alcohol 2009;44(2):148–54. [8] Chakraborty PP, Ghosh S. Wernicke’s encephalopathy. J Assoc Physicians India 2013;61(11):811–2. [9] Thomson AD, Marshall EJ. The natural history and pathophysiology of Wernicke’s encephalopathy and Korsakoff’s psychosis. Alcohol Alcohol 2006;41(2): 151–8.
[10] Galvin R, Brathen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol 2010;17(12):1408–18. [11] Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Intern Med J 2014;44(9):911–5. [12] Donnino MW, Vega J, Miller J, Walsh M. Myths and misconceptions of Wernicke’s encephalopathy: what every emergency physician should know. Ann Emerg Med 2007;50(6):715–21. [13] Day E, Bentham PW, Callaghan R, Kuruvilla T, George S. Thiamine for prevention and treatment of Wernicke– Korsakoff Syndrome in people who abuse alcohol. Cochrane Database Syst Rev 2013;7:CD004033. [14] Spruill SC, Kuller JA. Hyperemesis gravidarum complicated by Wernicke’s encephalopathy. Obstet Gynecol 2002; 99(5 Pt 2):875–7. [15] Togay-Isikay C, Yigit A, Mutluer N. Wernicke’s encephalopathy due to hyperemesis gravidarum and under-recognised condition. Aust N Z J Obstet Gynaecol 2001;41:453–6.
F. Jebali* S. Lejri Anesthesiology Department, University of Monastir, 5000 Monastir, Tunisia A.B. Salem Radiology Department, University of Monastir, 5000 Monastir, Tunisia L. Grati Anesthesiology Department, University of Monastir, 5000 Monastir, Tunisia *Corresponding author at: Anesthesiology Department, University of Monastir, cite´ Omrane, 5000 Monastir, Tunisia. E-mail address: [email protected] (F. Jebali) Received 17 January 2017 Received in revised form 6 March 2017 Accepted 31 March 2017 Available online xxx http://dx.doi.org/10.1016/j.neurol.2017.03.022 0035-3787/# 2017 Elsevier Masson SAS. All rights reserved.
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022
Available online at
ScienceDirect www.sciencedirect.com
Letter to the Editor
A rare complication of vomiting in pregnancy: Wernicke encephalopathy Introduction Wernicke encephalopathy (WE) is a rare, serious and acute neurological disorder resulting from vitamin B1 deficiency [1]. The mortality rate is estimated to be 30% [2]. It is mainly associated with excessive alcohol intakes, although several cases have been found in the context of hyperemesis gravidarum [3], a state of severe nausea and vomiting during pregnancy that leads to dehydration, electrolyte and acid–base disorders, malnutrition and weight loss [4]. The association of the two conditions was first described in 1939, and its incidence seems to be underestimated [2]. Traditionally, the clinical diagnosis of WE rests on a classic triad of ocular signs, altered consciousness and ataxia, as described by Wernicke in his original article [5]. In the present report, we describe four cases of WE revealed in the context of hyperemesis gravidarum (Table 1). The aim of this report is to demonstrate that this is a serious complication that can readily arise in the absence of adequate prevention, and also to describe our experience in terms of its clinical management and outcomes.
Case reports Case 1 A 21-year-old woman, who had already had one pregnancy and one delivery (G1P1), presented at 12 weeks of gestation with an altered mental state and intractable vomiting lasting for 6 weeks. The patient had received symptomatic treatment (rehydration with isotonic glucose solution, antiemetic treatment), but 3 days after admission, she presented with an altered mental state (disorientation). Physical examination revealed an ataxic gait, but neither diplopia nor nystagmus. She had no fever and no impairment of either her circulatory or respiratory function. Laboratory tests showed mild hypokalemia, cholestasis with cytolysis, a mild increase of pancreatic enzymes and collapsed levels of thyroid-stimulating hormone (TSH). Renal assessments were normal. Ultrasonography showed a normal singleton pregnancy in
accordance with gestational age. Six months after the onset of symptoms, she still had some memory disorder and ataxia. After intravenous (IV) thiamine supplementation, the pregnancy was uneventful, with vaginal delivery of a eutrophic baby at week 38. One year later, no neurological abnormalities were observed.
Case 2 A 28-year-old primigravida woman was hospitalized in our gynecology department at week 18 of gestation for intractable vomiting lasting 5 weeks, with clinical effects (asthenia, dehydration and poor general condition) and severe electrolyte disorders. The patient was managed with antiemetic treatment (metoclopramide) and proton pump inhibitors (PPIs) together with rehydration using isotonic glucose solution and polyionic infusion. Despite these measures, the symptoms and electrolyte disturbances persisted, prompting the patient to be transferred to the intensive care unit. Neurological examination revealed a static and kinetic cerebellar syndrome in association with a pyramidal syndrome (all tendon reflexes were hyperactive). Brain computed tomography (CT) was normal although, a few days later, the patient developed diplopia and nystagmus. Metabolic encephalopathy was suspected, but her brain magnetic resonance imaging (MRI) was normal. Vitamin B1 therapy was started. The pregnancy was carried to term and the patient gave birth, by vaginal delivery, to a eutrophic and healthy baby. By 6 months after delivery, the patient’s symptoms had completely disappeared. Confusion and ataxia had disappeared within the first week of treatment whereas nystagmus was the last to go.
Case 3 This 22-year-old primigravida woman was hospitalized at 15 weeks of gestation after 5 weeks of uncontrollable vomiting. She was admitted to our gynecology department and treated in the usual way (rehydration, glucose saline infusion, antiemetic, gastric protection with PPIs). She presented with a confusional state, cerebellar ataxia, diplopia and nystagmus.
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022
NEUROL-1771; No. of Pages 4
2
revue neurologique xxx (2017) xxx–xxx
Table 1 – Summary of four cases of Wernicke encephalopathy. Case
Weeks of gestation
1
12
2
18
3
15
4
16
Clinical triad Confusion Nystagmus Ataxia Confusion Nystagmus Ataxia Confusion Nystagmus Ataxia Confusion Nystagmus Ataxia
Radiological signs + + + + + + + +
Outcome
No magnetic resonance imaging (MRI)
Favorable
Normal cerebral MRI
Favorable
Bilateral T2 and FLAIR hyperintensities in mammillary bodies
Favorable
Normal cerebral MRI
Spontaneous abortion
+ +
Physiologically, the patient developed mild hepatic cytolysis, increased pancreatic enzymes and electrolyte disorders. Metabolic encephalopathy was suspected, and MRI showed bilateral and symmetrical signals on T2-weighted sequences and fluid-attenuated inversion recovery (FLAIR) hyperintensities in mammillary bodies (Fig. 1). Vitamin B1 supplementation was started. After 2 weeks of treatment, the patient had only lateral nystagmus, as the ataxia and diplopia had disappeared. She gave birth to healthy baby boy at 39 weeks of gestation, but with cesarean section because of acute fetal distress.
Case 4 A 23-year-old multiparous woman presented at gestational week 16 of a twin pregnancy with intractable vomiting lasting 8 weeks. The initial examination revealed an asthenic and dehydrated patient, with polypnea and sinus tachycardia, but no signs of low peripheral perfusion. Her physiological assessments showed severe hypokalemia (with electrical signs) and collapsed levels of TSH. Rehydration with isotonic saline glucose, potassium supplementation, antiemetic and gastro-protective PPIs were started to correct these disorders. However, after 10 days, the patient developed vertical nystagmus, ataxia without delirium and complete loss of deep tendon reflexes. Further assessments revealed hepatic cytolysis and cholestasis, and increased pancreatic enzymes. WE was suspected. Her brain MRI was normal, but vitamin B1 blood levels were low, so vitamin B1 supplementation was started. The outcome was marked by a spontaneous abortion at week 20 of gestation; her symptoms finally disappeared 1 year later.
Discussion WE is an acute neurological syndrome resulting from a deficiency of thiamine, a cofactor in several biochemical pathways in the brain [6]. Thiamine deficiency can arise under a number of circumstances, but typically with excessive alcohol intakes and after gastrectomy. However, it is also seen with prolonged fasting causing malnutrition, prolonged vomiting, gastrointestinal neoplasia, anorexia nervosa, malabsorption syndrome, bariatric surgery for morbid obesity, hemodialysis and peritoneal dialysis [2].
In cases of thiamine deficiency, the disorder is made acutely worse by the introduction of sweet foods and/or parenteral nutrition without vitamin supplementation, a complication due to the sweet solutes and subsequent brutal consumption of body reserves of thiamine via glucose metabolism [3]. This explains the aggravation of the secondary neurological status after infusions of IV glucose without thiamine supplementation in our present cases. Nevertheless, early detection of subclinical thiamine deficiency is a difficult task, as symptoms may be non-specific with, for example, headaches, fatigue, irritability and abdominal discomfort [7]. Definite thiamine deficiency presents with WE with an acute onset, and is characterized by changes in mental status, ocular abnormalities and ataxia. In spite of significant advances in imaging and laboratory assessments, the diagnosis remains clinical, with the classic triad, found in 66% of cases, of ophthalmological disorders (93%), confusion with temporospatial disorientation (80%) and ataxia (76%). More rarely, diminished deep tendon reflexes, peripheral polyneuropathy and decreased tone or dysarthria are also observed [8]. Brain CT has low sensitivity for detection of WE lesions, but can at least exclude any other possible pathologies responsible for symptoms [9]. Brain MRI offers better sensitivity and, while it cannot rule out WE, it is still probably the best way to confirm the diagnosis. Its specificity is estimated to be as high as 93%. Bilateral and symmetrical hyperintense lesions on T2-weighted and FLAIR sequences are mainly observed in periaqueductal gray matter, thalamus, mammillary bodies and around the third ventricle [9]. According to the European Federation of Neurological Societies (EFNS) guidelines [10], brain imaging investigations and measurement of total blood thiamine levels should be included in the paraclinical workup of all patients suspected to have WE, although it is important not to delay thiamine treatment while awaiting the results of investigations. According to many case reports, treatment with either 100 or 200 mg of IV thiamine may be curative in non-alcoholic patients (Table 2) [11]. Administration of thiamine improves the patient’s condition. However, neurological dysfunction may still persist [12]. A confusional state, ataxia and ophthalmoplegia usually resolve within hours of thiamine repletion if administered early in the disease course, whereas impaired memory and learning responds more slowly and often incompletely [13]. Also, WE can evolve into a chronic form of thiamine deficiency
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022
NEUROL-1771; No. of Pages 4 revue neurologique xxx (2017) xxx–xxx
3
Fig. 1 – Brain MRI shows hyperintense signals on (A) T2-weighted and (B) fluid-attenuated inversion recovery (FLAIR) sequences in mammillary bodies (arrows).
Table 2 – Recommended thiamine regimens for hospital inpatients with Wernicke encephalopathy (WE). Treatment of patients with definitive WE diagnosis Prophylactic treatment of patients with suspected or at risk of WE
At least 200–500 mg t.d.s. IV for 5–7 days, followed by oral thiamine, 100 mg t.d.s. for 1–2 weeks and 100 mg/day thereafter At least 100–200 mg t.d.s. IM or IV for 3–5 days, followed by oral thiamine 100 mg t.d.s. for 1–2 weeks and 100 mg/day thereafter
Source: Latt and Dore, 2014 [11]; IV: intravenous; IM: intramuscular.
known as Korsakoff’s psychosis, characterized by memory loss (global amnesia) and confabulation. Patients with Korsakoff’s psychosis often have permanent neurological disability and require long-term institutionalization. According to Spruill and Kuller [14], fetal outcome was favorable in various published cases when treatment was started within
24 h of the onset of neurological disorders. The treatment may also reduce the chances of spontaneous abortion [14]. The largest cohort in the literature, published in 2001 by TogayIsikay et al. [15], confirms our approach and recommends systematic thiamine supplementation as early as possible to prevent WE.
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022
NEUROL-1771; No. of Pages 4
4
revue neurologique xxx (2017) xxx–xxx
Conclusion Hyperemesis gravidarum can induce serious neurological complications. Thus, providing women with information about the condition, and the appropriate management of vomiting and thiamine supplementation in patients who have acute neurological symptoms, may preclude both maternal and fetal morbidity.
Disclosure of interest The authors declare that they have no competing interest.
references
[1] Adioui T, Nejjari F, Tamzaourte M, Basr H, Rouibaa F, Aourarh A. [Gayet–Wernicke encephalopathy: a rare complication of prolonged parenteral nutrition]. Presse Med 2015;44(5):561–4. [2] Kleinert-Altamirano AP, Juarez-Jimenez H. [Wernicke’s encephalopathy and Caine criteria. Report of six cases]. Rev Med Inst Mex Seguro Soc 2014;52(1):104–7. [3] Yahia M, Najeh H, Zied H, Khalaf M, Salah AM, Sofienne BM, et al. Wernicke’s encephalopathy: a rare complication of hyperemesis gravidarum. Anaesth Crit Care Pain Med 2015;34(3):173–7. [4] Jarraya A, Elleuch S, Zouari J, Trigui K, Sofiene A, Smaoui M, et al. [Hyperemesis gravidarum with severe electrolyte disorders: report of a case]. Pan Afr Med J 2015;20:264. [5] Behura SS, Swain SP. Neuropsychological functioning in Wernicke’s encephalopathy. Ind Psychiatry J 2015;24(1): 99–103. [6] Nardone R, Holler Y, Storti M, Christova M, Tezzon F, Golaszewski S, et al. Thiamine deficiency induced neurochemical, neuroanatomical, and neuropsychological alterations: a reappraisal. Sci World J 2013;2013:309143. [7] Kopelman MD, Thomson AD, Guerrini I, Marshall EJ. The Korsakoff syndrome: clinical aspects, psychology and treatment. Alcohol Alcohol 2009;44(2):148–54. [8] Chakraborty PP, Ghosh S. Wernicke’s encephalopathy. J Assoc Physicians India 2013;61(11):811–2. [9] Thomson AD, Marshall EJ. The natural history and pathophysiology of Wernicke’s encephalopathy and Korsakoff’s psychosis. Alcohol Alcohol 2006;41(2): 151–8.
[10] Galvin R, Brathen G, Ivashynka A, Hillbom M, Tanasescu R, Leone MA. EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. Eur J Neurol 2010;17(12):1408–18. [11] Latt N, Dore G. Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders. Intern Med J 2014;44(9):911–5. [12] Donnino MW, Vega J, Miller J, Walsh M. Myths and misconceptions of Wernicke’s encephalopathy: what every emergency physician should know. Ann Emerg Med 2007;50(6):715–21. [13] Day E, Bentham PW, Callaghan R, Kuruvilla T, George S. Thiamine for prevention and treatment of Wernicke– Korsakoff Syndrome in people who abuse alcohol. Cochrane Database Syst Rev 2013;7:CD004033. [14] Spruill SC, Kuller JA. Hyperemesis gravidarum complicated by Wernicke’s encephalopathy. Obstet Gynecol 2002; 99(5 Pt 2):875–7. [15] Togay-Isikay C, Yigit A, Mutluer N. Wernicke’s encephalopathy due to hyperemesis gravidarum and under-recognised condition. Aust N Z J Obstet Gynaecol 2001;41:453–6.
F. Jebali* S. Lejri Anesthesiology Department, University of Monastir, 5000 Monastir, Tunisia A.B. Salem Radiology Department, University of Monastir, 5000 Monastir, Tunisia L. Grati Anesthesiology Department, University of Monastir, 5000 Monastir, Tunisia *Corresponding author at: Anesthesiology Department, University of Monastir, cite´ Omrane, 5000 Monastir, Tunisia. E-mail address: [email protected] (F. Jebali) Received 17 January 2017 Received in revised form 6 March 2017 Accepted 31 March 2017 Available online xxx http://dx.doi.org/10.1016/j.neurol.2017.03.022 0035-3787/# 2017 Elsevier Masson SAS. All rights reserved.
Please cite this article in press as: Jebali F, Lejri S. A rare complication of vomiting in pregnancy: Wernicke encephalopathy. Revue neurologique (2017), http://dx.doi.org/10.1016/j.neurol.2017.03.022