Use of Thiamine Supplementation in Pregnant Women Diagnosed With Hyperemesis Gravidarum and Wernicke Encephalopathy.

Hyperemesis gravidarum is the most common condition requiring hospital care for women during the first 20 weeks of pregnancy and may lead to malnutrition, dehydration, and vitamin deficiencies. Depletion of vitamins such as thiamine may result in the development of Wernicke encephalopathy, a severe neurological disorder that can increase the risk for mortality and morbidity for the mother and fetus. A lack of awareness regarding the relationship of hyperemesis gravidarum and Wernicke encephalopathy may result in delayed treatment and disease management. Glucose administration in the presence of thiamine deficiency may induce Wernicke encephalopathy; protocols are needed to ensure dextrose is used for women with hyperemesis gravidarum in times of prolonged vomiting and poor oral intake only after first administering thiamine. This article includes a discussion of best practices for thiamine supplementation with hyperemesis gravidarum and Wernicke encephalopathy.

Fetal demise and Wernicke-Korsakoff syndrome in a patient with hyperemesis gravidarum: a case report.

BACKGROUND: Wernicke-Korsakoff syndrome is a neuropsychiatric disorder caused by thiamine deficiency composed of two related disorders accounting for an acute presentation and chronic progression. Hyperemesis gravidarum presents a significant risk factor for Wernicke-Korsakoff syndrome as symptoms may rapidly progress in the setting of pregnancy. We present the first-reported case of hyperemesis-gravidarum-associated Wernicke encephalopathy in a patient in the first half of pregnancy in which a missed diagnosis led to septic shock, fetal demise, and eventual profound Korsakoff syndrome. CASE PRESENTATION: We present the case of a 33-year-old primigravid African American woman at 15 weeks gestational age who initially presented at a community emergency department with nausea and vomiting that ultimately progressed to severe hyperemesis-gravidarum-associated Wernicke-Korsakoff syndrome, fetal demise, and septic shock. The patient received a total of 6 weeks of high-dose parenteral thiamine. Magnetic resonance imaging of the head and formal neuropsychological assessment following treatment plateau confirmed the diagnosis of Wernicke-Korsakoff syndrome. CONCLUSIONS: The multisystem complications seen in severe thiamine deficiency can delay timely administration of high-dose thiamine, particularly in pregnancy, in which the classic triad of Wernicke-Korsakoff syndrome may not raise clinical suspicion due to rapid progression of neurological sequelae in this population. We advise a low threshold for parenteral thiamine repletion in pregnant women with persistent vomiting as hyperemesis gravidarum-induced severe thiamine deficiency can result in Wernicke-Korsakoff syndrome, sepsis, and fetal demise.

Hyperemesis gravidarum and vitamin K deficiency: a systematic review.

Hyperemesis gravidarum (HG), severe nausea and vomiting in pregnancy, can lead to vitamin deficiencies. Little is known about HG-related vitamin K deficiency. We aimed to summarise available evidence on the occurrence of HG-related vitamin K deficiency and corresponding maternal and neonatal complications. A systematic review was conducted, searching Medline and EMBASE from inception to 12 November 2020. We identified 1564 articles, of which we included fifteen in this study: fourteen case reports (n 21 women) and one retrospective cohort study (n 109 women). Nine out of twenty-one women reported in case reports had a prolonged prothrombin time (PT). The cohort study measured PT in 39/109 women with HG, of whom 10/39 women (26 %) had prolonged PT. In total, 30-50 % women received vitamin K supplementation after vitamin K deficiency had been diagnosed. Four case reports (n 4 women) reported corresponding maternal complications, all consisting of coagulopathy-related haemorrhage. Nine case reports (n 16 neonates) reported corresponding neonatal complications including intracranial haemorrhage (n 2 neonates) and embryopathy (n 14 neonates), which consisted of Binder phenotype (n 14 neonates), chondrodysplasia punctata (n 9 neonates) and grey matter heterotopia (n 3 neonates). In conclusion, vitamin K deficiency and related complications occur among women with HG. In our systematic review, we were unable to assess the incidence rate.

Wernicke's encephalopathy in women with hyperemesis gravidarum - Case series and literature review.

Whilst nausea affects around 80% of pregnant women, hyperemesis gravidarum, an extreme form of the same, affects only 0.5% to 3%, but may lead to severe nutritional deficiency. Wernicke's encephalopathy is an acute neuropsychiatric disorder which occurs due to thiamine deficiency and needs emergency treatment to prevent neurological morbidity and mortality. Wernicke's encephalopathy is characterised by a clinical triad of oculomotor abnormalities, cerebellar dysfunction and altered mental state. Korsakoff's psychosis is a chronic condition and consequence of Wernicke's encephalopathy, resulting from its delayed treatment. Wernicke's encephalopathy is a well-known complication of chronic alcohol abuse. Not many are aware of its association with hyperemesis gravidarum. Although it is a rare complication, if not diagnosed and treated promptly, it may result in permanent and irreversible neurological sequelae. The objective of our retrospective observational study was to analyse the clinical profile and outcome (short and long term) in a rare yet preventable complication of pregnancy.

Wernicke's encephalopathy post hyperemesis gravidarum misdiagnosed as Guillain-Barre syndrome: lessons for the frontline.

We report a case of a 26-year-old pregnant woman, who presented with subacute limb weakness. This was initially suspected to be Guillain-Barre syndrome but subsequently found to be the motor neuropathy of dry beriberi (vitamin B1, thiamine deficiency) along with associated Wernicke's encephalopathy (WE). The underlying cause was revealed as hyperemesis gravidarum (HG). HG complicates up to 3% of pregnancies and if severe, without nutritional supplements, may lead to electrolyte disturbances, calorie loss and vitamin deficiency. Although the association of HG and WE was first reported in 1939, it remains an under diagnosed condition with potential for serious and permanent neurological deficits, and some mortality, in both mother and baby. Early recognition of the problem, with timely and careful fluid, electrolyte, glucose and vitamin replacement is needed to avoid complications. We highlight current best practice in the treatment of WE. An open mind to the possibility of HG complications in any pregnant woman presenting with neurological symptoms is probably the most important lesson to learn from the front line.

Reversible Wernicke encephalopathy caused by hyperemesis gravidarum in the second trimester of pregnancy: a case report.

Wernicke encephalopathy is a potentially life-threatening neurologic syndrome caused by acute thiamine (vitamin B1) deficiency. It is usually associated with excessive alcohol consumption. Less frequently, this syndrome can be caused by persistent vomiting. This is a case report of a 33-year-old woman diagnosed with Wernicke encephalopathy (WE) during the second trimester of pregnancy. The presence of neurological and ophthalmological symptoms in the context of hyperemesis gravidarum led us to evoke the diagnosis of WE, and it was confirmed when specific lesions were found in the brain magnetic resonance imaging (MRI). Luckily for our patient, WE was diagnosed promptly and the signs were reversible after thiamine supplementation. In conclusion, any first line care taker or midwife must know the symptoms of Wernicke encephalopathy because prompt diagnosis and treatment can lead to recovery.

Wernicke's encephalopathy in hyperemesis gravidarum: A systematic review.

Pregnant women have an increased demand for thiamine. In hyperemesis gravidarum (HG) thiamine rapidly depletes, which can lead to Wernicke's Encephalopathy (WE). Our objective was to systematically review the signs and symptoms of WE in HG. We conducted our search from inception using Mesh terms hyperemesis, Wernicke Encephalopathy, Korsakoff's syndrome, and pregnancy. We searched Pubmed, Embase, Cochrane, Web of Science, Psychinfo, PiCarta, and Cinahl. We defined WE as mental, oculomotor, and motoric alterations and thiamine deficiency; HG was defined as severe nausea, and vomiting during pregnancy; adequate WE treatment as >500 mg/day intramuscular or intravenous. Our search yielded 146 case studies reporting on 177 cases. Pregnant WE patients became thiamine depleted between 10-15 weeks of gestation. Patients had been vomiting for a median of 7 weeks before WE, and had lost 12.1 kg. Prodromal signs of WE were nausea and vomiting (100%), double vision (37.4%), and blurred vision (27.4%). Treatment with subtherapeutic thiamin dose was common (63.6%), WE was exacerbated by intravenous glucose administration (14.1%). We found chronic cognitive disorders occurred in 65.4%, pregnancy loss in 50%, and maternal death in 5% of cases. Thiamine supplementation was insufficient or absent from treatment plans. To eradicate WE in pregnancy, it is necessary to give 100 mg of intravenous or intramuscular thiamine in HG patients with persistent or severe late onset vomiting to prevent them from developing WE.

Hyperemesis gravidarum followed by refeeding syndrome causes electrolyte abnormalities induced rhabdomyolysis and diabetes insipidus.

Although hyperemesis gravidarum (HG), an extreme form of morning sickness, is a common complication during pregnancy, HG associated simultaneous onset of rhabdomyolysis and diabetes insipidus due to electrolyte abnormalities are rare. A 34-year-old woman with severe HG at 17 weeks of gestation complicated with appetite loss, weight reduction by 17 kg, general fatigue, myalgia, weakness and polyuria was identified to have simultaneous hypophosphatemia (1.6 mg/dL) and hypokalemia (2.0 mEq/L). Appetite recovery and the improvement of the hypophosphatemia (3.2 mg/dL) were observed prior to the first visit to our department. At the admission, she presented polyuria around 7,000~8,000 mL/day with impaired concentrating activity (U-Osm 185 mOsm/L), and abnormal creatine kinase elevation (4,505 U/L). The electrolyte disturbances and physio-metabolic abnormalities in undernourished state due to HG let us diagnose this case as refeeding syndrome (RFS). In this case, abnormal loss by vomiting, insufficient intake and previous inappropriate fluid infusion as well as the development of RFS may accelerate the severity of hypokalemia due to HG. Thus, as her abnormalities were considered as results of rhabdomyolysis and diabetes insipidus due to severe HG associated hypokalemia based on RFS, oral supplementation of potassium chloride was initiated. After 6 days of potassium supplementation, her symptoms and biochemical abnormalities were completely resolved. Severe HG followed by RFS can be causes of electrolyte abnormalities and subsequent complications, including rhabdomyolysis and renal diabetes insipidus. Appropriate diagnosis and prompt interventions including adequate nutrition are necessary to prevent electrolyte imbalance induced cardiac, neuromuscular and/or renal complications.

Complete recovery in Wernicke's encephalopathy complicating hyperemesis gravidarum.

Wernicke's encephalopathy (WE) is an uncommon neurological complication in pregnancies complicated with hyperemesis due to thiamine deficiency. In women with hyperemesis, inadvertent glucose administration prior to thiamine supplementation triggers the development of neurological manifestations. Delay in the diagnosis can lead to maternal morbidity, and in one-third of cases may lead to persistence of some neurological deficit. With early recognition and thiamine supplementation, complete recovery is reported. We report a case of WE complicating a case of triplet pregnancy with hyperemesis gravidarum, which highlights the importance of early recognition and treatment, resulting in complete recovery as in the index case.

Recurrent Wernicke's encephalopathy in pregnancy: A case report.

INTRODUCTION: Wernicke's encephalopathy (WE) is an acute neurologic syndrome resulting from a deficiency in thiamine, also known as Vitamin B1. Thiamine stores can be depleted rapidly in patients with severe hyperemesis. Treatment with thiamine typically results in complete resolution of the neurological abnormalities. CASE REPORT: A 15-year-old G2P0010 at 13.2 weeks gestation presented with altered mental status and transaminitis. She had a medical termination in her previous pregnancy following an admission for a similar clinical scenario. She was initially thought to have a postoperative surgical complication due to recent cholecystectomy, but further evaluation revealed thiamine depletion. Magnetic resonance imaging confirmed the diagnosis of WE. Repletion of thiamine and folic acid resulted in rapid clinical improvement. CONCLUSION: WE should be considered in the differential diagnosis of pregnant patients with hyperemesis and altered mental status. A prior history of WE increases the risk of recurrence during pregnancy. Severe hyperemesis during pregnancy increases the risk of thiamine deficiency and WE. Early thiamine supplementation may reduce the risk of WE in patients with a prior clinical history or in patients with severe hyperemesis gravidarum.

Characteristics and Outcomes of Ptyalism Gravidarum.

BACKGROUND: Ptyalism gravidarum (PG) is a condition of hypersalivation that affects pregnant women early in gestation. Symptoms include massive saliva volumes (up to 2 liters per day), swollen salivary glands, sleep deprivation, significant emotional distress, and social difficulties. OBJECTIVES: To examine maternal and fetal characteristics and pregnancy outcomes of patients with PG. METHODS: Patients diagnosed with PG in our clinic during the years 2001-2016 were identified and contacted. Demographic data were extracted from patient charts and clinical and outcome data was collected via telephone interviews. RESULTS: The incidence of PG was 1/963 (0.09%) in our sample. Eleven out of 22 women (40%) with PG were also diagnosed with hyperemesis gravidarum. Fetal gender did not increase the risk. Of the mothers presenting with PG, 37% had a positive family history for this condition. There was no associated increase in the rate of fetal or maternal complications. Two women reported a resolution of the symptoms immediately following hypnosis with acupuncture treatment. CONCLUSIONS: Although PG represents an unpleasant mental and physical condition, it does not pose any specific risk to the health of the mother or increase adverse perinatal outcomes for the fetus. Alternative medicine could play a role in the treatment of PG.

Clinical awareness for health care professionals: Fatal encephalopathy complicating persistent vomiting in pregnancy.

Women with persistent vomiting during pregnancy need early referral to appropriate health facilities. Delayed referral and inappropriate management may lead to metabolic encephalopathy from a variety of causes, including electrolyte derangements or thiamine deficiency (Wernicke's encephalopathy) (WE). We present a case of persistent vomiting in pregnancy in which there was delayed referral, inappropriate treatment and failure to associate neurological signs such as terminal neck stiffness with WE, resulting in poor fetomaternal outcomes. In this report, we discuss the following lessons: (i) the need for early transfer of a patient with persistent vomiting and enigmatic clinical features to a higher healthcare facility; (ii) failure to associate neurological signs with complications of hyperemesis gravidarum/WE; (iii) lack of thiamine supplementation; and (iv) the advantages of magnetic resonance imaging over a computed tomography scan in the diagnosis of WE.

Neurodevelopmental delay in children exposed in utero to hyperemesis gravidarum.

OBJECTIVE: The purpose of this study is to determine the frequency of emotional, behavioral, and learning disorders in children exposed in utero to hyperemesis gravidarum (HG) and to identify prognostic factors for these disorders. STUDY DESIGN: Neurodevelopmental outcomes of 312 children from 203 mothers with HG were compared to neurodevelopmental outcomes from 169 children from 89 unaffected mothers. Then the clinical profiles of patients with HG and a normal child outcome were compared to the clinical profiles of patients with HG and a child with neurodevelopmental delay to identify prognostic factors. Binary responses were analyzed using either a Chi-square or Fisher Exact test and continuous responses were analyzed using a t-test. RESULTS: Children exposed in utero to HG have a 3.28-fold increase in odds of a neurodevelopmental diagnosis including attention disorders, learning delay, sensory disorders, and speech and language delay (P<0.0005). Among characteristics of HG pregnancies, only early onset of symptoms (prior to 5 weeks gestation) was significantly linked to neurodevelopmental delay. We found no evidence for increased risk of 13 emotional, behavioral, and learning disorders, including autism, intellectual impairment, and obsessive-compulsive disorder. However, the study was not sufficiently powered to detect rare conditions. Medications, treatments, and preterm birth were not associated with an increased risk for neurodevelopmental delay. CONCLUSION: Women with HG are at a significantly increased risk of having a child with neurodevelopmental delay. Common antiemetic treatments were not linked to neurodevelopmental delay, but early symptoms may play a role. There is an urgent need to address whether aggressive treatment that includes vitamin and nutrient supplementation in women with early symptoms of severe nausea of pregnancy decreases the risk of neurodevelopmental delay.

A case of maternal vitamin K deficiency associated with hyperemesis gravidarum: its potential impact on fetal blood coagulability.

Vitamin K deficiency is associated with malnutrition in some complications, such as hyperemesis gravidarum, active gastrointestinal diseases, and psychological disorders. Maternal vitamin K deficiency can cause fetal bleeding, in particular, fetal intracranial hemorrhage. Although fetal hemorrhage is uncommon, severe damage to the fetus may be inevitable. We describe a pregnant woman with vitamin K deficiency possibly due to hyperemesis gravidarum. The patient was treated for the deficiency, and no fetal or neonatal hemorrhagic diseases were manifested.

Wernicke's encephalopathy following Hyperemesis gravidarum. A report of three cases.

Wernicke's encephalopathy (WE) due to causes other than chronic alcohol abuse is an uncommon and often misdiagnosed condition. In the setting of hyperemesis gravidarum, an acute deficiency of thiamine results from body stores being unable to meet increased metabolic demands. The condition produces typical clinical and radiological findings and when diagnosed early and treated promptly has a good prognosis. Magnetic resonance imaging (MRI) is sensitive and specific for diagnosis. We describe three patients with hyperemesis gravidarum who developed WE, and highlight a range of clinical and imaging features important for appropriate diagnosis. A high degree of clinical suspicion is essential. Treatment is often empirical pending results of investigation, and consists of parenteral repletion of thiamine stores. Reversal of MRI findings parallels clinical improvement. Neurologic outcomes are usually good, but half the pregnancies complicated by this condition do not produce healthy children.

Neurological complications in hyperemesis gravidarum.

Hyperemesis gravidarum can impair correct absorption of an adequate amount of thiamine and can cause electrolyte imbalance. This study investigated the neurological complications in a pregnant woman with hyperemesis gravidarum. A 29-year-old pregnant woman was admitted for hyperemesis gravidarum. Besides undernutrition, a neurological examination disclosed weakness with hyporeflexia, ophthalmoparesis, multidirectional nystagmus and optic disks swelling; the patient became rapidly comatose. Brain MRI showed symmetric signal hyperintensity and swelling of periaqueductal area, hypothalamus and mammillary bodies, medial and posterior portions of the thalamus and columns of fornix, consistent with Wernicke encephalopathy (WE). Neurophysiological studies revealed an axonal sensory-motor polyneuropathy, likely due to thiamine deficiency or critical illness polyneuropathy. Sodium and potassium supplementation and parenteral thiamine were administered with improvement of consciousness state in a few days. WE evolved in Korsakoff syndrome. A repeat MRI showed a marked improvement of WE-related alterations and a new hyperintense lesion in the pons, suggestive of central pontine myelinolysis. No sign or symptom due to involvement of the pons was present.

[Wernicke's encephalopathy due to hyperemesis gravidarum]. / Encefalopatia-Wernickego w przebiegu niepowsciagliwych wymiotów ciezarnych.

A report of 33 years old female with Wernicke's encephalopathy is presented. The disease was secondary to hyperemesis gravidarum, started from the 6th week of pregnancy. Neurological symptoms as nystagmus, headache, vertigo, disturbance of consciousness and ataxia are described, as well as difficulties in finding out the right diagnosis. We present the therapy with vitamin B1. The subsequent course of the pregnancy was uncomplicated and resulted in a birth--by caesarean section of a healthy male infant, weighted 2790 grams. However, four months later after the delivery, the patient is not yet completely recovered and still demands thiamine supplementation.