The Experts below are selected from a list of 30 Experts worldwide ranked by ideXlab platform
Aravindh Murugesan - One of the best experts on this subject based on the ideXlab platform.
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WERNICKE’S Encephalopathy IN A PREGNANT LADY WITH HYPEREMESIS GRAVIDARUM
University Journal of Medicine and Medical Specialities, 2016Co-Authors: Aravindh MurugesanAbstract:Wernicke's Encephalopathy is a metabolic disorder due to thiamine deficiency. Caseshave been described in situation where nutrition has been compromised .commonly seen in chronic alcoholism. Other conditions associated with Wernicke's Encephalopathy include starvation, anorexia nervosa, and malabsorption, hyperemesis gravidarum in pregnancy, AIDS (acquired immunodeficiency syndrome) patients, patients with malignancy and patients on hemodialysis. Expect in chronic alcoholism, its presences may not be easily recognized. Here we present one such rare occurrence of Wernickes Encephalopathy in a pregnant female with hyperemesis gravidarum in second trimester.
Jithin George - One of the best experts on this subject based on the ideXlab platform.
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hyperemesis gravidarum induced Wernickes Encephalopathy
Journal of Clinical and Medical Case Studies, 2018Co-Authors: Sriharsha Kulkarni, G R Suman, Jithin GeorgeAbstract:Introduction: Wernicke’s Encephalopathy (WE) is a condition caused by the depletion of Vitamin B1 levels. It causes neuropsychiatric symptoms. The triad includes Nystagmus and Ophthalmoplegia, mental status changes and Ataxia. Case description: 29 year old female, Gravida2 Para1 Live1, with 5 months of amenorrhea brought to the hospital with reduced responsiveness for 2 days. Patient had 8-10 episodes of vomiting per day. The vomitus was non-bilious and non-projectile for last 2 months. Patient had opthalmoplegia with restricted extraocular movements. All four limbs had reduced tone. MR imaging showed bilateral thalamus hyperintensities. Serum thiamine level was 2 nmol/L. Patient was treated with 350 mg of intravenous thiamine three times a day. Patient improved clinically. Conclusion: Hyperemesis Gravidarum is one of the rare causes of Wernicke’s Encephalopathy. This diagnosis should be brought to consideration when the neurological triad exist in women with hyperemesis gravidarum. Pregnant women who develop hyperemesis should be given thiamine supplementation, before intravenous or parenteral nutrition.
Michigan State University - One of the best experts on this subject based on the ideXlab platform.
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Walsh & Hoyt: Diagnosis
Spencer S. Eccles Health Sciences Library University of Utah, 2005Co-Authors: David I. Kaufman, Neurology & Ophthalmology, Michigan State UniversityAbstract:MFS should be considered in any patient who develops the rapidly progressive triad of ophthalmoparesis (with or without pupillary and eyelid involvement), ataxia, and areflexia, and also in patients who develop only a part of the syndrome such as an isolated unilateral or bilateral ophthalmoparesis, ophthalmoparesis and ataxia, ophthalmoplegia and areflexia, or ataxia and areflexia. Diagnoses to exclude in such cases are Wernickes Encephalopathy, vascular brainstem disease, botulism, multiple sclerosis, myasthenia gravis, brainstem neoplasm, and a variety of bacterial or viral brainstem encephalitides. EMG and lumbar puncture help confirm the diagnosis, particularly when neuroimaging studies show no evidence of overt CNS involvement
Sriharsha Kulkarni - One of the best experts on this subject based on the ideXlab platform.
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hyperemesis gravidarum induced Wernickes Encephalopathy
Journal of Clinical and Medical Case Studies, 2018Co-Authors: Sriharsha Kulkarni, G R Suman, Jithin GeorgeAbstract:Introduction: Wernicke’s Encephalopathy (WE) is a condition caused by the depletion of Vitamin B1 levels. It causes neuropsychiatric symptoms. The triad includes Nystagmus and Ophthalmoplegia, mental status changes and Ataxia. Case description: 29 year old female, Gravida2 Para1 Live1, with 5 months of amenorrhea brought to the hospital with reduced responsiveness for 2 days. Patient had 8-10 episodes of vomiting per day. The vomitus was non-bilious and non-projectile for last 2 months. Patient had opthalmoplegia with restricted extraocular movements. All four limbs had reduced tone. MR imaging showed bilateral thalamus hyperintensities. Serum thiamine level was 2 nmol/L. Patient was treated with 350 mg of intravenous thiamine three times a day. Patient improved clinically. Conclusion: Hyperemesis Gravidarum is one of the rare causes of Wernicke’s Encephalopathy. This diagnosis should be brought to consideration when the neurological triad exist in women with hyperemesis gravidarum. Pregnant women who develop hyperemesis should be given thiamine supplementation, before intravenous or parenteral nutrition.
Naidoo Dp - One of the best experts on this subject based on the ideXlab platform.
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Neurocirculatory Manifestations of Thiamine Deficiency
2015Co-Authors: Naidoo DpAbstract:The diagnosis of thiamine deficiency is essentially made on clinical grounds and may present with neurological deficit such as peripheral neuropathy and Wernicke’s Encephalopathy, or with high output heart failure (wet beriberi). This study was done to determine the frequency with which both the neurological and cardiovascular manifestations coexist in states of thiamine deficiency. The hospital records of 186 patients admitted on 200 occasions with a diagnosis of thiamine deficiency due to beriberi or Wernickes Encephalopathy were reviewed during the 7-year period (1994-2000). Cases were only included in the analysis if mental changes and neurological deficit (opthalmoplegia, ataxia, nystagmus) resolved rapidly after treatment with thiamine. Similar to the neurological recovery with thiamine, a rapid response in the cardiovascular state and in the metabolic acidosis to treatment with parenteral thiamine was taken as confirmatory evidence of thiamine deficiency. In all but 11 patients, complete recovery ensued within 1-3 days of treatment with parenteral thiamine. The 175 patients who responded dramatically to thiamine (67 Wernicke’s Encephalopathy and 108 cardiac beriberi) form the subject of this review. In total, 43/175 (25%) patients exhibited combined neurologic and circulatory manifestations of thiamine deficiency. Eighteen patients presented with overt coexisting neurocardiac manifestations, twelve of whom had acute pernicious beriberi with circulatory shock, metabolic acidosis and accompanying neurological deficit. There was one death due to circulatory shock and metabolic acidosis in patient who arrived in extremis with an unrecordable blood pressure at the emergency room. Cardiovascular/circulatory manifestations in patients presenting with acute neurological deficit are not infrequent and should raise suspicion of thiamine deficiency. Likewise patients with advanced thiamine deficiency states presenting with shock and metabolic acidosis not infrequently have coexistent signs of WE. Empiric therapy with thiamine in advanced stages of thiamine deficiency is life-saving and a rapid therapeutic response is confirmatory of the diagnosis.
