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Case Report
 
Severe hyponatremia: A physician's nightmare
Michele Carron1, Mariarosa Meneghetti2, Giuseppe Gagliardi2, Carlo Ori3
1Anesthesiologist and Intensivist, Assistant Professor, Department of Medicine, Anesthesiology and Intensive Care, University of Padova, Padova, Italy.
2Anesthesiologist and Intensivist, Intensive Care Unit, St. Antony Hospital, Via Jacopo Facciolati, 71 - 35127 Padova, Italy.
3Anesthesiologist and Intensivist, Professor and Chief, Department of Medicine, Anesthesiology and Intensive Care, University of Padova, Padova, Italy.

doi:10.5348/ijcri-2015111-CR-10572

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Michele Carron
Via C. Battisti, 267, Padova
Italy, 35121
Phone: +39 049 8213090
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How to cite this article
Carron M, Meneghetti M, Gagliardi G, Ori C. Severe hyponatremia: A physician's nightmare. Int J Case Rep Images 2015;6(11):694–697.


Abstract
Introduction: Osmotic demyelination syndrome is an uncommon neurological disease that may complicate the treatment of severe hyponatremia [1] [2] [3] [4]. In case of osmotic demyelination syndrome, the computed tomography and the magnetic resonance imaging scans are used for diagnosis. The experience with positron emission tomography with 18Fluoro-fluorodeoxyglucose is limited.
Case Report: We report the case of a 32-year-old female who presented to the emergency department with signs and symptoms of severe hyponatremia (104 mmol/L). Treatment with hypertonic saline allowed to increase her serum sodium level to 132 mmol/L in the following three days with initial clinical benefit. On the 3rd day, the patient showed neurological deterioration complicated by seizures requiring intensive care. The computed tomography and magnetic resonance imaging scans of her brain obtained in the first fifteen days from hospital admission were normal. Instead, positron emission tomography with 18Fluoro-fluorodeoxyglucose revealed an overall reduction in 18Fluoro-fluorodeoxyglucose uptake in the cortical area attributable to diffuse brain damage, confirmed by a subsequent third magnetic resonance imaging scan taken twenty days after the hospitalization. Osmotic demyelination syndrome was diagnosed. The patient did not recover neurologically as confirmed by a second positron emission tomography with 18Fluoro-fluorodeoxyglucose performed ninety days after hospitalization.
Conclusion: Great attention should be placed on treatment of severe hyponatremia. In case of osmotic demyelination syndrome, the use of positron emission tomography with 18Fluoro-fluorodeoxyglucose may be considered for diagnosis and for assessment of the degree and extent of cerebral damage over time.

Keywords: 18Fluoro-fluorodeoxyglucose, Hyponatremia, Osmotic demyelination syndrome, Positron emission tomography


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Author Contributions
Michele Carron – Substantial contributions to conception and design, Acquisition of data, Analysis and interpretation of data, Drafting the article, Revising it critically for important intellectual content, Final approval of the version to be published
Mariarosa Meneghetti – Analysis and interpretation of data, Revising it critically for important intellectual content, Final approval of the version to be published
Giuseppe Gagliardi – Analysis and interpretation of data, Revising it critically for important intellectual content, Final approval of the version to be published
Carlo Ori – Analysis and interpretation of data, Revising it critically for important intellectual content, Final approval of the version to be published
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The corresponding author is the guarantor of submission.
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Conflict of interest
Authors declare no conflict of interest.
Copyright
© 2015 Michele Carron et al. This article is distributed under the terms of Creative Commons Attribution License which permits unrestricted use, distribution and reproduction in any medium provided the original author(s) and original publisher are properly credited. Please see the copyright policy on the journal website for more information.