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Hypertonicity: Clinical entities, manifestations and treatment

Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water....

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Autores principales: Rondon-Berrios, Helbert, Argyropoulos, Christos, Ing, Todd S, Raj, Dominic S, Malhotra, Deepak, Agaba, Emmanuel I, Rohrscheib, Mark, Khitan, Zeid J, Murata, Glen H, Shapiro, Joseph I, Tzamaloukas, Antonios H
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Baishideng Publishing Group Inc 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5215203/
https://www.ncbi.nlm.nih.gov/pubmed/28101446
http://dx.doi.org/10.5527/wjn.v6.i1.1
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author Rondon-Berrios, Helbert
Argyropoulos, Christos
Ing, Todd S
Raj, Dominic S
Malhotra, Deepak
Agaba, Emmanuel I
Rohrscheib, Mark
Khitan, Zeid J
Murata, Glen H
Shapiro, Joseph I
Tzamaloukas, Antonios H
author_facet Rondon-Berrios, Helbert
Argyropoulos, Christos
Ing, Todd S
Raj, Dominic S
Malhotra, Deepak
Agaba, Emmanuel I
Rohrscheib, Mark
Khitan, Zeid J
Murata, Glen H
Shapiro, Joseph I
Tzamaloukas, Antonios H
author_sort Rondon-Berrios, Helbert
collection PubMed
description Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.
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spelling pubmed-52152032017-01-19 Hypertonicity: Clinical entities, manifestations and treatment Rondon-Berrios, Helbert Argyropoulos, Christos Ing, Todd S Raj, Dominic S Malhotra, Deepak Agaba, Emmanuel I Rohrscheib, Mark Khitan, Zeid J Murata, Glen H Shapiro, Joseph I Tzamaloukas, Antonios H World J Nephrol Review Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level. Baishideng Publishing Group Inc 2017-01-06 2017-01-06 /pmc/articles/PMC5215203/ /pubmed/28101446 http://dx.doi.org/10.5527/wjn.v6.i1.1 Text en ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
spellingShingle Review
Rondon-Berrios, Helbert
Argyropoulos, Christos
Ing, Todd S
Raj, Dominic S
Malhotra, Deepak
Agaba, Emmanuel I
Rohrscheib, Mark
Khitan, Zeid J
Murata, Glen H
Shapiro, Joseph I
Tzamaloukas, Antonios H
Hypertonicity: Clinical entities, manifestations and treatment
title Hypertonicity: Clinical entities, manifestations and treatment
title_full Hypertonicity: Clinical entities, manifestations and treatment
title_fullStr Hypertonicity: Clinical entities, manifestations and treatment
title_full_unstemmed Hypertonicity: Clinical entities, manifestations and treatment
title_short Hypertonicity: Clinical entities, manifestations and treatment
title_sort hypertonicity: clinical entities, manifestations and treatment
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5215203/
https://www.ncbi.nlm.nih.gov/pubmed/28101446
http://dx.doi.org/10.5527/wjn.v6.i1.1
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