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Erschienen in: Diabetes Therapy 4/2019

Open Access 01.07.2019 | Letter

Comment on “Excessive Sodium Bicarbonate Infusion May Result in Osmotic Demyelination Syndrome During Treatment of Diabetic Ketoacidosis: A Case Report” by Hsieh et al.

verfasst von: Luigi Mario Castello, Marco Baldrighi, Francesco Gavelli, Gian Carlo Avanzi

Erschienen in: Diabetes Therapy | Ausgabe 4/2019

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Dear Editor,
We read with great interest the case report recently published in Diabetes Therapy by Hsieh et al. [1], describing a paradigmatic case of diabetic ketoacidosis (DKA) complicated by osmotic demyelination syndrome (ODS). The initial estimate was based on a plasma sodium concentration (PNa) correction factor of 1.6 mEq/L every 100 mg/dL increase in plasmatic glucose above 100 mg/dL, but more recent evidence supports the use of higher correction factors (up to 4 mEq/L) [2]. This underestimation could be partially responsible for a liberal administration of sodium bicarbonate and hypertonic solutions during fluid therapy that led, despite the absence of hyponatremia, to an overly rapid PNa increase and to a fall in plasma osmolality (Posm) and, eventually, to ODS.
Although we find the possible correlation between ODS and hypokalemia mentioned by the authors [1] very fascinating, we would like to emphasize the importance of proper management of DKA and hyperglycemic hyperosmolar state (HHS), with a focus on the fluctuations of Posm and PNa. In our previous works, we set up several mathematical models that allowed us to develop a quantitative approach for the treatment of HHS with the aim of limiting the risk of harmful complications, notably ODS [3, 4]. Recently we proposed a “pragmatic approach” that, in our opinion, could represent a valuable tool in treating HHS patients [5]. Our method is based on a simple algorithm that provides the PNa expected on the basis of the water shift caused by hyperglycemia (PNaG); the difference between the PNaG and the measured PNa allows one to stratify patients into three groups: exclusive water shift, sodium deficit greater than water losses, and absolute water deficit. Further formulas allowed us to quantify the alteration. These data are useful in determining the appropriate treatment and, in our opinion, a therapeutic approach based on accurate quantitative estimate of water and solute imbalances should always be recommended since it represents the most reliable strategy to prevent ODS.

Acknowledgements

Funding

No funding or sponsorship was received for this study or publication of this article.

Authorship

All named authors meet the International Committee of Medical Journal Editors (ICMJE) criteria for authorship for this article, contributed to this manuscript, take responsibility for the integrity of the work as a whole, and have given their approval for this version to be published.

Disclosures

The authors Luigi Mario Castello, Marco Baldrighi, Francesco Gavelli, and Gian Carlo Avanzi have nothing to disclose.

Compliance with Ethics Guidelines

This letter is a response to a previously published article and does not contain any studies with human participants or animals performed by any of the authors.

Open Access

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://​creativecommons.​org/​licenses/​by-nc/​4.​0/​), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
Literatur
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Zurück zum Zitat Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Nephrol Dial Transpl. 2014;29(Suppl 2):i1–39.CrossRef Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Nephrol Dial Transpl. 2014;29(Suppl 2):i1–39.CrossRef
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Zurück zum Zitat Bartoli E, Sainaghi PP, Bergamasco L, Castello L. Computation of the excess glucose and Na deficit of hypo-osmolar hyponatremic hyperglycaemia. Acta Diabetol. 2010;47:147–54.CrossRef Bartoli E, Sainaghi PP, Bergamasco L, Castello L. Computation of the excess glucose and Na deficit of hypo-osmolar hyponatremic hyperglycaemia. Acta Diabetol. 2010;47:147–54.CrossRef
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Zurück zum Zitat Bartoli E, Sainaghi PP, Bergamasco L, Castello L. Hyperosmolar coma due to exclusive glucose accumulation: recognition and computations. Nephrology (Carlton). 2009;14:338–44.CrossRef Bartoli E, Sainaghi PP, Bergamasco L, Castello L. Hyperosmolar coma due to exclusive glucose accumulation: recognition and computations. Nephrology (Carlton). 2009;14:338–44.CrossRef
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Zurück zum Zitat Baldrighi M, Sainaghi PP, Bellan M, Bartoli E, Castello LM. Hyperglycemic hyperosmolar state: a pragmatic approach to properly manage sodium derangements. Curr Diabetes Rev. 2018;14:534–41.CrossRef Baldrighi M, Sainaghi PP, Bellan M, Bartoli E, Castello LM. Hyperglycemic hyperosmolar state: a pragmatic approach to properly manage sodium derangements. Curr Diabetes Rev. 2018;14:534–41.CrossRef
Metadaten
Titel
Comment on “Excessive Sodium Bicarbonate Infusion May Result in Osmotic Demyelination Syndrome During Treatment of Diabetic Ketoacidosis: A Case Report” by Hsieh et al.
verfasst von
Luigi Mario Castello
Marco Baldrighi
Francesco Gavelli
Gian Carlo Avanzi
Publikationsdatum
01.07.2019
Verlag
Springer Healthcare
Erschienen in
Diabetes Therapy / Ausgabe 4/2019
Print ISSN: 1869-6953
Elektronische ISSN: 1869-6961
DOI
https://doi.org/10.1007/s13300-019-0659-6

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