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Diabetic ketoacidosis in children and adolescents

Diabetic ketoacidosis (DKA) is considered to be a common presentation of both type 1 diabetes mellitus and type 2 diabetes mellitus in children and adolescents. DKA arises due to lack of adequate insulin in the body. Insulin stops the use of fat as an energy source by inhibiting the peptide hormone...

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Autor principal: Raghupathy, P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413392/
https://www.ncbi.nlm.nih.gov/pubmed/25941653
http://dx.doi.org/10.4103/2230-8210.155403
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author Raghupathy, P.
author_facet Raghupathy, P.
author_sort Raghupathy, P.
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description Diabetic ketoacidosis (DKA) is considered to be a common presentation of both type 1 diabetes mellitus and type 2 diabetes mellitus in children and adolescents. DKA arises due to lack of adequate insulin in the body. Insulin stops the use of fat as an energy source by inhibiting the peptide hormone glucagon. Without insulin, glucagon levels rise resulting in the release of free fatty acids from adipose tissue, as well as amino acids from muscle cells. Neurological observations should be made for warning signs and symptoms of cerebral edema, and capillary blood glucose concentration should be measured on an hourly basis. Every 2-4 h electrolytes, blood gases, and beta-hydroxybutyrate should be measured. Cerebral edema occurs in 0.5-0.9% of all episodes of DKA. It is considered to be a major cause of death in childhood DKA. Treatment of cerebral edema should be prompt and immediate. Successful DKA management in children depends upon swift diagnosis, meticulous monitoring of clinical and biochemical parameters with prompt intervention.
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spelling pubmed-44133922015-05-04 Diabetic ketoacidosis in children and adolescents Raghupathy, P. Indian J Endocrinol Metab Brief Communication Diabetic ketoacidosis (DKA) is considered to be a common presentation of both type 1 diabetes mellitus and type 2 diabetes mellitus in children and adolescents. DKA arises due to lack of adequate insulin in the body. Insulin stops the use of fat as an energy source by inhibiting the peptide hormone glucagon. Without insulin, glucagon levels rise resulting in the release of free fatty acids from adipose tissue, as well as amino acids from muscle cells. Neurological observations should be made for warning signs and symptoms of cerebral edema, and capillary blood glucose concentration should be measured on an hourly basis. Every 2-4 h electrolytes, blood gases, and beta-hydroxybutyrate should be measured. Cerebral edema occurs in 0.5-0.9% of all episodes of DKA. It is considered to be a major cause of death in childhood DKA. Treatment of cerebral edema should be prompt and immediate. Successful DKA management in children depends upon swift diagnosis, meticulous monitoring of clinical and biochemical parameters with prompt intervention. Medknow Publications & Media Pvt Ltd 2015-04 /pmc/articles/PMC4413392/ /pubmed/25941653 http://dx.doi.org/10.4103/2230-8210.155403 Text en Copyright: © Indian Journal of Endocrinology and Metabolism http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Brief Communication
Raghupathy, P.
Diabetic ketoacidosis in children and adolescents
title Diabetic ketoacidosis in children and adolescents
title_full Diabetic ketoacidosis in children and adolescents
title_fullStr Diabetic ketoacidosis in children and adolescents
title_full_unstemmed Diabetic ketoacidosis in children and adolescents
title_short Diabetic ketoacidosis in children and adolescents
title_sort diabetic ketoacidosis in children and adolescents
topic Brief Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413392/
https://www.ncbi.nlm.nih.gov/pubmed/25941653
http://dx.doi.org/10.4103/2230-8210.155403
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