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<article xlink="http://www.w3.org/1999/xlink" dtd-version="1.0" article-type="pediatrics" lang="en">
<front>
<journal-meta>
<journal-id journal-id-type="publisher">JOHS</journal-id>
<journal-id journal-id-type="nlm-ta">Journ of Health Scien</journal-id>
<journal-title-group>
<journal-title>Journal of HealthCare Sciences</journal-title>
<abbrev-journal-title abbrev-type="pubmed">Journ of Health Scien</abbrev-journal-title>
</journal-title-group>
<issn pub-type="ppub">2231-2196</issn>
<issn pub-type="opub">0975-5241</issn>
<publisher>
<publisher-name>Radiance Research Academy</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="publisher-id">405</article-id>
<article-id pub-id-type="doi">http://dx.doi.org/10.52533/JOHS.2025.50605</article-id>
<article-id pub-id-type="doi-url"/>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Pediatrics</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Diabetic Ketoacidosis in Pediatric Patients: Fluid Management and Cerebral Edema Risk
</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Alzamzami</surname>
<given-names>Abdulghani Abdulaziz</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alshab</surname>
<given-names>Duaa Ahmed</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alrabiea</surname>
<given-names>Mithaq Abdullah</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Mohammed</surname>
<given-names>Fidaa Saleh Al</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Albuainain</surname>
<given-names>Saad Fudail</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Mallawi</surname>
<given-names>Ola Ali</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alfehaid</surname>
<given-names>Rashed Saleh</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Almalki</surname>
<given-names>Abdullah Tariq</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Bagber</surname>
<given-names>Abdulrahman Abrahem</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Sabbagh</surname>
<given-names>Marwan Abdulmoomin</given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Alotaibi</surname>
<given-names>Khalid Fayez</given-names>
</name>
</contrib>
</contrib-group>
<pub-date pub-type="ppub">
<day>13</day>
<month>06</month>
<year>2025</year>
</pub-date>
<volume>5</volume>
<issue>6</issue>
<fpage>213</fpage>
<lpage>220</lpage>
<permissions>
<copyright-statement>This article is copyright of Popeye Publishing, 2009</copyright-statement>
<copyright-year>2009</copyright-year>
<license license-type="open-access" href="http://creativecommons.org/licenses/by/4.0/">
<license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.</license-p>
</license>
</permissions>
<abstract>
<p>Diabetic ketoacidosis represents a critical and potentially life-threatening complication associated with diabetes, predominantly encountered within pediatric populations. This condition is characterized by three key metabolic derangements: hyperglycemia, metabolic acidosis, and the presence of ketone bodies in both blood and urine. The pathophysiology of diabetic ketoacidosis is primarily driven by an absolute or relative deficiency of insulin, which subsequently triggers the secretion of counter-regulatory hormones, including glucagon, cortisol, growth hormone, and catecholamines. These hormonal responses facilitate processes such as gluconeogenesis, lipolysis, and ketogenesis, which collectively contribute to significant metabolic disturbances. A hallmark of diabetic ketoacidosis is the accompanying fluid depletion, which significantly exacerbates morbidity and mortality rates associated with the condition. Pediatric patients are at an increased risk of developing cerebral edema, an often-fatal complication, due to immature cerebral autoregulatory mechanisms. This review article meticulously examines the pathophysiological mechanisms, clinical manifestations, diagnostic criteria, and global prevalence of Diabetic ketoacidosis among children. The critical imperative for early identification and careful differentiation from hyperglycemic hyperosmolar state, particularly in atypical clinical presentations, is emphasized. The article provides a comprehensive overview of contemporary fluid management protocols, advocating for initial resuscitation with isotonic saline and outlining ongoing rehydration strategies tailored to individual weight or body surface area. It also underscores the necessity of vigilant monitoring of serum sodium concentrations, as these levels may appear elevated relative to declining serum glucose, erroneously suggesting hypernatremia. Furthermore, the review delves into the pathogenesis and clinical trajectory of cerebral edema in pediatric Diabetic ketoacidosis, evaluating evidence-based interventions such as intravenous mannitol and hypertonic saline. Recommendations for proactive monitoring and early treatment strategies are presented to mitigate neurologic damage and enhance patient outcomes. Given that pediatric Diabetic ketoacidosis continues to pose a significant global health challenge, targeted education, prompt diagnosis, and meticulous management are essential in reducing its associated complications.
</p>
</abstract>
<kwd-group>
<kwd>diabetic ketoacidosis</kwd>
<kwd> glucose</kwd>
<kwd> cerebral edema</kwd>
<kwd> insulin</kwd>
<kwd> fluid therapy</kwd>
</kwd-group>
</article-meta>
</front>
</article>