Diabetic ketoacidosis in children and adolescents

Abstract

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.

Daño renal agudo y cetoacidosis diabética en pacientes pediátricos: factores de riesgo

“…Un total de 70 pacientes ingresaron a la Unidad de Cuidados Intensivos Pediátricos con diagnóstico de diabetes mellitus tipo 1. 5 Asimismo, es una causa principal de morbilidad y mortalidad en los niños diabéticos en los países en vías de desarrollo. 6 Por lo anterior, es importante reconocer la presentación de daño renal agudo en los pacientes con diagnóstico de cetoacidosis diabética.…”

Association of diabetic ketoacidosis, severe hypoglycemia and glycemic control among children and young adults with type 1 diabetes mellitus treated with premixed versus basal-bolus insulin therapy

“…In addition, approximately 28%–65% of instances of DKA occurred in young T1DM patients due to omitted insulin injections; therefore, omitting insulin injection is the major cause of DKA in children and young adults with T1DM [13] , [21] , [22] , [23] , [24] , [25] . In patients with T1DM, after 4–6 h of withdrawal from insulin administration ketone bodies will increase, which eventually increases the risk of DKA [26] , [27] .After premixed insulin injection, serum insulin concentration may reach its maximum level 60–100 min after injection and down to relatively low level after around 15–18 h [28] , [29] , [30] , [31] .…”

Physiological effects of proinsulin-connecting peptide in human subcutaneous adipose tissue

“…On the other hand, insulin inhibits lipolysis by activating the phosphodiesterase-3B and consequently This effect is most probably mediated by activating phosphodiesterase-3B in adipocytes (20). Insulin deficiency as seen in type-1 diabetes is associated with increased lipolysis that ultimately results in severing fat loss and even diabetic ketoacidosis (22,43). Because of the antilipolytic property of C-peptide, coreplacement of insulin and C-peptide may prevent, retard, or ameliorate such diabetes-related complications.…”