Characteristics of Children with Diabetic Ketoacidosis Treated in Pediatric Intensive Care Unit: Two-Center Cross-Sectional Study in Croatia

Abstract

Background and objective: There is an increasing risk of type 1 diabetes mellitus (T1D) among children in Croatia. Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with T1D, with cerebral edema as the most severe complication. Since early recognition of cerebral edema leads to a better outcome, it is important that patients with moderate or severe DKA are closely monitored and treated in pediatric intensive care units (PICUs). The aim of this study is to investigate clinical and laboratory parameters, as well as complications in children treated in PICUs because of DKA. Materials and methods: Patients treated due to DKA in the PICU of the University Hospitals of Split and Osijek from 2013 to 2017 were included in this study. Retrospectively collected data included age, gender, clinical signs and symptoms, and various laboratory parameters. After dividing subjects into two groups: Newly diagnosed with T1D (NT1D) and previously diagnosed with T1D (PT1D), collected data were compared between the two groups. Results: A total of 82 patients were enrolled. Those with NT1D were more often treated in the PICU, with two of them developing cerebral edema. Dehydration was the most frequent clinical sign, found in 95% of patients at admission. Decreased consciousness level was found in 41.5% of patients, with majority of them being somnolent. No difference was found between NT1D and PT1D. Additionally, there was no significant difference regarding laboratory data at admission. Conclusions: More children with NT1D required treatment in the PICU due to DKA with two of them developing cerebral edema. Since cerebral edema is a life-threatening condition, treatment of patients with moderate or severe DKA in PICUs will provide necessary monitoring enabling early recognition, treatment, and better treatment outcome. To minimize the incidence of DKA among patients with NT1D, it is important to continuously carry out public health education programs aimed at early identification of signs and symptoms of T1D.

Fatal Cerebral Edema in a Young Adult with Diabetic Ketoacidosis: Blame the Bicarbonate?

“…Cerebral edema (CE) is a devastating complication of DKA. It is well-described in the pediatric population-it occurs in 0.2-1% of children with DKA and is the leading cause of diabetes-related death in this age group [7][8][9]. The rarity of CE in adults with DKA is illustrated by the fact that there are very few reported cases in this age group.…”

“…However, the addition of bicarbonate therapy to correct metabolic acidosis, particularly in DKA, has been shown to be unhelpful and in some cases even harmful [23]. Except in severely acidemic patients, it is believed that insulin therapy by inhibiting lipolysis will correct the acidosis without use of bicarbonate [6,9]. Bicarbonate administration in metabolic acidosis is associated with adverse effects such as hypokalemia, hypercapnia, ionized hypocalcemia, and the aforementioned CE [23].…”

Diabetic ketoacidosis: Our experiences

“…Među simptomima pacijenata lečenih u jedinicama intenzivne nege, slično našim pacijentima, pominju se polidipsija, poliurija, povraćanje, gubitak telesne mase, akutni bolovi u stomaku, slabost, glavobolja, koji do konačne dijagnoze obično traju oko desetak dana (14). Hrvatski autori navode dehidraciju i smanjen nivo svesti, dok kanadski noćno mokrenje u krevetu, neurološke simptome i povraćanje (15)(16). Oni izveštavaju da su u DKA kod NT1DM deca uglavnom posetila lekara u nedeljama pre dijagnoze, što nije bio slučaj s našim pacijentima (16).…”

Vasogenic edema in the medial temporal lobe during treatment of diabetic ketoacidosis in an elderly patient

“…Cerebral edema during the treatment of patients with diabetic ketoacidosis (DKA) has been reported in children and young adults 1‐7 . Possible mechanisms of this condition include initial cerebral vasoconstriction and hypoperfusion from hypocapnia, followed by reperfusion injury, and vasogenic edema associated with elevation of partial pressures of arterial carbon dioxide (PaCO 2 ) during treatment 2,8 .…”

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Cerebral edema during the treatment of patients with diabetic ketoacidosis (DKA) has been reported in children and young adults. [1][2][3][4][5][6][7] Possible mechanisms of this condition include initial cerebral vasoconstriction and hypoperfusion from hypocapnia, followed by reperfusion injury, and vasogenic edema associated with elevation of partial pressures of arterial carbon dioxide (PaCO 2 ) during treatment. 2,8 The apparent diffusion coefficient (ADC) values on MRI may elevate (suggesting vasogenic edema) in the frontal cortex, basal ganglia, thalamus, and hippocampus during treatment of DKA.

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