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PECARN Pie: DKA and Fluids Part 1

Nathan Kuppermann, MD, MPH and Solomon Behar, MD
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Sol and Nate Kuppermann, Professor of Emergency Medicine and Pediatrics at UC Davis, discuss fluid management and risk for cerebral edema in pediatric patients with DKA.

  • In a 2001 retrospective case control study, Dr. Glaser et al. found that the four risk factors associated with the development of cerebral edema in a child presenting with diabetic ketoacidosis (DKA) are:

    • degree of acidosis

    • severity of dehydration

    • failure of sodium to correct as the glucose normalizes

      • The thought is that these children have had a cerebral insult prior to presentation resulting in cerebral salt wasting. 

    • administration of bicarbonate 

    • Fluid was not a factor. 

  • Historically, we were taught that the cause of brain injury and subsequent edema that occurs during DKA is related to the difference in osmoles between the serum and the brain cells: as fluids are administered, the serum osmolarity drops causing fluid to move into the brain cell. 

  • The more current hypothesis is that DKA is an inflammatory state; the patient takes an insult with hypoperfusion in the setting of inflammation and it is these two factors that set them up for vasogenic edema (i.e. accumulation of fluid outside of the cell). Imaging confirms that the brain suffers a hypoperfusion-reperfusion type of injury during DKA.  

  • In 2018, a randomized control trial was done that examined the effects of the rate of administration and the sodium chloride content of IV fluids on neurologic outcomes in children with DKA.

    • Approximately 1,400 children presenting with DKA were randomly assigned to one of four treatment groups in a 2-by-2 factorial design (0.9% or 0.45% sodium chloride content and rapid or slow rate of administration). 

    • Clinically apparent brain injury during treatment for DKA occured in 12 patients (approximately 1%). 

    • The primary outcome looked at was a decline in mental status using a sustained Glasgow Coma Scale score of <14 as a surrogate measure. Additionally, short-term memory testing was followed as a secondary outcome given that the part of the brain that is most susceptible to hypoperfusion-reperfusion injury is the hippocampus.

  • The conclusion of the study was that neither the rate of administration nor the sodium chloride content of IV fluids significantly influenced neurologic outcomes in children with DKA.

    • The data suggests that in the sickest patients, faster fluids may be better. 

  • Dr. Kuppermann advises using an insulin drip instead of an insulin bolus given that the latter can cause rapid electrolyte changes. 

  • Monitor children presenting with DKA closely throughout treatment as 0.5 to 1% will have neurological decompensation. Watch not only the patient’s vital signs and mental status but also their sodium level because failure of the sodium to correct as blood sugar normalizes is one of the blood markers suggesting that cerebral insult has already happened.

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Hippo Peds RAP March 2021 Written Summary 177 KB - PDF

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