Online EMS & Fire CE Courses | 911 e-Learning Solutions LLC

Systematically Treating the Extra Sweet Pediatric Patient, Without Inadvertently Giving Them a Big Head

Home » 911 e-Learning News » Systematically Treating the Extra Sweet Pediatric Patient, Without Inadvertently Giving Them a Big Head

Roger L. Layell, AAS, FP-C, CCP-C, C-NPT, CCEMT-P, NRP

Kory A. Lane, MEd, NRP, FP-C, CCP-C, CCEMT-P, NCEE

Abstract

Treating pediatric patients with diabetic ketoacidosis (DKA) during transport can be complex and multifactorial. Cerebral edema is a frequent occurrence in pediatric patients with DKA; however, the signs often occur in a subtle manner. Overzealous correction of their blood glucose may result in cerebral edema as well as a cascade of electrolyte abnormalities. Pediatric patients with diabetes mellitus are prone to developing DKA. Serious complications from DKA in pediatrics often present acutely and rapidly.


© 2023 Air Medical Journal Associates. Published by Elsevier Inc. All rights reserved.

Treating pediatric patients with diabetic ketoacidosis (DKA) during transport can be complex and multifactorial. Overzealous correction of their blood glucose may result in cerebral edema as well as a cascade of electrolyte abnormalities. Pediatric patients with diabetes mellitus (DM) are prone to developing DKA. Serious complications from DKA in pediatrics often present acutely and rapidly. DKA can occur in those patients with pre-existing type 1 DM or new-onset DM.1 Recent reports have revealed that pediatric patients with type 2 diabetes who are non−insulin dependent have a higher incidence of DKA than those patients who are insulin dependent.1 DKA most often occurs because of a complete or respective lack in insulin. Unfortunately, DKA continues to be the leading cause of death in pediatric and younger adults with type 1 DM.2

Multiple factors can affect insulin requirements in the pediatric patient. Patients either do not manufacture insulin, they have a lack of insulin, or their bodies have become resistant to the insulin they produce. These patients display various baselines in their resistance to insulin and insulin requirements to maintain homeostasis.3 Insulin resistance is increased when the body is placed under a physiological stress load, inflammation, infection, or sudden acute fluid volume loss that increases cortisol and catecholamine levels. Cortisol, the main stress hormone of the body, elevates glucose in the bloodstream and magnifies the use of glucose by the brain. High blood glucose levels and metabolic acidosis are both particularly indicative of increasing insulin resistance.3 DKA can be defined as having a blood glucose level exceeding 200 mg/dL, an elevated anion gap acidosis revealing a pH below 7.3, and/or sodium bicarbonate below 15 mmol/L and beta-hydroxybutyrate above 3 mmol/L.4 The normal range of beta-hydroxybutyrate levels should be less than 0.4 to 0.5 mmol/L. When levels exceed 1 mmol/L, ongoing observation is required, and when reaching levels of 3 mmol/L expeditiously, expert attention is mandatory.

The primary treatment goals of patients with DKA are fluid volume resuscitation; augmenting insulin; and averting complications including cerebral edema, electrolyte deficiencies, and acute kidney injuries.4 Providers responsible for treating and transporting pediatric patients with DKA have long been cautioned on the complications of decreasing blood glucose levels too quickly, consequently causing cerebral edema.5 When there are excessive glucose particles in the bloodstream, the glucose cannot get into the cells to become available for use. Glucose molecules are particles that contain osmotic properties; therefore, the osmotic pressure is determined by the amount of glucose particles and the magnitude of ionization.6 Because these particles increase the osmolarity of the blood, they pull fluid out of the peripheral space and into the vascular space. When fluid moves from the extracellular space and into the intracellular spaces too quickly, brain cells are unable to adapt to the increasing intracellular volume, and cerebral edema in the brain cells results.6

A patient will start exhibiting signs of cerebral edema within the first 12 hours of treatment for hyperglycemia.7 One of the first clinical manifestations indicating the patient is developing cerebral edema is an acute change or decline in the patient’s mental status.6 Some additional signs and symptoms that the glucose is declining too rapidly, producing cerebral edema, include an acute headache or one that gets much worse shortly after beginning treatment, abnormal breathing patterns, intractable emesis, and a decline in heart rate.6 When decreasing blood glucose levels in pediatric patients, it is imperative that the glucose be decreased no faster than 100 mg/dL/h in order to avert causing cerebral edema.4 The initial fluid volume replacement therapy of the pediatric patient with DKA includes 10 to 20 mL/kg boluses of 0.9% sodium chloride or lactated Ringer’s solution over 30 minutes to 1 hour.4,7,8 If the initial fluid volume resuscitation does not improve the patient’s tissue perfusion status as evidence of improvement in the patient’s heart rate and peripheral perfusion, a second bolus of either of these fluids should be administered.7,8 If the blood glucose begins declining at a rate faster than 100 mg/dL/h, then a dextrose containing solution like 5% dextrose/0.9% sodium chloride or 5% dextrose/0.45% sodium chloride should be infused to slow the rate of decline.

Cerebral edema is an occasional occurrence in the pediatric patient with DKA; however, the signs often occur in a subtle manner. Cerebral edema is a clinical diagnosis, which is normal 40% of the time on neuroimaging.9 If cerebral edema is highly anticipated or there is evidence by imaging, then mannitol or hypertonic saline should be administered. Mannitol is the most frequently administered first-line treatment and should be administered at a dose of 1 g/kg. In the event mannitol is unavailable, then 3% sodium chloride of 5 to 10 mL/kg is the next available option.9

The International Society for Pediatric and Adolescent Diabetes provides the following additional guidelines in the treatment of pediatric patients with DKA. Additional maintenance fluid therapy containing a balanced sodium solution, such as 0.45% to 0.9% sodium chloride, may be used over 24 to 48 hours to correct any deficits.8 If the serum sodium content is low and does not increase judiciously when the glucose levels decline, then it is advocated to increase the sodium content in the fluid administration.8 Insulin infusion therapy should be established within 1 hour after correcting fluid volume resuscitation measures as an infusion of 0.05 to 0.1 U/kg/h. The administration of insulin therapy as a bolus is no longer recommended.8 The administration of sodium bicarbonate is no longer recommended in the standard treatment of DKA in the pediatric patient because of potential risk such as hypokalemia and no clear-cut benefit from routine use.10 However, sodium bicarbonate is advocated when life-threatening conditions like severe hyperkalemia or acidosis are present and cardiac contractility is jeopardized.8

The primary osmotic particle in the human body is sodium; therefore, massive sodium depletion results in a loss of intravascular fluid retention and causes third spacing of fluid. Hyponatremia when left untreated will inevitably result in cerebral edema and seizures. For every 100 mg/dL that the glucose level rises above the first 100 mg/dL, a decrease in the sodium content is lowered by 1.6 mEq/L, resulting in pseudohyponatremia.11 When acidosis occurs, potassium will initially shift extracellularly, thereby resulting in the potential of a false hyperkalemia. This results from a change in the pH of 0.1, which will produce an inverse effect on the potassium of about 0.6 in the opposite direction.12

Because these glucose particles increase the osmolarity in the blood, they pull fluid out of the peripheral space and into the vascular space. This causes the kidneys to sense an excess fluid load; therefore, they begin removing the fluid by diuresis. Potassium and phosphate losses to a certain level will occur with any form of diuresis or gastrointestinal loss.10 The kidneys can save or in some cases may limit the loss but cannot stop this from occurring. This will inevitably result in ongoing osmotic diuresis, causing the patients to lose large amounts of potassium, which is excreted in their urine.10 Treatment includes fluid volume resuscitation and insulin, which consequently shift the potassium back into the cell, therefore resulting in the patient becoming extremely hypokalemic as the acidosis is being corrected.

Any pediatric patient being treated for DKA who is acidotic with a normal or lower level of potassium should be considered high risk for becoming hypokalemic, and therefore should be considered strongly as a candidate for receiving prophylactic potassium replacement early on in their treatment.13 For every 10 mEq potassium administered, this will raise the overall mean serum potassium level by 0.14 mEq/L. Every drop in serum potassium of 0.3 mEq is equal to 100 mEq of total body potassium. Hypokalemia is often associated with hypomagnesemia. Magnesium and potassium, the 2 most abundant intracellular cations, together play a vital role in membrane potential stabilization, thereby reducing cellular excitability in the heart.12 Magnesium and potassium work in tandem and must be administered together. Intracellular potassium will not move intracellularly without concomitant repletion of magnesium.13 Under normal circumstances, there is approximately 98% of the total potassium found intracellularly, whereas the other 2% is located extracellularly.14 When blood specimens are obtained, the analyzed blood only accounts for extracellular potassium.15

Transport considerations of the pediatric patient with DKA with suspected cerebral edema should include keeping the head of the bed elevated at least 30 degrees. Maintaining normothermia in all patients should be prioritized, especially in these incidents involving pediatric patients. Constant re-evaluation of the Glasgow Coma Scale (GCS) and vital signs are a must, including heart rate, blood pressure, end-tidal carbon dioxide, and oxygen saturation to identify any subtle or acute changes. Monitoring of end-tidal carbon dioxide is imperative in these transports because for every change in the end-tidal carbon dioxide of 1 mm Hg, there is a subsequent change in the cerebral blood flow of 3% to 4%. Additionally, glucose checks should occur at a minimum of 1 hour to ensure that glucose drops are not occurring any faster than 100 mg/dL per hour.

The normal intracranial pressure (ICP) range is between 0 and 10 mm Hg. Using the GCS can help guide the provider in estimating the ICP. Mild ICP is defined as an ICP of 10 to 20 mm Hg.16 When the GCS is in a range of 13 to 14, this can be correlated with a mild increase in ICP. Moderate ICP is defined as an ICP of 20 to 30 mm Hg.16 When the GCS is in a range of 9 to 12, this can be correlated with a moderate increase in ICP. Severe ICP is defined when the ICP exceeds 40 mm Hg. When the GCS is less than 9, it is correlated with an increase in ICP above 40 mm Hg.16 The threshold for ICP is generally targeted at 20 mm Hg; however, with younger pediatric patients a lower threshold is more appropriate.17 Should the patient’s GCS decline more than 2 points before or during transfer, the administration of mannitol at a dose of 1 g/kg is indicated. If mannitol is not available, then 5 to 10 mL/kg 3% sodium chloride is the best choice.9 If patients’ cerebral edema worsens to the point that they become comatose, then they have lost their ability to maintain and protect their airway, and endotracheal intubation and mechanical ventilation will be required.17

In conclusion, we have observed that pediatric patients with DM are prone to the development of DKA, which can result in serious complications that present acutely and rapidly. Treating the pediatric patient with DKA in transport has been shown to be complex and multifactorial. Providing the appropriate care while systematically lowering their blood glucose will prevent the overzealous correction of their glucose, which can combat the effects that produce cerebral edema, along with causing a cascade of electrolyte abnormalities. The provider should recognize the most subtle changes in the GCS because this can be an ominous sign that the patient has developed cerebral edema.

References

  1. Bonadio W. The evaluation and management of pediatric diabetic ketoacidosis: a comprehensive review [e-pub ahead of print]. Clin Pediatr (Phila). https://doi.org/ 10.1177/00099228221139982, accessed January, 2023.
  2.    Dhatariya KK. Defining and characterising diabetic ketoacidosis in adults. Diabetes Res Clin Pract. 2019;155:107797.
  3.   Glaser NS, Ghetti S, Casper TC, Dean JM, Kupperman N. Pediatric Emergency Care Applied Research Network (PECARN) DKA FLUID Study Group. Pediatric diabetic ketoacidosis, fluid therapy, and cerebral injury: the design of a factorial randomized controlled trial. Pediatr Diabetes. 2013;14. 453-446.
  4.   Ravikumar N, Bansal A. Application of bench studies at the bedside to improve outcomes in the management of severe diabetic ketoacidosis in children—a narrative review. Transl Pediatr. 2021;10:2792–2798.
  5. Azova S, Rapaport R, Wolfsdorf J. Brain injury in children with diabetic ketoacidosis: review of the literature and a proposed pathophysiologic pathway for the development of cerebral edema. Pediatr Diabetes. 2021;22: 148–160.
  6. Varela D, Held N, Linas S. Overview of cerebral edema during correction of hyper-glycemic crises. Am J Case Rep. 2017;19:562–566. https://doi.org/10.12659/ AJCR.908465.
  7.   Glaser N, Kuppermann N. Fluid treatment for children with diabetic ketoacidosis: how do the results of the pediatric emergency care applied research network fluid therapies under investigation in diabetic ketoacidosis (fluid) trial change our perspective? Pediatr Diabetes. 2019;20(1):10–14.
  8. Dhatariya KK, Glaser NS, Codner E, Umpierrez GE. Diabetic ketoacidosis. Nat Rev Dis Primers. 2020;6:40.
  9. Long B, Koyfman A. Emergency medicine myths: cerebral edema in pediatric diabetic ketoacidosis and intravenous fluids. J Emerg Med. 2017;53:212–221. https:// doi.org/10.1016/j.jemermed.2017.03.014.
  10. Grams ME, Hoenig MP, Hoorn EJ. Evaluation of hypokalemia. JAMA. 2021;325: 1216–1217. https://doi.org/10.1001/jama.2020.17672
  11. Bhasin-Chhabra B, Veitla V, Weinberg S, Koratala A. Demystifying hyponatremia: a clinical guide to evaluation and management. Nutr Clin Pract. 2022;37:1023–1032.
  12. Mount DB, Sterns RH, Foreman JP. Potassium balance in acid-base disorders. 2022. Available  at:  https://www.uptodate.com/contents/potassium-balance-in-acid- base-disorders#:»:text=Acid%2Dbase%20disturbances%20cause%20potassium,the%20extracellular%20pH%20%5B3%5D. Accessed January, 2023.Frenkel A, Hassan L, Segal A, et al. Estimation of potassium changes following potassium supplements in hypokalemic critically ill adult patients−a patient personalized practical treatment formula. J Clin Med. 2021;10:1986. https://doi.org/ 10.3390/jcm10091986.
  13. De Baaij JH, Hoenderop JG, Bindels RJ. Magnesium in man: implications for health and disease. Physiol Rev. 2015;95:1–46.
  14. Palmer BF, Clegg DJ. Physiology and pathophysiology of potassium homeostasis: Core Curriculum 2019. Am J Kidney Dis. 2019;74:682–695. https://doi.org/10.1053/ j.ajkd.2019.03.427.
  15. Aries MJ, Czosnyka M, Budohoski KP, et al. Continuous determination of optimal cerebral perfusion pressure in traumatic brain injury. Crit Care Med. 2012;40: 2456–2463.
  16. Kochanek PM, Tasker RC, Carney N, et al. Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, Third Edition: Update of the Brain Trauma Foundation Guidelines. Pediatr Crit Care Med. 2019;20:S1–S82. https://doi.org/10.1097/ PCC.0000000000001735.


© 2023 Air Medical Journal Associates. Published by Elsevier Inc. All rights reserved.

https://www.airmedicaljournal.com/