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Pediatric Diabetic Ketoacidosis Emergency Department Care Treatment & Management

  • Author: Grace M Young, MD; Chief Editor: Stephen Kemp, MD, PhD  more...
 
Updated: Dec 16, 2015
 

Prehospital Care

Provide oxygen and advanced airway management in patients with diabetic ketoacidosis (DKA), if needed.[7]

Monitor the patient.

Provide isotonic intravenous fluids (eg, isotonic sodium chloride solution or lactated Ringer solution).

Perform fingerstick glucose testing.

Consider empiric naloxone if altered mental status is present.

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Emergency Department Care

Multiple goals are noted for the acute treatment of diabetic ketoacidosis (DKA), including volume resuscitation, identification and treatment of the precipitant event, insulin therapy, hourly monitoring of serum markers of diabetic ketoacidosis, and prevention of complications from rapid decreases in serum osmolarity. Each aspect of diabetic ketoacidosis management must be closely monitored.[8, 9, 10]

Alter fluid, glucose, and insulin administration in response to the dynamic and often volatile metabolic changes that occur during treatment.[11] A flow sheet is invaluable to monitor and document the progression of diabetic ketoacidosis management and is shown in the image below.

Sample diabetic ketoacidosis flow sheet. Sample diabetic ketoacidosis flow sheet.

Concurrent with management of diabetic ketoacidosis are basics of emergency resuscitation (eg, management of urgent airway, breathing, and circulation).

In addition to these basics, patients with diabetic ketoacidosis should remain on a diet of nothing by mouth (NPO), receive supplemental oxygen and, if bacterial infection is suspected, empiric antibiotic therapy.

The goal of the first hour of treatment is volume resuscitation and confirmation of diabetic ketoacidosis by laboratory studies, as follows:

  • Fluids - Isotonic sodium chloride solution bolus, 20 mL/kg intravenously over an hour or less
  • Glucose - None, unless serum glucose level falls to 250-300 mg/dL during rehydration

The goals of the second and succeeding hours are slow correction of hyperglycemia (with glucose level falling at a rate < 100 mg/dL/h), metabolic acidosis, and ketosis, in addition to continued volume replenishment.

Goals

These goals must be met in a manner that prevents too rapid a decrease in serum osmolarity.

This usually requires several hours and meticulous attention to the patient's response to therapy.

Careful observation is warranted to ensure that the patient does not become hypoglycemic.

Hypoglycemia may occur abruptly as insulin resistance resolves.

To this end, maintain glucose levels above 150-250 mg/dL.

During this period, admit the patient to an inpatient setting.

Fluids

Give isotonic sodium chloride solution or 0.45 isotonic sodium chloride solution (0.45% NaCl) with supplemental potassium at twice maintenance rate.

Add potassium as KCl, potassium phosphate, or potassium acetate.

If serum potassium level is in the low life-threatening range, consider replenishing potassium orally (or by nasogastric tube) in a liquid (not tablet) formulation. This corrects hypokalemia much more rapidly than intravenous replenishment, the rate of which must be reduced because of cardiac considerations.

If serum potassium level is less than 3.5, add 40 mEq/L to intravenous fluids.

If serum potassium level is 3.5-5, add 30 mEq/L to intravenous fluids.

If serum potassium level is 5-5.5, add 20 mEq/L to intravenous fluids.

If serum potassium level is greater than 5.5, do not add additional potassium to intravenous fluids.

If serum potassium level is not immediately available, perform an ECG to search for electrocardiographic signs of hyperkalemia.

Insulin

Do not give insulin until severe hypokalemia is corrected.

Then give 0.1 U/kg intravenous bolus; follow with insulin 0.1 U/kg/h intravenously by constant infusion. Prime all intravenous tubing before the bolus because insulin binds to intravenous tubing.

As a result of the potential for hypoglycemia, forego the insulin bolus if the serum glucose level is less than 500 mg/dL or if the child is known to be hypersensitive to exogenous insulin.

To prepare the insulin drip, add units of regular insulin equal to the patient's kilogram weight to 100 mL saline. Saturate the intravenous tubing with 20 mL of the insulin solution, and set the infusion rate equal to 10 mL/h. This provides 0.1 U/kg/h.

Use regular human insulin, unless the patient uses bovine insulin.

Glucose

Add 5% dextrose (D5 or D10) to intravenous fluids, if the child remains in ketoacidosis and serum glucose level approaches 250-300 mg/dL.

Do not discontinue the insulin drip, as the child remains in ketoacidosis for some time and insulin is critical in eliminating ketoacidosis.

Maintain the serum glucose concentration at 150-250 mg/dL during insulin infusion.

Titrate the insulin and glucose infusions, noting that 1 unit of regular insulin metabolizes 3 g of glucose.

The final goal is to obtain a serum glucose concentration within the reference range (serum glucose level, 100-150 mg/dL), to obtain neutral blood pH (pH =7.4; serum bicarbonate = 15-18 mEq/dL), and to eliminate serum ketones. This phase includes the transition from parenteral to subcutaneous insulin and from a fasting state to oral fluids. It usually occurs in the inpatient setting (see Further Inpatient Care) under the direction of a pediatric endocrinologist.

Fluids

Give 0.45% sodium chloride solution with dextrose and potassium up to twice maintenance rate.

Consider oral fluids if nausea is absent.

Insulin

Set the intravenous infusion at 0.05-0.10 U/kg/h.

Glucose

Consider 5-10% dextrose in intravenous fluids to maintain serum glucose level at least 150 mg/dL.

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Consultations

A pediatric endocrinologist may be useful in complicated cases.

Transfer to a pediatric intensive care unit is prudent for the patient with persistent altered mental status, resistant acidosis, and hemodynamic instability, and for the first-time newly diagnosed patient.

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Complications

Cerebral edema

Cerebral edema occurs in 0.7-1% of children with diabetic ketoacidosis.

Causes are multifactorial but may include too-rapid infusion of fluids and electrolytes, overhydration, and overly aggressive correction of acidosis or hyperglycemia.

Treatment includes intubation, hyperventilation, and mannitol 0.25-1 g/kg intravenously.

Hypoglycemia

Causes include increased sensitivity to exogenous insulin and insufficient serum glucose for insulin to metabolize.

Treatment includes adding 5-10% dextrose to intravenous fluids when serum glucose level is 250-300 mg/dL.

Hypokalemia

Serum potassium begins to reflect actual total body potassium depletion as volume depletion and acidosis resolve.

Add potassium to intravenous fluids (see Emergency Department Care) when urine output is present and results of serum potassium level are available.

Cardiac dysrhythmia

Causes include hyperkalemia, hypokalemia, and hypocalcemia.

Treatment involves correcting the specific cause.

Pulmonary edema

Causes include low plasma oncotic pressure and increased pulmonary capillary permeability.

Treatment includes oxygen and diuresis.

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Prevention

If the patient is known to have diabetes, maintain compliance with an insulin therapy regimen and close contact with the treating physician. This is especially important in the presence of nausea, vomiting, and abdominal pain.

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Long-Term Monitoring

Admit children with diabetic ketoacidosis (DKA) for further evaluation, observation, management, diabetes education, and assessment of compliance by responsible caretakers.

Assess the need for social service intervention.

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Contributor Information and Disclosures
Author

Grace M Young, MD Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Wayne Wolfram, MD, MPH Professor, Department of Emergency Medicine, Mercy St Vincent Medical Center; Chairman, Pediatric Institutional Review Board, Mercy St Vincent Medical Center, Toledo, Ohio

Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

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Sample diabetic ketoacidosis flow sheet.
 
 
 
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