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Pediatrics, Diabetic Ketoacidosis: Treatment & Medication

Author: Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Contributor Information and Disclosures

Updated: Jun 16, 2008

Treatment

Prehospital Care

  • Provide oxygen and advanced airway management, if needed.
  • 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.

Emergency Department Care

Multiple goals exist 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 DKA, and prevention of complications from rapid decreases in serum osmolarity. Each aspect of DKA management must be closely monitored.

Alter fluid, glucose, and insulin administration in response to the dynamic and often volatile metabolic changes that occur during treatment. A flow sheet is invaluable to monitor and document the progression of DKA management (see Media file 1).

  • Concurrent with management of DKA are basics of emergency resuscitation (eg, management of urgent airway, breathing, and circulation).
  • In addition to these basics, patients with DKA 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 DKA by laboratory studies.
    • 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.

    • Consultations

    • A pediatric endocrinologist may be useful in complicated cases.

    Medication

    Medical therapy centers on fluid and electrolyte replacement. Initiate insulin therapy after beginning fluid replacement and serum potassium correction.

    Antidiabetic Agent

    Insulin suppresses the formation of ketone bodies.


    Insulin (Humulin, Novolin)

    Stimulates proper utilization of glucose by the cells and reduces blood sugar levels.
    Adjust infusion rate based on blood glucose level.

    Adult

    0.05-0.1 U/kg/h IV/IO

    Pediatric

    Administer as in adults

    Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid hormones, estrogens, ethacrynic acid, calcitonin, oral contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin; medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone

    Documented hypersensitivity; hypoglycemia

    Pregnancy

    B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

    Precautions

    Only regular insulin may be given intravenously; do not give before treating life-threatening hypokalemia; monitor serum glucose level during administration (a too-rapid drop in blood glucose levels can produce cerebral edema); hyperthyroidism may increase renal clearance of insulin and may need more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of insulin may be necessary in patients diagnosed with renal and hepatic dysfunction

    More on Pediatrics, Diabetic Ketoacidosis

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    Follow-up: Pediatrics, Diabetic Ketoacidosis
    Multimedia: Pediatrics, Diabetic Ketoacidosis
    References
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    References

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    28. Sema A, Puliyel JM. Cerebral edema in diabetic ketoacidosis with serum sodium <135 mEq/L. J Pediatr. Jan 2008;152(1):145-6; author reply 147-9. [Medline].

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    30. Takaya J, Ohashi R, Harada Y, Yamato F, Higashino H, Kobayashi Y, et al. Cerebral edema in a child with diabetic ketoacidosis before initial treatment. Pediatr Int. Jun 2007;49(3):395-6. [Medline].

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    Further Reading

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    Keywords

    diabetic ketoacidosis, DKA, hyperglycemia, ketosis, acidosis, ketone bodies, diabetes, type 1 diabetes mellitus, type 2 diabetes mellitus, insulin deficiency, diabetic ketoacidosis in children, lactic acidosis, hypokalemia, cerebral edema

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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 and American College of Emergency Physicians
    Disclosure: Nothing to disclose.

    Medical Editor

    James Li, MD, Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine
    Disclosure: Nothing to disclose.

    Pharmacy Editor

    Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
    Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

    Managing Editor

    Wayne Wolfram, MD, MPH, Clinical Associate Professor, Departments of Pediatrics, Children's Hospital and University of Cincinnati
    Wayne Wolfram, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, and Society for Academic Emergency Medicine
    Disclosure: Nothing to disclose.

    CME Editor

    John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
    John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
    Disclosure: Nothing to disclose.

    Chief Editor

    Richard G Bachur, MD, Assistant Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
    Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
    Disclosure: none None None

     
     
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