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Pediatrics, Diabetic Ketoacidosis

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

Updated: Jun 16, 2008

Introduction

Background

Diabetic ketoacidosis (DKA) is a complex metabolic state of hyperglycemia, ketosis, and acidosis. DKA results from untreated absolute or relative deficiency of insulin in type 1 or type 2 diabetes mellitus, respectively.

Pathophysiology

Hyperglycemia results from impaired glucose uptake because of insulin deficiency and excess glucagon with resultant gluconeogenesis and glycogenolysis. Glucagon excess also increases lipolysis with the formation of ketoacids. Ketone bodies provide alternative usable energy sources in the absence of intracellular glucose. The ketoacids (acetoacetate, beta-hydroxybutyrate, acetone) are products of proteolysis and lipolysis.

Hyperglycemia causes an osmotic diuresis that leads to excessive loss of free water and electrolytes. Resultant hypovolemia leads to tissue hypoperfusion and lactic acidosis.

Ketosis and lactic acidosis produce a metabolic acidosis; however, supplemental bicarbonate is not recommended. Acidosis usually resolves with isotonic fluid volume replenishment and insulin therapy. A pediatric trial of bicarbonate in severe metabolic acidosis during DKA (pH <7.15) showed no benefit when compared with placebo.1 Indeed, multiple studies suggest that bicarbonate therapy may cause paradoxical intracellular acidosis, worsening tissue perfusion and hypokalemia, and cerebral edema.

As acidosis corrects, acetoacetate and acetone levels increase in proportion to beta-hydroxybutyrate. As it worsens, the reverse occurs. Routine laboratory testing for ketones measures only the presence of acetoacetate and acetone, not beta-hydroxybutyrate. Therefore, ketosis may appear to be absent in early DKA and to worsen as severe DKA resolves.

Electrolyte imbalances are the consequences of hyperglycemia, hyperosmolality, and acidosis.

Despite what may be severe total body potassium depletion, apparent serum hyperkalemia often is observed in patients with DKA prior to volume resuscitation. Serum hyperkalemia occurs as potassium ions shift from the intracellular to extracellular space because of acidosis from insulin deficiency and decreased renal tubular secretion. Similar decreases in serum phosphate and magnesium concentrations are the result of ion shifts.

Hyponatremia results from a dilutional effect as free water shifts extracellularly because of high serum osmolarity. True serum sodium values can be calculated by adjusting measured sodium levels upward 1.6 mEq/L for every 100 mg/dL increase in serum glucose concentration.

As serum osmolarity increases from hyperglycemia, intracellular osmolality in the brain also increases. Overly rapid correction of serum hyperglycemia and osmolarity may create a large gradient between intracerebral and serum osmolarity. Free water then shifts into the brain and may cause cerebral edema with herniation. Therefore, fluid resuscitation and correction of hyperglycemia should be gradual and closely monitored.

Frequency

United States

Incidence of type 1 diabetes mellitus is 2 per 1000. The exact incidence of DKA is unknown but is estimated to be 4-8 per 1000. DKA occurring at the time of diagnosis of diabetes mellitus is more common in younger children. In the United States, the rate of DKA is about 25% at the time of diagnosis.

International

Exact incidence is unknown.

Mortality/Morbidity

With current medical therapy, DKA has a 2-5% mortality rate. Mortality results from the precipitating underlying cause, which is primarily cerebral edema. Cerebral edema occurs in 0.3-1% of all episodes of DKA.

Race

Because of an association with human leukocyte antigen (HLA) groups DR3 and DR4 (which occur more commonly in white populations), type 1 diabetes mellitus and DKA are more common in white children. The exact racial frequency is unknown.

Clinical

History

Classic symptoms of diabetic ketoacidosis (DKA) are often absent in toddlers. If a patient has known diabetes, obtain a history for compliance with insulin regimens and the name of the patient's endocrinologist.

  • Often insidious
  • Fatigue and malaise
  • Nausea/vomiting
  • Abdominal pain
  • Polydipsia
  • Polyuria
  • Polyphagia
  • Weight loss
  • Fever

Physical

  • Altered mental status without evidence of head trauma
  • Tachycardia
  • Tachypnea or hyperventilation (Kussmaul respirations)
  • Normal or low blood pressure
  • Increased capillary refill time
  • Poor perfusion
  • Lethargy and weakness
  • Fever
  • Acetone odor of the breath reflecting metabolic acidosis

Causes

  • DKA is the presenting complaint in approximately one fourth of newly diagnosed patients with type 1 diabetes mellitus.
  • Infection is the most frequent cause of DKA, particularly in patients with known diabetes.
    • Aggressive evaluation for infection always is warranted.
    • Strongly consider empiric antibiotic therapy until cultures return.
  • Patient has poor compliance with existing insulin regimens.
  • Patient exhibits underlying endocrine changes of adolescence (thelarche, adrenarche, menarche).
  • Caregiver's lack of competence may be a cause.
  • Pump failure may occur (insulin pumps are increasingly in use).

More on Pediatrics, Diabetic Ketoacidosis

Overview: Pediatrics, Diabetic Ketoacidosis
Differential Diagnoses & Workup: Pediatrics, Diabetic Ketoacidosis
Treatment & Medication: Pediatrics, Diabetic Ketoacidosis
Follow-up: Pediatrics, Diabetic Ketoacidosis
Multimedia: Pediatrics, Diabetic Ketoacidosis
References
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References

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  27. Rosenbloom AL. Treatment of diabetic ketoacidosis and the risk of cerebral edema. J Pediatr. Jan 2008;152(1):146-7; author reply 147-9. [Medline].

  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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