Diabetic Ketoacidosis

Headshot of Chris Anderson, Vice Chair, Pediatrics
Chris Anderson
Vice Chair, Pediatrics
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Headshot of Hinah Parker, MD Ā· Assistant chair, Pediatrics
Hinah Parker
MD Ā· Assistant chair, Pediatrics
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Table of Contents

Ketoacidosis is responsible for the initial presentation of insulin dependent diabetes (IDDM) in up to 25% of children. It is the triad of hyperglycemia (above 200mg/dL), systemic ketosis (with ketones present in the urine or a beta-hydroxybutyrate (BOHB) over 3mmol/L), and acidosis (pH of <7.3 or bicarb <15mmol/L). It can be classified as either mild, moderate, or severe, based on the clinical and lab criteria. Early manifestations are mild and include vomiting, polyuria, polydipsia, weight loss, and dehydration. More severe cases include Kussmaul (shallow and rapid) respirations, alterations to mentation, and seizures, as well as an odor of acetone on the breath. Abdominal pain or rigidity may be present and mimic acute appendicitis or pancreatitis.

Etiology

Approximately one third of children with Type 1 diabetes present in DKA at time of diagnosis. Younger patients are also higher risk to present in DKA. Those with prior episodes of DKA (excluding initial presentation) are also higher risk to have recurrent episodes.

For all patients there should be a detailed history addressing any acute illness, recent trauma, new medications, possible ingestions or drug/alcohol use.

Pathophysiology

DKA results in altered lipid metabolism. There is an increased concentrations of total lipids, cholesterol, triglycerides, and free fatty acids. Free fatty acids are shunted into ketone body formation due to lack of insulin; the rate of formation exceeds the capacity for their peripheral utilization and renal excretion leading to accumulation of ketoacids and therefore systemic metabolic acidosis. With progressive dehydration, acidosis, hyperosmolality, and diminished cerebral oxygen utilization, consciousness becomes impaired, and the patient ultimately becomes comatose.

Diagnosis

Important history to get from family when the patient is a known diabetic includes insulin regimen, most recent dose, whether the patient has an insulin pump and if so have there been issues charging it, home glucose levels and whether they have been checking ketones at home, type of diabetes and how many prior episodes of DKA they have had.

Vitals and exam may show tachypnea, tachycardia, poor perfusion, decreased skin turgor, and altered mental status. Lab work to diagnose must include hyperglycemia >200mg/dL, ketones present in the urine or serum (BOHB > 3mmol/L), and acidosis (venous pH of <7.3 or bicarb <15mmol/L).

Management

Goals are to accurately diagnose (mild, moderate, severe), hydrate, give insulin to correct acidosis and ketosis, and lastly stabilize glucose levels.

  • Intravascular volume expansion: dehydration is most commonly in the order of 10%.
  • Initial hydrating fluid should be isotonic saline, this alone will often slightly lower the blood glucose.
  • DKA is hypertonic dehydration, and therefore plasma volume is fairly well preserved.Ā  It is rare, even in severe DKA, that a patient will present hypotensive from hypovolemia and dehydration. Therefore, there is rarely a need for large volumes (> 40 cc/kg) of fluid in the acute setting.
  • Once initial fluid bolus is given, a two-bag system is set up with electrolyte containing fluids. One bag will also contain dextrose while the other will not, and the rates will be adjusted to allow for normoglycemia while the patient is on their insulin drip.
    • Examples of the two bag system include:
      • D10+NS+20meq/L KCl.
      • NS+20meq/L KCl.
      • Hold potassium if serum potassium is > 5.5, or there has not been any urine output in the past 12 hours.
    • Based on the blood glucose check after the initial IVF bolus:
      • For blood glucose is already < 300 or falling by more than 100mg/dL/hr, start the dextrose containing bag (D10), or
      • For glucose 200-299 run them at equivalent rates, and then once the glucose is <200 you can switch over to just the D10 bag.
      • For glucose <150, start with the dextrose containing bag but increase to D12.5.
  • Serum potassium is often elevated, though total body potassium is depleted, and thus you should expect the serum potassium to drop as the acidosis corrects.
  • Phosphate is depleted and may be added as potassium phosphate (KPO4), especially if serum chloride is already elevated.
  • ā€œPseudohyponatremiaā€ is often present and the sodium level should be expected to rise during treatment. If Na+ does not rise, true hyponatremia may be present (possibly increasing cerebral edema risk) and should be treated
    • Corrected Na+ = Measured Na+Ā  + 0.016(measured glucose – 100).
  • Bicarbonate: The risks of bicarbonate administration are high, as it leads to increased risk of cerebral edema.
    • HCO3- combines with H+ and dissociated to CO2 and H2O. Whereas HCO3- passes through the blood-brain barrier slowly, CO2 diffuses freely and thus it can exacerbate cerebral acidosis and cerebral depression.
    • Indications for bicarbonate administration include severe acidosis leading to cardiorespiratory compromise.
  • Do not bolus insulin.
  • Start insulin drip after normal saline bolus. There are a few different ways to choose your starting drip dose, one of them being dosing based on age and weight.
    • For children <5 yr old start at 0.05 U/kg/hr.
    • For children >5 yr old start at 0.1 U/kg/hr.
      • Mild DKA can be treated with aggressive subcutaneous regimen.
      • The goal is to correct the acidosis and ketosis, which is done primarily through insulin. The goal of insulin in this acute situation is not to treat hyperglycemia. While that is happening, you want to make sure the glucose is slowly decreasing by < 100 mg/dL/hr as a more precipitous drop increases the risk of cerebral edema.
      • When the acidosis is corrected, with goal bicarb being >15 and BHOB <2mmol/L and anion gap <10, the continuous insulin infusion may be discontinued and subcutaneous insulin initiated.

Conclusion

DKA is a potentially life-threatening complication of IDDM, however with prompt management most children will improve within 24–48 hours. The risk of cerebral edema is very real, but when management is done thoughtfully that risk can be minimized. Although this guideline pertains more to moderate-severe DKA, mild–moderate DKA can sometimes be treated with subcutaneous insulin rather than a drip.

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