TREATMENT
■ DKA treatment encompasses a multisystem approach including hydration,
electrolyte replacement, and insulin administration under careful monitoring.
■ Rehydration
■ Patients are usually significantly dehydrated. Most patients will benefit
from an initial 2-L saline bolus followed by additional fluids to total
4–6 L in the first 6 hours.
■ Use 0.9 NS unless the patient is severely dehydrated where 0.45 NS or
combination are acceptable as well.
■ Once the patient’s glucose falls <250 mg/dL switch to a glucose solu-
tion to avoid hypoglycemia and cerebral edema.
■ In pediatric patients, overly aggressive fluid resuscitation has been associ-
ated with cerebral edema. Do not exceed 40 mL/kg in the first 4 hours.
■ Insulin
■ Bolusing large doses of insulin may cause hypoglycemia and hypo-
kalemia. Instead infusing 0.1 units/kg/hr is a safe and effective way to
initiate insulin. If the patient fails to respond after a few hours, infusion
rates may be increased. Do not initiate insulin therapy until you know
the patient’s serum potassium. Giving insulin to a DKA patient with low
serum potassium is a way to stop his heart. If the serum potassium is
low, replace potassium before initiating insulin treatment.
■ Potassium replacement
■ DKA may causes significant hypokalemia that is sometimes only un-
masked once the acidosis is reversed and the remaining extracellular K+
shifts back into the cell.
■ After the initial fluid bolus patients with normal K+should receive at
least 20–40 mEq/L in infusion fluids.
■ Sodium bicarbonate should be reserved for critically ill patients with a
pH<7.0 and evidence of shock, renal failure, or respiratory depression.
Risks of sodium bicarbonate administration include:
■ Paradoxical CSF acidosis
■ Hypokalemia
■ Hyperosmolarity from sodium overload worsening dehydration
■ Decreased O 2 dissociation from red blood cells, ie, leftward shift of the
oxyhemoglobin dissociation curve delaying O 2 deliver and recovery
■ Phosphate replacement
■ Not routinely given 2°to possibly disposing patients to seizures
■ Do not give as initial management and reserve for levels below 1 mg/dLCOMPLICATIONS
■ DKA has a host of life-threatening complications that result from the
1 °disease as well as the treatment.
■ Primary-disease related:
■ MI and cardiovascular collapse
■ DIC
■ Cerebral edema
■ Rhabdomyolysis
■ Therapy-related
■ Hypoglycemia (from insulin)
■ Hypokalemia
■ Hypophosphatemia
■ Cerebral edema (insulin)
■ Alkalosis and paradoxical CSF acidosis (from bicarbonate)
■ CHF and ARDS (fluids)ENDOCRINE, METABOLIC, FLUID, AND
ELECTROLYTE DISORDERSIn DKA, insulin should start
late and end late.
Start insulin late because you
need to wait for the serum
potassium. End insulin late
because you need to close the
anion gap (not just bring
down the glucose).The most common cause of
death in children with DKA is
cerebral edema, which is
associated with bicarbonate
therapy and overly aggressive
fluid resuscitation.