Pediatric emergency medicine trisk 1868 1868
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counterregulatory hormones). It is unnecessary and possibly detrimental to give an initial bolus
of insulin. The dose for the hourly intramuscular (IM) injection, used if IV access cannot be
obtained, is 0.1 Unit/kg/hr.
Once the blood glucose approaches 300 mg/dL, dextrose should be added to the IV fluids.
As long as the child remains acidotic, insulin infusion should be not be stopped; instead, the
amount of dextrose in the IV infusion should be increased in stepwise fashion up to a
concentration of 12.5 g/dL to maintain the blood glucose between 200 and 300 mg/dL. If the
blood glucose continues to drop, the rate of IV fluid administration should be increased to
twice maintenance. If the blood glucose still cannot be maintained, the insulin infusion should
be decreased by increments of 0.025 Unit/kg/hr. One efficient system to maintain an
acceptable range of blood glucose is the “two bag system” in which two bags of the selected
IV fluid solution are infused concurrently, one with 10% to 12.5% dextrose and the other
without dextrose, both with electrolytes including sodium, chloride, potassium, acetate, and
phosphate. The rates of fluid infused from each bag can be adjusted to allow varying rates of
dextrose infusion without change in electrolyte concentration or overall rate of fluid
administration.
When the child is able to eat and the anion gap has closed (normal = 10 to 12), IV infusion
of insulin can be discontinued. If hourly IM injections are used, they should be continued until
the blood glucose is less than 300 mg/dL and acidosis is correcting. Because IV insulin is
metabolized rapidly, subcutaneous insulin must be given 30 minutes prior to the
discontinuation of the infusion. The initial dose of subcutaneous insulin should be calculated,
with consultation by a pediatric endocrinologist, based on a daily dose of 0.75 Unit/kg/day in
the prepubertal child up to 1.0 Unit/kg/day in the pubertal child and beyond. The total daily
dose must be divided into long-acting and short-acting insulins.
Cerebral Edema
Despite several investigations of the causes and risk factors for clinically significant cerebral
edema in patients with DKA, and subsequent modifications in therapy, the incidence of the
complication has not changed significantly during the past 20 years and remains at
approximately 0.5% to 1%. Table 89.3 lists the leading risk factors published in more recent
years. Clinical signs and symptoms of significant cerebral edema include abnormal motor or
verbal response to pain, decorticate or decerebrate posturing, new cranial nerve palsy, and
abnormal respiratory pattern. Other concerning signs are decrease or fluctuation in level of
consciousness (e.g., Glasgow Coma Scale), age-inappropriate incontinence, vomiting,
headache, and heart rate deceleration.
If these signs are noted by the physician at the bedside, a clinical diagnosis of cerebral
edema must be made and treatment initiated without any diagnostic imaging. The patient
should receive mannitol 1 g/kg IV over 10 minutes. There is some evidence that mannitol is
the preferred first-line agent, but that hypertonic saline (3%) may be an appropriate secondline agent; however, only a large retrospective study and case series data are currently
available.
Endotracheal intubation should be considered rarely: primarily if the patient’s mental status
does not assure a safe airway, and secondarily if the patient is not able to maintain a
respiratory alkalosis to partially compensate for the metabolic acidosis. Noninvasive
