Pediatric emergency medicine trisk 1867 1867
Bạn đang xem bản rút gọn của tài liệu. Xem và tải ngay bản đầy đủ của tài liệu tại đây (102.73 KB, 1 trang )
potassium acetate (or chloride) and potassium phosphate in equal amounts. If the initial serum
[K+ ] is less than 4 mEq/L, potassium replacement should be initiated promptly; if less than 3
mEq/L, IVF concentrations of K+ of 60 mEq/L or greater may be necessary. With the higher
concentrations of potassium, the phosphate component must be adjusted not to exceed the
maximum allowable phosphate infusion rate. If the K+ initial concentration is low, monitoring
via an electrocardiogram (ECG) is indicated.
Phosphate depletion is almost universal in patients with DKA; however, the clinical
significance of this reaction remains uncertain. As noted earlier, half of the K+ replacement is
with potassium phosphate, up to a maximum of 20 mEq potassium phosphate per liter except
in the rare situation of severe hypophosphatemia (serum phosphate less than 2 mEq/L).
Infusion of excess phosphate results in hypocalcemia, which may be complicated by tetanic
seizures.
Bicarbonate Therapy
In retrospective reviews of patients with DKA who developed significant cerebral edema,
bicarbonate administration was identified as a significant risk factor ( Table 89.3 ). This may
be because the sickest patients are the ones most likely to have received bicarbonate therapy;
however, without further clarification of the pathophysiology, bicarbonate therapy is reserved
for patients with both severe acidosis (pH <6.9) and secondary hemodynamic compromise that
is unresponsive to inotropic agents.
A theoretical mechanism for the complications observed with bicarbonate therapy is the
development of a paradoxical acidosis of the central nervous system (CNS) and resultant
cerebral depression. Paradoxical acidosis occurs because administered HCO3 − combines with
excess H+ ions in the bloodstream to form H2 O and CO2 . Because the blood–brain barrier is
relatively more permeable to CO2 than to HCO3 − , CO2 accumulates in the CNS, resulting in
further exacerbation of acidosis in this compartment, while acidosis is being corrected
systemically.
Insulin and Glucose
Regular insulin is used for the treatment of ketoacidosis, but it should not be administered until
the initial isotonic fluids have been administered for 1 hour. Insulin is initially necessary to
stop ongoing ketone body production, the primary cause of the acidosis. Insulin should be
started after 1 hour of initial fluid expansion to steadily correct the acidosis and may be either
infused intravenously or, if necessary, injected intramuscularly at hourly intervals. Intermittent
injections of insulin should be avoided because of the uncertainties of absorption in a
dehydrated patient, although in a resource-limited setting, hourly intramuscular injections may
be a suitable substitution for continuous intravenous dosing. The starting dose of insulin for
continuous infusion is 0.1 Unit/kg/hr, infused by a regulated pump. Small studies comparing
low-dose insulin infusions (0.05 Unit/kg/hr) with this standard infusion rate found no
difference in rate of blood glucose decline or time to achieve blood glucose target in mild
DKA (pH ≥7.2), however, larger randomized trials are needed for full understanding of
benefits and risks of these different insulin infusion rates. Failure of the glucose to decrease in
response to insulin suggests improper insulin preparation, inadequate hydration, or serious
underlying disease (e.g., appendicitis or fasciitis with resultant significant increases in
