Hiperkalemia pada

pediatrik

Hyperkalemia is generally due to one or a

combination of the following mechanisms:
Excessive increase in potassium intake
Transcellular movement of intracellular potassium
into the extracellular space (eg, rhabdomyolysis
from crush injury or exercise, tumor lysis
syndrome, massive transfusion, and metabolic
acidosis)
Decreased renal excretion of potassium (impaired
effective arterial perfusion, renal dysfunction, or
hypoaldosteronism)

 cardiac status (rate and rhythm)

determines the care of children with
hyperkalemia
In children with hyperkalemia, the
appearance of peaked T waves is
followed by lengthening of the PR
interval and widening of the QRS
complex until P waves are lost
Finally, the QRS complex merges
with its T wave to produce a
sinusoidal pattern

Treatment
Emergent therapy is first directed toward
antagonism of potassiums cardiac effects by
administration of calcium
Serum potassium is then reduced by returning
potassium to the intracellular space by correcting
acidosis through administration of sodium
bicarbonate (1-2 mEq/kg)
To maintain potassium in the intracellular space,
glucose and insulin are administered by infusion
(0.5-1 g/kg glucose with 0.1 U/kg insulin over 3060 minutes).
Cote, 2009

Cardiac membrane stabilization

Calcium directly antagonizes the hyperkalemia-induced
depolarization of the resting cardiac membrane
Calcium therapy results in decreased membrane
excitability and reduces the risk of developing cardiac
conduction abnormalities and arrhythmias .
It should be givenonlyfor hyperkalemia with
significant ECG findings (eg, widening of the QRS
complex or loss of P waves, butnotpeaked T waves
alone), with severe arrhythmias thought to be caused
by hyperkalemia or in patients with a potassium level
greater than 7mEq/L
In children,calcium gluconate10 percent solution is
given at a dose of 0.5mL/kg(maximum dose 20 mL [2
g]) by intravenous slow infusion over five minutes

Sodium bicarbonate
Increasing the extracellular pH with sodium
bicarbonate leads to hydrogen ion movement
from the cell into the extracellular
spaceextracellular potassium moves into the
cell to maintain electroneutrality
it shouldnotbe the only therapy used in the
management of hyperkalemia
In children, the dose of bicarbonate is
1mEq/kg(maximum dose 50 mEq) administered
over 10 to 15 minutes
It can be given as 1mL/kgof an 8.4 percent
solution or, for children less than six months of
age, as 2mL/kgof a 4.2 percent solution.

Insulin and glucose

With intravenous access, infusion of insulin and
glucose can be given to mobilize extracellular
potassium into the cells
Insulin
administration
drives
extracellular
potassium into the cells by enhancing the activity
of the Na-K ATPase pump in skeletal muscles
Glucose is given concomitantly to prevent
hypoglycemia
The effect of insulin begins in 10 to 20 minutes
and peaks at 30 to 60 minutes
The major adverse effect is hypoglycemia, and
serum glucose level should be measured one
hour after the administration of insulin

 In children,regular insulin(dose of 0.1 units per

kg, maximum dose of 10 units) is given along
with a dextrose (glucose) dose of 0.5g/kgover 30
minutes
The administration of dextrose is based upon the
age of the patient as follows:
Children younger than five years of age: Give 10
percent dextrose (100mg/mL)at a dose of
5mL/kg
Children five years of age and older: Give 25
percent dextrose (250mg/mL)at a dose of
2mL/kg(maximum dose 25 g)

 The knowledge that -adrenergic stimulation

modulates the translocation of potassium into the
intracellular space has prompted the consideration
of agonists in the treatment of acute hyperkalemia
a single infusion of salbutamol (5 g/kg over 15
minutes) has been shown to effectively lower
serum potassium concentrations within 30 minutes
In addition to intravenous therapy, both salbutamol
and albuterol have been found to be effective when
given by inhalation
Inhalation of albuterol during such an event in the
operating room may speed the reduction in serum
potassium
Cote, 2009

Dosing ofalbuterolis based on the childs weight as

follows:
Neonates: 0.4 mg in 2 mL of saline.
Infants and small children <25 kg: 2.5 mg in 2 mL
of saline.
Children between 25 and 50 kg: 5 mg in 2 mL of
saline.
Older children and adolescents >50 kg: 10 mg in
2 to 4 mL of saline (doses up to 20 mg have been
used). Inhaledalbuterolmay also be administered
by metered dose inhaler (MDI) as 4 to 8 puffs with
a spacer.

Diuretics
Loop and thiazide diuretics can improve urinary
potassium excretion in children with adequate
effective volume and renal function
This intervention may be useful in children with
persistently elevated but nonurgent levels of
hyperkalemia (5.5 to 6.5mEq/L),and as an
adjunct in those with more severe hyperkalemia.
In general, furosemide, a loop diuretic, at a dose
of 1mg/kgintravenously, maximum dose in
children with normal renal function is 40 mg
in children with renal insufficiency, higher doses
(up to 80 mg) may be required
If effective, furosemide may be given every six
hours.

Hirchprung disease
Anesthetic concerns for patients with Hirschsprungs
disease are similar to those for any child having surgery
Maintaining body temperature and providing
appropriate fluid therapy (for replacement of large
thirdspace losses) are the major challenges for the
anesthesiologist

Smith, 2011

 Anesthesia induction can be either by inhalation or IV

means.
Because of the surgical bowel manipulation and the
relatively obstructive nature of the underlying disease,
nitrous oxide is discontinued after induction, and
anesthesia is maintained with a mixture of air, oxygen,
and potent inhalation agent
Long-term follow-up of patients with Hirschsprungs
disease suggests that 25% of patients will require
reoperation, and that 19% to 25% of patients will
develop enterocolitis

Smith, 2011

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