DEPARTMENT Pharmacology Continuing Education

Hypokalemia and
Hyperkalemia in Infants and
Children: Pathophysiology
and Treatment
Kayleen Daly, PharmD, & Elizabeth Farrington,
PharmD, FCCP, FCCM, FPPAG, BCPS

Section Editors
Teri Moser Woo, PhD, RN, ARNP, CNL, CPNP,
FAANP
Corresponding Editor
Pacific Lutheran University
Tacoma, Washington
Elizabeth Farrington, PharmD, FCCP, FCCM,
FPPAG, BCPS
University of North Carolina, Eshelman School of
Pharmacy
Chapel Hill, North Carolina
New Hanover Regional Medical Center
Wilmington, North Carolina
Brady S. Moffett, PharmD, MPH
Clinical Pharmacy Specialist-Pediatric Cardiology
Texas Children’s Hospital, Department of Pharmacy
Houston, Texas
Kayleen Daly, Pharmacist II, New Hanover Regional Medical
Center, Wilmington, NC.
Elizabeth Farrington, Pharmacist III, Pediatrics, New Hanover
Regional Medical Center, Wilmington, NC.
Conflicts of interest: None to report.
Correspondence: Kayleen Daly, PharmD, New Hanover Regional
Medical Center, 2131 S 17th St, Wilmington, NC 28401; e-mail:
kayleen.daly@nhrmc.org.
0891-5245/$36.00
Copyright Q 2013 by the National Association of Pediatric
Nurse Practitioners. Published by Elsevier Inc. All rights
reserved.
http://dx.doi.org/10.1016/j.pedhc.2013.08.003
ABSTRACT
Potassium is the second most abundant cation in the body.
About 98% of potassium is intracellular and that is particu-
larly in the skeletal muscle. Electrical disturbances associated
with disorders of potassium homeostasis are a function of
both the extracellular and intracellular potassium concentra-
tions. Clinical disorders of potassium homeostasis occur with
some regularity, especially in hospitalized patients receiving
many medications. This article will review the pathophysiol-
ogy of potassium homeostasis, symptoms, causes, and treat-
ment of hypo- and hyperkalemia. J Pediatr Health Care.
(2013) 27, 486-496.
KEY WORDS
Hypokalemia, hyperkalemia, treatment
OBJECTIVES
1. Describe the pathophysiology of potassium ho-
meostasis.
2. Explain the role of potassium in the human body.
3. List the symptoms of hypokalemia and hyperkale-
mia.
4. Recommend the treatment for hyperkalemia and
explain why one treatment regimen might be pre-
ferred over another.
5. Recommend the treatment for hypokalemia and ex-
plain when one would use intravenous versus oral
replacement.
Healthy persons are in potassium balance, which
means that the daily intake of potassium is equal to
the amount excreted. In children, normal daily potas-
sium requirements vary by age. However, they are esti-
mated at approximately 2 mEq per 100 kcal of energy

486 Volume 27  Number 6 Journal of Pediatric Health Care

 BOX 1. Foods high in potassium
Fruits
Bananas, oranges (citrus), cantaloupe, watermelon,
apricots, raisins, prunes, pineapples, cherries, and
tomatoes
Vegetables
Green and leafy, potatoes, avocados, artichokes, lentils,
beets, white mushrooms, and onions
Meats/Fish
All contain potassium (the lowest levels are in chicken liver,
shrimp, and crab)
Breads/Flours
Pumpernickel, buckwheat, and soy
Miscellaneous
Chocolate, cocoa, brown sugar, molasses, nuts, peanut
butter, French fries, and whole milk
Data from Potassium content of selected foods per
common measure, sorted by nutrient content (USDA
National Nutrient Database for Standard Reference,
Released 2012). Retrieved from http://lpi.oregonstate.
edu/infocenter/minerals/potassium/ and Bakris, G. L., &
Olendzki, B. (2012). Patient information: Low potassium
diet. Retrieved from http://www.uptodate.com/contents/
low-potassium-diet-beyond-the-basics.
requirement throughout most of childhood (Linshaw,
1987). An adult’s dietary intake varies from approxi-
mately 50 to 150 mEq per day. Potassium is present in
sufficient quantities in most fruits, vegetables, meat,
and fish (Box 1 and Table 1). Nutrition labels typically
do not list the amount of potassium that is present in
foods. In this article we will review a clinical approach
to the treatment of both hyperkalemia and hypokale-
mia in the pediatric population. Treatment of hyperka-
lemia in newborns is the same as for infants and
children but may be initiated at a slightly higher serum
potassium level because of differences in normal serum
potassium values in newborns.
PHYSIOLOGY OF POTASSIUM
Potassium is the second most abundant cation in the
body. About 98% of potassium is intracellular, particu-
larly in skeletal muscle, where the concentration ranges
from 140 to 150 mEq/L. Only about 2% of the body’s po-
tassium is in the extracellular fluid, where the concen-
tration is tightly regulated at 3.5 to 5.5 mEq/L (Kraft,
Btaiche, Sacks, & Kudsk, 2005). Therefore a gradient
exists for the diffusion of potassium from intracellular
to extracellular fluid. The gradient is the reverse of
that for sodium, which is present in high extracellular
concentration and low intracellular concentration.
Diffusion occurring along both the sodium and po-
tassium gradients is mainly controlled by the sodium–
potassium–adenosine triphosphate (ATP) pump. This
ion pump uses ATP to pump three sodium ions out of
the cell and two potassium ions into the cell, which cre-
www.jpedhc.org
TABLE 1. Potassium content in popular foods
and beverages
Food/beverage Potassium content (mEq)
French fries 17.7
Small banana 8.6
White mushrooms 8.1
Orange juice (200 ml) 7.9
Whole milk (200 ml) 7.7
Broccoli 5.8
Potato chips 5.1
Green beans 3.9
Milk chocolate bar (20 g) 2.4
Onions, cooked 1.5
Coca-Cola (200 ml) 0.1
Data from Potassium content of selected foods per common
measure, sorted by nutrient content (USDA National Nutrient Da-
tabase for Standard Reference, Released 2012). Retrieved from
http://lpi.oregonstate.edu/infocenter/minerals/potassium/
ates an electrochemical gradient over the cell mem-
brane (Nyirenda, Tang, Padfield, & Seck, 2009). Many
factors affect the activity of this pump, such as insulin,
glucagon, catecholamine, aldosterone, acid-base sta-
tus, plasma osmolality, and intracellular potassium
levels (Baumgartner, Bailey, & Caudill, 1997). The pres-
ence of these pumps and the concentration of potas-
sium inside the cell are critical because potassium
performs an essential role in numerous physiologic
and metabolic processes, including regulation of cell
volume; influencing osmotic balance between cells
and the interstitial fluid; renal function; carbohydrate
metabolism; contraction of cardiac muscle; and the reg-
ulation of the electrical action potential across cell
membranes, especially in the myocardium (Schaefer
& Wolford, 2005).
Under normal physiological conditions, 80% of po-
tassium is excreted through the kidneys, with at least
90% actively reabsorbed along the kidney tubule.
About 15% of potassium is excreted in feces, and 5%
is lost in sweat. The balance of both cations, sodium
and potassium, is maintained by the kidneys. The kid-
neys can adjust to increased intake by increasing potas-
sium excretion, but they cannot prevent depletion in
the absence of potassium ingestion. Most drugs that in-
duce hyperkalemia/hypokalemia alter the renal elimi-
nation or reabsorption of potassium, and therefore
the kidney is unable to prevent the electrolyte imbal-
ance. The kidneys of a healthy person usually reabsorb
all but 10% of filtered potassium (Greger & G€ ogelein,
1987). However, during osmotic diuresis, the kidney re-
absorbs less potassium, and thus hypokalemia may oc-
cur. This mechanism of hypokalemia is seen in persons
with diabetic ketoacidosis.
Clinical disorders of potassium homeostasis occur
with some regularity, especially in hospitalized patients
receiving many medications. Clinically significant
symptoms caused by disturbances in potassium
November/December 2013 487
 BOX 2. Causes of hyperkalemia BOX 3. Drug-induced hyperkalemia

Pseudo hyperkalemia Increased potassium input

 Use of tourniquet when drawing blood  Potassium chloride supplements (including salt substi-
 Hemolysis of drawn blood tutes)
 Leukocytosis (white blood cell count >50,000/mm3 or  Potassium penicillin
thrombocytosis [platelets >1,000,000/mm3]) Decreased potassium output
Increased efflux from intracellular fluid
 Potassium sparing diuretics (e.g., spironolactone,
 Due to redistribution: acidosis, especially inorganic triamterine, and amiloride)
 Hyperkalemic familial periodic paralysis  Cyclosporine
Increased potassium load endogenous  Angiotensin-converting enzyme inhibitors
 Nonsteroidal antiinflammatory drugs
 Extensive tissue injury, burns, heat stroke, or trauma  Heparin
 Hemolysis  Tacrolimus
 Rhabdomyolysis  Pentamidine
 Tumor lysis syndromes  Trimethoprim
 Tissue necrosis
 Hemolytic uremic syndrome Data from Lehnhardt & Kemper (2011).
Increased potassium load exogenous
 Diet, dietary salt substitutes duce clinically significant signs and symptoms
 Banked blood transfusions (Lehnhardt & Kemper, 2011).
 Gastrointestinal hemorrhage Hypokalemia, defined as a serum potassium level 3.5
 Poisoning mEq/L or lower, is perhaps the most common electro-
Decreased excretion with or without increased lyte abnormality encountered by clinicians (Smellie
intake et al., 2007). Hyperkalemia is defined in children and
adults as a potassium level greater than 5.5 mEq/L. In
 Acute renal failure and severe chronic renal failure
 Mineralocorticoid deficiency
newborns, hyperkalemia is defined as a serum potas-
— Addison’s disease sium level more than 6 mEq/L. Although hyperkalemia
— Selective aldosterone deficiency is less common than hypokalemia, it is equally impor-
 Hyporeninemic hypoaldosteronism tant by virtue of its inherent dangers.
 Hereditary enzyme deficiencies
 Tubulo-interstitial disease HYPERKALEMIA
 Type IV renal tubular acidosis Although hyperkalemia is defined as a serum potas-
 Obstruction sium concentration of > 5.5 mEq/L, it is moderate (6
 Sickle cell disease to 7 mEq/L) and severe (> 7 mEq/L) cases of hyperkale-
 Systemic lupus erythematosus mia that are life threat-
Data from Lehnhardt & Kemper (2011). ening and require The most common
immediate therapy. cause of
The most common
balance are due to potassium’s role in regulating ‘‘bio- cause of hyperkalemia
hyperkalemia in
logic electricity.’’ An alteration in electrical conduction in infants and children infants and children
within a nerve or muscle can cause signs and symptoms is ‘‘pseudo hyperkale- is ‘‘pseudo
that range from subtle muscle weakness to more obvi- mia’’ from hemolysis
ous cardiac arrhythmias. of the blood sample
hyperkalemia’’
It is important to point out that the electrical distur- when the sample is ob- from hemolysis of
bances associated with disorders of potassium homeo- tained from a heel stick the blood sample
stasis are a function of both the extracellular and or a small bore intrave-
intracellular potassium concentrations. In clinical nous line. When
when the sample is
conditions leading to chronic potassium depletion, pseudo hyperkalemia obtained from
both the extracellular and intracellular potassium con- is suspected, the test a heel stick or
centrations will be decreased. In addition, in persons to determine the serum
with chronic potassium depletion, potassium shifts potassium level should
a small bore
out of the cells, and thus the alteration in electrical con- be repeated from intravenous line.
duction is minimized; therefore, disturbances com- a free-flowing venous
monly associated with disorders in potassium balance sample before any treatment is administered. Other-
are less noticeable or absent. In contrast, acute changes wise, hyperkalemia is most commonly seen in patients
in potassium homeostasis are much more likely to pro- with end-stage renal disease or in those who

488 Volume 27  Number 6 Journal of Pediatric Health Care

 TABLE 2. Electrocardiographic manifestations for hypokalemia and hyperkalemia
Serum potassium
concentration Hypokalemia
< 3.5 mEq/L; does not Increased P wave amplitude
correlate with specific
potassium levels Prolonged PR interval, ST
segment depression
QT prolongation, reduction
in T wave amplitude
T wave inversion, U waves
Note. Data from Taketomo, Hodding, & Kraus (2013) and Sood, Sood, & Richardson. (2007). Emergency management and commonly en-
countered outpatient scenarios in patients with hyperkalemia. Mayo Clinic Proceedings, 82(12), 1553-1561.
experience acute renal failure (Masilamani & Van der
Voort, 2012). The causes of hyperkalemia are summa-
rized in Boxes 2 and 3. Identification of potential
causes of hyperkalemia will be beneficial when
determining optimal treatment.
Clinical manifestations of hyperkalemia include
weakness, confusion, and muscular or respiratory paral-
ysis (Kleinman et al., 2010). Early electrocardiographic
(ECG) changes seen with an increase in the potassium
level include peaked T waves followed by a decrease
in R wave amplitude, widened QRS complex, and a
prolonged PR interval. This scenario may ultimately
progress to complete heart block with absent P waves
and finally a sine wave. Ventricular arrhythmias or
cardiac arrest may ensue if no effort is made to lower
the serum potassium level. Although the sequences of
ECG abnormalities correlate with the serum potassium
concentrations, the potassium levels at which specific
ECG abnormalities are seen vary widely from patient
to patient.
Treatment of hyperkalemia depends on the serum
potassium level, as well as the presence or absence of
symptoms and ECG changes. Table 2 includes a list of
ECG changes based on hypokalemia and hyperkalemia
serum concentrations. Treatment is recommended
when ECG changes are present or when serum potas-
sium levels are greater than 6 to 6.5 mEq/L, regardless
of the ECG findings. The first step is to identify and re-
move all sources of oral or parenteral potassium intake
(oral potassium supplements and intravenous mainte-
nance fluids or parenteral nutrition must be consid-
ered) and evaluate drugs that can increase the serum
potassium level (e.g., potassium-sparing diuretics,
angiotensin-converting enzyme inhibitors, and nonste-
roidal antiinflammatory agents). A list of commonly
used medications that can increase serum potassium
is provided in Box 3.
The goals of hyperkalemia treatment are to antago-
nize the cardiac effects of potassium, reverse symp-
toms, and return the serum potassium level to normal
www.jpedhc.org
Serum potassium
concentration Hyperkalemia
5.5-6.5 mEq/L Tall, peaked, ‘‘tented’’ T waves, normal or decreased
QT, PR interval shortening
6.5-7.5 mEq/L Widening of QRS complex, increased PR interval
7.0-8.0 mEq/L Broad, low-amplitude P waves, QT prolongation,
ST elevation or depression
> 8 mEq/L P waves disappear, marked widening of QRS + ‘‘sine
wave’’ pattern, high risk for ventricular fibrillation or
asystole
while avoiding overcorrection. Three principle
methods are used to treat hyperkalemia. First, calcium
is administered to counteract the effects of excess po-
tassium on the heart. Second, medications can be
used to shift potassium from extracellular to intracellu-
lar fluid compartments. Third, exchange resins, di-
uretics, or dialysis are used to remove potassium from
the body (Farrington, 1991). Table 3 lists treatment op-
tions for hyperkalemia.
CALCIUM
Calcium increases the cellular threshold potential,
thereby restoring the normal difference between
the resting membrane potential and the firing thresh-
old, which is elevated abnormally in persons with
hyperkalemia. This type of treatment is temporary
to antagonize the effects of hyperkalemia on cardiac
muscle and will not remove potassium from the body
(Schaefer & Wolford, 2005). Calcium should be ad-
ministered intravenously to symptomatic patients or
those with ECG changes. In the presence of a life-
threatening arrhythmia, 20 mg/kg of calcium chloride
(with a maximum dose of 1 g) or 100 mg/kg of cal-
cium gluconate (with a maximum dose of 1 g) may
be given intravenously over 2 to 5 minutes to reduce
the effects of potassium at the myocardial cell mem-
brane (Taketomo, Hodding, & Kraus, 2013). The
dose may be repeated in 5 minutes; continuous mon-
itoring of the ECG is mandatory. The cardiac re-
sponse to an injection of calcium is seen within 5
minutes and may last for up to 1 hour (Farrington,
1991). Calcium must be administered with caution
to patients receiving digitalis glycosides because the
cardiac glycosides are synergistic with parenteral cal-
cium salts and thus the combination of digitalis and
calcium may increase the risk of precipitating
hypokalemia-related arrhythmias (Taketomo et al.,
2013). Because the administration of calcium does
not lower serum potassium, other modes of treat-
ment must be initiated.
November/December 2013 489
490
Volume 27  Number 6

TABLE 3. Treatment of hyperkalemia

Pediatric dose Adult Administration Length
Drug (max: adult dose) dose Route time Onset of effect Notes Adverse effects
Calcium 20 mg/kg/ dose 1-2 g IV, IO 2-5 min 5 min 30-60 min May repeat in 5 min Burning at the infusion site
chloride 10% if necessary
Calcium 60-100 mg/kg/dose 1-2 g IV, IO 2-5 min 5 min 30-60 min May repeat in 5 min Burning at the infusion site
gluconate 10% if necessary
Sodium 1-2 mEq/kg/dose 50-100 mEq IV, IO 2-5 min 15-60 min Various May repeat every Hypernatremia, metabolic alkalosis
bicarbonate depending on 5-10 min
acid base status
of the patient
50% dextrose 102 ml/kg 50 ml IV, IO 5 min 20 min 6 hr Administer with insulin Hypoglycemia, hyperosmolarity,
volume overload
10% dextrose 5-10 ml/kg 250 ml IV, IO 5 min 20 min 6 hr Administer with insulin Hypoglycemia, hyperosmolarity,
volume overload
Regular insulin 0.2 units/kg 5-10 units IV, IO 5 min 20 min 2-6 hr Administer with glucose Hypoglycemia, hyperosmolarity,
volume overload
Kayexalate 1 g/kg 60 g Oral or rectal N/A Oral: 1-2 hr Rectal: 4-6 hr Effective but slow Nausea and vomiting
< 30 min
Albuterol 10-20 mg (use 10-20 mg (use Inhale by 10 min 30 min 2 hr Efficacy demonstrated in Tachycardia, vasomotor flushing,
concentrated concentrated nebulizer patients with renal mild tremor
form, 5 mg/ml) form, 5 mg/ml) insufficiency
Furosemide 1 mg/kg 40 mg IV 1-2 min 5-30 min 4 hr Amount of potassium Volume depletion
excretion is unreliable
and does not correlate
Journal of Pediatric Health Care

to furosemide dose
Hemodialysis N/A N/A N/A N/A Hypotension Volume depletion
Note. IO = interosseous; IV = intravenous; N/A = not applicable. Data from Taketomo, Hodding, & Kraus (2013).
TREATMENT THAT SHIFTS POTASSIUM INTO
CELLS
Increasing the Serum pH of the Acidotic Patient
The most rapid treatment for hyperkalemia in an aci-
dotic patient is hyperventilation. However, the de-
crease in serum potassium level seen with acute
increases in pH resulting from decreases in partial pres-
sure of carbon dioxide (PCO2) may be less than that seen
with comparable improvements in pH obtained with
intravenously administered sodium bicarbonate
(NaHCO3; Lehnhardt & Kemper, 2011). Classically, it
has been taught that for every 0.1 increase in serum
pH, serum potassium will decrease by approximately
0.6 mEq/L. However, observed changes in serum potas-
sium concentrations vary widely, depending, in part,
on the origin of the acid or base load. Hyperventilation,
or a decrease in the PCO2 (respiratory alkalosis), is asso-
ciated with a decrease in serum potassium of only 0.1 to
0.3 mEq/L for each 0.1 pH unit change (Lehnhardt &
Kemper, 2011).
Sodium Bicarbonate
NaHCO3 is used because the alkaline systemic pH it
produces favors the shift of potassium intracellularly,
and the sodium load enhances distal tubular potas-
sium secretion (Galla, 2000). Thus the administration
of sodium bicarbonate is most effective in a patient
who is acidotic and will have less of an effect on a non-
acidotic hyperkalemic patient. In addition, NaHCO3 ad-
ministration can cause an ‘‘overshoot’’ alkalosis in an
oliguric patient who is unable to excrete the adminis-
trated NaHCO3. The dose of NaHCO3 is 1 to 2 mEq/kg
injected intravenously over 1 to 5 minutes (with a max-
imum dose of 50 to 100 mEq; Taketomo et al., 2013).
This treatment may be repeated every 5 to 10 minutes
as needed to reverse ECG abnormalities (Farrington,
1991). Administration of NaHCO3 can have a rapid ef-
fect; however, it only causes a temporary redistribu-
tion of potassium into the intracellular space and
does not change total body potassium levels
(Masilamani & Van der Voort, 2012). Therefore addi-
tional therapy should be administered to remove se-
rum potassium. Patients with coexisting respiratory
failure should not be given NaHCO3. Because patients
with respiratory failure cannot eliminate the increase
of CO2 production that results from NaHCO3 metabo-
lism, respiratory acidosis will develop. For each 1
mEq of NaHCO3 that is administered, the patient re-
ceives 1 mEq of sodium. Therefore NaHCO3 should
be used with caution in patients with heart failure or
renal failure because of its sodium content, which
could exacerbate fluid retention.
Glucose Plus Insulin
Glucose plus insulin infusions shift potassium intracel-
lularly. Insulin stimulates cellular uptake of glucose
with potassium following, thus lowering its serum con-
www.jpedhc.org
centration (Palmer, 2010). However, if the patient is hy-
perglycemic, only the administration of insulin is
recommended to treat the hyperkalemia. Remember
that the effects of intravenously administered insulin
frequently extend several hours after the dextrose has
been consumed, which may result in delayed hypogly-
cemia. Glucose, 500 mg/kg (maximum dose 25 g), and
insulin, 0.2 units/kg (5 to 10 units), are administered
over a 5-minute period (Farrington, 1991; Taketomo
et al., 2013). The hypokalemic effect of this treatment
can be seen within 20 minutes, peaks between 30 and
60 minutes, and may last for up to 6 hours. A
continuous infusion of glucose and insulin may be
initiated after the initial glucose/insulin bolus (10
units of regular insulin in 500 ml dextrose 10%). This
is a ratio of 0.2 units of regular insulin per 1.0 g of
glucose (Parham, Mehdirad, Biermann, & Fredman,
2006). It is recommended that finger-stick tests for
blood glucose levels be checked hourly for at least 6
hours after insulin and dextrose have been adminis-
tered.
b-Adrenergic Agonists
Albuterol and other b-adrenergic agents induce the in-
tracellular movement of potassium via the stimulation
of the sodium/potassium–adenosine triphosphate
pump. Inhaled b2 agonists have a rapid onset of action.
The effect of b2 agonists is additive to that of insulin or
NaHCO3 administration, and they can be administered
concurrently.
The majority of published data concerning the effi-
cacy of albuterol in persons with hyperkalemia has
been in patients with chronic renal failure. Intrave-
nous administration of salbutamol at a dose of 5 mg/
kg over 15 minutes has demonstrated a predictable
decrease in serum potassium with a mean decrease
of 1.6 to 1.7 mEq/L after 2 hours (Kember, Harps,
Hellwege, & Mueller-Wiefel, 1996). Injectable salbuta-
mol is not available in the United States; however,
nebulized albuterol has demonstrated efficacy
(Weisberg, 2008). Studies show that a nebulization of
10 mg of albuterol leads to a decline in serum
potassium of 0.6 mmol/kg and a nebulized dose of al-
buterol 20 mg demonstrates a decline in pharmacoki-
netics (about 1 mmol/L; Weisberg, 2008). Note that the
effective dose of albuterol for hyperkalemia is at least
four times higher than that typically used for broncho-
dilation. The clinical effect of high-dose albuterol is
apparent at 30 minutes and persists for at least 2 hours
(Weisberg, 2008). A single study demonstrated that the
administration of subcutaneous terbutaline (7 mg/kg)
reduces serum potassium in patients undergoing dial-
ysis by an average of 1.3 mEq/L within 60 minutes
(Sowinski, Cronin, Mueller, & Kraus, 2005). Mild
tachycardia is the most common reported adverse ef-
fect of high-dose nebulized albuterol or terbutaline.
It is unlikely that patients who take nonselective
November/December 2013 491
b-blockers will have a hypokalemic effect from nebu-
lized albuterol. Approximately 40% of patients who do
not take b-blockers seem to be resistant to the hypoka-
lemic effect of albuterol. The mechanism for this resis-
tance is currently unknown, and there is no basis for
predicting which patients will respond. Because of
this uncertainty, albuterol should never be used as
a single agent for the treatment of urgent hyperkale-
mia in patients with renal failure (Nissenson & Fine,
2005).
TREATMENT THAT REMOVES POTASSIUM
Exchange Resins
Sodium polystyrene sulfonate or Kayexalate mixed in
sorbitol is a cation-exchange resin that binds potassium
in the gastrointestinal tract and eliminates it from the
body. Each gram of resin will bind approximately 1
mEq of potassium and release 2 to 3 mEq of sodium.
It should be given at a dose of 1 g/kg orally or per rec-
tum (maximum dose: 60 g) and repeated every 1 to 2
hours until the serum potassium level is lowered
(Taketomo et al., 2013). The onset of action of sodium
polystyrene sulfonate administered orally is at least 2
hours, and the maximal effect may take 6 hours
(Hollander-Rodriguez & Calvert, 2006).
Although the oral administration of Kayexalate is of-
ten considered unpalatable, it should not be mixed with
citrus juices or solutions that contain high concentra-
tions of potassium because doing so will reduce the ef-
fectiveness of the resin. Because this resin exchanges
sodium for potassium, consideration should be given
to patients with congestive heart failure, elevated blood
pressure, or severe hepatic disease (Farrington, 1991).
Lastly, because of complications of hypernatremia
and necrotizing enterocolitis, Kayexalate use in neo-
nates should be reserved for refractory cases
(Taketomo et al., 2013).
Diuretics
For patients who are not experiencing renal failure, the
administration of furosemide, a loop diuretic, will pro-
duce an increase in the renal excretion of potassium.
The onset of action of parenteral furosemide is within
5 minutes; the peak effect is observed within 30 min-
utes. The furosemide dose for children is 1 mg/kg/
dose (maximum 40 mg/dose; Taketomo et al., 2013).
The amount of potassium excreted is unreliable and
does not correlate with the diuretic dose; therefore,
the administration of diuretics should only be used as
an adjunct to other modes of therapy (Lehnhardt &
Kemper, 2011).
Renal Replacement Therapy
Renal replacement therapy is used when conservative
methods fail or for patients with life-threatening hyper-
kalemia. Hemodialysis (or continuous venovenous he-
mofiltration in hemodynamically unstable patients) is
492 Volume 27  Number 6
more effective than peritoneal dialysis and is the pre-
ferred method when hyperkalemia is the result of cell
breakdown (Weisberg, 2008). To be most effective,
peritoneal dialysis
must be started early, Hemodialysis is
because potassium
clearance rates by the
much more
peritoneal membrane efficient at
are limited by the limi- removing
tations on dialysate
flow rates inherent to
potassium from the
the peritoneal dialysis patient than all
system. Hemodialysis other treatment
is much more efficient
at removing potassium
modalities
from the patient than
all other treatment modalities. In patients with life-
threatening levels of hyperkalemia, hemodialysis
should be the treatment of choice (Lehnhardt &
Kemper, 2011).
Prevention of Recurrence
After hyperkalemia is treated, it is essential to determine
the cause and implement measures to prevent recur-
rence. In patients with renal dysfunction, management
for sustained hyperkalemia is to reduce the overall total
dietary potassium intake, which includes restriction in
the use of salt substitutes because they contain potas-
sium chloride (KCl). In some studies it has been found
that fludrocortisone, an oral mineralocorticoid, is effec-
tive in lowering serum potassium levels in patients with
hyporenin hypoaldosteronism (Hollander-Rodriguez
& Calvert, 2006; Kim, Chung, Yoon, & Kim, 2007).
Fludrocortisone, an endogenous mineralocorticoid,
mimics the actions of aldosterone, and hence
hyperkalemia is reversed. The patient’s medication
regimen should be evaluated to see if it is causing
hyperkalemia, including over-the-counter medications
and herbal and dietary supplements. In patients with re-
nal dysfunction, it may not be prudent to discontinue
therapy with an angiotensin-converting enzyme inhib-
itor or angiotensin receptor blocker because they slow
progression of renal dysfunction. Instead, it may be in
the patient’s best interest to use oral Kayexalate daily,
which is effective in reducing the incidence of severe
hyperkalemia (Gennari, 2002).
Monitoring
In the acute management of hyperkalemia, the fre-
quency of monitoring depends on the potassium level,
any underlying comorbidities experienced by the pa-
tient, and the physician’s preference. Once initial inter-
ventions have been made, the serum potassium level
should be rechecked within 1 to 2 hours to ensure the
effectiveness of the correction. Depending on the un-
derlying cause of the hyperkalemia and the level
when the potassium is rechecked, the physician may
Journal of Pediatric Health Care
 The clinical manifestations of hypokalemia involve
BOX 4. Causes of hypokalemia
changes to muscle and cardiovascular function because
hypokalemia results in membrane hyperpolarization
Intracellular shifts of potassium
and impairs muscle contraction. Mild hypokalemia (3
 Metabolic alkalosis (respiratory and metabolic) to 3.5 mEq/L) may not cause symptoms. Moderate hy-
 b-Adrenergic agonists: albuterol, insulin, theophylline, pokalemia, with serum potassium concentrations of
caffeine, and epinephrine 2.5 to 3 mEq/L, may cause muscular weakness, myalgia,
 Hyperthyroidism muscle cramps (as a result of disturbed function of the
 Delirium tremens
skeletal muscles), and constipation (as a result of dis-
 Barium poisoning
 Therapy of hyperglycemia
turbed function of smooth muscles). With more severe
Increased losses of potassium hypokalemia, flaccid paralysis and hyporeflexia may
result. Reports have been made of rhabdomyolysis oc-
 Sodium polystyrene sulfonate, corticosteroids, and curring with profound hypokalemia with serum potas-
magnesium depletion sium levels less than 2 mEq/L. Respiratory depression
 Renal replacement therapy from severe impairment of skeletal muscle may occur
 Hemodialysis
with severe potassium depletion (Schaefer & Wolford,
 Continuous renal replacement therapy
2005).
Decreased intake/gastrointestinal losses
 Diarrhea TREATMENT OF HYPOKALEMIA
 Vomiting Treatment depends on the serum level of potassium, as
 Increased colostomy output well as the presence or absence of symptoms and ECG
 Nasogastric drainage changes (Table 2). Early ECG changes include ST seg-
Inadequate potassium intake (< 40 mEq/L) ment depression, T wave flattening, and the presence
 Eating disorders of U waves. Like hyperkalemia, the sequence of ECG
 Alcoholism abnormalities corre-
Urinary loss lates with serum con- Patients with
centrations, but the
 Diuretics: loop and thiazide symptomatic
 Antimicrobials: amphotericin B, cisplatin, aminoglyco- potassium levels at
side—piperacillin, ticarcillin which specific ECG ab- hypokalemia
 Diabetic ketoacidosis normalities are seen should be treated
 Osmotic dieresis (diabetic ketoacidosis, mannitol) vary widely from pa-
with
 Hypomagnesemia tient to patient. The
 Cushing syndrome goals of therapy for hy- pharmacologic
 Primary mineralocorticoid excess pokalemia include therapy, because
 Bartter syndrome or Gitelman syndrome avoidance or resolu-
increasing the
Data from Gennari (2002) and Linshaw (1987). tion of symptoms and
return of the serum po- intake of
tassium concentration potassium-rich
choose to decrease or increase the frequency of potas- to normal (Gennari,
foods only is
sium checks (Elliott et al., 2010). 1998).
If potassium were unlikely to resolve
HYPOKALEMIA to be removed from symptoms in
Hypokalemia occurs when a serum potassium concen- the diet, a minimum
potassium-
tration is < 3.5 mEq/L, and it can become life- kidney excretion of
threatening when the serum potassium concentration about 200 mg per depleted patients.
falls below 2.5 mEq/L (Table 2). Hypokalemia can day would continue
result from intracellular shifts of potassium, increased to occur. The serum potassium level would decline
losses of potassium, or decreased ingestion or adminis- to 3.0 to 3.5 mEq/L in about 1 week. If the serum po-
tration of potassium (Box 4). The main cause of tassium was not supplemented, the patient would ex-
hypokalemia in pediatric patients is excessive gastroin- perience further depletion in serum potassium levels
testinal losses such as diarrhea or vomiting. Because se- and could ultimately experience death. A potassium
rum potassium levels do not correlate with intracellular intake sufficient to support life can in general be
potassium levels, hypokalemia does not reflect total guaranteed by eating a variety of foods. Patients
body potassium stores. Clear cases of potassium defi- with symptomatic hypokalemia should be treated
ciency, defined by symptoms, signs, and a low potas- with pharmacologic therapy, because increasing the
sium level, are rare in healthy persons (Kleinman intake of potassium-rich foods only is unlikely to re-
et al., 2010). solve symptoms in potassium-depleted patients.

www.jpedhc.org November/December 2013 493

 TABLE 4. Oral potassium replacement products
Salt form (mg)/miscellaneous
Potassium chloride preparations # mEq/mg potassium information
Tablets, controlled release/extended 8 600 KCl
release
Tablets, controlled release/extended 10 750 KCl
release
Tablets, extended release 15 1125 KCl
Tablets, controlled release/extended 20 1500 mg KCl
release
Tablets, effervescent 25 Chloride and bicarbonate salts
Capsules, controlled release 8 600 mg KCl
Capsules, controlled release 10 750 mg KCl
Liquid 20 mEq/15 ml 1125 mg/15 ml
Liquid 40 mEq/15 ml 2250 mg/15 ml
Powder packets 20 mEq/packet 1500 mg KCl
Powder packets 25 mEq/packet 1875 mg KCl
Potassium gluconate preparations
Caplet 99 mg potassium 595 mg potassium gluconate
Capsule 99 mg potassium 595 mg potassium gluconate
Tablets 99 mg potassium/ 595 mg potassium gluconate/550 mg
90 mg potassium potassium gluconate
Tablets, timed-release 95 mg potassium
Liquid 20 mEq/15 ml As the gluconate salt
Liquid 20 mEq/15 ml A mixture of gluconate and citrate salts
Potassium bicarbonate
Tablets, effervescent 25 Orange flavor
Potassium bicarbonate and potassium citrate
Tablets, effervescent 10 Unflavored and cherry vanilla flavor
Tablets, effervescent 20 Unflavored and orange cream flavor
Tablets, effervescent 25 Unflavored, orange, lemon citrus and
cherry berry flavor AND sugar free;
orange flavor
Potassium phosphate
Tablet (K-Phos original) 3.7 mEq 114 mg potassium and 114 mg phosphate
per tablet
Powder packet (Neutral-Phos K) 14 mEq KCl 8 mmol phos
Powder packet (Neutral-Phos) 7 mEq KCl 8 mmol phos, 7 mEq NaCl
Potassium citrate
Tablet, extended release 5 mEq 540 mg potassium citrate
Tablet, extended release 10 mEq 1080 mg potassium citrate
Tablet, extended release 15 mEq 1620 mg potassium citrate
Potassium citrate and citric acid
Liquid 2 mEq/mL 2 mEq/mL NaHCO3
Powder packets 30 mEq 30 mEq NaHCO3
Note. KCl = potassium chloride; NaCl = sodium chloride; NaHCO3 = sodium bicarbonate. Data from Taketomo, Hodding, & Kraus (2013).

Dietary potassium is predominantly in the form of
potassium phosphate or potassium citrate, which re-
sults in the retention of only 40% as much potassium
as KCl (Sanguinetti & Jurkiewicz, 1992). Therefore
pharmacotherapy of symptomatic hypokalemia
should be with KCl.
In the presence of cardiac arrhythmias, extreme mus-
cle weakness, or respiratory distress, KCl should be ad-
ministered intravenously with cardiac monitoring. The
intravenous dose of KCl is 0.5 mEq/kg (maximum 20
mEq/dose) administered over 1 to 2 hours based on
the severity of the patient’s symptoms (Taketomo
et al., 2013). Once the serum potassium level is stabi-
lized, the oral route of administration is preferable
(Schaefer & Wolford, 2005).
Oral potassium supplements are available as chloride,
bicarbonate, citrate, gluconate, and phosphate salts. Po-
tassium bicarbonate is preferred in patients with hypo-
kalemia and metabolic acidosis because of their renal
tubular acidosis or diarrhea. Administration of potas-
sium phosphate should be considered only in patients
with hypokalemia and hypophosphatemia, which might
occur in patients with proximal renal tubular acidosis as-
sociated with Fanconi syndrome and phosphate wast-
ing. Use of potassium chloride is preferred in patients
with hypokalemia, hypochloremia, and metabolic

494 Volume 27  Number 6 Journal of Pediatric Health Care


TABLE 5. Intravenous potassium replacement
products
Infusion, premixed Central or peripheral
in water for injection line recommended
10 mEq/50 mL Central
10 mEq/100 mL Peripheral
20 mEq/50 mL Central
20 mEq/100 mL Central
30 mEq/100 mL Central
40 mEq/100 mL Central
Mixed by pharmacy
# 0.1 mEq/mL Peripheral
> 0.1 mEq/mL with a maximum Central
of 0.4 mEq/mL
Note. Data from Taketomo, Hodding, & Kraus (2013).
alkalosis because of diuretic therapy or vomiting. Chlo-
ride depletion contributes to maintenance of the meta-
bolic alkalosis by enhancing renal bicarbonate
reabsorption and may contribute to potassium wasting
as sodium is reabsorbed in exchange for secreted potas-
sium rather than with chloride. Compared with potas-
sium bicarbonate, KCL raises the serum potassium
concentration more quickly (Schaefer &Wolford,
2005). Chloride is primarily an extracellular anion that
does not enter cells to the same extent as bicarbonate,
thereby promoting maintenance of the administered po-
tassium in the extracellular fluid (Sanguinetti &
Jurkiewicz, 1992). The single oral dose of KCl is 1 to
1.5 mEq/kg/dose (maximum 40 mEq/dose; Taketomo
et al., 2013). If potassium deficits are severe or ongoing,
scheduled potassium doses may be necessary (Gennari,
1998). Potassium salts available for potassium replace-
ment are summarized in Tables 4 and 5.
Patients with hypokalemia may also have hypomag-
nesemia as a result of concurrent loss of magnesium
with diarrhea or diuretic therapy or medications such
as cisplatin, carboplatin, and amphotericin B, which
cause renal magnesium wasting. In addition, magne-
sium depletion may cause renal potassium wasting. Be-
cause the major site of potassium reabsorption occurs in
the ascending loop of Henle and reabsorption at this
site is driven by a magnesium-dependent, sodium–po-
tassium–adenosine triphosphatase pump, cellular de-
pletion of magnesium in these cells prevents
potassium reabsorption (Schaefer & Wolford, 2005).
Treating the hypokalemia without addressing the hypo-
magnesemia will be ineffective. The measurement of
serum magnesium should be considered in patients
with hypokalemia, and if hypomagnesemia is present,
it should be treated prior to the administration of potas-
sium. The recommended initial treatment is intrave-
nous magnesium sulfate, 50 mg/kg/dose (maximum
dose: 2 g) administered over 2 hours (Taketomo et al.,
2013). This dose can be repeated if the hypomagnese-
mia persists.
www.jpedhc.org
Monitoring
The timing of a repeat serum potassium level depends
on the severity of the initial value, the patient’s symp-
toms, and the form of potassium administered to the pa-
tient. In a symptomatic patient who receives an
intravenous dose of KCl, the dose should be repeated
without measuring a serum value if the patient’s symp-
toms persist. If the symptoms resolve, the serum potas-
sium level can be obtained 1 hour after completion of an
intravenous dose (Schaefer & Wolford, 2005). In clinical
situations in which an oral dose is administered based
on a low serum value, in the absence of clinical symp-
toms, the serum level can be repeated the next day.
After hypokalemia is treated, it is essential to deter-
mine the cause and implement measures to prevent re-
currence. Patients who receive diuretics or other
medications that cause a depletion of serum potassium
(Box 4) may need to begin taking a scheduled oral sup-
plement.
CONCLUSION
Derangements in potassium homeostasis affect the
body’s bioelectric process, including muscle contrac-
tion, nerve conduction, and myocardial electrical activ-
ity. Alterations in the potassium level, whether it be
hyperkalemia or hypokalemia, may cause serious
symptoms in the patient. Knowledge of the causes of
hypokalemia and hyperkalemia and the therapeutic in-
terventions recommended for their treatment can be
lifesaving for the patient.
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