Emergency Management of Hyperkalaemia

Paediatric Intensive Care Unit

Royal Hospital for Sick Children

Emergency
Mangement
Hyperkalaemia
Author: A McKie, D Ellis
Date of Review: Oct 2012

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Contents
1.
2.
3.
4.
5.
6.
7.
8.

Methodology
Background
Management
Review
Monitoring
Implementation
References
Treatment Algorithm

Page Number(s)
2-3
3-8
9-14
14
14
15
15-16
17

1 Methodology
1. Rationale/Purpose/Objective
-

to standardise the emergency management of hyperkalaemia in children

within the PICU
provide an evidence base for the proposed guideline
provide background information to allow the practitioner to understand the
principles of the therapy

2. Scope

- emergency management of hyperkalaemia

- this guideline is intended for the management of hyperkalaemia
in patients in paediatric critical care. Transfer to an HDU or PICU
environment should be considered depending on where the patient
is located. It may be appropriate to initiate and complete
management within the A+E Department or on the renal ward.
Renal patients may have their own treatment algorithm. Chronic
renal patients should be discussed with both consultant renal and
consultant PICU staff as a matter of urgency. If there are ECG
abnormalities then follow this emergency protocol.

3. Roles and Responsibilities

-

critical care personnel managing a child who develops

hyperkalaemia on the critical care unit at Yorkhill Chidrens
Hospital Glasgow.

4. Evidence

- constructed after review of standard textbooks, pub med and

Google scholar search (interrogation of quoted references), using
the search terms, hyperkalaemia or hyperkalemia, therapy or
treatment or management or guideline. Only articles in English
were reviewed. Evidence available is mostly level 3 and 4.

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Mangement
Hyperkalaemia
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This guideline is proposed acknowledging that

there is little evidence base
there is significant variation in how drugs are used, despite
acceptance of their efficacy
there is a lack of agreement on treatment thresholds.
Any chosen threshold value for commencing treatment is by
definition arbitrary.

5. Methods

prior to publication the proposed guideline was reviewed by PICU

consultants, the ward pharmacist and nursing education staff.

2. Background
Potassium is a mostly intracellular cation with approximately 98% of the
total being within the intracellular fluid (ICF) compartment (mainly
muscle) and only 2% in the extracellular fluid (ECF). This ratio of ECF:ICF
potassium is a primary determinant of resting membrane potential in all
electrically active cells and a small absolute change in extracellular
potassium can alter the resting membrane potential of these cells. This
can have dramatic effects on cell function including altering myocardial
cell conduction velocity, repolarisation, preventing normal muscle
contraction and nerve functioning. Therefore the body maintains tight
control of extracellular potassium in a variety of ways including altering
renal and gut excretion and the flux of potassium into or out of the
intracellular compartment (mainly via the sodium potassium pump).

Potassium is retained in cells by a negative voltage, generated by the

active transport of Na out of cells by Na/K-ATPase. Both insulin and
catecholamines cause a potassium shift into cells. Insulin stimulates the
NA/H exchanger, the intracellular Na is now available for exchange with
Potassium via Na/K-ATPase, whilst catecholamines directly activate the
Na/K-ATPase via adenlate cyclase activation, which in turn stimulates cAMP which is utilised by Na/K-ATPAse . The concentration gradients of Na
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Mangement
Hyperkalaemia
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and K produce an electrical potential across the myocyte leading to a

resting membrane potential of -90mV.
As ECF K content increases the concentration gradient across the myocyte
decreases and the resting membrane potential is lowered (Fig.1) The rate
of rise of phase 0 of the action potential (Vmax) is directly proportional to
the value or the resting membrane potential at the onset of phase 0
(Fig.2). The decrease in Vmax slows conduction and prolongs membrane
depolarisation. In addition the duration of the action potential is
decreased. Initially hyperkalaemia increases excitability by shifting the
resting membrane potential to a less negative value i.e. nearer to the
threshold potential. Subsequently Vmax continues to decrease and myocyte
depression occurs.

Fig. 1

Fig. 2

Hyperkalaemia is defined as a potassium level greater than the upper limit

of normal for age. Normal serum (extracellular) potassium levels are age
dependant in children, within the range 3.5 to 5 mEq/l (mmol/l), but can
be as high as 6.mEq/L in premature infants [1]. There is no universally
accepted definition for mild, moderate, or severe hyperkalaemia. [2]
Some authors suggest mild to be 5.5 to 6 moderate 6.1 to 7, and severe
hyperkalaemia to be greater than 7mEq/l (mmol/l) [3].
Hyperkalaemia is not uncommon with some reports suggesting up to 10%
of hospitalised adult patients being affected [4], though in reality the
incidence in the paediatric population is unknown. It can be a serious and
potentially life threatening condition and may necessitate urgent
intervention that often precedes complete investigation of the cause.
Unfortunately, serum potassium does not always correlate with severity of
the clinical picture and other factors such as rapidity of rise, acid-base
status and pre-morbid condition of the patient also need to be considered.
Classic electrocardiogram changes associated with hyperkalaemia are well
described in the literature [5]. However, it is important to appreciate that
the relationship between serum potassium and ECG changes varies
between individuals particularly in mild to moderate elevation of
potassium. In some patients with severe hyperkalaemia, particularly of a
more chronic nature, minimal ECG changes may be evident [5] [6]. As
such ECG changes should not be taken in isolation to determine
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Mangement
Hyperkalaemia
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management and it is important to note that a normal ECG should not

preclude need for treatment

Aetiology of hyperkalaemia
The most common cause of hyperkalaemia in paediatric practice is
pseudo-hyperkalaemia or a spuriously elevated result. The clearest
indicators of probable spurious hyperkalaemia are clinical context and
renal function [7]. Therefore, if the patient has normal renal function and
no risk factors for hyperkalaemia it is likely that the result is spurious.
(1) Pseudo-hyperkalaemia may be due to:

Excessive tourniquet time, fist clenching

Squeezing related to capillary blood letting
Sampling proximal to a line taking potassium containing fluid
Sampling a line with potassium containing fluid
Sampling from a central line lumen distal to lumen containing
potassium infusate
Vigorous shaking of sample
Contamination of sample by potassium EDTA from FBC bottle
Injection of serum through narrow bore needle into sample bottle
Delay in processing of sample
Cold storage/transport of sample (big issue in primary care)

Some of these situations cause red cell haemolysis. This in vitro

haemolysis causing potassium to leach out of red cells can usually be
detected in the laboratory by a pinkish tinge to the serum.
True hyperkalaemia is due to a combination of increased intake,
transcellular shift and decreased excretion.
(2) Renal dysfunction or renal tract obstruction:
This can be chronic and includes patients on various dialysis regimens, or
acute in which case it may not be known at presentation that the patient
has renal dysfunction.
(3) Conditions that cause cellular potassium leakage including:

Marked leucocytosis/leukaemia
Thrombocytosis (potassium released during clot formation-plasma
levels normal serum levels raised)
Hereditary and acquired red cell disorders causing in vivo
haemolysis
Tumour lysis syndrome
Trauma, burns, surgery, crush injury, rhabdomyolysis

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Mangement
Hyperkalaemia
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Compartment syndrome

(4) Causes of increased potassium intake or reduced excretion including:

Excessive potassium in diet usually able to be accommodated for

by increased secretion by normally functioning kidneys
Potassium sparing diuretics e.g. spironolactone
Potassium containing medications such as potassium
supplementation, lo salt (replaces sodium salt with potassium),
trimethoprim, Movicol, Fybogel
Drugs that interfere with the renin-angiotensin system: heparin,
NSAIDs, ACE inhibitors, angiotensin II blockers
Iatrogenic excess e.g. IV fluid / TPN
Blood transfusion (risk increases with irradiation and age of blood)
Rapid administration of blood via hand held syringes and small
gauge needles

(5) Causes of transcellular shift of potassium out of cells:

Acidosis
*
Some drugs e.g. -blockers, suxamethonium , propofol
Digoxin toxicity
Insulin deficiency
Cessation of -adrenergic agonists, followed by leaching of K+ out
of cells

Suxamethomium can cause a transient rise in serum potassium of 0.51mmol/l for up to half an hour [8][9][10]
(6) Rare conditions such as:

Hyperkalaemic familial periodic paralysis

Disorders of adrenal insufficiency, hypoaldosteronism and Addisons
(inadequate aldosterone driven excretion of potassium)
Malignant hyperthermia

Patient Assessment
Hyperkalaemia may be entirely asymptomatic and detected coincidentally
during blood testing for another reason or the patient may have
symptoms such as tiredness, nausea, vomiting, muscle weakness,
palpitations or very rarely flaccid paralysis.
Even in the absence of symptoms a high potassium level particularly in
conjunction with supportive ECG changes is a medical emergency. A
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Mangement
Hyperkalaemia
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totally asymptomatic patient can rapidly progress to develop a life

threatening arrhythmia in this condition. It is therefore vital that the
diagnosis is reached rapidly and that appropriate therapeutic measures
are undertaken immediately.
As already mentioned in paediatric practice spuriously high potassium
levels are a regular occurrence often due to difficulty obtaining blood
samples. However these possibly spurious results must never simply be
ignored, and should always be repeated.
The clinician should determine whether the patient has any signs of renal
dysfunction or if any other features in the history or examination make
him at risk of hyperkalaemia (e.g. drug history, known diabetic, patient
receiving chemotherapy). Indicators of renal function including urea and
creatinine will usually be available concurrent with the potassium result to
provide some guidance.
In most cases of unexpected hyperkalaemia it is prudent to rapidly repeat
the test whilst preparing treatment, though treatment should not be
delayed awaiting the result, especially if there are ECG changes supportive
of elevated potassium [11]. In many acute paediatric assessment areas
there is now the ability to measure a potassium level on a blood gas
analyser which will take a matter of minutes. Whilst a specimen should
also be sent to the laboratory for confirmation, therapy if needed should
not be withheld awaiting the formal laboratory result.

ECG Monitoring:
Whilst confirming the diagnosis and during therapy, the patient should
have continuous ECG monitoring, to detect any of the classic changes
associated with hyperkalaemia. Whilst there is a recognised progression of
ECG changes from mild through to severe hyperkalaemia, there is a poor
correlation between ECG changes and serum potassium concentration,
and the progression of rhythm abnormalities is unpredictable in any
individual. ECG changes are dependent on both the absolute value and the
rate of increase of potassium levels. Some patients with severe
hyperkalaemia may have no identifiable ECG changes and others may
have changes at surprisingly low potassium levels. The absence of ECG
changes in cases of moderate or severe hyperkalaemia does not obviate
the need for therapy. The presence of ECG changes, even in mild
hyperkalaemia, should encourage prompt and aggressive treatment.

Emergency
Mangement
Hyperkalaemia
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Early ECG changes in mild hyperkalaemia (>5.5mEq/l) include peaking or

tenting of the T-wave. Thereafter as levels exceed 6.5mEq/l there is
reduction in conduction velocity resulting in prolonged PR interval and
progressive widening of the QRS complex and nodal and ventricular
arrhythmias may occur. Ultimately the p-waves disappear and the QRS
complexes combine with the T-wave to form a sine-wave appearance with
ventricular fibrillation or asystole ensuing.

Investigations
Regular monitoring of serum potassium, electrolytes, glucose and blood
gas are useful especially as hyperkalaemia is frequently associated with
acidosis and hyperglycaemia. In some cases it may be useful to perform:

Full blood count with differential and film to look for haemolysis,
leucocytosis and thrombocytosis
Creatinine kinase in cases of possible tissue injury, trauma, burns
Urinary potassium excretion
Bilirubin, reticulocytes and haptoglobin in suspected haemolysis
Renal ultrasound if suggestion of renal dysfunction or obstruction

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Mangement
Hyperkalaemia
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These investigations depend upon the individual clinical situation and must
never delay acute treatment once it is deemed necessary.

3. Management
Airway, Breathing, Circulation.
Repeat serum potassium should be ordered urgently, especially if
hyperkalaemia is an unexpected or isolated finding and there are no ECG
signs of hyperkalaemia, to exclude pseudohyperkalaemia. This can be run
on the gas machine and should not preclude starting preparation of
definitive therapy.
Hypoxia potentiates the risk of cardiac dysrhythmia, so all patients (unless
there is an associated cardiac lesion requiring low FiO2) should be
administered oxygen.
The response of an individual patient to any of the following proposed
therapies is unpredictable, so frequent repeated monitoring of potassium
is mandatory.
ECG monitoring should be continuous once hyperkalaemia is suspected
and treatment is commenced. Emergency treatment is required in any
patient with ECG changes, is symptomatic or who has a true potassium
level above 6.5mmol/l regardless of ECG appearance. Between 6 and
6.5mmol/l calcium may be withheld at the discretion of senior medical
staff but other therapy should be commenced. Even lower levels of
hyperkalaemia may require treatment particularly in the setting of a rapid
or acute rise when it is less well tolerated. Arrhythmia control is difficult
without lowering the serum potassium level.
Ideally calcium and glucose 50% should be administered centrally. If
central access is unavailable then it may be appropriate to give larger
volumes of a more dilute concentration. Preparation time and risk of
injuries secondary to extravasation must be weighed against the risk of
cardiac instability.
Bradycardia secondary to hyperkalaemia presents a conundrum and
mandates the PICU consultant being informed. It is unlikely to resolve
without correcting the hyperkalaemia but therapy with calcium salts may
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Mangement
Hyperkalaemia
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exacerbate the bradycardia, or produce AV block and asystole. The effect

of atropine and phenylepherine is blunted. Pacing may prove ineffective
because of increased stimulation thresholds secondary to hyperkalaemia.
Standby ECMO may have to be considered.
There are four components to the acute management of hyperkalaemia:
1. Antagonize the membrane toxic effects of potassium
2. Promote rapid cellular uptake of potassium
3. Remove potassium directly from the body
4. Discontinue source of exogenous potassium (drugs, fluids)
1.

Antagonize the membrane toxic effects of potassium

Calcium salts antagonise the effects of hyperkalaemia on the cardiac

membrane. They increase the threshold potential, restoring the gap
between the resting membrane potential and the threshold potential. In
addition it restores Vmax at higher resting membrane potentials,
normalising the rate of myocyte depolarisation, and normalises impulse
propagation in the SA and AV nodes. There is no effect on serum
potassium levels and other therapies that lower serum potassium levels
should be administered concomitantly.
Either 10% calcium gluconate or 10% calcium chloride can be used
depending on availability. Calcium chloride has 3 times more elemental
calcium than an equal volume of calcium gluconate, so if volume
administration/tolerance is a problem then theoretically calcium chloride
may be preferred. Calcium chloride is more likely to cause extravasation
injury.
The benefits of this treatment are usually evident with improvement in
ECG changes within a few minutes and last 30-60 minutes.

IV Calcium Gluconate 10%, 0.5 -1ml/kg (0.11-0.22mmol/kg) [max

4.4mmol]
IV Calcium Chloride 10%, 0.2ml/kg (0.14mmol/kg) [max 1.4mmol]

Administer over 5minutes and repeat as necessary after 5 minutes, if ECG

fails to improve or deteriorates. The initial dose can be given over 1-3
minutes if life threatening arrhythmias or sine wave ECG changes are
present. (Stop infusion if bradycardia develops) Administration should be
over 30 minutes if the patient is on digoxin, to avoid hypercalcaemia that
may potentiate the myocardial toxicity of digoxin.
2.

Promote rapid cellular uptake of potassium

These interventions buy time for more definitive therapy but they do not
remove potassium from the body. Beta-blockers and digoxin may reduce
the effectiveness of insulin-glucose and beta-2 agonists.
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Hyperkalaemia
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a)

Insulin

Insulin stimulates the Na-K ATP pump to promote intracellular potassium

uptake. It is thought to recruit intracellular pump components into the
cellular membrane and increase availability of intracellular Na by its effect
on the Na/H exchanger. It is indicated in every case of hyperkalaemia that
requires treatment [11]. Insulin is co administered with glucose to
prevent hypoglycaemia. Blood glucose should be checked at the end of
the infusion and then every 15 minutes for an hour after administration as
delayed hypoglycaemia is common.

The onset of action is around 15 minutes and the effect lasts for over 1
hour. Potassium levels have been shown to fall by up to 0.5mmol/l in
20minutes and 1mmol/l by an hour, so it is an effective temporising
manoeuvre [11] [14]. Dosing can be repeated after 30 minutes. The
effect lasts up to 4 hours.

2ml/kg 50% dextrose (1g/kg) and 0.1units/kg of fast acting

Insulin over 5-10 minutes (mixed in same syringe) [13].

Theoretically one could give a dextrose load alone as this will increase the
childs own insulin production and promote intracellular uptake of
potassium, however the potassium lowering effect is likely to be greater if
glucose and insulin are used in combination. Also the endogenous insulin
response may be inadequate and the resultant hypertonic state may
exacerbate hyperkalaemia due to solvent drag with efflux of water from
the intracellular to extracellular compartment.
Glucose may not need to be given if the serum glucose is > 16mmol/dl,
this should be discussed with the consultant.
b)

-adrenergic agonist.

Several paediatric studies, although small, advocate the use of salbutamol

as a safe and effective measure to temporarily reduce serum potassium
levels [15][16][17]. Salbutamol, (IV or nebulised), indirectly, via cyclicAMP, stimulates the cell membrane Na-K ATP pump in hepatic and muscle
cells to promote cellular potassium uptake. In addition it increases
endogenous insulin secretion. This is secondary to hepatic
gluconeogenesis derived hyperglycaemia, and is not a dominant
mechanism for reducing potassium levels Salbutamol is equally effective
in diabetic and non diabetic patients and in diabetic patients where cpeptide levels are not elevated. [18]
There is controversy regarding use of salbutamol as some studies suggest
it to be arrythmogenic at high dose. There is also a significant proportion
of patients (up to 20-40%) who are non-responders to this treatment with
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Hyperkalaemia
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no or minimal reduction in serum potassium. The mechanism is unclear

and unpredictable. For this reason it is recommended that salbutamol not
be used alone in the treatment of hyperkalaemia.

4mcg/kg IV salbutamol over 5 minutes repeated as required

or
2.5mg (<5 years) or 5mg (>5years) nebulised salbutamol

It is unlikely to be effective if the patient is on beta blockade for renal

failure associated hypertension. Both of these have been proven to be
effective in reducing potassium levels by up to 1.4mmol/l if intravenous
route used and up to 1mmol/l if nebulised. The onset of action is around
30 minutes lasting 2-3 hours. [15][16][17]
A few studies suggest a synergistic effect in using salbutamol combined
with insulin/glucose with greater reduction in potassium level than either
used alone. [14][18]. They are equally efficacious in lowering plasma
potassium. The effect of salbutamol is delayed slightly relative to insulin
but this is likely to be secondary to the mode of administration ie slow
nebulisation as opposed to IV bolus. In addition salbutamol may offset the
hypoglycaemic effect of insulin. This is consistent with 2-agonistic
activity on the liver where stimulation of
gluconeogenesis and glycogenolysis occurs. [18]
A Cochrane review suggests that Dextrose/Insulin and salbutamol are the
first line therapies most supported by evidence, and that a combination of
the two therapies may be more effective than either alone. [19] There is
no statistically significant difference between the effectiveness of
intravenous, nebulised or inhaled salbutamol in the limited number of
studies to date. It is likely to be easier and quicker to nebulise a patient in
the short term, though in the emergency situation in a non ventilated
patient, delivery may be erratic. Under such circumstances intravenous
follow up can be considered. Salbutamol can cause a transient
release of potasssium from liver causing a small increase in
potassium
c) Sodium Bicarbonate
The use of sodium bicarbonate is no longer advocated in the absence of
significant metabolic acidosis. It has little effect in lowering serum
potassium levels within 60 minutes when studied in adult populations with
chronic renal failure [20][21]. It may offer slight reduction in potassium
levels over a period of several hours particularly on the background of
proven metabolic acidosis with pH < 7.2 [22]. Acidosis may inhibit the
physiologic response to catecholamines and insulin, and using bicarbonate
in conjunction with insulin or salbutamol may be of some benefit.
There is a risk of hypocalcaemia because alkalosis decreases the levels of
ionised calcium, which may be poorly tolerated and potentiate
arrhythmias. It should not be administered at the same time via the same
line as calcium or calcium bicarbonate may precipitate.
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Hyperkalaemia
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It is unclear whether any reduction in potassium is due to intracellular

shift of potassium with alkalinisation or if it is related to the large
hypertonic load from large quantities of sodium in the preparation with
ensuing fluid shifts. Regardless, the significant side effects such as
volume and sodium overload, particularly in patients with renal
dysfunction, along with the knowledge that it is poorly effective, probably
preclude its use in most situations. The evidence is sufficiently
inconclusive in cases of co-existing acidosis that some centres continue to
use bicarbonate to manage hyperkalaemia in combination with other
therapy. [23].

3.

1mmol/kg over 10 minutes (repeat in 10 minutes as

required; monitor blood gases to maintain pH <7.55

Remove potassium directly from the body

a)
Cation exchange resins e.g. calcium resonium and Resonium A
the degree of benefit of these treatments in hyperkalaemia remains
controversial.
Cation exchange resins remove potassium directly from the body through
the gut mucosa of the large bowel and ileum. Approximately one gram of
resin exchanges 1mmol sodium or 2mmol calcium for 1mmol of
potassium. This potassium is then bound by the resin in the intestinal
lumen and excreted. The onset of action is slow, in the order of 1-2
hours, with peak of 4-6 hours so the temporising steps in point 2 must be
undertaken in the first instance.
The resins can be administered rectally or orally. The preferred route is
oral (except in neonates) if administered rectally the resin should be
mixed with methylcellulose and retained for at least 60 minutes.
Recommended doses are: 250mg/kg (max 15g) 3-4 times per day orally
or rectally, repeated every 6-8 hours if required for children over 1 month
of age. [13] The resin must not be combined with fruit juices as they
contain high levels of potassium. If the rectal route is used the colon
must be irrigated 6-12 hourly to prevent faecal impaction. Side effects
include rectal mucosal irritation and ulceration, faecal impaction,
constipation and rarely bowel perforation. Hypercalcaemia may occur
especially in patients on dialysis.
The data regarding the effectiveness of exchange resins is conflicting. It
is possible to excrete up to 12 mmol/l potassium via the gastro-intestinal
tract in healthy adults however this is limited by stool volume. This is
especially pertinent in a paediatric population who obviously have much
lower stool volumes. Some authors also suggest that resins do not
contribute to faecal potassium excretion above the effect of laxatives
alone [24]

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In spite of these reservations the GAIN (Guidelines and Audit

Implementation Network) in Northern Ireland still advocate the use of
exchange resins to remove potassium from the gut though accept that
other measures must be used in the first instance due to delayed onset of
action [4]
b)

Loop diuretic e.g. Furosemide

These drugs increase urine flow and delivery of sodium to distal tubular
potassium excreting sites. This is likely to be less effective in patients
with renal dysfunction who may have limited response to diuretics
c)

Haemodialysis

This is the definitive method of removal of potassium from the body. It is

used in cases of severe hyperkalaemia or when other treatments have
failed to provide a sustained reduction in potassium. Serum potassium
can be lowered by 1-1.5mmol/l for every hour of dialysis although some
rebound is expected on completion of dialysis. Rapid liaison with tertiary
paediatric nephrologists or intensive care specialists capable of providing
this treatment modality is necessary when potassium is very high, other
treatments appear to be failing, or if ongoing tissue damage and
continued release of intracellular potassium is expected.
Treatment that causes intracellular shifts of potassium decreases the
efficacy of potassium clearance by dialysis because they decrease the
concentration gradient between plasma and the dialysate. It may be
necessary to redialyse this patient group as the effects of agonists
wear of and potassium returns to the extracellular compartment. [25]
Potassium free dialysate will maximise potassium clearance.
Long term management
Review diet and reduce potassium intake - in normal individuals the
kidneys can adapt to excrete excess potassium intake however this is not
the case if there is kidney dysfunction or the patient is taking medications
that alter potassium excretion such as potassium sparing diuretics.
Notably Lo salt replaces sodium salt with potassium salt and may be an
occult contributory factor.
Review of medications and fluid/nutrition prescriptions - potassium
sparing diuretics, ACE inhibitors, heparin, trimethoprim and other
potassium containing antibiotics, Fybogel and Movicol all act by various
mechanisms to increase extracellular potassium levels.
Haemodialysis the definitive treatment of hyperkalaemia. Particularly
useful in cases of acute or chronic renal failure or when other treatments
have failed and the potassium level remains high. If a potassium free
diasylate is used, serum potassium may decrease as much as 1.2 to 1.5
mmol/l per hour however there will be rebound in potassium levels on
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completion of dialysis. Peritoneal dialysis is poorly effective at lowering

serum potassium levels in comparison.
Longer term treatment must be individual patient based, dependent upon
the cause of the hyperkalaemia. It may simply be a case of dietary
restriction or alteration to drug regime though in other cases, such as
hypoaldosteronism, mineralocorticoid replacement therapy would be
necessary or haemodialysis may be required for renal dysfunction.

4. Review:
This guideline should be reviewed every 2 years from date of approval

5. Monitoring
An audit of adherence to the guidelines can be performed.

6. Implementation plan
-

Education and training for nursing staff

Education for PICU trainees

Guideline to be put on electronic clinical information system

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7. References
1. Shaffer SG, Kilbride HW, Hayen LK, Meade VM, Warady
BA. Hyperkalemia in Very Low Birth Weight Infants. J Pediatr,
1992;121:275-9.
2. Brenner: Brenner & Rector's The Kidney, 7th ed.
Copyright 2004 Saunders, An Imprint of Elsevier
3. Mandal AK. Hypokalemia and hyperkalemia. Med Clin North Am
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Hyperkalaemia Algorithm
(PICU)

K+ > 5.5
mmol/l

Regular Monitoring During Therapy

(Genuine Result)

A,B,C, Oxygen, cardiac monitoring

Consider and address

precipitating factors
Stop potassium containing
fluids

Does Patient Have Chronic Renal

Failure?
Yes

No

Asymptomatic and
Normal ECG
Symptomatic or
abnormal ECG
Discuss with renal and
ICU consultant , follow
patient protocol

Stabilise Cardiac Membrane

K+ 6mmol/l
or abnormal ECG
or symptomatic

IV Calcium Gluconate 10%, 0.5 -1ml/kg

(0.11-0.22mmol/kg) [max 4.4mmol]
or
IV Calcium Chloride 10%, 0.2ml/kg
(0.14mmol/kg) [max 1.4mmol]

K+ <6mmol/l and
normal ECG
and asymptomatic

Discuss with
consultant

over 2-3 minutes (can repeat after 10 mins)

Shift Potassium Into Cells

IV glucose 50% 2ml/kg + 0.1 units/kg Actrapid insulin over 5-10

minutes (mixed in same syringe)
AND
Nebulised salbutamol: <5Years 2.5mg, >5 years 5mg
Or
IV salbutamol 4mcg/kg over 5minutes
Consider Sodium Bicarbonate 8.4%, 1mmol/kg if pH < 7.2

IV Furosemide 0.5mg/kg

Calcium Resonium 250mg Oral or PR 6-8 hourly

Remove Potassium From Body

CONSIDER HAEMODIALYSIS HAEMOFILTRATION