YOR-PICU-007 Hyperkalaemia Guideline Oct 2010

8/10/2019 YOR-PICU-007 Hyperkalaemia Guideline Oct 2010

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Emergency Management of Hyperkalaemia

Paediatric Intensive Care Unit

Royal Hospital for Sick Children

Emergency Mangement of

Hyperkalaemia

Version: 1 Page 1 of 19

Author: A McKie, D Ellis Authorised by: PICU Guideline

Group

Issue Date: Oct 2010

Date of Review: Oct 2012 Q-Pulse Ref: YOR-PICU-007


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Contents Page Number(s)

1. Methodology 2-3

2. Background 3-8

3. Management 9-14

4. Review 14

5. Monitoring 146. Implementation 15

7. References 15-16

8. Treatment Algorithm 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 hyperkalaemiain patients in paediatric critical care. Transfer to an HDU or PICU

environment should be considered depending on where the patientis 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. Chronicrenal patients should be discussed with both consultant renal andconsultant 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 ChidrensHospital Glasgow.

4. Evidence- constructed after review of standard textbooks, pub med andGoogle scholar search (interrogation of quoted references), usingthe search terms, hyperkalaemia or hyperkalemia, therapy ortreatment or management or guideline. Only articles in English

were reviewed.Evidence available is mostly level 3 and 4.


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This guideline is proposed acknowledging that there is little evidence base

there is significant variation in how drugs are used, despiteacceptance of their efficacy

there is a lack of agreement on treatment thresholds.

Any chosen threshold value for commencing treatment is bydefinition arbitrary.

5. Methods

- prior topublication the proposed guideline was reviewedby PICUconsultants, 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 (mainlymuscle) and only 2% in the extracellular fluid (ECF). This ratio of ECF:ICF

potassium is a primary determinant of resting membrane potential in allelectrically active cells and a small absolute change in extracellularpotassium can alter the resting membrane potential of these cells. Thiscan have dramatic effects on cell function including altering myocardial

cell conduction velocity, repolarisation, preventing normal musclecontraction and nerve functioning. Therefore the body maintains tight

control of extracellular potassium in a variety of ways including alteringrenal and gut excretion and the flux of potassium into or out of theintracellular 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 andcatecholamines cause a potassium shift into cells. Insulin stimulates theNA/H exchanger, the intracellular Na is now available for exchange withPotassium via Na/K-ATPase, whilst catecholamines directly activate the

Na/K-ATPase via adenlate cyclase activation, which in turn stimulates c-AMP which is utilised by Na/K-ATPAse . The concentration gradients of Na


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and K produce an electrical potential across the myocyte leading to aresting membrane potential of -90mV.

As ECF K content increases the concentration gradient across the myocytedecreases and the resting membrane potential is lowered (Fig.1) The rateof 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 membranedepolarisation. In addition the duration of the action potential isdecreased. Initially hyperkalaemia increases excitability by shifting the

resting membrane potential to a less negative value i.e. nearer to thethreshold potential. Subsequently Vmaxcontinues to decrease and myocytedepression occurs.


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

of normal for age. Normal serum (extracellular) potassium levels are agedependant in children, within the range 3.5 to 5 mEq/l (mmol/l), but canbe as high as 6.mEq/L in premature infants [1]. There is no universallyaccepted 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].

Fig. 1 Fig. 2

Hyperkalaemia is not uncommon with some reports suggesting up to 10%

of hospitalised adult patients being affected [4], though in reality theincidence in the paediatric population is unknown.It can be a serious andpotentially 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 ofthe 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 welldescribed in the literature [5]. However, it is important to appreciate that

the relationship between serum potassium and ECG changes variesbetween individuals particularly in mild to moderate elevation ofpotassium. In some patients with severe hyperkalaemia, particularly of a

more chronic nature, minimal ECG changes may be evident [5] [6]. Assuch ECG changes should not be taken in isolation to determine


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management and it is important to note that a normal ECG should notpreclude need for treatment

Aetiology of hyperkalaemia

The most common cause of hyperkalaemia in paediatric practice is

pseudo-hyperkalaemia or a spuriously elevated result. The clearestindicators of probable spurious hyperkalaemia are clinical context and

renal function [7]. Therefore, if the patient has normal renal function andno 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 bedetected 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, oracute 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-plasmalevels 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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Compartment syndrome

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

Excessive potassium in diet usually able to be accommodated forby 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 0.5-

1mmol/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 coincidentallyduring 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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totally asymptomatic patient can rapidly progress to develop a lifethreatening arrhythmia in this condition. It is therefore vital that the

diagnosis is reached rapidly and that appropriate therapeutic measuresare undertaken immediately.

As already mentioned in paediatric practice spuriously high potassiumlevels are a regular occurrence often due to difficulty obtaining bloodsamples. However these possibly spurious results must never simply beignored, and should always be repeated.

The clinician should determine whether the patient has any signs of renaldysfunction or if any other features in the history or examination make

him at risk of hyperkalaemia (e.g. drug history, known diabetic, patientreceiving chemotherapy). Indicators of renal function including urea andcreatinine 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 bedelayed awaiting the result, especially if there are ECG changes supportiveof elevated potassium [11]. In many acute paediatric assessment areasthere is now the ability to measure a potassium level on a blood gas

analyser which will take a matter of minutes. Whilst a specimen shouldalso be sent to the laboratory for confirmation, therapy if needed shouldnot be withheld awaiting the formal laboratory result.

ECG Monitoring:

Whilst confirming the diagnosis and during therapy, the patient shouldhave continuous ECG monitoring, to detect any of the classic changesassociated with hyperkalaemia. Whilst there is a recognised progression of

ECG changes from mild through to severe hyperkalaemia, there is a poorcorrelation between ECG changes and serum potassium concentration,

and the progression of rhythm abnormalities is unpredictable in anyindividual. ECG changes are dependent on both the absolute value and the

rate of increase of potassium levels. Some patients with severehyperkalaemia may have no identifiable ECG changes and others may

have changes at surprisingly low potassium levels. The absence of ECGchanges in cases of moderate or severe hyperkalaemia does not obviate

the need for therapy. The presence of ECG changes, even in mildhyperkalaemia, should encourage prompt and aggressive treatment.


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Early ECG changes in mild hyperkalaemia (>5.5mEq/l) include peaking ortenting of the T-wave. Thereafter as levels exceed 6.5mEq/l there is

reduction in conduction velocity resulting in prolonged PR interval andprogressive widening of the QRS complex and nodal and ventricular

arrhythmias may occur. Ultimately the p-waves disappear and the QRScomplexes 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 withacidosis 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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These investigations depend upon the individual clinical situation and must

never delay acute treatmentonce it is deemed necessary.

3. Management

Airway, Breathing, Circulation.

Repeat serum potassium should be ordered urgently, especially ifhyperkalaemia is an unexpected or isolated finding and there are no ECGsigns of hyperkalaemia, to exclude pseudohyperkalaemia. This can be runon the gas machine and should not preclude starting preparation ofdefinitive therapy.

Hypoxia potentiates the risk of cardiac dysrhythmia, so all patients (unlessthere 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 potassiumis mandatory.

ECG monitoring should be continuous once hyperkalaemia is suspectedand treatment is commenced. Emergency treatment is required in anypatient with ECG changes, is symptomatic or who has a true potassiumlevel above 6.5mmol/l regardless of ECG appearance. Between 6 and

6.5mmol/l calcium may be withheld at the discretion of senior medicalstaff but other therapy should be commenced. Even lower levels ofhyperkalaemia 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. Ifcentral access is unavailable then it may be appropriate to give larger

volumes of a more dilute concentration. Preparation time and risk ofinjuries 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 resolvewithout correcting the hyperkalaemia but therapy with calcium salts may


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exacerbate the bradycardia, or produce AV block and asystole. The effectof 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 potassium2. Promote rapid cellular uptake of potassium

3. Remove potassium directly from the body4. Discontinue source of exogenous potassium (drugs, fluids)

1. Antagonize the membrane toxic effects of potassium

Calcium salts antagonise the effects of hyperkalaemia on the cardiacmembrane. They increase the threshold potential, restoring the gap

between the resting membrane potential and the threshold potential. Inaddition it restores Vmax at higher resting membrane potentials,

normalising the rate of myocyte depolarisation, and normalises impulsepropagation in the SA and AV nodes. There is no effect on serumpotassium levels and other therapies that lower serum potassium levelsshould be administered concomitantly.

Either 10% calcium gluconate or 10% calcium chloride can be useddepending on availability. Calcium chloride has 3 times more elementalcalcium 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 extravasationinjury.

The benefits of this treatment are usually evident with improvement inECG changes within a few minutes and last 30-60 minutes.

IV Calcium Gluconate 10%, 0.5 -1ml/kg (0.11-0.22mmol/kg) [max4.4mmol]

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

Administer over 5minutes and repeat as necessary after 5 minutes, if ECGfails to improve or deteriorates. The initial dose can be given over 1-3

minutes if life threatening arrhythmias or sine wave ECG changes arepresent. (Stop infusion if bradycardia develops)Administration should beover 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 notremove potassium from the body. Beta-blockers and digoxin may reducethe effectiveness of insulin-glucose and beta-2 agonists.


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a) Insulin

Insulin stimulates the Na-K ATP pump to promote intracellular potassiumuptake. It is thought to recruit intracellular pump components into thecellular membrane and increase availability of intracellular Na by its effect

on the Na/H exchanger. It is indicated in every case of hyperkalaemia thatrequires treatment [11]. Insulin is co administered with glucose toprevent hypoglycaemia. Blood glucose should be checked at the end ofthe 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 1hour. Potassium levels have been shown to fall by up to 0.5mmol/l in20minutes and 1mmol/l by an hour, so it is an effective temporising

manoeuvre [11] [14]. Dosing can be repeated after 30 minutes. Theeffect lasts up to 4 hours.

2ml/kg 50% dextrose (1g/kg) and 0.1units/kg of fast actingInsulin over 5-10 minutes (mixed in same syringe) [13].

Theoretically one could give a dextrose load alone as this will increase thechilds own insulin production and promote intracellular uptake ofpotassium, however the potassium lowering effect is likely to be greater ifglucose 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 fromthe 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 potassiumlevels [15][16][17]. Salbutamol, (IV or nebulised), indirectly, via cyclic-AMP, stimulates the cell membrane Na-K ATP pump in hepatic and musclecells to promote cellular potassium uptake. In addition it increases

endogenous insulin secretion. This is secondary to hepaticgluconeogenesis derived hyperglycaemia, and is not a dominant

mechanism for reducing potassium levels Salbutamol is equally effectivein diabetic and non diabetic patients and in diabetic patients where c-peptide levels are not elevated. [18]

There is controversy regarding use of salbutamol as some studies suggestit 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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no or minimal reduction in serum potassium. The mechanism is unclearand 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 (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 beeffective in reducing potassium levels by up to 1.4mmol/l if intravenousroute 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 combinedwith insulin/glucose with greater reduction in potassium level than eitherused alone.[14][18]. They are equally efficacious in lowering plasma

potassium. The effect of salbutamol is delayed slightly relative to insulinbut this is likely to be secondary to the mode of administration ie slow

nebulisation as opposed to IV bolus.In addition salbutamol may offset thehypoglycaemic effect of insulin. This is consistent with 2-agonisticactivity on the liver where stimulation ofgluconeogenesis and glycogenolysis occurs. [18]

A Cochrane review suggests that Dextrose/Insulin and salbutamol are thefirst line therapies most supported by evidence, and that a combination ofthe 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 ofstudies to date. It is likely to be easier and quicker to nebulise a patient inthe short term, though in the emergency situation in a non ventilatedpatient, delivery may be erratic. Under such circumstances intravenousfollow up can be considered. Salbutamol can cause a transient

release of potasssium from liver causing a small increase inpotassium

c) Sodium Bicarbonate

The use of sodium bicarbonate is no longer advocated in the absence ofsignificant metabolic acidosis. It has little effect in lowering serum

potassium levels within 60 minutes when studied in adult populations withchronic renal failure [20][21]. It may offer slight reduction in potassiumlevels over a period of several hours particularly on the background of

proven metabolic acidosis with pH < 7.2[22]. Acidosis may inhibit thephysiologic response to catecholamines and insulin, and using bicarbonatein conjunction with insulin or salbutamol may be of some benefit.

There is a risk of hypocalcaemia because alkalosis decreases the levels ofionised calcium, which may be poorly tolerated and potentiatearrhythmias. It should not be administered at the same time via the same

line as calcium or calcium bicarbonate may precipitate.


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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 largehypertonic load from large quantities of sodium in the preparation withensuing fluid shifts. Regardless, the significant side effects such as

volume and sodium overload, particularly in patients with renaldysfunction, along with the knowledge that it is poorly effective, probablypreclude its use in most situations. The evidence is sufficientlyinconclusive in cases of co-existing acidosis that some centres continue to

use bicarbonate to manage hyperkalaemia in combination with othertherapy.[23].

1mmol/kg over 10 minutes (repeat in 10 minutes asrequired; monitor blood gases to maintain pH


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In spite of these reservations the GAIN (Guidelines and AuditImplementation Network) in Northern Ireland still advocate the use of

exchange resins to remove potassium from the gut though accept thatother measures must be used in the first instance due to delayed onset ofaction[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 patientswith renal dysfunction who may have limited response to diuretics

c) Haemodialysis

This is the definitive method of removal of potassium from the body. It isused in cases of severe hyperkalaemia or when other treatments have

failed to provide a sustained reduction in potassium. Serum potassiumcan be lowered by 1-1.5mmol/l for every hour of dialysis although some

rebound is expected on completion of dialysis. Rapid liaison with tertiarypaediatric nephrologists or intensive care specialists capable of providingthis treatment modality is necessary when potassium is very high, othertreatments 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 theefficacy 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 agonistswear of and potassium returns to the extracellular compartment. [25]Potassium free dialysate will maximise potassium clearance.

Long term management

R ev i e w d i e t a n d r e d u c e p o t a s si u m i n t a k e - in normal individuals thekidneys can adapt to excrete excess potassium intake however this is notthe 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 anoccult contributory factor.

R ev i e w o f m e d i ca t i o n s

a n d f l u i d / n u t r i t io n p r e s c r i p t i o n s -potassiumsparing diuretics, ACE inhibitors, heparin, trimethoprim and otherpotassium containing antibiotics, Fybogel and Movicol all act by various

mechanisms to increase extracellular potassium levels.

H a em o d i a l y s is the definitive treatment of hyperkalaemia. Particularlyuseful in cases of acute or chronic renal failure or when other treatments

have failed and the potassium level remains high. If a potassium freediasylate 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 loweringserum potassium levels in comparison.

Longer term treatment must be individual patient based, dependent uponthe cause of the hyperkalaemia. It may simply be a case of dietary

restriction or alteration to drug regime though in other cases, such ashypoaldosteronism, mineralocorticoid replacement therapy would benecessary 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 Am1997;81:61139

4. Guidelines for the Treatment of Hyperkalaemia in Adults GAIN

(Guidelines and Audit Implementation Network- Northern Ireland)December 2008

5. Webster A, Brady W, Morris F. Recognising Signs of Danger: ECGChanges Resulting From an Abnormal Serum Potassium Concentration.Emerg Med J 2002;19:7477

6. Martinez-Vea A, Bardaji A, Garcia C, Oliver J A. Severe HyperkalemiaWith Minimal Electrocardiographic Manifestations. Journal ofElectrocardiology1999 32 1 45-49

7.Stuart W, Smellie A. Spurious Hyperkalaemia. BMJ 2007;334:693-5

8. Day S. Plasma Potassium Changes Following Suxamethonium And

Suxethonium In Normal Patients And In Patients In Renal FailureBr.J. Anaesth. 1976;48: 1011-15

9. List W F. Serum Potassium Changes During Induction Of Anaesthesia.Brit. J. Anaesth. 1967;39: 480-484

10. Weintraub H D, Heisterkamp D V, Cooperman L H. Changes InPlasma Potassium Concentration After Depolarizing Blockers In

Anaesthetized Man. Brit. J. Anaesth. 1969;41:1048-10511. Ahee P, Crowe AV. The Management Of Hyperkalaemia In TheEmergency Department. J Accid Emerg Med 2000;17:188191

12. Noyan A, Anarat A, Pirti M, et al. Treatment Of Hyperkalemia InChildren With Intravenous Salbutamol. Acta Paediatr Jpn 1995;37:3557

13. Martin J (ed) BNF for Children 2010. London: Pharmaceutical Press

2010

14. Lens XM, Montoliu J, Cases A, et al. Treatment Of Hyperkalemia In

Renal Failure: Salbutamol V Insulin. Nephrol Dial Transplant 1989;4:22832
http://www.mdconsult.com/about/book/saunders.htmlhttp://www.mdconsult.com/about/book/saunders.html


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15. Murdoch IA, Dos Anjos R, Haycock GB. Treatment Of HyperkalemiaWith Intravenous Salbutamol. Arch Dis Child. 1991;66:527-8

16. Kemper MJ, Harps E, Hellwege HH, et al. Effective Treatment Of AcuteHyperkalaemia In Childhood By Short term Infusion Of Salbutamol. Eur J

Pediatr 1996;155:4957

17. McClure RJ, Prasad VK, Brocklebank JT. Treatment OfHyperkalaemia Using Intravenous And Nebulised Salbutamol.

Arch Dis Child 1994;70:1268

18. Allon M, Copkney C. Albuterol And Insulin For Treatment Of

Hyperkalemia In Hemodialysis Patients. Kidney Int 1990;38:86972

19.Mahoney BA, Smith WAD, Lo D, Tsoi K, Tonelli M, Clase C. EmergencyInterventions For Hyperkalaemia (Review).

Cochrane Collaboration July 2009

20. Allon M, Shanklin N. Effect Of Bicarbonate Administration On PlasmaPotassium In Dialysis Patients: Interactions With Insulin And Albuterol.Am J Kidney Dis 1996;28:50814

21. Blumberg A, Weidmann P, Shaw S, et al. Effect Of Various TherapeuticApproaches On Plasma Potassium And MajorRegulating Factors In Terminal Renal Failure. Am J Med 1988;85:50712

22. Allon M. Treatment And Prevention Of Hyperkalemia In Endstage

Renal Disease. Kidney Int 1993;43:1197209

23. Kamel K S, Wei C. Controversial Issues In The Treatment OfHyperkalaemia. Nephrol Dial Transplant 2003; 18: 22182221

24. Gruy-Kapral C, Emmett M, Santa Ana CA. Effect Of Single Dose Resin-Cathartic Therapy On Serum Potassium Concentration In Patients WithEnd-Stage Renal Disease. J Am Soc Nephrol 1998; 9: 19241930

25. Allon M, Shanklin N. Effect Of Albuterol Treatment On Subsequent DialyticPotassium Removal. Am J Kidney Dis 1995;26:607-1


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Hyperkalaemia Algorithm(PICU)

Regular Monitoring During TherapyK+

> 5.5mmol/l

Genuine Resul t

Consider and addressprecipitating factors

Stop potassium containingfluids

A,B,C, Oxygen, cardiac monitor ing

Does Patient Have Chronic RenalFailure?

Yes

Asymptomatic andNormal ECG

Discuss with renal andICU consultant , follow

patient protocol

Symptomatic orabnormal ECG

No

K+ 6mmol/lor abnormal ECG

or symptomatic

K+

YOR-PICU-007 Hyperkalaemia Guideline Oct 2010

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Transcript of YOR-PICU-007 Hyperkalaemia Guideline Oct 2010