23/03/2023, 13:58 Potassium - Hyperkalaemia | Emergency Care Institute

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 /  For clinicians /  Clinical Tools /  Electrolytes /  Potassium - Hyperkalaemia

Potassium - Hyperkalaemia
Background:
Hyperkalaemia defined as serum K+ >5.5mEq/L
Hyperkalaemia is potentially life threatening, and can result in cardiac arrythmias and sudden death

Causes:

MECHANISM CAUSE

Pseudo hyperkalaemia Blood sample handling

Haemolysis

Thrombocytosis

Severe leukocytosis

Cellular potassium Tissue damage

release
Rhabdomyolysis

Insulin deficiency

Metabolic acidosis

Hypoaldosteronism Primary adrenal insufficiency

Pseudo hypoaldosteronism

Hyporeninaemia (diabetes, interstitial kidney disease)

Adrenal enzyme defect

Heparin

HIV

Renal failure Reduced potassium excretion

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Volume depletion Reduced excretion K due to reduced sodium and water delivery to distal
tubules

Drug induced Potassium supplements

Potassium sparing diuretics

ACE inhibitors

Angiotensin II receptor blockers (ARBs)

NSAIDs

Trimethoprim

Ciclosporin

Pentamidine

Other Hyperkalaemic periodic paralysis

Table 1. Causes of hyperkalaemia

Assessment:

History and examination:

Clinical manifestations of hyperkalaemia are uncommon with values < 6.0mmol/L.

Common acute manifestations of significant hyperkalaemia include muscle weakness or paralysis and
cardiac conductions abnormalities. Physiologically, one will find a reduced urinary acid excretion resulting in
a normal anion gap metabolic acidosis (due to decreased renal ammonia-genesis)

Hyperkalaemia can be initially asymptomatic or can presents with severe symptoms/signs:

Severe muscle weakness or paralysis.

Ascending muscle weakness or paralysis that begins with the legs and progresses to the trunk and
arms. Can progress to flaccid paralysis. Sphincter tone and cranial nerve function typically intact.
Respiratory muscle weakness is rare.

Cardiovascular

Electrocardiographic changes (as above) that may suggest the diagnosis before the blood test
results.
Conduction abnormalities (bradycardia) and arrhythmias (as above).

Management

Investigation
Any potassium abnormalities found on either a venous blood gas - or serum blood sample, should be re-
confirmed on a serum sample. Do not let this delay treatment in clear cases of hyperkalaemia
(consistent history, ECG changes).

In significant hyperkalaemia, an urgent ECG should be obtained to establish whether cardiotoxicity is

present, and continuous ECG monitoring should occur until serum potassium values are brought into a
safer range and resolution of cardiotoxicity is observed.

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After confirming the diagnosis of hyperkalaemia, assessing the following is essential for optimal choice of
therapy:

Volume status: volume depletion should be corrected to ensure kidney function is optimised
Kidney function: exclude acute kidney injury (AKI).
ECG changes: conduction disturbances are more likely when there is a rapid risk in potassium
Digoxin levels: in appropriate context i.e., acute, or chronic digoxin toxicity
Check for adrenal insufficiency
FBC: looking for normocytic, normochromic anaemia, which may suggest acute haemolysis),
thrombocytosis and/or leucocytosis.
Venous blood gas: looking for metabolic acidosis and a comparable potassium level.
Glucose

ECG Findings
Several characteristic electrocardiogram (ECG) abnormalities associated with hyperkalaemia exist, such as:

Tall, peaked T waves and shortened QT intervals (earliest waveform changes).

Progressive lengthening of the PR interval and QRS duration.
Loss of the P wave morphology with progressive lengthening of the QRS interval into a sine wave.

The above ECG changes can progress to life-threatening arrhythmias including, and not limited to:

bradycardia, sinus arrest, slow idioventricular rhythms

ventricular tachycardia, ventricular fibrillation
asystole with ventricular standstill - a flat line – showing complete absence of electrical activity.

K+ (mmol) ECG changes

5.5 – 6.5 Peaked T waves

6.5 – 7.5 Flattening then loss P wave

>7.5 Widening QRS

>8.0 Sine wave, VT, VF

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Treatment
Emergency treatment for life-threatening hyperkalaemia is:

1. Calcium gluconate (stabilise myocardium, not lower serum K)

2. Salbutamol (temporising measure, not definitive)
3. Correct any volume depletion (optimise kidney function)
a. metabolic acidosis is present, intravenous bicarbonate
4. Insulin and glucose
a. Monitor for hypoglycaemia and correct as necessary
5. Removing potassium from bowel (less urgent, slower acting)
6. Dialysis (in severe cases, none of above approaches may be effective)
7. Medication review
8. Seek and treat cause

Specific cases:

Primary adrenal insufficiency/hypoaldosteronism - give hydrocortisone and NOT insulin

Digoxin toxicity (https://tgldcdp.tg.org.au.acs.hcn.com.au/viewTopic?topicfile=toxicology-chronic-
digoxin&sectionId=ttg1-c68-s3#toc_d1e181) - use of digoxin immune Fab (digibind) if severe life threatening
arrythmia or severe ECG changes due to hyperkalaemia, use treatment as below.

TREATMENT DOSING

Calcium gluconate Calcium gluconate 10% 10 mL IV over 2-3 mins into

a large vein

May need repeat 30-60min

Salbutamol Salbutamol 10mg via intermittent nebulisation

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Correct any volume depletion (a) N. Saline iv – titrate to level depletion

(a) No acid-base disturbance (b) Sodium bicarbonate 8.4%, 50 mL IV over 5-10

min
(b) Metabolic acidosis present

Insulin and glucose (a) Short-acting insulin 10 units IV bolus

(a) Standard therapy PLUS

(b) Higher risk hypoglycaemia Glucose 50% 50 mL IV over 5 min

(https://tgldcdp.tg.org.au.acs.hcn.com.au/viewTopic?
OR
topicfile=hypoglycaemia-in-patients-with-
diabetes&sectionId=dbg1-c16-s1#dbg1-c16-box1) Glucose 10% 250 mL IV over 15 min (if 50%
causing vascular irritation)

(b) Glucose 10% IV infusion at 75 to 100 mL/hour

*rule out hypoglycaemia

(https://tgldcdp.tg.org.au.acs.hcn.com.au/viewTopic?
topicfile=hypoglycaemia-in-patients-with-diabetes) prior
commencing treatment. Monitor and treat for
hypoglycaemia every 30mins for 2hrs, then hourly
for 4hrs.

**Remove Potassium from bowel Sodium polystyrene sulfonate 15 g PO, TDS OR 30g
PR OD

OR

Calcium polystyrene sulfonate 15 g PO TDS OR 30g

PR OD

Dialysis If none of above approaches effective

Medication review Stop drugs causing hyperkalaemia – see table 1.

**Gastrointestinal cation exchangers - use contentious

(https://www.uptodate.com.acs.hcn.com.au/contents/treatment-and-prevention-of-hyperkalemia-in-
adults/abstract/31,32,35,36) in patients not requiring dialysis. Discuss with inpatient team prior to administration

Consider consultation with critical care team:

Severe hyperkalaemia
Requiring dialysis

References:
LITFL (https://litfl.com/hyperkalaemia-ecg-library)

UpToDate (https://www.uptodate.com.acs.hcn.com.au/contents/treatment-and-prevention-of-hyperkalemia-in-adults?
search=hyperkalaemia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1)

ETG (https://tgldcdp.tg.org.au.acs.hcn.com.au/viewTopic?topicfile=electrolyte-
abnormalities&guidelineName=Other#toc_d1e1118)

Patient Uk (https://patient.info/doctor/hyperkalaemia-in-adults)
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Deranged physiology (https://derangedphysiology.com/main/required-reading/electrolytes-and-

fluids/Chapter%206.2.2/hyperkalemia)

European journal of emergency medicine (https://journals.lww.com/euro-

emergencymed/Fulltext/2020/10000/Acute_hyperkalemia_in_the_emergency_department__a.10.aspx)

Renal guidelines
(https://renal.org/sites/renal.org/files/RENAL%20ASSOCIATION%20HYPERKALAEMIA%20GUIDELINE%202020.pdf)

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