Hyperkalaemia: quick reference for emergency treatment

Emergency management in brief

The intensity of treatment is governed by ECG changes, symptoms, the rate of rise, renal function and the clinical context, not by the potassium value alone. A normal ECG does not exclude dangerous hyperkalaemia. Record a 12-lead ECG and start cardiac monitoring at a plasma potassium above 6.0 mmol/L, and at lower values if the rise is rapid, the patient has symptoms, or the clinical risk is high [1,2].

1. Perform an ABCDE assessment, attach cardiac monitoring, secure intravenous access and record an ECG.
2. Confirm the potassium with a repeat sample, but do not delay treatment when there are ECG changes, circulatory compromise or a very strong clinical suspicion.
3. Give intravenous calcium in the presence of hyperkalaemic ECG changes or arrhythmia.
4. Shift potassium into the cells with insulin and glucose. Add high-dose salbutamol in marked hyperkalaemia if there is no contraindication.
5. At the same time, start treatment that eliminates potassium from the body.
6. Check the plasma potassium after about 1 hour and follow the plasma glucose closely for at least 6 hours after insulin.
7. Contact nephrology early in anuria, in a dialysis patient, in severe acute kidney injury, in treatment failure or in ongoing massive potassium release.

In cardiac arrest with suspected hyperkalaemia, advanced life support is followed while the hyperkalaemia is treated. Calcium chloride is then usually the first choice, since it provides more elemental calcium per millilitre and can be given rapidly through secure intravenous or intraosseous access.

Grading

There is no entirely uniform international grading. The following division is clinically useful and is consistent with commonly used guidelines [1,3].

ECG changes or serious neuromuscular symptoms mean a high risk even if the plasma potassium is below 6.5 mmol/L. Conversely, patients with chronic renal failure may have very high values without the classical ECG findings. A rapidly rising potassium is usually more dangerous than a corresponding stable chronic value [4].

The grading must not be used mechanically. A patient with a plasma potassium of 6.2 mmol/L, new bradycardia and acute kidney injury may be at greater immediate risk than a stable dialysis patient with a plasma potassium of 6.6 mmol/L and an unchanged ECG. Both, however, need rapid assessment and an active treatment plan.

Initial assessment and sampling

Immediate measures

• Assess airway, breathing and circulation.
• Attach continuous ECG monitoring and pulse oximetry.
• Measure the blood pressure repeatedly as clinically indicated.
• Record a 12-lead ECG.
• Insert at least one functioning intravenous cannula.
• Stop potassium infusions and temporarily withdraw drugs that can raise the potassium.
• Assess the urine output and ask when the patient last passed urine.
• Contact intensive care in circulatory compromise, serious arrhythmia, marked QRS widening, a sine wave pattern, or a need for repeated calcium treatment.

Urgent investigations

As a rule, take:

• Plasma potassium as a central laboratory sample.
• A blood gas with pH, bicarbonate, potassium and glucose if a rapid result is needed.
• Creatinine, urea, sodium, calcium and magnesium.
• Full blood count.
• Plasma glucose before insulin.
• Creatine kinase in suspected rhabdomyolysis.
• Phosphate, urate and lactate dehydrogenase in suspected tumour lysis syndrome.
• A digoxin level when toxicity is possible.
• Cortisol in suspected acute adrenal insufficiency, without delaying steroid treatment in a clinical crisis.

Potassium from a blood gas analyser is useful for rapid triage but should normally be verified. A blood gas analyser cannot detect haemolysis, which is an important cause of a falsely raised potassium [5]. The difference between point-of-care and central measurement is often small, but the sample type and pre-analytical errors can be decisive when the result does not fit the clinical picture [1].

With a clearly hyperkalaemic ECG, circulatory failure or cardiac arrest, treatment must not await the central laboratory result. In a stable patient without risk factors and with an unexpectedly high blood gas potassium, by contrast, a correctly taken repeat sample should take priority before insulin is given.

The ECG in hyperkalaemia

The classical sequence is useful for teaching but is not reliable in the individual patient:

1. Tall, symmetrical, peaked and narrow-based T waves, sometimes with a shortened QT interval.
2. A prolonged PR interval and a reduced P wave amplitude.
3. The P wave disappears.
4. QRS widening.
5. Bradycardia, conduction block, bundle branch block or a junctional escape rhythm.
6. Fusion of the QRS complex and the T wave into a sine wave pattern.
7. Ventricular tachycardia, ventricular fibrillation, pulseless electrical activity or asystole.

Hyperkalaemia can also mimic ST elevation myocardial infarction or a Brugada pattern. QRS widening, marked bradycardia and a junctional rhythm appear to be particularly worrying findings [1,2].

The ECG has low sensitivity and limited specificity. In a retrospective study, fewer than half of the patients with hyperkalaemia had typical changes, while 24 per cent of normokalaemic patients showed at least one finding that could be interpreted as hyperkalaemic [6]. In a more recent study of 1,608 emergency department patients, the sensitivity of physicians' ECG assessment was 39 to 47 per cent and the specificity 76 to 81 per cent [7]. A normal ECG must therefore never be used as grounds for withholding investigation or necessary treatment.

The ECG should chiefly be used to identify cardiotoxicity and to guide the need for calcium, not as a stand-alone diagnostic test for hyperkalaemia. Compare with previous ECGs where possible. New QRS widening or bradycardia in an at-risk patient is more worrying than a previously known bundle branch block pattern.

The treatment sequence

The measures should often be given in parallel. Calcium protects the heart, insulin and salbutamol buy time, while diuresis, potassium binders or dialysis eliminate potassium. The evidence for many emergency measures rests on small studies and physiological endpoints. Randomised trials have as a rule measured the change in potassium, not mortality or arrhythmias [8,9].

An important note on calcium dosing

Ten millilitres of calcium chloride 10 per cent contains approximately three times as much elemental calcium as 10 mL of calcium gluconate 10 per cent. The doses are therefore not interchangeable by volume. About 30 mL of calcium gluconate 10 per cent corresponds approximately to the amount of calcium in 10 mL of calcium chloride 10 per cent [1,2].

Swedish local protocols sometimes use 10 mL of calcium gluconate as the initial dose with rapid repetition according to the ECG response. Follow the locally determined preparation and dose, but be aware of the difference in elemental calcium. If wide QRS complexes or other clear hyperkalaemic changes persist, calcium must be repeated and not regarded as a single dose.

Always check which salt, which concentration and which volume have been prescribed. Confusion between calcium gluconate and calcium chloride can lead to substantial under- or overdosing.

Step 1: stabilise the cardiac membrane with calcium

Indications

Give intravenous calcium immediately in:

• QRS widening judged to be due to hyperkalaemia.
• Loss of P waves or marked conduction disturbance.
• Hyperkalaemic bradycardia or a junctional rhythm.
• Ventricular arrhythmia.
• A sine wave pattern.
• Cardiac arrest in which hyperkalaemia is known or strongly suspected.

Calcium may also be considered at a plasma potassium of at least 6.5 mmol/L if an ECG or monitoring cannot be obtained immediately [1].

Calcium is not needed routinely in every patient with moderate hyperkalaemia and a normal ECG. The potential benefit must be weighed against the risk of extravasation and of overtreatment. The threshold should, however, be low when ECG changes or circulatory compromise are present.

Choice of calcium salt

Calcium gluconate is suitable for a peripheral vein, since the tissue toxicity on extravasation is lower than that of calcium chloride.

Calcium chloride provides more elemental calcium per millilitre and is often used in cardiac arrest or through secure central access. Peripheral administration carries a greater risk of serious tissue injury on extravasation.

With peripheral administration the cannula must be checked carefully. Stop the infusion if there is pain, swelling or suspected extravasation.

Assessing the response

An effect on the ECG should be seen within a few minutes. If the ECG does not improve within 5 to 10 minutes, or if the changes recur, give a further dose. The effect usually lasts 30 to 60 minutes [1,2].

Calcium stabilises the membrane but does not lower the plasma potassium. It must therefore be followed by an intracellular shift and a plan for elimination.

Digitalis and digoxin toxicity

The historical notion that calcium is always contraindicated in digoxin toxicity has weak support. Human studies have not shown increased mortality or more life-threatening arrhythmias after calcium [1,2]. Where acute digoxin toxicity is strongly suspected, a toxicologist or your national or regional poison control centre should be contacted immediately and digoxin antibodies considered. If calcium is required because of life-threatening hyperkalaemic cardiotoxicity, it should not be withheld as a matter of routine, but it can be given more slowly under close monitoring.

In acute digoxin toxicity, hyperkalaemia is a marker of severe poisoning. Digoxin antibodies are the causal treatment and must not be delayed by the discussion about calcium.

Step 2: shift potassium into the cells

Insulin and glucose

Insulin activates the sodium–potassium pump, above all in skeletal muscle, and moves potassium from the plasma into the cells. The effect usually begins within 10 to 20 minutes, is greatest after about 30 to 60 minutes, and can persist for 4 to 6 hours [2,3].

A common adult regimen is:

• 10 units of short-acting or rapid-acting insulin intravenously.
• 25 g of glucose intravenously, for example 50 mL of glucose 500 mg/mL or 250 mL of glucose 100 mg/mL.

Check that the insulin really is prescribed in units and that the correct syringe is used. Confusion between units and millilitres can cause catastrophic overdosing. Standardised prescription templates reduce the risk.

Measure the plasma glucose before treatment. In marked hyperglycaemia the glucose dose may need to be reduced or omitted, but the glucose-lowering effect of insulin remains and monitoring is required in any case. In diabetic ketoacidosis or hyperosmolar hyperglycaemic state, the specific treatment protocol must govern insulin, fluid and potassium monitoring.

Systematic data show that 10 units of intravenous insulin lower the plasma potassium by approximately 0.8 mmol/L after 60 minutes, but the variation is wide. Almost one in five developed hypoglycaemia in the systematic review [10]. A lower insulin dose, for example 5 units or 0.1 units/kg up to 10 units, is used in some protocols for patients of low body weight or with marked renal failure. The evidence is not sufficient for a universal change of dose, and the local protocol should therefore be followed.

Preventing hypoglycaemia

The risk is higher in:

• Renal failure or dialysis treatment.
• A low plasma glucose before treatment.
• The absence of diabetes.
• Low body weight or little muscle mass.
• Repeated doses of insulin.
• Poor nutritional intake.
• Sepsis or liver failure.

With a low or normal baseline glucose, particularly below about 7 mmol/L, a total of 50 g of glucose or a subsequent infusion of glucose 100 mg/mL may be needed according to the local protocol. A prospective study in which patients received 10 units of insulin and 25 g of glucose found hypoglycaemia in 44 per cent within 3 hours, of whom 10 per cent had a glucose below 3.0 mmol/L. The median time to hypoglycaemia was 2 hours [11]. This underlines that an initial dose of glucose does not replace continued monitoring.

Extra glucose must not, however, be given as a matter of routine to markedly hyperglycaemic patients. Marked hyperglycaemia can increase the osmolality and thereby contribute to an extracellular shift of potassium. Glucose treatment must therefore be individualised according to the baseline value and the subsequent measurements.

Salbutamol

Salbutamol stimulates beta-2 receptors and the sodium–potassium pump. Give 10 to 20 mg by nebuliser. This is considerably higher than the usual bronchodilator dose.

The effect begins after about 30 minutes and is usually greatest after 60 to 120 minutes. In small studies, 10 to 20 mg of nebulised salbutamol lowered the plasma potassium by approximately 0.6 to 1.2 mmol/L. The combination with insulin is more effective than either treatment alone [8,9].

Use salbutamol as an adjunct in marked hyperkalaemia, not as sole treatment. Some patients respond inadequately. Beta blockade could theoretically reduce the effect, but the degree is hard to predict in the individual patient. Adverse effects include:

• Tachycardia.
• Tremor.
• Myocardial ischaemia.
• Arrhythmia.
• Hyperglycaemia.
• A raised lactate.

Take care in unstable ischaemic heart disease, marked tachycardia or another ongoing arrhythmia. An intravenous beta-2 agonist causes more cardiovascular adverse effects, and nebulised treatment is therefore usually preferable.

Sodium bicarbonate

Sodium bicarbonate has a small and unpredictable acute potassium-lowering effect in the absence of metabolic acidosis. It must therefore not be used routinely as a substitute for insulin and salbutamol [8,9].

Consider sodium bicarbonate in marked metabolic acidosis, particularly at a pH below about 7.2, if the patient can tolerate the sodium and volume load [2]. The benefit is probably greatest in a mineral acidosis, for example hyperchloraemic acidosis. The effect is less predictable in ketoacidosis and lactic acidosis, since organic anions affect the distribution of potassium differently [12].

Risks:

• Hypernatraemia.
• Fluid overload.
• Metabolic alkalosis.
• A fall in ionised calcium.
• Worsening heart failure.

Check the blood gas and consider measuring the ionised calcium after larger doses. Bicarbonate must not be given through the same line at the same time as calcium, since precipitation can occur.

Step 3: eliminate potassium

An intracellular shift lowers the plasma potassium temporarily but does not change the total body potassium. Rebound can begin as early as 2 to 3 hours later if potassium is not eliminated at the same time [1].

Sodium zirconium cyclosilicate

Sodium zirconium cyclosilicate binds potassium in the gastrointestinal tract and increases faecal excretion. A common correction regimen is 10 g three times daily, according to the licensed dosing of the product and the local protocol.

An effect can be demonstrated within 1 to 2 hours, but the initial reduction is limited. In a meta-analysis the mean reduction after 1 hour was about 0.17 mmol/L [13]. In the ENERGIZE trial of 70 emergency department patients, adding sodium zirconium cyclosilicate to insulin and glucose produced a greater reduction after 2 hours than placebo, but no statistically significant difference after 4 hours. The trial had substantial loss to follow-up and many missing samples [14].

The drug should therefore be regarded as an adjunct for elimination and for reducing rebound, not as a substitute for calcium, insulin or urgent dialysis.

Monitor:

• Fluid status.
• Blood pressure.
• Signs of oedema or worsening heart failure.
• Plasma potassium, since the combination with other treatments can cause hypokalaemia.

The risk of oedema is dose-dependent and is probably related to the sodium content [15]. Separate the drug from other oral preparations according to the current product information and the local protocol.

Patiromer

Patiromer has a slower onset than sodium zirconium cyclosilicate and is chiefly established in subacute or chronic hyperkalaemia. Hypomagnesaemia and gastrointestinal adverse effects can occur. The drug must not replace standard emergency treatment in life-threatening hyperkalaemia [13,16].

Patiromer can bind other drugs in the gut. Check the recommended dosing interval relative to other oral preparations in the current product information.

Older ion exchange resins

Sodium polystyrene sulfonate and calcium polystyrene sulfonate act slowly and unpredictably and are not sufficient as emergency treatment. Randomised data have not shown a definite effect within the first 4 hours [9]. Sodium polystyrene sulfonate has in addition been associated with serious gastrointestinal injury, including colonic necrosis, both with and without sorbitol [17].

Avoid them particularly in:

• Ileus or bowel obstruction.
• Recent bowel surgery.
• Ischaemia or shock.
• Marked constipation.
• Markedly reduced bowel motility.

Older ion exchange resins must not be given as a measure that delays dialysis or creates false reassurance in life-threatening hyperkalaemia.

Loop diuretic

An intravenous loop diuretic can increase renal potassium excretion when the patient has:

• Preserved urine output.
• An adequate intravascular volume.
• Fluid overload or heart failure.

The effect is uncertain in acute kidney injury and absent in anuria. Diuretics must not delay dialysis. Monitor the urine output, fluid balance, creatinine, sodium and magnesium. In hypovolaemic patients the circulation must be restored before diuretics are considered [2].

Balanced crystalloids can be used in hypovolaemia despite containing a small amount of potassium. They do not necessarily cause more hyperkalaemia than sodium chloride, which can cause a hyperchloraemic acidosis and thereby increase the extracellular potassium [18].

The absence of a diuretic response after an adequate dose argues against continued diuretic treatment alone resolving the hyperkalaemia. Contact nephrology at that point and reconsider the need for dialysis.

Dialysis

Haemodialysis is the fastest and most predictable method of removing potassium. Contact nephrology early in:

• Anuria or marked oliguria.
• A dialysis patient with significant hyperkalaemia.
• Persistent or recurrent marked hyperkalaemia despite medical treatment.
• Severe acute kidney injury.
• Marked hyperkalaemia with concomitant severe acidosis or fluid overload.
• Rhabdomyolysis, tumour lysis syndrome, burns or other ongoing tissue breakdown.
• Hyperkalaemia in which rapid and durable elimination cannot be achieved by other means.

Intermittent haemodialysis lowers the plasma potassium within minutes, but rebound can occur after treatment ends as intracellular potassium redistributes into the plasma. Continued or repeated dialysis may be needed with ongoing potassium release [2,18].

Do not give less emergency membrane stabilisation merely because dialysis is planned. Calcium must be given for ECG changes, and insulin or salbutamol may be needed if dialysis cannot be started immediately.

In a dialysis patient who can be dialysed immediately, repeated doses of insulin should be avoided unless they are needed to stabilise the patient. An intracellular shift before dialysis can reduce the amount of potassium immediately available for dialytic removal and contribute to later rebound.

Monitoring after treatment

Plasma glucose

After intravenous insulin:

• Check the plasma glucose before treatment.
• Check every 30 minutes for the first 2 hours.
• Thereafter check at least hourly for up to 6 hours.
• Continue for longer in renal failure, after repeated doses of insulin, with a low baseline glucose, poor nutritional intake or previous hypoglycaemia.

Give glucose immediately in hypoglycaemia and continue monitoring, since the hypoglycaemia may recur. Symptoms may be hard to identify in a patient with a reduced level of consciousness, a sedated patient or one on a beta blocker, which makes scheduled measurements necessary.

Plasma potassium

• Check about 1 hour after insulin and salbutamol.
• Check again after 2 to 3 hours.
• Thereafter continue according to the potassium value, renal function, treatment and the risk of rebound.
• Take a repeat sample sooner if the ECG deteriorates, or in arrhythmia or circulatory compromise.
• Continue monitoring after dialysis, since rebound can occur.

If the plasma potassium does not fall as expected, check that the treatment really has been given, exclude continued potassium administration, and contact nephrology. Consider also ongoing cellular injury, absent urine output, inadequate dialysis access, or a laboratory result that is not comparable with the first sample.

Avoid repeated doses of insulin without planned glucose monitoring. The potassium-lowering effect of insulin may have worn off while the glucose-lowering effect persists.

ECG and other monitoring

Continue continuous ECG monitoring in:

• A plasma potassium of at least 6.5 mmol/L.
• Hyperkalaemic ECG changes.
• A rapidly rising potassium.
• Ongoing tissue breakdown.
• Renal failure requiring dialysis.
• A need for repeated calcium treatment.

Record a new 12-lead ECG after calcium if the original ECG was abnormal. Recurrent ECG changes may mean that the effect of the calcium has worn off before the potassium has been lowered.

Look for and correct the cause

Hyperkalaemia is usually due to several interacting factors. A high potassium intake alone rarely causes marked hyperkalaemia if renal function and the aldosterone system are intact [12].

Diabetes can cause hyperkalaemia through insulin deficiency, hyperosmolality, diabetic kidney disease and hyporeninaemic hypoaldosteronism. Combination with RAAS blockade, an MRA or trimethoprim increases the risk further [19].

Consider urinary tract obstruction in new-onset oliguria, particularly in older patients, after surgery or in neurogenic bladder dysfunction. A bladder scan and, where needed, ultrasound of the kidneys and urinary tract can rapidly identify a treatable cause.

Medication review

Temporarily withdraw drugs contributing to the acute situation. Document explicitly:

• Which drug has been paused.
• Why it has been paused.
• When the potassium and creatinine are to be checked.
• Who is responsible for restarting it.
• What potassium value and what renal function are required before restarting.

RAAS blockade and MRAs improve the prognosis in, among other conditions, heart failure with reduced ejection fraction and proteinuric kidney disease. They must therefore not be stopped permanently without review. Observational studies show an association between a low dose or withdrawal of RAAS inhibitors and worse cardiorenal outcomes, although residual confounding cannot be excluded [20,21].

Newer potassium binders, correction of acidosis, optimised diuretic treatment and more frequent sampling can sometimes make it possible to continue prognostically important treatment [22]. A more recent meta-analysis of randomised trials found that patiromer and sodium zirconium cyclosilicate increased the ability to maintain or optimise RAAS-inhibiting treatment, but the follow-up periods were limited and the effect on mortality remains uncertain [26].

Pseudohyperkalaemia

Suspect pseudohyperkalaemia when:

• The patient has no plausible cause for hyperkalaemia.
• Renal function is normal.
• The ECG is normal and the patient has no symptoms.
• The sample is flagged as haemolysed.
• The potassium value is unexpected or markedly different from previous values.
• There is thrombocytosis or marked leucocytosis.
• The sample was taken with a prolonged tourniquet time or with repeated clenching of the fist.

Common causes are haemolysis during sampling, a thin needle, forceful aspiration, shaking of the tube, a prolonged tourniquet time, repeated clenching of the fist, delayed centrifugation and an unsuitable temperature during transport. Contamination with potassium-containing EDTA, or sampling close to a potassium infusion, are other possible causes.

In thrombocytosis or leucocytosis, comparison between serum, heparinised plasma and rapidly analysed whole blood can be informative [12,23]. Serum potassium is normally somewhat higher than plasma potassium, since platelets release potassium during clotting. The difference can become marked in pronounced thrombocytosis. In extreme leucocytosis, mechanical handling and centrifugation can also damage fragile leucocytes.

Repeat the sample with a short tourniquet time, without pumping the hand, and with rapid transport. A point-of-care blood gas can be valuable but cannot reveal haemolysis [5].

Do not wait for a repeat sample when there are hyperkalaemic ECG changes, circulatory compromise or a strong clinical suspicion. Treating pseudohyperkalaemia in error can, on the other hand, cause dangerous hypokalaemia, and clinically stable patients without risk factors should therefore have the value verified before aggressive treatment.

Special situations

BRASH syndrome

Think of BRASH in the combination of:

• Marked bradycardia.
• Acute deterioration in renal function.
• Treatment with an AV nodal blocking drug, usually a beta blocker, verapamil or diltiazem.
• Hypotension or shock.
• Hyperkalaemia, which is sometimes only moderate.

Hyperkalaemia and accumulation of AV nodal blocking drugs reinforce one another. The bradycardia may therefore be disproportionately marked in relation to the potassium value. In a systematic review, more than half had a plasma potassium below 6.5 mmol/L, while the mean heart rate was 36 beats per minute [24].

Treat the hyperkalaemia, pause AV nodal blocking drugs, correct hypovolaemia where present, and provide circulatory support. Atropine may have limited effect, since the mechanism is not primarily vagal. Adrenaline or another catecholamine may be needed to support the rate and perfusion. Pacing or dialysis may become necessary, but a permanent pacemaker is rarely needed once the metabolic and pharmacological cause has been corrected.

Diabetic ketoacidosis and hyperosmolar hyperglycaemic state

The plasma potassium can be high despite a marked total body deficit. Insulin deficiency and hyperosmolality move potassium out of the cells, while osmotic diuresis causes large total body losses of potassium. Insulin treatment, fluid and correction of the acidosis can therefore lower the plasma potassium rapidly.

Follow the specific protocol for ketoacidosis or hyperosmolar hyperglycaemic state. As the plasma potassium falls, potassium replacement may be needed even though the initial value was high [19]. Potassium binders and dialysis must not be used routinely on the basis of an initially high potassium alone if the patient has a marked total body potassium deficit and is responding to standard treatment.

Rhabdomyolysis and tumour lysis syndrome

The potassium may continue to rise despite an initial response to treatment. Repeat the samples frequently and contact nephrology early. A temporary fall after insulin does not exclude the need for dialysis.

In tumour lysis syndrome, phosphate, calcium, urate, creatinine and fluid balance are also monitored. In rhabdomyolysis, creatine kinase, creatinine, calcium, phosphate, acid–base status and urine output are monitored. Oliguria, acidosis and continued tissue breakdown lower the threshold for dialysis.

The dialysis patient

Contact the dialysis unit or nephrology immediately. Establish:

• The most recent dialysis session and any missed treatment.
• The type of dialysis and the prescribed schedule.
• Access function.
• The most recent post-dialysis potassium.
• Diet and use of salt substitutes.
• Constipation.
• Medication.
• Signs of ongoing cellular injury or bleeding.

If dialysis can be started immediately it is definitive treatment, but give calcium for ECG changes and use temporising treatment if a delay is expected. Continue potassium monitoring after dialysis because of the risk of rebound.

Acute adrenal insufficiency

Consider adrenal insufficiency in hyperkalaemia combined with hypotension, hyponatraemia, hypoglycaemia, abdominal symptoms or known steroid treatment. Take a cortisol level if this can be done without delay, but do not delay hydrocortisone and fluid treatment in a clinical adrenal crisis.

Red flags

The following findings warrant immediate senior assessment and often contact with intensive care or nephrology:

• A plasma potassium of at least 6.5 mmol/L.
• A rapidly rising plasma potassium.
• QRS widening, loss of the P wave or a sine wave pattern.
• Bradycardia, a junctional rhythm, high-grade AV block or ventricular arrhythmia.
• Syncope, shock or cardiac arrest.
• Marked muscle weakness or progressive paralysis.
• Anuria or marked oliguria.
• Severe acute kidney injury.
• Rhabdomyolysis, tumour lysis syndrome or massive tissue injury.
• Recurrent hyperkalaemia after an initial response to treatment.
• An inadequate response to insulin and salbutamol.
• A need for repeated doses of calcium.
• Severe metabolic acidosis or concomitant pulmonary oedema.
• Suspected digoxin toxicity.
• Marked bradycardia during treatment with an AV nodal blocking drug.

Common pitfalls

• Being reassured by a normal ECG. The ECG can be normal even in marked hyperkalaemia [6,7].
• Treating on the basis of the ECG alone. Typical findings also occur in normokalaemic patients.
• Delaying treatment while awaiting a repeat sample. Treat first when there are ECG changes or circulatory compromise.
• Treating an unexpected blood gas potassium aggressively in a stable low-risk patient without verification. Blood gas analysers cannot detect haemolysis.
• Giving too small a dose of calcium. Calcium gluconate and calcium chloride contain different amounts of elemental calcium.
• Confusing calcium gluconate with calcium chloride. Check the salt, the concentration, the volume and the route of access.
• Giving calcium and then waiting. Calcium does not lower the plasma potassium.
• Giving insulin without planned glucose checks. Hypoglycaemia can occur several hours later.
• Repeating insulin too frequently. A cumulative insulin effect can cause serious hypoglycaemia.
• Giving extra glucose as a matter of routine in marked hyperglycaemia. This can worsen the hyperosmolality.
• Using salbutamol as sole treatment. The response is variable.
• Giving bicarbonate routinely in the absence of metabolic acidosis. The effect is then small and the sodium load can do harm.
• Regarding potassium binders as immediate rescue treatment. They do not replace calcium, insulin or dialysis.
• Giving older ion exchange resins in ileus or when there is a risk of bowel ischaemia.
• Giving diuretics to an anuric or hypovolaemic patient and then waiting for an effect.
• Not planning for elimination. Rebound is to be expected after temporising treatment.
• Permanently stopping prognostically important RAAS blockade without a plan for restarting it.
• Missing BRASH. Marked bradycardia can occur even with moderate hyperkalaemia.
• Missing pseudohyperkalaemia. Unnecessary treatment can cause life-threatening hypokalaemia.
• Using suxamethonium in a high-risk patient. Suxamethonium can raise the plasma potassium and should be avoided in known hyperkalaemia, extensive burns, denervation, prolonged immobilisation and other states of receptor upregulation [2].
• Stopping monitoring as soon as the potassium has normalised. Rebound and late hypoglycaemia can occur after an initial response to treatment.

Discharge and continuing plan

Discharge from emergency care should be considered only when:

• The plasma potassium has fallen and is stable on repeat measurement.
• The ECG is stable.
• No significant rebound is expected.
• The cause has been identified or sufficiently investigated.
• Potassium-raising drugs and supplements have been dealt with.
• Renal function is stable.
• Repeat sampling has been arranged.
• The clinician responsible for follow-up has been identified.
• The patient is able to follow instructions and to seek help promptly if they deteriorate.

Patients who have required intravenous calcium, repeated doses of insulin, urgent dialysis or treatment for marked ECG changes should as a rule not be discharged directly from the emergency department.

Recurrence is common. In patients with heart failure, hyperkalaemia recurs in approximately one quarter to two fifths of cases, and the risk increases after every episode [25]. The timing of follow-up must therefore be individualised. After moderate or severe hyperkalaemia, a check within 24 to 72 hours is often needed, and sooner in renal failure, when a risk factor persists, or after a change of medication.

Dietary advice should be targeted and not consist merely of a general restriction of fruit and vegetables. Ask specifically about:

• Potassium supplements.
• Salt substitutes containing potassium chloride.
• Concentrated fruit juices and smoothies.
• Nutritional drinks.
• Dried fruit.
• Large quantities of nuts.
• Processed foods with potassium additives.
• Dietary supplements and herbal remedies.

In chronic kidney disease a dietitian with renal expertise should be involved. The evidence for broad and strict potassium restriction is limited, and unnecessarily restrictive advice can worsen nutrition. Modern guidance instead emphasises individualised advice, treatment of constipation, correction of metabolic acidosis, and reduction of readily absorbed potassium additives in processed food [22,27].

References

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