Investigations

1st investigations to order

serum potassium

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Result
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Order serum potassium in all patients.[12]​ In an emergency setting, measure potassium using arterial or venous blood gas while waiting for the results from formal laboratory measurement.[1]

There is no universally accepted definition of hyperkalaemia. However, many guidelines use a threshold of serum potassium ≥5.5 mmol/L (≥5.5 mEq/L) and the European Resuscitation Council classification of severity of hyperkalaemia, which is as follows:[1][2][3]

  • 5.5 to 5.9 mmol/L (5.5 to 5.9 mEq/L) - mild

  • 6.0 to 6.4 mmol/L (6.0 to 6.4 mEq/L) - moderate

  • ≥6.5 mmol/L (≥6.5 mEq/L) - severe.​​​​​​​

Note that Kidney Disease: Improving Global Outcomes (KDIGO) uses a similar scale but also adds ECG changes to categorise severity; according to the KDIGO scale, mild hyperkalaemia with ECG changes increases the severity level to moderate, and moderate hyperkalaemia with ECG changes increases the severity level to severe.[4]

For more information on severity thresholds, see Criteria.

It is useful to know whether serum or plasma was used for potassium measurement. Plasma potassium concentrations are on average usually 0.1 to 0.4 mmol/L (0.1 to 0.4 mEq/L) lower than serum levels due to release of potassium from platelets during coagulation.[1]

If serum potassium is elevated, exclude pseudohyperkalaemia and spurious hyperkalaemia.[1][2]​​​​​ Assess the probability of these by reviewing the medical history (e.g., for diabetes, heart failure, chronic kidney disease), drug history, and other blood results (e.g., FBC).[2] 

Result

mild: 5.5 to 5.9 mmol/L (5.5 to 5.9 mEq/L); moderate: 6.0 to 6.4 mmol/L (6.0 to 6.4 mEq/L); severe: ≥6.5 mmol/L (≥6.5 mEq/L)

12-lead ECG

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Obtain an urgent 12-lead ECG in all hospitalised patients with a serum potassium level of ≥6.0 mmol/L (≥6 mEq/L; or use the threshold in your local protocol) to assess for changes associated with hyperkalaemia, which can help to determine the urgency and type of treatment required.[1][2]

Note that the ECG is often normal in hyperkalaemia.[12]​​​ If hyperkalaemia-related changes are present, they may correlate with the severity and rate of rise of serum potassium.[1][4]​​ ECG changes may progress from peaked T waves to prolonged PR interval and progressive widening of QRS complex, followed by sine wave patterns, ventricular fibrillation, and asystole.[4]

However, be aware that ECG changes are dependent on a variety of other factors (e.g., concurrent electrolyte abnormalities, acid-base status, prior cardiac injury), and relying on or expecting progressive ECG changes with increasing severity of hyperkalaemia may be misleading and potentially dangerous.[2]

[Figure caption and citation for the preceding image starts]: ECG changes in people with hyperkalaemiaBMJ 2009; 339:b4114. Copyright ©2009 by the BMJ Publishing Group [Citation ends].com.bmj.content.model.Caption@564e1c4

Result

tall peaked T waves, shortened QT interval, ST segment depression, prolonged PR interval, disappearing P wave, widening of QRS (progressive QRS widening may be seen with higher levels of hyperkalaemia), amplified R wave, arrhythmias (atrial fibrillation, bradycardia, ventricular tachycardia)

blood gas

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Order if metabolic acidosis is suspected.

In addition, in an emergency setting, measure potassium using arterial or venous blood gas while waiting for the results from formal laboratory measurement.[1]

Result

pH <7.35, low bicarbonate, and/or marked increase in serum anion gap indicates metabolic acidosis

FBC

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Result
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Order (or review a recent) FBC if you suspect pseudohyperkalaemia (due to potassium released from blood cells during in vitro coagulation) to exclude a haematological disorder.[1]​ Hyperkalaemia in the setting of significantly elevated white cell count or platelet count with no obvious risk factor for hyperkalaemia (i.e., normal renal function, no ECG changes) indicates pseudohyperkalaemia.

Result

no significant leukocytosis or thrombocytosis

plasma glucose

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Result
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Always order plasma glucose to exclude hyperglycaemia, which causes cellular redistribution of potassium. Useful in patients with known or suspected diabetes and when diabetic ketoacidosis is likely.

Result

elevated in poorly controlled diabetes or diabetic ketoacidosis

renal chemistry

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Result
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Always order to check for kidney dysfunction as a cause of hyperkalaemia, and to exclude cellular redistribution of potassium due to metabolic acidosis. Includes, in addition to potassium as discussed above, sodium, chloride, bicarbonate, urea, and creatinine.

Result

creatinine, urea (elevated if kidney dysfunction present); bicarbonate (low if metabolic acidosis present)

serum calcium

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Result
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Always order serum calcium. Check for hypocalcaemia because this will potentiate the toxicity of hyperkalaemia.[69]​ Calcium will also be low in rhabdomyolysis, which is a cause of hyperkalaemia.

Result

baseline level; low in rhabdomyolysis

Investigations to consider

uric acid and phosphorus

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Result
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Order uric acid and phosphorus if there is history of malignancy and/or treatment is being initiated for malignancy to check for tumour lysis syndrome.​[70]

Result

elevated in tumour lysis syndrome

creatine kinase

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Result
Test

Order creatine kinase if rhabdomyolysis is a possibility.[64][65]​​

Result

elevated if rhabdomyolysis present

serum digoxin level

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Result
Test

Order if the patient is taking digoxin or if suicide is known to have been attempted with digoxin ingestion.​

Result

normal or elevated

cortisol and aldosterone levels

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Result
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Order cortisol and aldosterone levels if you suspect mineralocorticoid deficiency (e.g. primary adrenal insufficiency [Addison's disease]) and other potential causes of hyperkalaemia have been excluded.

Result

normal or low

24-hour urine potassium excretion

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Result
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Consider 24-hour urine potassium excretion to distinguish renal from extrarenal causes of hyperkalaemia. However, urinary potassium measurements may prove difficult to interpret because multiple factors influence these values independent of level of renal function.

Result

<20 mmol/L (<20 L mEq/L) indicates renal cause of hyperkalaemia; >40 mmol/L (>40 mEq/L) indicates extrarenal cause of hyperkalaemia

plasma and urine potassium and osmolality

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Plasma and urine potassium and osmolality is used to calculate transtubular potassium gradient (TTKG). Calculate TTKG if values from 24-hour urine potassium secretion are difficult to interpret. TTKG (TTKG = [K+] urine/(U/P)osm/plasma K+) corrects urinary potassium for changes in osmolality that occur with absorption of water in the collecting duct. TTKG can identify impaired distal tubular secretion of potassium, which can be secondary either to hypoaldosteronism or to aldosterone resistance.

For this formula to be accurate, urine osmolality should be equal to or greater than plasma osmolality and urine sodium should be greater than 25 mmol/L.[71]​​

Result

<7 suggests impaired distal tubular secretion of potassium; >10 suggests increased intake and intact distal tubular handling of potassium

urine pH

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Result
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Order urine pH if you suspect renal tubular acidosis, which is suggested by inappropriately elevated value (pH >5.5) in the setting of hyperchloraemic metabolic acidosis.​[66][67][68]

Result

urine pH >5.5 in renal tubular acidosis

plasma renin activity

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Result
Test

Measure plasma renin activity if you suspect pseudohypoaldosteronism.

Result

usually elevated in pseudohypoaldosteronism

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