Pseudohyperkalaemia

Also known as: Pseudohyperkalemia, Spurious hyperkalaemia, Factitious hyperkalaemia

Pseudohyperkalaemia is a spuriously raised serum potassium caused by potassium release from cells after the blood sample is taken, rather than any true elevation in the patient. It matters because treating it is both unnecessary and potentially harmful: a patient given insulin, calcium and a potassium binder for a laboratory artefact gains only the risk of hypoglycaemia and hypokalaemia.

Recognised causes include haemolysis during difficult venepuncture, prolonged tourniquet time, fist clenching during sampling, delayed sample processing or transport, sample refrigeration, and marked thrombocytosis or leucocytosis, where potassium is released from the very high cell mass during clotting.

The essential clinical judgement is whether the result fits the patient.

A high potassium in a well patient with entirely normal renal function, no relevant drugs and a completely normal ECG should prompt suspicion before it prompts treatment
Ask the laboratory whether the sample was haemolysed, which is the single most useful piece of information and is usually flagged automatically
Review the FBC: a platelet count above roughly 500 × 10⁹/L or a very high white cell count supports pseudohyperkalaemia by this mechanism
Repeat the sample with good technique: free-flowing venepuncture, minimal or no tourniquet, no fist clenching, prompt transport to the laboratory without refrigeration
A plasma sample (lithium heparin, which does not clot) rather than a serum sample avoids the clot-related potassium release seen in thrombocytosis, and is the definitive way to resolve the question in patients with high platelet counts
A venous or arterial blood gas gives a rapid potassium result on a heparinised sample and is a practical immediate cross-check

Crucially, none of this should delay treatment when the patient is unwell, the ECG is abnormal, or the clinical context makes genuine hyperkalaemia plausible. Suspicion of an artefact is not a reason to ignore a dangerous result — it is a reason to confirm it quickly while remaining prepared to treat.

Do not treat a suspected artefact in a well patient with a normal ECG and no plausible cause; repeat the sample correctly instead
Where there is genuine doubt, treat as real hyperkalaemia while the repeat is processed, since the consequences of missing true hyperkalaemia far outweigh those of a single unnecessary dose of calcium
Correct the sampling technique for future draws, and document the tendency in the notes for patients with known thrombocytosis or difficult venous access, so the same investigation is not repeated at every admission
In patients with myeloproliferative disease and persistent pseudohyperkalaemia, arrange for potassium to be measured on plasma or blood gas samples routinely
Communicate clearly with the laboratory, since flagging the clinical question often produces a faster and more useful answer than simply resending the sample

Referral: haematology if an unexplained marked thrombocytosis or leucocytosis is newly identified during the workup.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Hypokalaemia

Also known as: Hypokalemia, Low potassium

Hypokalaemia is a serum potassium below the reference range, graded as mild (3.0–3.4 mmol/L), moderate (2.5–2.9 mmol/L) and severe (<2.5 mmol/L).

It is among the commonest electrolyte abnormalities in hospital practice and is a well recognised precipitant of arrhythmia, particularly in patients on digoxin or with underlying cardiac disease.

Causes include renal loss (diuretics, particularly thiazides and loop diuretics, hyperaldosteronism, Cushing's syndrome, renal tubular acidosis, Bartter and Gitelman syndromes, hypomagnesaemia), gastrointestinal loss (vomiting, diarrhoea, laxative misuse, fistulae, villous adenoma), transcellular shift (insulin, beta-agonists, alkalosis, refeeding, thyrotoxic periodic paralysis) and, less commonly, inadequate intake alone.

Frequently asymptomatic, particularly with mild or gradually developing hypokalaemia, and detected incidentally
Neuromuscular: weakness (typically proximal and ascending), fatigue, cramps, myalgia, and in severe cases paralysis and respiratory muscle involvement
Gastrointestinal: constipation, abdominal distension, and ileus
Cardiac: palpitations and arrhythmia, with ECG changes including T wave flattening, ST depression, and prominent U waves, and, in severe cases, ventricular ectopics, ventricular tachycardia and torsades de pointes
Renal: polyuria and polydipsia from a nephrogenic diabetes insipidus effect, and, in prolonged hypokalaemia, structural tubular changes
Rhabdomyolysis in severe depletion

Symptoms correlate poorly with the absolute value, and severe weakness or arrhythmia can occur at levels that seem only moderately low, particularly if the fall has been rapid.

Correcting magnesium is the step most often missed and the commonest reason potassium replacement fails. Hypomagnesaemia promotes renal potassium wasting, and until magnesium is replaced, potassium will continue to be lost no matter how much is given. Check magnesium in every case of hypokalaemia, and replace it in parallel rather than sequentially.

Oral replacement is preferred where the patient is stable, tolerating oral intake, and the deficit is mild to moderate: potassium chloride, in divided doses, with the deficit typically being far larger than the serum value suggests (a fall of 1 mmol/L may represent a total body deficit of 200–400 mmol).

Intravenous replacement is indicated for severe hypokalaemia, symptomatic patients, arrhythmia, or where oral intake is not possible:

Peripheral infusion should not exceed 10 mmol/hour and concentrations above 40 mmol/L are painful and sclerosing
Faster rates (up to 20 mmol/hour) require central access and continuous cardiac monitoring, and are reserved for life-threatening hypokalaemia
Never give potassium as a bolus or undiluted push — this is a well documented cause of fatal cardiac arrest
Use saline rather than dextrose as the carrier where possible, since dextrose stimulates insulin release and drives potassium further into cells

Alongside:

Recheck potassium regularly during replacement, at least every few hours during intravenous correction
Identify and treat the cause: review diuretics, consider hyperaldosteronism in hypokalaemia with hypertension, and consider surreptitious vomiting or laxative use where the cause is unclear
ECG monitoring for severe hypokalaemia
In digoxin-treated patients, maintain potassium in the upper part of the reference range, since hypokalaemia potentiates digoxin toxicity

Referral: endocrinology if hyperaldosteronism or Cushing's syndrome is suspected; nephrology for renal tubular causes or recurrent unexplained hypokalaemia.

Pseudohyperkalaemia

Overview

Diagnosis

Management

Overview

Clinical Features

Management