Pseudohypokalemia

Pseudohypokalemia is seen in

A. Conn’s syndrome

B. Diabetic ketoacidosis

C. Sampling errors

D. Cushing’s syndrome

ANSWER

C. Sampling errors.

Sampling errors – particularly if a blood sample is taken upstream of an infusion of saline, dextrose, or other fluids that contain little or no potassium.

Most common cause of ‘Pseudohypokalemia’

A. Diarrhea

B. Excessive perspiration

C. Muscle-crush injury

D. Acute leukemia

ANSWER

D. Acute leukemia.

Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells in a blood sample after it has been drawn.

What is ‘Pseudohypokalemia’?

Pseudohypokalemia – serum potassium decreases, artifactually, after phlebotomy.

Pseudohypokalemia is a decrease in the amount of potassium that occurs due to excessive uptake of potassium by metabolically active cells in a blood sample after it has been drawn.

It is a laboratory artifact that may occur when blood samples remain in warm conditions for several hours before processing

What is the most common cause of ‘Pseudohypokalemia’?

Most common cause of ‘Pseudohypokalemia’ is acute leukemia.

Large numbers of abnormal leukocytes take up potassium when the blood is stored in a collection vial for prolonged periods at room temperature.

How pseudohypokalemia is diagnosed?

Rapid separation of plasma and storage at 4° C is used to confirm this diagnosis

This method should be used for subsequent testing once pseudohypokalemia is diagnosed, to avoid this artifact leading to inappropriate treatment.

What is seasonal pseudohypokalemia?

It is found to increase during the summer season- seasonal pseudohypokalemia.

The activity of sodium-potassium exchange ATPase is increased by an increase in the temperature and presence of glucose.

Prolonged exposure of the blood sample to a higher than normal temperature stimulates the metabolism of glucose (blood sugar) thus increasing the uptake of potassium by the cells due to activation of the sodium-potassium exchange ATPase.

There is an increased incidence of pseudohypokalemia during the summer (seasonal pseudohypokalemia) in samples from primary care.

This is an in vitro pseudo-phenomenon mediated by sodium-potassium-exchanging-ATPase.

What is the mechanism of action of Sodium-potassium exchange ATPase?

Na+K+-ATPase pump helps to maintain osmotic equilibrium and membrane potential in cells.

The sodium and potassium move against the concentration gradients.

The Na+ K+-ATPase pump maintains the gradient of a higher concentration of sodium extracellularly and a higher level of potassium intracellularly.

Sodium-potassium exchange ATPase – an enzyme present on the outer surface of a cell that helps in maintaining a proper concentration of sodium and potassium ions within and outside of the cell.

1) What is pseudohypokalemia?

A) True low plasma potassium causing weakness

B) Artifactual low serum potassium due to in vitro factors or handling

C) Low potassium caused by diuretic overuse only

D) A form of hyperaldosteronism

Pseudohypokalemia is a lab artifact — measured K is low but true plasma K is normal.

2) Which blood sample artifact commonly causes pseudohypokalemia?

A) Hemolysis releasing intracellular K

B) In vitro uptake of K by very high WBC or platelets

C) Lipemia interfering with the assay

D) High plasma free hemoglobin

Marked leukocytosis or thrombocytosis can lower measured serum K via cellular uptake or processing artifact.

3) Which CBC finding raises suspicion for pseudohypokalemia?

A) Mild anemia

B) Normal platelet and WBC counts

C) Very high WBC (>50×10^9/L) or platelets (>1000×10^9/L)

D) Isolated lymphopenia

Extremely elevated cell counts predispose to in vitro K shifts in the tube.

4) A clue that low K is pseudohypokalemia is:

A) Normal ECG and no hypokalemia symptoms

B) Prominent U waves on ECG

C) Muscle weakness and ileus

D) Constipation

If ECG and clinical picture don’t fit, consider lab artifact and repeat with proper handling.

5) Best initial test to confirm pseudohypokalemia?

A) 24-hour urine potassium

B) Repeat K on plasma (heparin tube) processed immediately

C) Serum magnesium

D) Oral potassium load

Plasma K on promptly processed heparinized sample avoids in vitro uptake seen in serum/clotted samples.

6) Delayed processing affects potassium measurement by:

A) Causing hemolysis and falsely high K

B) Allowing cells to uptake K, lowering measured K

C) Increasing plasma glucose

D) Reducing platelet count

If blood sits at room temp, metabolically active cells take up K, causing artifactual low values.

7) Which sample type is least likely to show pseudohypokalemia?

A) Serum (clotted tube)

B) Arterial whole blood (on ABG analyser immediately)

C) Serum sent with long transport

D) Clotted tube left at room temp

Bedside arterial blood gas potassium measured immediately avoids in vitro artifacts.

8) Which condition can cause ‘cold-aggravated’ familial pseudohypokalemia?

A) Inherited RBC membrane K transport defect

B) Gitelman syndrome

C) Liddle syndrome

D) Bartter syndrome

Rare familial forms involve temperature-sensitive RBC K flux leading to low sample K when cooled.

9) Which action is safest when pseudohypokalemia is suspected?

A) Give IV potassium immediately

B) Repeat potassium on plasma and check ECG

C) Start oral potassium supplements without repeat

D) Ignore the lab value

Confirm true hypokalemia before replacement to avoid dangerous hyperkalemia.

10) Thrombocytosis affects potassium measurement because:

A) Platelet activation/release during clotting alters serum K

B) Platelets consume K in vivo only

C) Platelets cause assay interference always increasing K

D) Platelets have no effect

During clotting, platelets can release or alter K levels causing spurious results in serum.

11) Which lab should be notified if pseudohypokalemia is suspected?

A) Microbiology

B) Clinical chemistry/biochemistry

C) Hematology only

D) Blood bank

Clinical chemistry can advise on appropriate sample type and rapid processing.

12) Which electrolyte finding would you expect if true hypokalemia existed?

A) Tall peaked T waves

B) U waves and flattened T on ECG

C) Short QT interval

D) PR prolongation

ECG changes such as U waves and T flattening support true hypokalemia.

13) Which transport process in circulating cells causes in vitro K uptake?

A) Na+/K+ ATPase activity in metabolically active leukocytes

B) Passive diffusion only

C) Chloride channel opening

D) K efflux pumps

Metabolically active cells continue to transport ions in collected blood, causing artefactual shifts.

14) How does using plasma (heparin tube) help?

A) Prevents clotting-related platelet K changes and allows rapid centrifugation

B) Causes hemolysis

C) Increases pseudohypokalemia risk

D) Is irrelevant

Heparinized plasma reduces cellular K changes seen with serum from clotted tubes.

15) In severe leukemias, measured K may:

A) Be falsely high only

B) Be falsely low due to cellular uptake during clotting

C) Not change

D) Always be artifactual high

High leukocyte counts in leukemia often cause pseudohypokalemia if samples aren’t processed rapidly.

16) Which bedside measure gives the fastest reliable K result?

A) Arterial blood gas analyzer K (immediate)

B) Serum sent to central lab with delays

C) 24-hour urine K

D) Fingerstick glucose

ABG analyzers give rapid potassium measurements minimizing in vitro shifts.

17) If treating suspected true hypokalemia, what is safest?

A) Large IV K bolus without ECG

B) Check ECG and confirm with repeat rapid plasma K before aggressive replacement

C) Ignore ECG and give oral K only

D) Give calcium gluconate

Confirmatory testing and ECG monitoring prevent iatrogenic hyperkalemia and arrhythmia.

18) Which medication can cause true hypokalemia (not pseud) requiring K replacement?

A) ACE inhibitor

B) Loop diuretics (e.g., furosemide)

C) Spironolactone

D) ACE inhibitor with K-sparing

Diuretics can cause genuine renal K loss, differentiating from lab artifacts.

19) Platelet count >1,000×10^9/L commonly affects:

A) Serum potassium more than plasma potassium

B) Plasma potassium more than serum

C) No difference between serum and plasma

D) Only affects sodium

Platelet activation during clotting alters serum K, so serum may be artifactually different from plasma.

20) Key lab instruction to prevent pseudohypokalemia:

A) Use heparinized plasma tube and centrifuge/process immediately

B) Leave blood at room temp for 2 hours

C) Use clotted tube and delay transport

D) Freeze sample before analysis

Rapid processing and appropriate tube choice minimize in vitro K shifts.

Pseudohypokalemia	Anaswers
What is pseudohypokalemia?	Artifactual low serum K caused by in vitro cellular uptake or sample handling.
Main lab clues?	Very high WBC/platelet counts, normal ECG, discrepancy between serum and plasma K.
Best confirmatory test?	Repeat K on heparinized plasma processed immediately or ABG K bedside.
Why avoid immediate IV K?	Risk of iatrogenic hyperkalemia if low K is artifactual.
Key prevention?	Use plasma tubes, rapid centrifugation, and inform lab of high cell counts.

#	Pseudohypokalemia -Fact
1	Pseudohypokalemia is an artifactual low serum potassium measurement.
2	Common in marked leukocytosis and thrombocytosis.
3	In vitro cellular uptake (Na+/K+ ATPase) lowers measured K if sample delays occur.
4	Serum (clotted) samples are more susceptible than plasma to this artifact.
5	Delayed centrifugation/transport increases risk.
6	ECG is often normal in pseudohypokalemia; ECG changes suggest true hypokalemia.
7	Compare serum vs plasma K to identify discrepancy.
8	Arterial blood gas analyzers provide rapid bedside K to minimize artifact.
9	Familial cold-aggravated pseudohypokalemia is rare (RBC membrane transport defects).
10	Platelet counts >1,000×10^9/L can significantly affect serum K.
11	WBC counts >50×10^9/L are a red flag for pseudohypokalemia.
12	Notify the lab when high cell counts are present so they can process appropriately.
13	Do not treat lab K without confirming true hypokalemia (use ECG and repeat testing).
14	Heparinized plasma tubes reduce clotting-related K shifts.
15	Cooling of samples can unmask familial cold-aggravated forms—handle appropriately.
16	Pseudohypokalemia can coexist with true hypokalemia—clinically correlate.
17	Check for hemolysis: hemolysis causes hyperkalemia, not pseudohypokalemia.
18	ABG K is not perfect but is useful for rapid confirmation.
19	Lab assays may vary—consult lab on best sampling practice.
20	Early recognition prevents harmful unnecessary potassium replacement.

"Infographic showing pseudohypokalemia: blood sample delayed → in vitro cellular uptake by leukocytes causes spuriously low lab potassium; recommended actions: repeat on iced heparinized plasma and correlate with ECG."

Pseudohypokalemia