Low potassium (hypokalemia) symptoms

Short answer

Hypokalemia is a fall in serum potassium below the normal range; the NIH defines it as below 3.6 mmol/L and EFSA as below 3.5 mmol/L. ^{[1] [3]} It is rare in healthy people with normal kidney function; it is mostly associated with losses such as diuretics, diarrhea, vomiting and low magnesium, and inadequate food intake alone rarely causes it. This page is not for diagnosis and treatment; assessment belongs to the physician.

At how many mmol/L does hypokalemia begin?

The threshold varies somewhat by source and depends on the laboratory’s reference range. The NIH counts serum potassium below 3.6 mmol/L as hypokalemia; it separates moderate-to-severe hypokalemia as below about 2.5 mmol/L. ^[1] The review by Kardalas and colleagues takes the normal range as 3.5–5.0 mEq/L (for potassium, mEq/L equals mmol/L) and defines below 2.5 as severe, potentially life-threatening hypokalemia; the review’s treatment table separates mild (3.0–3.4), moderate (2.5–2.9) and severe (below 2.5 or symptomatic). ^[2]

Kardalas and colleagues report that mild hypokalemia can be found in about 14% of outpatients who have laboratory tests, and that hypokalemia is found in up to 20% of hospitalized patients but is clinically significant in only 4–5% of them; the NIH reports that it is seen in up to 21% of hospitalized patients, mostly due to diuretics and other medications. ^{[2] [1]}

What are the symptoms?

According to the NIH, mild hypokalemia is characterized by constipation, fatigue, muscle weakness and malaise. Moderate-to-severe hypokalemia (below about 2.5 mmol/L) can cause frequent urination (polyuria), encephalopathy in kidney patients, glucose intolerance, muscle paralysis, respiratory failure and, particularly in people with underlying heart disease, heart rhythm disorders; severe hypokalemia can be life-threatening because of its effects on muscle contraction and therefore on heart function. ^[1]

Kardalas and colleagues report that the severity of clinical symptoms is proportional to the degree and duration of the potassium drop, and that symptoms generally do not appear until potassium falls below 3.0 mEq/L (unless there is a facilitating factor such as a rapid fall or use of digitalis (digoxin)). In the neuromuscular system, leg cramps, weakness, paresis or ascending paralysis; in digestion, constipation or intestinal paralysis; in the heart and vessels, U waves, T wave flattening and ST changes on the ECG, rhythm disorders and heart failure; and in the kidney, in severe cases, rhabdomyolysis can be seen. ^[2]

None of these symptoms is specific to hypokalemia; muscle cramps or malaise can have many other causes. The diagnosis is made by measuring blood potassium, and a symptom alone is not considered evidence of potassium deficiency.

What causes hypokalemia?

According to the NIH, hypokalemia rarely results from low dietary potassium intake alone. Diarrhea causes potassium loss through the intestine, and vomiting causes potassium loss through the kidneys via metabolic alkalosis. Refeeding syndrome (because potassium moves into cells), laxative misuse, diuretic use, clay eating (pica), heavy sweating and dialysis are also among the causes. ^[1] EFSA likewise states that hypokalemia is usually due to increased potassium loss (diarrhea, vomiting, kidney losses) or to potassium shifting into cells (for example in alkalosis), that hypokalemia due to inadequate intake is rare, and that it can be associated with very-low-calorie diets or with increased requirement during recovery from malnutrition. ^[3]

Among medications, the NIH says that loop diuretics such as furosemide and thiazide-type diuretics can cause hypokalemia by increasing urinary potassium loss; that in inflammatory bowel disease (Crohn’s disease, ulcerative colitis) potassium secretion increases and chronic diarrhea increases the loss further. Large doses of laxatives and repeated enema use also increase loss in stool. ^[1]

Kardalas and colleagues list insulin administration, stimulation of the sympathetic nervous system, thyrotoxicosis and familial periodic paralysis, which cause potassium to shift into cells, and also mention endocrine diseases among the causes of hypokalemia. The review states that licorice root, through its active ingredient glycyrrhetinic acid, can reversibly suppress the enzyme 11β-HSD2 and produce the findings of apparent mineralocorticoid excess (AME) (hypertension, hypokalemia), and that people suspected of AME should not consume licorice root. The same review reports that screening for primary aldosteronism (excess aldosterone production by the adrenal gland) is recommended in everyone with hypokalemia that develops spontaneously or with a diuretic together with high blood pressure. ^[2] That is, unexplained low potassium together with high blood pressure may be related not only to diet but also to a hormonal cause, and the physician makes this distinction.

What is the connection with magnesium?

The NIH reports that magnesium depletion can contribute to hypokalemia by increasing urinary potassium loss and, by reducing intracellular potassium, can also increase the risk of heart rhythm disorders. More than 50% of people with clinically significant hypokalemia may have magnesium deficiency; in those with both hypomagnesemia and hypokalemia, both need to be corrected together. ^[1] Kardalas and colleagues likewise state that accompanying magnesium deficiency aggravates hypokalemia and that in this case hypokalemia often does not respond to potassium alone. ^[2] The decision on testing and treatment is individual and is made by the physician.

Detailed guideMagnesium deficiency symptoms and what the test means→

How is it assessed and treated?

Kardalas and colleagues state that an ECG is recommended for everyone with hypokalemia. According to the review, there are two main components to the diagnosis: assessment of urinary potassium excretion (to distinguish kidney losses from other causes) and assessment of acid-base status. The basis of treatment is management of the underlying disease or contributing factors; potassium is replaced, where possible, by the oral route and gradually, and in severe or symptomatic cases and with cardiac involvement it is given intravenously with continuous ECG monitoring. ^[2] Viera and Wouk likewise state that hypokalemia is treated with oral or intravenous potassium, and that severe or symptomatic lowering, abrupt changes and ECG changes require urgent treatment. ^[4] This page does not give the dose or duration of potassium supplementation; the decision on supplementation and follow-up in hypokalemia belongs to the physician.

In which situations is urgent assessment needed?

Marked muscle weakness or paralysis, palpitations and rhythm irregularity, breathing difficulty, malaise after heavy vomiting-diarrhea, or the development of these symptoms together with a known low potassium value may require urgent medical assessment. The risk of rhythm disorders is higher in people with heart disease and in those using digitalis. ^[2]

Detailed guidePotassium guide: functions, reference intakes and supplement safety→ Detailed guideHigh potassium (hyperkalemia): causes, ECG risk and urgent signs→ Detailed guideWhich foods contain potassium? Serving table and the DASH pattern→

Main guide: What is potassium? This guide does not recommend a personal dose.