Potassium
| Type | Recommendation |
|---|---|
| When to deprescribe | |
| CBR |
To minimise potential prescribing cascades and risk of adverse outcomes associated with electrolyte imbalance, especially in people with an increased risk of hyperkalaemia (e.g. renal impairment, concurrent use of medicines affecting serum potassium levels), we suggest deprescribing be offered to older people taking long-term potassium:
|
| Ongoing treatment | |
| CBR |
We suggest continuing potassium in older people with persistent potassium depletion due to causes that cannot be resolved:
provided treatment aligns with the individual's goals and preferences, following informed consent. |
| How to deprescribe | |
| CBR |
We suggest discontinuing potassium without the need for tapering with the possibility of restarting if needed. If tapering is preferred [e.g. for people taking a high dose (i.e. > 1200 mg three times daily) prior to deprescribing], we suggest reducing the dose by 50%* every two weeks to minimise the risk of hypokalaemia. Once the lowest dose is reached, we suggest discontinuing potassium completely. *Tapering can be performed by reducing the dosing frequency. Effervescent tablet formulation is available, presenting additional options for tapering doses. |
| Monitoring | |
| CBR |
We suggest closely monitoring serum potassium concentration with the time frame to be determined by the baseline dose. In general, we suggest reassessing serum potassium concentration once, one week after deprescribing. We suggest periodic monitoring for dietary changes (i.e. intake of potassium-containing foods), and symptoms or signs attributable to hypokalaemia (e.g. muscle weakness, cramps, spasms, fatigue, and palpitations). |
CBR, consensus-based recommendation; GPS, good practice statement
Hypokalaemia is widely defined as a serum potassium concentration of < 3.5 mmol/L [222]. A cross-sectional study reported that hypokalaemia is significantly more prevalent in older people with a diagnosis of hypertension, especially those taking potassium-losing diuretics [222]. In contrast, the incidence of hypokalaemia did not significantly differ between older people with heart failure and those without [222]. Mild-to-moderate hypokalaemia is typically treated with an oral potassium supplement. Enteral preparations are often poorly tolerated due to common gastrointestinal side effects including nausea, vomiting, diarrhoea, and abdominal pain [223].
Refer to the narrative evidence summary, the GRADE Summary of Findings table in the guidelines, and the Technical Report for a complete presentation of the deprescribing evidence based on the GRADE framework (including other factors considered in developing the recommendations).
The benefits of potassium supplements and medicines that increase serum potassium levels must be carefully balanced against the risk of hyperkalaemia, as the risk of hyperkalaemia becomes more pronounced with advancing age and the presence of comorbidities such as chronic kidney disease and diabetes [224].
Maintaining serum potassium within the optimal range is essential as dyskalaemia (encompassing both hypokalaemia and hyperkalaemia) can cause neuromuscular, gastrointestinal, and cardiac abnormalities [225]. In people with heart failure, hypokalaemia is associated with a higher risk of morbidity and mortality [225]. Similarly, both hypokalaemia and hyperkalaemia are linked to increased mortality risks in people with arrhythmias or acute myocardial infarction [226, 227].
People with persistent potassium depletion due to irreversible causes (e.g. advanced liver disease, secondary hyperaldosteronism with renovascular hypertension, gastrointestinal losses) may require ongoing potassium supplementation to maintain adequate levels [228].
The major risk factors for hyperkalaemia are renal impairment, history of diabetes mellitus, adrenal disease and concurrent use of medicines affecting serum potassium levels such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and potassium-sparing diuretics [229]. A common example of a prescribing cascade involves lower extremity oedema, which may occur as a side effect of a calcium channel blocker. Rather than discontinuing the causative medicine, a diuretic is often added, followed by potassium supplementation to counteract diuretic-induced potassium loss [230]. In some cases, the original medication affecting serum potassium levels may be discontinued, yet potassium supplementation is unnecessarily continued as a 'relic' of prior prescribing [231]. In individuals with normal serum potassium levels and no clear ongoing indication, deprescribing may be appropriate to reduce the risk of dyskalaemia.
If potassium is considered suitable to deprescribe, monitoring serum potassium concentration is necessary along with dietary changes (i.e. intake of potassium-containing foods), and symptoms or signs attributable to hypokalaemia [228]. It may be helpful to provide examples of common symptoms of hypokalaemia (e.g. muscle weakness, cramps, spasms, fatigue, and palpitations) when encouraging individuals to self-monitor and report symptoms to their healthcare professionals. As some symptoms are non-specific, many individuals may not recognise that they could be indicative of hypokalaemia.
We identified one before-and-after study related to deprescribing potassium from the systematic review and meta-analysis. The current evidence for deprescribing potassium is based on a single-arm study. Although approximately half of the participants on diuretics for heart failure were able to discontinue potassium without a significant change in their mean erythrocyte potassium level, the certainty of the evidence is of very low certainty due to a surrogate outcome, very small sample size, lack of a comparison group, and other methodological limitations. The evidence at this stage is insufficient to inform evidence-based recommendations.
Key study characteristics and results
Henschke 1981 conducted a before-and-after study that involved 14 male veterans living in a veterans’ care complex who were taking diuretics for heart failure as well as potassium supplements as routine prophylaxis against potassium depletion. All 14 veterans received an average daily potassium content of 100 mEq and had their oral potassium supplements withdrawn [232]. Six weeks after withdrawal of potassium supplements, plasma potassium levels significantly fell by a mean of 0.37 mmol/L (p < 0.001) but there was no significant change in mean erythrocyte potassium level (from 107.3 ± 6.3 mmol/L and 105.7 ± 7.4 mmol/L). No deaths were reported. For a further six weeks after the withdrawal period, seven participants (50%) were given a combination of 25 mg spironolactone (potassium-sparing diuretic) and 25 mg hydrochlorothiazide. Plasma potassium level increased significantly but the erythrocyte potassium level remained unchanged. None of the participants reported adverse effects or symptoms attributable to hypokalaemia during the period of study.
The method of deprescribing was not specified in the study, but it appears to have involved abrupt discontinuation.