Description of the condition
Hyperkalaemia is defined as an excess concentration of potassium ions in the extracellular fluid compartment. Acute hyperkalaemia, as opposed to chronic hyperkalaemia, occurs over hours to days, and depending on the degree of hyperkalaemia requires rapid treatment. Hyperkalemia occurs in both outpatients and hospitalised patients, often due to kidney failure, drugs or disorders that inhibit the renin-angiotensin-aldosterone axis, insulin deficiency or direct tissue trauma. Patients with hyperkalaemia may experience muscle weakness, fatigue, distal paraesthesias and respiratory depression (Freeman 1993). The most feared consequence of hyperkalaemia is cardiac arrhythmias. Electrocardiogram (ECG) changes include peaked T waves, QRS widening and diminished P waves. Severe hyperkalaemia may lead to a sine wave ECG pattern, ventricular tachycardia, ventricular fibrillation and death (Browning 1981).
Description of the intervention
A number of different pharmacologic interventions are used to treat patients with hyperkalaemia. Intravenous (IV) calcium salts are believed to stabilise the cardiac membrane, thereby reducing the risk of fatal arrhythmias even in the absence of any effect on serum potassium levels (Greenberg 1998; Schwartz 1978). IV bicarbonate lowers the serum hydrogen ion concentration, thereby promoting an intracellular shift of potassium ions in exchange for hydrogen ions. Beta-2 agonists and insulin enhance the activity of the Na-K-ATPase pump in skeletal muscle and drive potassium intracellularly (Williams 1985; Zierler 1987). Diuretics can enhance the loss of potassium from the kidneys. Cation exchange resins are also thought to bind potassium in the intestinal tract and remove it from the body via faecal excretion (Berlyne 1966; Johnson 1976).
The evidence for renal replacement therapy (RRT) will not be discussed in detail in this review. Dialysis is known to be effective in both acute and chronic hyperkalaemia in patients with kidney failure. In an acute situation, the decision to use dialysis depends on the severity and aetiology of the hyperkalaemia, the safety and effectiveness of alternate therapies, as well as availability of dialysis (Evans 2005; Putcha 2007). Pharmacological interventions are used in patients with hyperkalaemia to either prevent the need for dialysis or to prevent complications until dialysis can be performed. In this review, the need for dialysis will be treated as an outcome rather than a treatment (Carvalhana 2006).
Although the evidence for RRT is outside the scope of this review, it is worth noting that dialysis is generally considered the definitive treatment for hyperkalaemia. Conventional haemodialysis causes the most rapid decrease in serum potassium levels. Other forms of dialysis (peritoneal dialysis, continuous venovenous haemofiltration or continuous venovenous haemodialysis) are also effective. The amount of potassium removed during dialysis depends on dialysis duration, dialysate potassium concentration, dialyser membrane, and patient characteristics such as baseline serum potassium (Evans 2005).
Why it is important to do this review
Hyperkalaemia is a commonly encountered, potentially life-threatening clinical event that requires prompt and effective treatment to prevent serious complications. This review will summarise and synthesise the literature published on the pharmacological management of hyperkalaemia to help clinicians best treat their patients. This review is a derivative of a Cochrane systematic literature review first published in 2005 (Clase 2005), but has narrowed the focus to the effectiveness and safety of the pharmacological management of hyperkalaemia in adults.