23rd June 2023

Specific complications

Hyperkalaemia

The degree of hyperkalaemia tolerated by a patient will vary – patients with a chronically raised potassium level may tolerate hyperkalaemia better than those with an acute kidney injury. Additional factors such as a very quick rise in serum potassium, low serum calcium and coexisting acidosis may also exacerbate the problem. The most serious consequence of hyperkalaemia is cardiac dysrhythmias; it is essential to perform an ECG to identify abnormalities from mild changes (peaking or ‘tenting’ of T waves, P wave flattening, prolonged PR interval) to those approaching life-threatening (widening of the QRS complex, sine wave pattern, ventricular fibrillation).

Management of hyperkalaemia focuses on initial stabilisation of the myocardium, followed by measures to lower serum potassium:

• Calcium – intravenous calcium, often in the form of calcium chloride or calcium gluconate, acts quickly to stabilise the myocardium. It should be given if the potassium level is very high (>6.5mmol/L) or if there are ECG changes present; it can be repeated after 5 minutes if there is no ECG improvement. Caution is advised in patients taking digoxin as toxicity can be induced. Time to effect = minutes, duration of effect = <1 hour.
• Insulin and glucose – insulin acts to move potassium into cells. Monitor for and treat any resulting hypoglycaemia. The effect is temporary and can result in rebound hyperkalaemia. Time to effect = 15-30 minutes, duration of effect = 4-6 hours.
• Salbutamol – nebulised beta-2 agonists will act to move potassium into cells. Caution in patients with underlying cardiac disease and note that salbutamol use can increase serum lactate levels. This should be considered in addition to insulin/glucose, not given alone.
• Sodium bicarbonate – serum potassium is inversely related to serum pH, therefore, correcting an acidosis can reduce serum potassium. However, caution should be taken with the accompanying salt and fluid load in a patient at risk of volume overload.
• Diuretics – can be helpful in removing potassium through the urine if a patient has urine output and if there is accompanying volume overload. Note that higher doses of drugs like furosemide will be required as GFR worsens.
• Gut – potassium binders such as calcium Resonium® will exchange other cations (sodium/calcium) for potassium in the gut and aid its removal. They can result in constipation which will reduce efficacy.
• Further steps include ensuring that intravenous fluid prescriptions do not contain potassium, that a dietitian is involved in care to ensure a low potassium diet and that offending drugs such as ACE-inhibitors have been suspended.

Pulmonary oedema

Pulmonary oedema is a significant risk in patients with poor urine output who will be prone to fluid retention. Alongside standard supportive measures, such as oxygen therapy, the mainstay of treatment is diuretics. Patients with renal impairment will often require a high initial bolus dose, which can be continued if it causes a diuresis. However, if a high bolus dose results in no effect, escalation of care will be required (see below).

Metabolic acidosis

A metabolic acidosis can contribute to cardiac instability and hyperkalaemia. If severe, it can be treated with sodium bicarbonate, but this does carry a risk of salt and fluid overload. It is also important to ensure that other causes of metabolic acidosis have been ruled out, e.g. ketoacidosis.