Hyperkalaemia

From Ganfyd

A [K+] over 6.5 mmol/l is a medical emergency and should be investigated and treated rapidly. Consult local guidelines on precise emergency management. Be aware that its the plasma potassium that determines toxicity not the usual surrougate of serum potassium

Introduction

If no local guidelines available suggest urgent confirmation at [K+] > 6.0 mmol/l, with ECG, independent sample(in case of haemolysis), and venous blood gas sample (to exclude pseudohyperkalaemia on a serum specimen) and start treating pending confirmation. Below this level decide if problem chronic, subacute or acute, and react in an appropriate timescale.

Potassium is the major intracellular cation.

• Hyperkalaemia is regarded as a plasma [K⁺] > 5.0 mmol/l
• Severe hyperkalaemia is regarded as a plasma [K⁺] > 6.5 mmol/l and is considered to be a medical emergency as it can lead to cardiac arrest.

Clinical

Heart failure patients most at risk of hyperkalaemia are those with[1]: GFR < 45 ml/min - quadruples relative risk Diabetes mellitus - triples relative risk NYHA class III-IV failure - doubles relative risk In hospital practice the following characteristics in order are predictive of fastest evolution of hyperkalaemia. Two or more of these make progression rate even faster[2]. Use of potassium supplements Severe renal failure Use of ACE inhibitors or ARBs Use of potassium-sparing diuretics Diabetes mellitus

Symptoms

• Asymptomatic
• Non specific malaise
• Acute renal failure
• Cardiac arrest presentation

Investigations

Plasma [K⁺]

• Ensure it is not haemolysed and is a fresh sample
• Also look for biochemical evidence of ARF

ECG will show changes

• Tenting of T waves
• P wave amplitude reduced
• lengthened PR interval
• Broadening of QRS
• Ventricular tachycardia
• Ventricular fibrillation

Causes

Hyperkalaemia is always an indication for careful review of recent drug and fluid therapy. Common is ACE or angiotension II inhibitors combined with diuretic (especially potassium retaining ones) and/or NSAIDs.

• Spurious - Check no sample haemolysis and no thrombocytosis. Hyperkalaemia related to increased platelets is easy to detect by looking at a heparinised arterial or venous (blood gas) potassium or sending a lithium heparin plasma sample to the lab.
• Acute renal failure
• Cell damage - trauma, burns, rhabdomyolysis, massive blood transfusion
• Addison's disease
• K⁺ sparing diuretics
  • Spironolactone
  • Eplerenone
  • Amiloride, Co-amilofruse, Co-amilozide, Co-triamterzide, Co-flumactone
  • Triamterene,
• Metabolic acidosis
• Excess IV or Oral K⁺ (Some antacids introduce a fair potassium load)
• genetic
  • Hyperkalemic periodic paralysis
• Pseudohyperkalaemia can be caused by thrombocytosis
• Reverse pseudohyperkalaemia can be caused by heparin used to collect plasma lysing sensitized blood cells.

Treatment

Calcium resonium is powerful and patients have had a hypokalaemic cardiac arrest from 72 hours treatment when the acute cause of the hyperkalaemia was removed on presentation

1. Remove underlying cause.
2. Calcium (either as gluconate or chloride) gives cardioprotection (but does not lower K⁺)
3. Insulin + glucose to shift K⁺ back into cells
4. Salbutamol nebuliser will also shift K⁺ back into cells
5. Binding resins such as calcium resonium
6. Haemofiltration and Dialysis

Cochrane has published a systematic review on emergency interventions for hyperkalaemia [1]. They conclude that inhaled or nebulised, or IV insulin-and-glucose are the first-line therapies for the management of emergency hyperkalaemia that are best supported by the evidence. In combination they may be more effective than either alone, and should be considered when hyperkalaemia is severe. In the presence of arrhythmias anecdotal evidence suggests that IV calcium is effecting in treating arrhythmia.

External links

Guidelines for the treatment of hyperkalaemia in adults.

References