Introduction

Hyperkalaemia is a potentially life-threatening condition that can be difficult to diagnose because of a paucity of distinctive signs and symptoms. Physicians must have a high index of suspicion as hyperkalaemia can lead to sudden death from cardiac arrhythmias. Any suggestion of hyperkalaemia requires an immediate electrocardiogram (ECG) to ascertain whether electrocardiographic signs of electrolyte imbalance are present.

Case report

A 72 years old gentleman was diagnosed with ischaemic heart disease, congestive heart failure, mild renal impairment and gout 5 years ago. Percutaneous transluminal cardioangioplasty was done for his triple vessels disease 2 years later. In a cardiac rehabilitation programme, he received comprehensive education, and exercised regularly under close supervision. His medication included digoxin 62.5mcg daily, furosemide 80mg daily, isosorbide mononitrate 60mg daily, atorvastatin 10mg daily, aspirin 80mg daily, and perindopril 8mg daily. Since then, he had been admitted to hospital six times for congestive heart failure secondary to ischaemic heart disease. The latest echocardiography one year ago showed a dilated left ventricle with markedly impaired function (ejection fraction of <10%), mild mitral regurgitation and moderate tricuspid regurgitation compatible with ischaemic dilated cardiomyopathy. Spironolactone 25mg daily and carvedilol 3.125mg daily were added to optimise the regime. Renal function was monitored (sodium 135mmol/L, potassium 4.4mmol/L, urea 13.7mmol/L, creatinine 141ol/L).

Earlier this year, during walking exercise under supervision, he collapsed suddenly. He became unconscious with no detectable pulse and blood pressure. ECG showed ventricular fibrillation (VF). Cardiopulmonary resuscitation (CPR) was started immediately. Defibrillation and antiarrhythmic drugs were given repeatedly to no avail, VF persisted. Meanwhile, he was put on mechanical ventilation and received continuous external cardiac massage. Results of laboratory tests showed sodium 132mmol/L, potassium 7.4mmol/L, urea 23.2mmol/L and creatinine 217ol/L. Continuous dextrose-insulin infusion, ion exchange enema and intravenous sodium bicarbonate were given to correct the hyperkalaemia with repeated monitoring of his potassium levels. The patient finally regained sinus rhythm and measurable blood pressure after he was given a total of 40 units of soluble insulin intravenously and 60g of ion exchange enema. The resuscitation process lasted for three hours.

After resuscitation, he regained consciousness and obeyed commands. Potassium level was around 6.5mmol/L. A further 40 units of soluble insulin infusion was given to bring the potassium down to normal level. On the next day, mechanical ventilation was stopped successfully. All his medications were resumed except perindopril and spironolactone in view of their association with hyperkalaemia. His general condition improved and his renal function was stable: sodium 141mmol/L, potassium 4.5mmol/L, urea 11.2mmol/L and creatinine 102ol/L. Eighteen days later, he was discharged home and continued to participate in the rehabilitation programme.

The patient suffered from refractory VF, which was probably caused by hyperkalaemia. He had mild chronic renal failure, on perindopril and spironolactone, all of which are known to increase the risk of hyperkalaemia. On detailed review of his diet, he disclosed that he took a lot of fruits, about 10 oranges and 5 bananas, every day. Oranges and bananas have high potassium content; one medium orange contains 6.5mmol, one medium banana contains 8mmol.¹ The large amount of fruit intake was likely to contribute to the occurrence of hyperkalaemia in this patient who was already at high risk.

Discussion

There are many causes of hyperkalaemia (Table 1).² The usual daily dietary intake of potassium varies between 80 and 150mmol depending on the amount of fruit and vegetable. Foods with high potassium content are shown in Table 2. Treatment of hyperkalaemia depends on the urgency of the clinical status, potassium level, cardiac symptomatology, and the rate at which the hyperkalaemia evolved. Emergency treatment of hyperkalaemia consists of two phases. The first is to rapidly counteract the effects of hyperkalaemia, and to induce an intracellular shift of the ion, these effects are transient. The second phase is the removal of potassium from the body. Diuresis, ion exchange resin and dialysis are definitive means of eliminating potassium from the body. Concerning the ion exchange resin, more rapid effect is achieved with rectal rather than with oral administration. Each enema should be retained for 30 minutes and may decrease serum potassium level by 0.5 - 2mEq/L.³ Resonium C removes potassium from the body by exchanging it within the gut for calcium. This action occurs in the large intestine, which excretes potassium to a greater degree than does the small intestine. Resin is not selective for potassium. The efficacy of potassium exchange is unpredictable and variable.

• All meats, poultry and fish
• Apricots (fresh more so than canned)
• Avocado
• Banana
• Cantaloupe
• Honeydew
• Kiwi
• Lima beans
• Milk
• Oranges and orange juice
• Potatoes (can be reduced to moderate by soaking peeled, sliced potatoes overnight before cooking)
• Prunes
• Spinach
• Tomatoes
• Vegetable juice
• Winter squash

Schepkens Hans et al. suggested that a combination of angiotensin-converting enzyme inhibitors (ACEIs) and spironolactone should be used with caution and monitored closely in patients with renal insufficiency, diabetes, older age, worsening heart failure, at risk for dehydration, and in combination with other medications that may cause hyperkalaemia.^4-6 Patients with creatinine levels of 120 to 150 ol/L represent a loss of glomerular filtration function of more than 50%.⁷ Perazella, Mark A. cited that the high rate of polypharmacy also contributed to hyperkalaemia. In addition, many patients ingest over-the-counter medicines, nutritional supplements, and unknown herbal remedies in an unregulated fashion, which can further increase the risk of serious hyperkalaemia. Doctors must recognise the patients at risk of hyperkalaemia and avoid medications or drug combinations that may exacerbate the problem. Patients should be educated to avoid non-prescriptive sources of potassium supplements.⁸

Our experience with this patient emphasises the importance of obtaining a detailed history in patients who have serious hyperkalaemia that is not readily attributable to acute renal failure, or other known predisposing factors. Patients who are predisposed to hyperkalaemia should avoid eating excess amount of fruit, particularly if they have impaired renal function or are taking medications with potassium sparing effects such as ACEIs and angiotensin II antagonists. Starting CPR promptly in case of cardiac arrest has been proven to be effective in improving the outcome of prolonged VF.⁹ It is also important to monitor the renal function closely if they are taking ACEIs, potassium sparing diuretics and/or angiotensin II antagonists.

Key messages

1. Treatment of hyperkalaemia depends on the urgency of the clinical status.


2. A combination of ACEIs and spironolactone should be used with caution and monitored closely in patients with renal insufficiency, older age, and in combination with other medications that may cause hyperkalaemia.


3. Doctors must recognise the patients at risk of hyperkalaemia and avoid medications or drug combinations that may exacerbate the problem.


4. Patients should be educated to avoid non-prescriptive sources of potassium supplements.

References