antagonizes the action of potassium on the cell membrane, although it does not reduce the serum potassium level. In general, it is used in intermittent doses for 30-60 minutes and it buys time until other conservative measures take effect or until haemodialysis is available. We describe a patient with severe hyperkalemia treated with a continuous infusion of calcium gluconate.
A 79-year-old woman came in due to reduced dieresis and lower extremity weakness. Five days prior to arrival, a
cardiac catheterisation has been made with placement of 2 stents. The medical history included: ischemic heart disease with 3 myocardial infarctions, dyspnea on minimum effort, diabetes mellitus, chronic renal failure (baseline creatinine 1.5-2 mg/dl), hypertension under treatment with ramipril, obesity and polyarthrosis. Physical examination: BP 130/60 mmHg, afebrile, CA: rhythmic at 60 bpm; PA: rhonchi and isolated crepitants, generalized oedema. Laboratory results: haemoglobin 8.7 g/dl, glucose 173 mg/dl, BUN 249 mg/dl, creatinine 9.31 mg/dl, normal CK and troponin-I, sodium 124 meq/l, potassium 8.89 meq/l, pH 7.3, bicarbonate 17.3 meq/l; following bladder catheterisation, a scant amount of urine was recovered, the analysis of which revealed: SG 1.005, urine protein 30-70 mg/dl, sediment: 4-6 RBC/hpf, leukocyturia. ECG: wide QRS complexes measuring 160-200 milliseconds a 60 bpm and absent P waves. Renal ultrasound: kidneys of normal size without ectasia. Chest x-ray: vascular redistribution. The patient and the family were informed of the severity of the situation and the possible need for dialysis. The family refused haemodialysis and requested conservative treatment that does not cause suffering to space out laboratory testing. The patient was initially administered seguril 250 mg bolus and 20 ml of 10% calcium gluconate over 30 minutes. Later, she was treated with 24-hour continuous infusions of seguril 250 mg, 500 ml of D10W with 10 U of rapid-acting insulin and 250 ml of D5W with 60 ml of 10% calcium gluconate plus oral Resonium ®. A day later, dieresis was 500 ml, potassium 8.59 meq/l, total calcium 9.63 mg/dl; the ECG showed narrow QRS complexes; the treatment ordered was continued. Subsequent progress was good with a progressive increase in dieresis and a reduction in creatinine and potassium. After 3 weeks of hospitalisation, the creatinine was 1.72 mg/dl and the potassium was 4 meq/l.
Once haemodialysis was ruled out in our patient, we considered different conservative measures for her situation.
Hypertonic glucose with insulin temporarily reduces serum potassium by facilitating cell uptake. There are different
guidelines, but hypoglycaemia is not uncommon, which is why infusion of hypertonic glucose solution at a variable
rate (50-75 ml/h)1-3 is recommended after initial treatment, a method that could have exacerbated the patient¿s
hypervolaemia. Sodium bicarbonate can also cause volume overload and its use is also controversial.1,2 β2-antagonists can produce tachyarrhythmia and lead to myocardial ischemia at the dosages needed to reduce potassium.1 In this patient with a significant history of ischemic heart disease, hypervolaemia and anuria, we considered to be less of a risk to use continuous infusion of calcium and wait for restoration of dieresis.
Intravenous calcium antagonises the effects of hyperkalaemia on the heart; on the one hand, it reduces threshold
potential electronegativity, restores the difference between the membrane and reduces myocyte excitability; on the
other hand, it increases the maximum velocity of the action potential and improves cardiac conduction.4 It has been
suggested that continuous calcium infusion will lead to more stable levels and better results than intermittent dosages.5
In summary, continuous calcium infusion is a therapeutic option that may offer advantages over other conservative
treatment measures in extreme patients with severe hyperkalaemia.