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We read with interest the problem solving article by Tse et al. looking at the management of infants presenting with hyponatraemia plus hyperkalaemia1. They recommend the administration of intravenous 0.9% NaCl to correct hyponatraemia until oral feeds can be given. We are concerned that this protocol will produce a rise in serum [Na+] faster than recommended. The guidance is that once any acute symptoms have been addressed the rise in serum [Na+] should not exceed 8 mmol/L/day in order to minimise the risk of developing Osmotic Demyelination Syndrome (ODS). Certainly the rise should be less than 10-12 mmol/L in any 24-hour period or 18 mmol/L in any 48-hour period2.
No specific comment is made about the speed of correction of the serum sodium concentration in case 1 other than that there was "gradual resolution of both the hyponatraemia and hypokalaemia". However in case 2 the serum sodium concentration is said to have normalised within 48 hours. The starting sodium concentration was 108 mmol/L and the normal quoted as 133-146 mmol/L so the minimum rate of rise was 12.5 mmol/L/day, exceeding the recommended rate of rise.
As illustrated by the two cases, these patients usually present with extracellular fluid (ECF) contraction and require replacement of the ECF volume deficit. This should be with a fluid that matches the electrolyte composition of the ECF but we tend to only cater for a normal ECF [Na+] and use 0.9% NaCl. However i...
As illustrated by the two cases, these patients usually present with extracellular fluid (ECF) contraction and require replacement of the ECF volume deficit. This should be with a fluid that matches the electrolyte composition of the ECF but we tend to only cater for a normal ECF [Na+] and use 0.9% NaCl. However in patients with hyponatraemia, 0.9% NaCl is hypertonic and tends to lead to a rise in serum sodium concentration in excess of that which is desired. In an acute situation this is usually unavoidable but must be taken into consideration when prescribing further fluids if too rapid a rise in serum [Na+] is to be avoided.
Once euvolaemia has been established a gradual correction of serum [Na+] is best effected by administering a fluid which contains a slightly higher [Na+] than that in the fluids being lost from the body. The main fluid loss, in the absence of diarrhoea or vomiting, is urine. Greater control of the rise in serum sodium concentration is obtained by measuring the [Na+] of the urine and adjusting the [Na+] of the intravenous fluid accordingly. Once the underlying pathology has been corrected, in these two case, by steroid replacement and treatment of urine infection and urinary obstruction, the kidneys will start to hold onto sodium, particularly while hyponatraemic. Fluids containing relatively low concentrations of sodium will then be sufficient to raise the serum sodium concentration.
A more appropriate management scheme is highlighted by a recent case we had:
A 4 month old boy presented with poor feeding. He had been born at 38 weeks gestation and remained well, and growing appropriately for the first few months of life. Antenatal scans had demonstrated hydronephrosis but he had not attended for a post natal scan. A good urinary stream had been observed. Prior to presentation he had been unwell for one week with an URTI and slightly loose stools. He was noted to normally take 6-7 ounces of milk every 3-4 hours.
On admission, he was alert and active, warm and well perfused. Observations: Weight 5.89 kg, Temperature 35.2°C; Pulse 134 bpm; Respiration 36 bpm; O2 saturation 100% in air; Blood pressure 80/47
Examination was unremarkable.
He was initially started on oral Dioralyte and blood sent for routine investigations:
Hb 143 g/L, WCC 19.9x109/L, Na+ 113 mmol/L, K+ 8.1 mmol/L, Urea 24.4 mmol/L, Creatinine 93 µmol/L, CRP 5 mg/L. A venous blood gas revealed a metabolic acidosis: pH 7.25, pCO2 3.0 kPa, BE -17.1, HCO3- 10.1 mmol/L. Urine was positive for leucocytes on dipstick testing. A renal ultrasound was carried out. It showed moderate bilateral hydronephrosis and both ureters were significantly dilated down to the vesicoureteric junction. There was layering of echogenic material in the distal left ureter.
The hyperkalaemia was managed with salbutamol nebulizers, calcium gluconate and sodium bicarbonate (half correction with 28 mmol). A bolus of 10 ml/kg 0.9% NaCl was also given. These equated to a total of 37 mmol of sodium which is already a significant proportion (47%) of the calculated sodium deficit (0.6 × Wt (kg) × (desired serum [Na+] - current serum [Na+]) of approximately 78 mmol.
Antibiotics were started for a presumed urinary tract infection and a urinary catheter passed in case of urethral obstruction.
On consultation with the regional paediatric nephrology team a plan was put in place to achieve a gradual correction of the hyponatraemia over a minimum period of 72 hours. A presumptive diagnosis of type 4 renal tubular acidosis was made while blood was sent to exclude congenital adrenal hyperplasia. The initial urine [Na+] was 54 mmol/L in keeping with an inability to hold on to sodium despite hyponatraemia. As already mentioned, 37 mmol of sodium had already been prescribed so it was important to slow down sodium administration if too rapid a rise in serum [Na+] was to be avoided and to allow the intracellular compartment to adapt to the rise that had already taken place. The intravenous fluid prescribed was therefore 0.45% NaCl + 5% Dextrose at a rate equivalent to urine output + 4 ml/h to cover insensible losses. Four hourly biochemistry was carried out. Six hours into the management the urine [Na+] had dropped to 25 mmol/L and in order to maintain the gradual correction the intravenous fluid was changed to a mixture of 0.45% NaCl and 5% dextrose in a ratio of 2:1, giving a solution containing 50 mmol/L of sodium. This still contained an excess of sodium compared to the fluid being lost from the body, to facilitate correction of the hyponatraemia. After 24 hours the serum [Na+] had risen to 126 mmol/L (still above the ideal) but the curve had flattened with most of that rise taking place in the first 12 hours (reaching 124 mmol/L) due to the initial fluid boluses.
On day 2 oral feeds were started, initially at 10 ml/h and gradually increased as tolerated. The sodium content of formula milk is around 1 mmol/100ml so an intake of 100ml/kg/d gives 1 mmol/kg/d. This was therefore supplemented with an additional 1 mmol/100ml of sodium chloride. By day 3 he was on full feeds and the sodium supplements were stopped on day 4 when the serum [Na+] had reached 131 mmol/L.
It is important to recognise that in the two cases described by Tse et al.1, when the underlying problem is addressed, the kidneys ability to retain sodium will start to recover and continued administration of 0.9% NaCl will produce too rapid a rise in serum [Na+] and risk causing ODS. Healthy kidneys can cut urinary sodium losses to almost zero. Initial resuscitation often gives a significant amount of sodium over a short period of time and it is important therefore to rein back on replacement in order to allow the adaptive mechanisms that the body has put in place, to correct. I would urge clinicians faced with such cases to measure urinary [Na+] and adjust intravenous replacement fluids accordingly.
1. Tse Y, et al. Problem solving in clinical practice: the sick infant with low sodium and high potassium. Arch Dis Child Educ Pract Ed 2020; 0: 1–5.
2. Verbalis JG, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013; 126 (10 suppl 1): S1–S42.