Most patients in PICU should have at least daily U+Es checked, and also Magnesium and Calcium. The Na, K and Ca are checked as part of a blood gas, but abnormal values should be verified by sending a lab sample, as the gas machine is less accurate.
Use the tabbed panel below for guidance in dealing with electrolyte and acid-base balance issues
Bear in mind that 'normal' ranges of lab reference results are based on healthy populations. The range that PICU accepts as 'normal' will be different to the range that you are used to. A sodium of 152mmol/l found in a patient on the paeds ward would normally provoke a bit of excitement. On PICU in a patient being prepared for ventilation, the same sodium concentration might only stimulate a yawn.
Click on the appropriate tabbed panels above for advice on the management of common electrolyte problems.
Cause cannot be established without examining the patient and reviewing the drug chart and fluid chart
Most common cause is SIADH - the treatment then is to restrict fluid and sometimes to give frusemide
SIADH is essentially a diagnosis of exclusion. The following are required to make the diagnosis: -
- Serum osmolality <270
- Urine concentrated (>100mosm/kg)
- Clinical euvolaemia
- Increased urinary [Na]
- Absence of hypothyroidism, hypoadrenalism,renal insufficiency or diuretic use
Another common cause is iatrogenic - using very hypotonic saline solutions. 0.18% saline should never be routinely used - 0.45%/ with 5% dextrose is the usual maintenance, although 0.9%/ with 5% dextrose may be preferable
Frusemide does not usually cause hyponatraemia - it causes excretion of water in excess of Na, so usually causes hypernatraemia.
Urinary sodium or osmolarity may give useful information (urine osmolarity has to be interpreted in light of serum osmolarity)
- Urine Na > 20 - renal failure, SIADH, diabetes insipidus
- Urine Na < 20 - dehydration, extra-renal sodium loss
Rapid correction avoided - max rate of increase aim for 0.5mmol/l/hr. Over-rapid correction has been reported to cause central pontine myelinolysis in neonates and the elderly.
Exception is symptomatic severe hyponatraemia (Na < 120 + seizures or coma) - give 3% saline as 4 -6ml/kg boluses until Na > 125.
The patient has a Na of 128, what do you want to do about it?
The patient has a Na of 128, they appear euvolaemic, and their serum osmolarity is 265, with a urine Na of 42mmol/L. They have a positive fluid balance, and are receiving 0.9% saline/5% dextrose at 100% of maintenance requirements. Urine output is 1.1 ml/kg/hr. Urea and creatinine are not raised. I suspect it may be SIADH or a degree of iatrogenic fluid overload - I planned to restrict IV input to 60% of maintenance and see if the Na increased over the next few hours - would you agree?
Commonest causes in our population of patients are dehydration, frusemide and diabetes insipidus.
Frusemide may be used to correct fluid overload in septic patients in the recovery phase of their illness, and Na concentrations are often in the low 150s - it generally self corrects when the diuresis is stopped once the patients are extubated.
Treating severe hypernatraemia is done slowly - correct at a rate no greater then 0.5mmol/l/hr. 0.45% saline/5% dextrose solution is used to provide maintenance and correct any suspected dehydration, and the serum sodium measured initially 2 hourly. Fluid composition is adjusted according to response. Over-rapid correction may cause cerebral oedema if the hypernatraemia has been long standing (a few days).
If salt poisoning is part of the differential diagnosis, serial urine samples should be taken for Na analysis until the hypernatraemia has resolved.
Sarnaik AP, Meert K, Hackbarth R, Fleischmann L.Management of hyponatremic seizures in children with hypertonic saline: a safe and effective strategy. Crit Care Med. 1991 Jun;19(6):758-62.
Potassium < 3.5 mmol/L
Increase KCl content of IV fluids, or give enteral K supplements
Ensure Spironolactone or amiloride is being used if the patient is on another diuretic.
IV infusion of KCl is only used in severe hypokalaemia in children with poor cardiac function or a tendency to arrhythmia, and usually only if K < 2.5mmol/l. Max rate is 0.5mmol/kg/hr, and it is given only via central access. Maximum concentration 1mmol per 1 mL. (On the rare occasions it has to be given peripherally, the maximum concentration is 6mmol/100ml).
Emergency treatment required for K>7mmol/l with ECG changes (tall T waves, broad QRS complex).
- Calcium gluconate 10% 0.5ml/kg slow IV AND
- Salbutamol 5mg nebulized (or 4mcg/kg IV over 20 mins)
Additional treatment may involve giving 1mmol/l NaHCO3 and a glucose and insulin infusion. This will be determined by aetiology and response to the above.
Treat Ca2+ < 1.0 mmol/l with Calcium gluconate 10% 0.5ml/kg over 30 mins.
Treat Mg2+ < 0.7mmol/l with Magneium sulphate 20% 0.5ml/kg over 30 mins.
Phosphate < 1.3mmol/l may need to be corrected, but is not an acute problem and can be discussed on a ward round. In some conditions, eg DKA it is common, but not treated.
Enteral 2 - 3mmol/kg/day in 2 - 4 divided doses
Intravenous Dilute injection to 0.1 mmol sodium acid phosphate in 1 mL with Sodium Chloride 0.9% or 0.45% or Glucose 5% or 10%. Administration rate should not exceed 0.05 mmol/kg/hour. Rarely may increase rate to 0.5 mmol/kg/hour via central venous catheter only
Results can only be interpreted properly with knowledge of the patient’s haemodynamic status, urine output, urine pH, lactate, chloride and anion gap.
Anion gap = [Na + K] - [Cl + HCO3]
Normal range < 16mmol/l
Normal anion gap
Usually with hyperchloraemia (> 105mmol/l). This is commonly due to administration of boluses of normal saline or albumin. No specific treatment required, although further boluses of fluid should can be given as Hartmann's solution.
- Bicarbonate loss (diarrhoea, renal tubular acidosis, enterostomies)
High anion gap - other acid present
- Lactate - measure it!
- Other unmeasured organic acids
- Think about poisoning (aspirin, alcohol, methanol, glycol)
- Think about inborn errors of metabolism
- Ketosis - DKA is obvious, but starvation may also cause severe ketosis
The patient has a pH of 7.24, what do you want to do about it?
The patient has a pH of 7.24, is well perfused with a good urine output, has a chloride of 114, a lactate of 1.3 and an anion gap of 14. I thought I would use Hartmann's for any further boluses but otherwise just observe - do you agree?