Hyponatraemia is a common problem in hospitalised patients.
It is defined by a sodium concentration <135 mmol/l.
Even mild degrees of hyponatraemia are associated with increased mortality.

Plasma sodium is proportional to total body OSMOLALITY.
Plasma sodium concentration us NOTHING about the patient's volume status.

Two mechanisms underlie almost all cases of hyponatraemia:
  1. Accumulation of excess free water
  2. A defect in renal free water excretion

The exception to point 2 is primary polydipsia where water consumption is so great it exceeds normal excretory capacity.
Thiazide diuretics work by mechanism 2.

  1. Determine volume status by clinical assessment.
  2. Review fluid balance and medication charts over the last few days.
  3. Decide if the patient is volume overloaded, euvolaemic or volume depleted.
  4. Check:
    • Plasma EUC, glucose and osmolality.
    • Urine Na, creatinine and osmolality (at the same time as the plasma sample)
    • Morning cortisol and thyroid function.
  5. Once plasma osmolality falls <270mOsm/Kg then the urine should be maximally dilute i.e. approx 100mOsm/Kg.
    • This assumes that renal and tubule function is normal and the patient is not taking diuretics.

Volume overloaded patients
Typical conditions in this group include heart failure, cirrhosis and nephrotic syndrome.

These patients should be managed by:
  • Salt restriction - no added salt diet.
  • Water restriction - 1L per day initially.
  • Judicious use of diuretics e.g. frusemide.
  • Monitor electrolytes and renal function as this group is prone to developing acute renal failure.

Volume depleted patients
Typical conditions in this group include vomiting, diarrhoea, and intestinal obstruction with 'third-space' fluid losses.
In this group the urine Na should be <25 mmol/L if renal tubule function is preserved.

These patients should be managed by:
  • Replacement of volume deficit with 0.9% 'normal' saline
  • At the same time restrict access to free water (if able to tolerate oral fluids)
  • These patients can have liberal salt intake - this can stimulate thirst so beware of excess water intake.
  • Correct hypokalaemia if also present as this may be contributing to hyponatraemia.

Euvolaemic patients
In this group the activity of ADH means that water excretion is impaired even though sodium excretion is normal.
ADH release is commonly stimulated by surgery, pneumonia, HIV infection and CNS disorders eg stroke, meningitis or brain tumours. SIADH refers to those patients where this leads 'inappropriate' hyponatraemia.

These patients should be managed by:
  • Water restriction - 800mL per day initially.
  • 3% 'hypertonic' saline in select cases with severe or symptomatic hyponatraemia. A consultant should ALWAYS be involved.

If using 3% saline ALWAYS check plasma Na every 4-6h during the first 12-18h.
Do not correct plasma sodium by >12 mmol/L/day or >2mmol/L/hour.
More rapid correction increases the risk of pontine demyelination syndromes.
3% saline contains 540mmol/L of sodium.

Calculating the sodium deficit

Na deficit = (desired Na - current Na) x total body water

Total body water is 60% of lean body mass in men and 50% of lean body mass in women.
Take the example of a 70kg man with sodium 110mmol/L and we want to raise it to 120mmol/L over 24h.
Sodium deficit = (120 - 110) x (70 x 0.6) = 420 mmol
The volume of 3% saline required = 420/540 = 780 mL which would be 32mL/h over 24h.
Therefore we would chart 3% saline, 780mL @ 30mL per hour (to give a margin of safety).