Why it’s tricky
- Serum sodium concentration is linked to water content – it’s not simply a matter of considering sodium intake or losses. Sodium (and chloride) contribute predominantly to the ECF osmolarity and therefore ECF water content has a marked effect on concentration
- Fluid/electrolyte shifts have an important role on serum concentration – just like any other electrolyte e.g. potassium into cells, calcium/magnesium/phosphate into bone. But it’s water shifts (rather than sodium shifts) that mainly affect sodium concentration (remember most of the sodium stays in the ECF)
- Hormones act on the renal system to control fluid/electrolyte balance – but the role of hormones (e.g. aldosterone) on sodium balance tends to result in only isotonic gains or losses. Therefore, concentration doesn’t alter. Aldosterone affects blood volume without affecting sodium concentration. However, ADH which selectively controls water gains or losses does have a major effect on serum sodium concentration. After the thirst mechanism (that controls water intake) it is the other main controller of water balance (via water output) which in turns alters sodium concentration (and ultimately ECF osmolarity)
- The cause of hyponatraemia is often multifactorial which complicates the assessment. An example is a patient on diuretics who loses water and salt. They may also be concurrently placed on a salt-restrictive diet and only replacing their fluid/electrolyte losses with water. Furthermore, an acute illness might trigger inappropriate section of ADH. The combined effects thus overcomes any of the homeostatic responses to correct the sodium
Here is a clinical approach in the light of this
- Determine if there is a hyponatraemic medical emergency – A patient with severe hypontraemia is at risk of cerebral oedema. As mentioned, sodium is an important contributor to ECF osmolarity, holding water in that compartment. If it falls, water can flow into cells. In most places of the body, this has no acute effect. But within the closed box where the brain sits, the risk is of herniation. It tends to be a problem when concentrations falls into the teens (i.e. < 120mmol/L) Any patient who is significantly drowsy or has an acute seizure warrants urgent attention and prompt administration of hypertonic saline. A good rule is 3ml/kg of 3% hypertonic saline over 30 minutes (but you should have called a MET by this time)
- Clinically evaluate the volume status – Most importantly if the patient is shocked (due to a combination of sodium and water loss) they need fluid resuscitation until vital signs and perfusion normalises. However, if they are oedematous this opens a whole range of possibilities in which the underlying medical condition (which predisposes to water retention) or its therapy (which contributes to sodium loss) is contributing to hyponatraemia. Generally, it is difficult or inadvisable to directly correct their serum sodium. Instead their underlying disease should be optimised.
- Check there is a low measured osmolarity to confirm it is a “True hyponatraemia”. Since sodium (and chloride) are usually the main osmotically active particles in ECF, a measured drop in osmolarity confirms this. The opposite is a ‘Hyperosmolar Hyponatraemia” or “Pseudo Hyponatraemia”. A common cause is hyperglycaemia which is also osmotically active and draws water into the circulation and temporarily dilutes the sodium concentration. The answer isn’t to change sodium or water balance but to address the hyperglycaemia (e.g. insulin). As it falls, the water moves out in reverse without having to do anything else. A rare cause of hyponatraemia is “Iso-osmolar hyponatraemia” or “Factitious hyponatramia” which is not really a disorder of sodium at all, but a lab measurement error. It is rare with modern labs but essentially the equipment gets confused when there are other constituents in the blood sample that interfere with the calculation. Examples are hypertriglyceridaemia and hyperproteinaemia. They just alert you to a problem that has nothing to do with serum sodium concentration. Using another lab technique indicates normal concentrations.
- Check the urine sodium concentration and osmolarity – Urine electrolytes are useful to determine if dysfunctional renal/endocrine homeostatic mechanisms are the cause of the problem. It should be expected that if the serum sodium is low that the kidney will respond by producing a urine with low sodium or high water content. If that is not the case then the inappropriate sodium loss (or water retention) has been identified as originating from the kidneys or by hormonal dysfunction. Linking this with the clinical evaluation of volume status, the cause would be diuretic use or polyuric renal failure (if hypovolaemic), SIADH (if normovolaemic), nephrotic syndrome (if oedematous)
- Eliminating the cause and water restriction usually solves the issue – Despite the complexity of the evaluation and the various causes, as long as the patient is confirmed to have true hyponotraemia, is not shocked and has normal renal function, the usual treatment is just to fluid restrict the patient to less than one litre a day. But remember there is a subset of patient due to a variety of reasons that have chronic asymptomatic hyponatraemia due to a reset of their hypothalamic osmostat which don’t benefit or resist treatment. It only becomes a problem if they suffer a further acute deterioration.
In summary, consider
- The effect of water intake/output/shifts
- The combination of sodium loss combined with inadequate intake
- The impact of ADH affecting this balance
- Confirming the issue with serum osmolarity
- Identifying a renal/endocrine issue with urine electrolytes
- Drug can interfere with renal/endocrine homeostatic function
- After resuscitation, treating the cause fluid restriction is all that is needed
- Beware of over treating chronic hyponatraemia