(From Pulse learning module)
- Mild hyponatraemia: 130 – 132
- Moderate hyponatraemia: 125 – 129
- Severe/profound hyponatraemia: <125 (some experts use ‘profound’ for <110). This category was picked on the basis of patients being increasingly likely to be symptomatic below this figure.
Patients are better able to compensate for hyponatraemia in cases where it comes on more gradually; hence cerebral oedema is more of a risk in acute cases (<24 hrs).
Hyponatraemia is in fact caused by excess of water; sodium depletion may or may not be present as well, but the key issue is water excess. This is almost always due to vasopressin release, with the exception being hyperglycaemia; in that situation, osmotic pressure draws water out of cells. To calculate the extent to which this is playing a part, reckon on a drop of 1 mmol/l Na for every 3 mmol/l rise of glucose.
One other thing to consider here is pseudohyponatraemia, caused by marked hyperlipidaemia or very high proteinaemia in the case of multiple myeloma. In that case, the volume is artificially increased by the sheer volume of lipid molecules, causing the sodium concentration to look artificially low. No treatment is needed other than treatment of the hyperlipidaemia.
Hyponatraemia caused by vasopressin secretion –> water retention (i.e. all cases except hyperglycaemia-induced hyponatraemia and pseudohyponatraemia) is referred to as hypotonic hyponatraemia. (I think this is because the osmolality is reduced in all other cases; it’s high in hyperglycaemia and normal in pseudohyponatraemia.) It can be subdivided according to whether the blood volume is reduced, normal, or increased.
This is caused when a loss of water and usually also sodium causes a drop in fluid volume, triggering ADH secretion (appropriate secretion of ADH, in other words). Causes include:
- Diuretics (typically thiazide or potassium sparing; despite what we learned at medical school, it is uncommon for loop diuretics to do so)
- Adrenal failure
- Severe gastrointestinal loss (fistula, severe diarrhoea)
This is typically caused by SIAD, although severe hypothyroidism can cause something similar; however, to have any more than a slight effect on sodium concentration, hypothyroidism has to be practically at the coma level, so is going to be very obvious clinically. (Nevertheless, TSH levels are recommended as part of the investigations of hyponatraemia.)
- SIAD due to vasopressin secretion from a tumour (small cell carcinoma of the lung is the most common)
- SIAD due to triggering of vasopressin secretion from the pituitary due to lung disease (including COPD) or hypothalamic dysfunction
- SIAD due to the ‘reset osmostat’ syndrome; in the elderly, the setting for triggering vasopressin release can be reset to an abnormally low level.
- SIAD due to drug-induced vasopressin release; a wide range of drugs will do this.
Drugs that cause SIAD:
- Antidepressants: tricyclics, SSRIs, venlafaxine
- Anticonvulsants: lamotrigine, sodium valproate, carbamazepine
- Antineoplastic drugs: methotrexate was the one that stood out for me here, though there are various others which I’m less likely to be dealing with. Interesting; obviously lots of emphasis on monitoring the LFTs/FBC with methotrexate, but I actually hadn’t realised we were meant to monitor the sodium as well (luckily the practice nurses take U&Es anyway!)
- Tolbutamide (does anyone ever still use that these days?)
- Random: PPIs, amiodarone, NSAIDs, opiates, interferon, ecstasy, levamisole (not even sure what that one is, but it’s on the list)
This occurs when marked oedema, due to severe CCF, nephrotic syndrome, or liver cirrhosis, causes a large movement of water and sodium from the vascular to the extracellular space, causing arterial hypovolaemia and triggering vasopressin release. This leads to the paradoxical situation of hyponatraemia in a situation of total body excess.
History and examination
Look for any obvious causes (medication, lung disease) and for signs of hypovolaemia (postural hypotension, tachycardia), marked oedema, or lung disease. Ask about nausea, headache and confusion as these are symptoms of cerebral oedema. Note that severe cerebral oedema can lead to stupor, convulsions, coma and death.
If sodium is below 110, admit. If between 110 – 125, consider admission. Mild or moderate hyponatraemia is not an emergency, but is not as benign as once thought either; it’s now known to be a risk factor for death, MI, falls, and fracture. Therefore, where possible stop any medication that may be causing the problem.
- Repeat U&Es. (Note that raised urea/creatinine in a patient without kidney disease can point to volume loss via gastrointestinal or renal route, and hyperkalaemia can point to adrenal dysfunction.)
- Serum osmolality (will be high in hyperglycaemia, normal in pseudohyponatraemia, and low in other cases)
- Urinary osmolality and sodium (random but concurrent sample)
- Random cortisol – and if low or low-normal, follow up with short Synacthen test
Urinary osmolality will normally be high – if it’s low, that’s a clue that the problem is inappropriately high fluid consumption.
Urinary sodium will normally be low in hypovolaemic or hypervolaemic causes, except for in cases of diuretic use or adrenal failure as the normal response is blocked. Urinary sodium >30 mmol/l in the absence of diuretics is typically due to SIAD, as is urinary osmolality >100.
SIAD is a diagnosis of exclusion. Obviously, once it’s reached it’s wise to check a CXR for lung causes (urgently, to exclude small cell carcinoma).
If the cause of mild or moderate hyponatraemia can’t be reversed and the problem is therefore chronic, do check U&Es in the case of any intercurrent illness, particularly pulmonary; this can cause an acute exacerbation of the hyponatraemia.