Serum sodium below <130mmol/L occurs in up to 30% of hospital inpatients and many older patients. However, sudden and dramatic falls in sodium to <120mmol/L can be life-threatening and requires evaluation of fluid status to determine emergency management.
As well as assessing the sodium level, potassium needs to be documented.
Hyperkaleamia should increase the suspicion of glucocorticoid deficiency.
Hypokalaemia raises the possibility of diuretic use, or cardiac failure as an underlying cause.
Renal function is also useful as elevated urea and creatinine make hypovolaemia more likely.
Useful general screen e.g. for infection or haemorrage.
Useful screen for liver disease. Hypoalbuminaemia may occur in any very sick patient but may also be associated with nephrotic syndrome, hepatic synthetic failure and fluid overload.
Heavy proteinuria raises the possibility of nephrotic syndrome.
Factitious hyponatraemia may be seen with very high glucose levels.
Not usually useful if the patient is on diuretics or an ACE inhibitor.
Not indicated in a patient which is clearly hypovolaemic.
Useful in patients in whom SIADH is suspected. A sodium over 30mmol/l is supportive of SIADH or other causes of eu- or hyper-volaemic hyponatraemia. A urinary sodium below 30mmol/l should prompt reassessment of the patient as it suggests hypovolaemia with renal retention of sodium.
Repeat urinary sodium may also be helpful to assess response in the patient initialy thought to be hypovolaemic whose serum sodium has not improved after giving IV saline. Urine sodium rises and serum sodium falls in patients with SIADH if they are given fluids. Reassess the patient and reconsider the diagnosis in this case.
Not necessary in the hypovolamic patient, but paired osmolalities are useful to confirm a clinical suspicion of the syndrome of inappropriate antidiurectic hormone (SIADH).
Essential to document normal thyroid function in the eu- or hyper-volaemic patient before a confident diagnosis of SIADH can be made.
Glucocorticoid defiency is associated with hyponatraemia which may be hypo- or eu-volaemic and must be ruled out before a confident diagnosis of SIADH can be confirmed.
Random admission cortisol is useful in very unwell patients. In less acute patients, a 9am cortisol or synacthen test should be performed.
Some laboratory assays still report factitious hyponatraemia in the face of extreme hyperlipidaemia. It is useful to document lipids to rule out this phenomenon, though this does not need to be performed in all units, and not in the acute setting.
A CT scan should be considered in patients with acute confusion, neurological signs or an altered GCS.
This should also be performed if a subsequent diagnosis of SIADH with no obvious respiratory or pharmacological cause has been identified.
Useful aid to diagnose pulmonary oedema which would indicate hypervolaemia, or respiratory pathologies which might have triggered SIADH.
This should be performed in patients with electrolyte abnormalities or with collapse.