SIADH and disorders of water balance — viva

Opening (must-hit)

"I am worried about hyponatraemic encephalopathy: he is drowsy and vomiting with a sodium that has dropped to 121 mmol/L on hypotonic-type fluids, so I will treat this as an emergency. I will assess his airway and conscious level, stop any hypotonic fluid, and prepare hypertonic 3 per cent saline. If he seizes or deteriorates I will give it aiming to raise the sodium by only 4 to 6 mmol/L, and I will call for senior and intensive care help. The likely mechanism is hospital-acquired hyponatraemia from an ADH stimulus plus free water." [7][6]

Branch A — Recognition and mechanism

Examiner: Why has his sodium fallen so fast? Candidate: He has a strong non-osmotic stimulus to ADH — the bronchiolitis and the associated stress and vomiting — so his kidney cannot excrete free water. Given a hypotonic maintenance fluid, that free water is retained and dilutes his serum sodium directly. This is hospital-acquired hyponatraemia: the combination of an ADH stimulus and a hypotonic fluid load. It is common, preventable, and can be fatal, which is why isotonic maintenance fluid is now the standard. [6][8]

Branch B — Emergency management

Examiner: He now has a generalised seizure. What do you do? Candidate: This is hyponatraemic encephalopathy. I give intravenous hypertonic 3 per cent saline at about 2 mL/kg over 10 to 15 minutes, capped near 100 mL, and repeat if he keeps seizing. The target is to raise the sodium by only 4 to 6 mmol/L to reverse the cerebral oedema and stop the fit — not to normalise it. Each 2 mL/kg bolus raises the sodium by roughly 2 mmol/L. I manage the airway and seizure, stop the hypotonic fluid, and check the sodium every 2 to 4 hours. [7][3]

Branch C — The correction-rate ceiling

Examiner: The seizure stops after the sodium rises by 5. The intern wants to keep the saline running to get him to 135. Your response? Candidate: No — I stop the rapid correction now. The emergency correction has done its job. Continuing to push the sodium risks osmotic demyelination syndrome, because a hyponatraemia of uncertain duration must be assumed chronic and the adapted brain is vulnerable to a fast rise. The ceiling is a total rise of no more than 8 mmol/L in 24 hours. I switch to slow management, monitor closely, and if we overshoot I re-lower the sodium with 5 per cent dextrose and desmopressin. [10][3]

Branch D — Confirming the diagnosis

Examiner: How do you confirm this is SIADH rather than something else? Candidate: I confirm true hypotonicity with a serum osmolality, then read his volume status. SIADH is a low serum sodium and osmolality with an inappropriately concentrated urine (over 100 mOsm/kg) and a high urine sodium (over 30 mmol/L), in a euvolaemic child who is not on diuretics. Because it is a diagnosis of exclusion, I check cortisol and thyroid function to exclude adrenal insufficiency and hypothyroidism, which mimic it exactly. The bronchiolitis is the trigger. [8][12]

Branch E — Cerebral salt wasting

Examiner: Suppose instead this were a child six days after a brain tumour resection, dry, with a high urine output and weight loss. How would that change your thinking? Candidate: That points to cerebral salt wasting, not SIADH. The biochemistry can look identical — low sodium, high urine sodium — but the child is volume depleted with a negative fluid balance, because the primary problem is renal salt loss, not water retention. The urine sodium cannot separate them; volume status does. The treatment inverts: I give salt and volume, not fluid restriction. Restricting fluid in a salt-waster deepens the deficit and, in a brain-injured child, risks cerebral ischaemia. [9][3]

Branch F — Definitive SIADH management

Examiner: Back to the SIADH child. He is stable. What is the definitive plan? Candidate: Fluid restriction below insensible plus urinary losses, treat the trigger (the bronchiolitis), and use isotonic fluid if intravenous therapy continues. I recheck the sodium every 2 to 4 hours while correcting, then space it out as it stabilises. Most hospital SIADH resolves as the illness resolves. For chronic or refractory SIADH I would add oral salt and consider oral urea under specialist care, but that is not needed here. [8][12]

Branch G — Prevention

Examiner: How could this have been prevented? Candidate: By using isotonic maintenance fluid from the start, which removes the free-water load that turns a physiological ADH surge into a dangerous dilutional fall, and by checking the sodium in any child on intravenous fluids who deteriorates neurologically. Isotonic maintenance fluid is now the standard of care for hospitalised children for exactly this reason. [6][7]

Examiner traps

• Continuing to correct the sodium after the seizure has stopped, risking osmotic demyelination. [10]
• Restricting fluid in a child who is actually cerebral salt wasting. [9]
• Using urine sodium to try to separate SIADH from salt wasting. [12]
• Diagnosing SIADH without excluding adrenal insufficiency and hypothyroidism. [8]
• Continuing hypotonic maintenance fluid in a sick child and manufacturing the hyponatraemia. [6]