Hyponatraemia and hypernatraemia — viva

Opening (must-hit)

"This is severe symptomatic hyponatraemia with a seizure at a sodium of 117, which means cerebral oedema and raised intracranial pressure. This is a neurological emergency. My first action is to give intravenous 3 percent hypertonic saline at 2 mL per kilogram over 10 minutes, repeated up to three times if the seizure continues, aiming for a 4 to 6 mmol per litre rise or seizure control. I secure the airway, breathing, and circulation, stop the hypotonic maintenance fluid immediately, and check the sodium after each bolus. The likely cause is hospital-acquired hyponatraemia: the pneumonia has driven non-osmotic ADH, and the hypotonic fluid has provided the free water the kidney retains." [5][11]

Examiner: "Why hypertonic saline, and what exactly does it do?"

"3 percent hypertonic saline raises the serum osmolality and pulls water out of the swollen brain cells, relieving the cerebral oedema and the raised intracranial pressure within minutes. It does not normalise the sodium, and it should not — a 2 mL per kilogram bolus gives a measured 2 to 4 mmol per litre rise, and the target is seizure control or a 4 to 6 rise, not 140. The fear of osmotic demyelination has led to under-use of hypertonic saline, and Ayus and Moritz have documented that this has caused more deaths from untreated cerebral herniation than ODS itself causes. A single bolus in a seizing child is safe and life-saving; the risk of ODS is from sustained over-correction over 24 hours, not a measured bolus now." [11][6]

Examiner: "What is your correction-rate ceiling over the next 24 hours, and why?"

"Once the brain is safe, I correct slowly at no more than 8 mmol per litre in 24 hours. The reason is brain cell volume adaptation. Over hours to days of hyponatraemia the brain extrudes intracellular osmoles — first potassium, then organic osmolytes — to shed water and limit the oedema. If I correct the sodium too quickly, the serum becomes hypertonic relative to the newly depleted brain cells, water rushes out, and the cells shrink and demyelinate, producing osmotic demyelination syndrome. I check the sodium every 2 to 4 hours during active correction and adjust the rate to stay within the ceiling. If I over-correct, the rescue is to lower the sodium back down with desmopressin and free water or 5 percent dextrose." [5][6]

Examiner: "How would you classify the cause, and what would the urine show?"

"I classify hyponatraemia by volume status, and here the child is clinically euvolaemic. The urine osmolality is inappropriately concentrated (above 100 mOsm per kilogram) and the urine sodium is high (above 40), which is the SIAD pattern — non-osmotic ADH release driven by the pneumonia. If she were hypovolaemic with a low urine sodium, I would think of extrarenal salt and water loss; if she were hypervolaemic with oedema, heart failure or renal failure. The single pair of urine osmolality and urine sodium, read with the volume status, sorts most hyponatraemias at the bedside." [3][1]

Examiner: "How would you prevent this from happening again?"

"I would switch the ward default to isotonic maintenance fluid. The McNab JAMA trial and the systematic reviews showed that isotonic maintenance fluid prevents hyponatraemia without increasing hypernatraemia or fluid overload, because it removes the free-water load that the non-osmotically driven ADH retains. Hypotonic maintenance fluid in a sick child is the commonest cause of hospital-acquired hyponatraemia, and the move to isotonic as the default is among the most important preventable-harm interventions in paediatric inpatient care. I would also ensure any child at risk has the sodium monitored daily while on intravenous fluids." [7][8]

Examiner: "Final corner — turn it around. A neonate presents with a sodium of 162 and a dilute urine. What is the principle there?"

"That is hypernatraemia with inappropriately dilute urine, which is diabetes insipidus, and it is the mirror image of the hyponatraemia problem. Here the brain has generated idiogenic osmoles to hold onto water, so rapid correction would flood the adapted cells and cause cerebral oedema. The correction ceiling for hypernatraemia is 0.5 mmol per litre per hour, or 10 to 12 mmol per litre in 24 hours, over 48 hours. The free-water deficit is calculated and replaced slowly, with oral or nasogastric water preferred. Central DI responds to desmopressin; nephrogenic DI does not and is managed with solute reduction and a thiazide or indometacin. The unifying principle for both sodium disorders is that the brain adapts slowly, so correction must be slow." [5][1]

Closing summary

"In summary: severe symptomatic hyponatraemia — 3 percent saline 2 mL per kilogram bolus first, then correct no faster than 8 mmol per litre in 24 hours. Hospital-acquired hyponatraemia — prevent with isotonic maintenance fluid. SIAD is euvolaemic and fluid-restricted, cerebral salt wasting is hypovolaemic and salt-replaced. Hypernatraemia — correct at 0.5 mmol per litre per hour to avoid cerebral oedema. The brain adapts slowly, so correct slowly." [5][11]