Hyponatraemia and hypernatraemia — formative SAQs

SAQ 1 (10)

A 3-year-old boy is admitted with pneumonia. On day two of his admission he has a generalised seizure. He has been receiving 0.45 percent saline with dextrose as maintenance fluid. His serum sodium is 116 mmol/L, serum osmolality 258 mOsm per kg, urine osmolality 340 mOsm per kg, and urine sodium 52 mmol/L. He is post-ictal but arousable. [3][7]

1. Classify this child's hyponatraemia and explain the mechanism by which it developed. (3) [1][8]
2. Give the emergency management in the first hour, naming each step, drug, dose, route, and the specific goal. (5) [5][11]
3. Outline the definitive management over the next 24 hours, including the correction-rate ceiling and the safety pitfalls, and state how you would prevent recurrence. (2) [6][7]

Model answer

Classification and mechanism. This is hypotonic, euvolaemic hyponatraemia (low serum osmolality of 258) with the SIAD pattern: an inappropriately concentrated urine (340 mOsm per kg, above 100) and a high urine sodium (52, above 40). The mechanism is hospital-acquired hyponatraemia: the pneumonia drives non-osmotic arginine vasopressin release, and the hypotonic maintenance fluid (0.45 percent saline) provides free water that the ADH-activated kidney retains, diluting the serum sodium. The acute fall has not given the brain time to adapt, which is why he has seized from cerebral oedema. [1][8]

Emergency management (first hour). This is severe symptomatic hyponatraemia with cerebral oedema, a neurological emergency. First, secure the airway, breathing, and circulation and attach cardiac and neurological monitoring. Second, give intravenous 3 percent hypertonic saline at 2 mL per kg over 10 minutes, repeated up to two or three times if seizures continue, aiming for a 4 to 6 mmol per litre rise or seizure control, whichever comes first. The goal is not normalisation but a measured rise sufficient to pull water out of the swollen brain and relieve the cerebral oedema. A 2 mL per kg bolus raises the sodium by roughly 2 to 4 mmol per litre. Stop the hypotonic maintenance fluid immediately. Check the serum sodium after the first bolus. [5][11]

Definitive management and pitfalls. Once the brain is safe, switch to slow correction at no more than 8 mmol per litre in 24 hours to avoid osmotic demyelination syndrome, with the sodium checked every 2 to 4 hours. Change the maintenance fluid to isotonic (0.9 percent saline with dextrose), and fluid-restrict if the SIAD persists. Two pitfalls: (1) over-correcting beyond 8 mmol per litre in 24 hours risks osmotic demyelination, and if it happens the rescue is to lower the sodium with desmopressin and free water; (2) fear of osmotic demyelination must never delay 3 percent saline in a seizing child, because cerebral herniation kills faster than ODS. Recurrence is prevented by using isotonic maintenance fluid as the default, as proven by the McNab trial. [6][7]

SAQ 2 (10)

A 4-week-old exclusively breastfed infant presents with poor feeding, lethargy, and a 13 percent weight loss from birth. Serum sodium is 162 mmol/L, and the urine osmolality is 800 mOsm per kg. The infant is tachycardic with a sunken fontanelle and reduced skin turgor. [2][10]

1. What is the most likely diagnosis, and what does the urine osmolality tell you about the kidney's concentrating ability? (3) [2]
2. Give the immediate and definitive management, including the free-water deficit principle, the correction rate, and the route of choice. (5) [2][10]
3. Explain why the correction must be slow, and state two complications of over-rapid correction. (2) [2][10]

Model answer

Diagnosis and the urine osmolality. This is breastfeeding-associated hypernatraemia, presenting in the first weeks of life with inadequate intake, weight loss over 10 percent, and a serum sodium above 150. The concentrated urine (800 mOsm per kg) confirms that the kidney is responding normally to the hypernatraemia by maximally conserving water, so the loss is extrarenal (inadequate free-water intake), not diabetes insipidus (which would show a dilute urine despite the high sodium). The infant is hypovolaemic as well as hypernatraemic. [2]

Immediate and definitive management. If the infant is shocked, restore intravascular volume first with isotonic saline boluses (10 to 20 mL per kilogram) until perfusion is restored, because the immediate threat is shock and isotonic saline does not significantly change the sodium. Once perfused, correct the free-water deficit over 48 hours. Estimate the deficit: in infants the body water fraction is high (around 0.7 to 0.75), so the deficit is roughly 0.7 times body weight times the sodium minus 140 divided by 140, plus ongoing losses. Correct at a maximum of 0.5 mmol per litre per hour (10 to 12 mmol per litre in 24 hours). The preferred route is oral or nasogastric free water, because the gut controls the rate far better than an intravenous line and lowers the risk of cerebral oedema; intravenous fluids are used when enteral is not feasible, and the sodium is checked every 2 to 4 hours during active correction. [2][10]

Why correction must be slow and its complications. Over the days of hypernatraemia, the brain has generated idiogenic osmoles to hold onto water and protect its volume. If the sodium is corrected rapidly, the serum becomes hypotonic relative to the adapted brain cells, water rushes back into them, and the brain swells inside the rigid skull, causing cerebral oedema. Two complications of over-rapid correction are therefore cerebral oedema with seizure, herniation, and death, and the related risk of intracranial haemorrhage from the rapid fluid shift. The 0.5 mmol per litre per hour ceiling is the hard limit that protects the adapted brain. [2][10]