Phys · renal
Sodium Disorders — Hyponatraemia and Hypernatraemia
Also known as hyponatraemia · hyponatremia · hypernatraemia · hypernatremia · SIADH · syndrome of inappropriate antidiuresis · osmotic demyelination syndrome · central pontine myelinolysis · diabetes insipidus · arginine vasopressin deficiency · arginine vasopressin resistance · cerebral salt wasting · psychogenic polydipsia · tea and toast hyponatraemia · beer potomania · reset osmostat
Consultant-physician-depth guide to sodium and water homeostasis. Covers hyponatraemia (the commonest inpatient electrolyte disorder): symptom-stratified urgency, volume-status classification, serum and urine osmolality with urine sodium interpretation, severe symptomatic management with 3% hypertonic saline boluses, the 8-10 mmol/L in 24 hours correction ceiling and osmotic demyelination syndrome, SIADH, and the euvolaemic/hypervolaemic differentials. Covers hypernatraemia as a water-deficit state: central versus nephrogenic diabetes insipidus, the water deprivation test and copeptin, free water deficit calculation, and slow oral or D5W correction over 48-72 hours. Structured for FRACP DWE and DCE preparation.
Checked against its sources on 3 Sept 2026
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Red flags
- Severe symptomatic hyponatraemia (seizure, coma, signs of cerebral oedema) — give 3% saline 100 mL bolus over 10 minutes immediately; do not wait for investigations
- Acute hyponatraemia developing in under 48 hours (post-operative, MDMA, primary polydipsia, colonoscopy prep) — high risk of cerebral herniation; correct promptly
- Na less than 105 mmol/L — extreme hyponatraemia, high risk of seizure and respiratory arrest; treat in ICU
- Rapidly rising sodium above 8-10 mmol/L in 24 hours — risk of osmotic demyelination syndrome; relower with DDAVP and free water
- Chronic hyponatraemia over-correcting after cessation of a provoking drug (thiazide, SSRI) — autonomous water diuresis can overshoot
- Hypernatraemia with altered conscious state — reflects severe free water deficit or acute brain injury (hypodipsia, central DI post-neurosurgery)
- Central DI in the post-pituitary-surgery patient — triphasic response can produce dangerous hyper- then hyponatraemia within days
Sodium Disorders — Hyponatraemia and Hypernatraemia
The answer first
Sodium disorders are water disorders. Serum sodium reflects the ratio of total body exchangeable sodium to total body water — it tells you about water balance, not sodium balance. A normal sodium means water and sodium are matched; an abnormal sodium means they are mismatched. The clinician's job is to work out which side of the equation is wrong. [1]
Hyponatraemia (Na less than 135 mmol/L) is the commonest electrolyte disorder in hospitalised patients, present in 15 to 30 percent of inpatients [4]. It is almost always a problem of relative water excess — the kidney cannot excrete free water because arginine vasopressin (AVP, also called antidiuretic hormone or ADH) is inappropriately present. Even hypovolaemic hyponatraemia is driven by non-osmotic AVP release: the body defends circulating volume at the cost of tonicity.
Hypernatraemia (Na greater than 145 mmol/L) is almost always a problem of relative water deficit, and it almost always implies impaired access to water — the very old, intubated, neurologically impaired, post-operative. A patient with an intact thirst mechanism and free access to water does not develop sustained hypernatraemia. Hypernatraemia is iatrogenic more often than it is admitted [5].
The two clinical questions that dominate management: [1]
- How fast did it develop, and is the brain threatened? Acute hyponatraemia (under 48 hours) risks cerebral oedema and herniation — correct promptly. Chronic hyponatraemia (over 48 hours) risks osmotic demyelination if corrected too fast — correct slowly.
- What is the volume status, and what is driving the abnormal vasopressin? That single bedside assessment — hypovolaemic, euvolaemic, or hypervolaemic — divides the differential into three families and determines treatment. [1]
The management mandate, in priority order: [1]
- Severely symptomatic hyponatraemia (seizure, coma) is an emergency — give 3% hypertonic saline, 100 mL bolus over 10 minutes, repeat up to three times, aiming for a 4 to 5 mmol/L rise in the first 4 hours. Do not wait for bloods.
- Respect the correction ceiling — no more than 8 to 10 mmol/L in 24 hours, and 18 mmol/L in 48 hours, to avoid osmotic demyelination syndrome (ODS) [1][2].
- Treat the cause — stop the thiazide, the SSRI, the carbamazepine; give glucocorticoids for adrenal insufficiency; treat heart failure; remove the water load.
The single most important exam principle: the risk of treating hyponatraemia is ODS, and the risk of not treating it is cerebral herniation. Both kill. The skill is judging which risk dominates for the patient in front of you, based on symptoms and chronicity. [1]
References8ShowHide
- [1]Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia Nephrol Dial Transplant, 2014.PMID 24569496
- [2]Sterns RH Disorders of plasma sodium--causes, consequences, and correction N Engl J Med, 2015.PMID 25551526
- [3]Sterns RH, Riggs JE, Schochet SS Jr Osmotic demyelination syndrome following correction of hyponatremia N Engl J Med, 1986.PMID 3713747
- [4]Adrogué HJ, Madias NE Hyponatremia N Engl J Med, 2000.PMID 10824078
- [5]Adrogué HJ, Madias NE Hypernatremia N Engl J Med, 2000.PMID 10816188
- [6]Schrier RW, Gross P, Gheorghiade M, et al. Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia N Engl J Med, 2006.PMID 17105757
- [7]Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations Am J Med, 2013.PMID 24074529
- [8]Sterns RH, Nigwekar SU, Hix JK The treatment of hyponatremia Semin Nephrol, 2009.PMID 19523575