Hyponatraemia & Hypernatraemia
Medicine · Nephrology · lean revision notes
Hyponatraemia & Hypernatraemia
Disorders of plasma sodium are fundamentally disorders of water balance, not of sodium content. Sodium is the principal determinant of plasma tonicity, so dysnatraemias reflect a mismatch between body water and solute. This topic is a perennial NEET PG favourite because of its tidy diagnostic algorithm, the deadly traps of correction rate, and the named syndromes (SIADH, ODS, cerebral salt wasting).
Core concepts: tonicity vs sodium
The cardinal rule: serum sodium tells you about water, serum osmolality tells you about effective solute. A patient can have a high total body sodium (oedema) yet still be hyponatraemic because free water is retained in excess.
Plasma osmolality is calculated as:
High-yield: Calculated osmolality = 2 × [Na⁺] + [Glucose mg/dL ÷ 18] + [Urea mg/dL ÷ 2.8]. Normal = 275–295 mOsm/kg. Urea is an ineffective osmole (crosses membranes freely) so it does NOT cause water shifts; glucose and mannitol are effective osmoles.
The osmolar gap = measured − calculated osmolality (normal < 10). A raised gap suggests unmeasured osmoles (methanol, ethylene glycol, mannitol).
| Term | Meaning | Clinical relevance |
|---|---|---|
| Osmolality | Total solute per kg water | Includes ineffective osmoles (urea) |
| Tonicity (effective osmolality) | Solute that draws water across membranes | Drives cellular swelling/shrinkage |
| Effective osmoles | Na, glucose, mannitol | Cause symptoms |
| Ineffective osmoles | Urea, ethanol | Raise osmolality but not tonicity |
Hyponatraemia (Na⁺ < 135 mmol/L)
The commonest electrolyte abnormality in hospitalised patients. Severe = Na⁺ < 120 mmol/L. The diagnostic engine is a three-step algorithm: serum osmolality → volume status → urine sodium/osmolality.
Stepwise diagnostic approach
Step 1 — Measure serum osmolality → classify into hypotonic, isotonic, or hypertonic hyponatraemia.
Step 2 (if hypotonic) — Assess volume status → hypovolaemic, euvolaemic, or hypervolaemic.
Step 3 — Urine sodium and urine osmolality → localise the cause.
So the flow is: Serum osmolality → Volume status → Urine Na⁺ & urine osmolality → Diagnosis.
Step 1: Classify by osmolality
| Type | Serum osmolality | Causes |
|---|---|---|
| Hypotonic (true) | < 275 | The "real" hyponatraemia — bulk of cases |
| Isotonic (pseudo) | 275–295 | Hyperlipidaemia, hyperproteinaemia (paraproteinaemia) — lab artefact with flame photometry |
| Hypertonic (translocational) | > 295 | Hyperglycaemia, mannitol — water drawn out of cells diluting Na |
High-yield: In hyperglycaemia, correct measured Na by adding 1.6 mmol/L for every 100 mg/dL glucose above 100 (some texts use 2.4 for glucose > 400). DKA hyponatraemia is usually translocational, not true.
High-yield: Pseudohyponatraemia (isotonic) classically appears in multiple myeloma and severe hypertriglyceridaemia. Modern direct ion-selective electrodes minimise this artefact.
Step 2 & 3: Hypotonic hyponatraemia by volume status
| Volume status | Urine Na⁺ | Examples | Treatment principle |
|---|---|---|---|
| Hypovolaemic | < 20 (renal loss > 20) | Vomiting/diarrhoea (extra-renal), diuretics/Addison's/salt-wasting nephropathy/CSW (renal) | Isotonic (0.9%) saline |
| Euvolaemic | > 20–40 | SIADH, hypothyroidism, glucocorticoid deficiency, psychogenic polydipsia, beer potomania | Fluid restriction ± vaptan |
| Hypervolaemic | < 20 (renal failure > 20) | CCF, cirrhosis, nephrotic syndrome, advanced renal failure | Fluid + salt restriction, treat cause |
High-yield: Urine osmolality < 100 mOsm/kg with hyponatraemia = appropriately dilute urine = primary polydipsia or beer potomania / "tea-and-toast" diet (low solute intake limits free-water excretion). Urine osmolality > 100 = ADH is active (SIADH, hypovolaemia, etc.).
SIADH — the examiner's darling
Syndrome of Inappropriate Antidiuretic Hormone secretion: ADH released despite low plasma osmolality, causing water retention and dilutional hyponatraemia with euvolaemia.
Bartter & Schwartz diagnostic criteria
- True hypotonic hyponatraemia (serum osm < 275).
- Inappropriately concentrated urine (urine osm > 100, usually > 300).
- Clinical euvolaemia (no oedema, no dehydration).
- Urine sodium > 30–40 mmol/L on normal salt/water intake.
- Normal thyroid and adrenal function.
- Normal renal function, no recent diuretics.
High-yield: SIADH triad to memorise — euvolaemia + low serum osmolality + inappropriately concentrated urine (urine osm > serum osm) with high urine sodium. Serum uric acid and urea are characteristically LOW in SIADH (dilution + increased clearance).
Causes (mnemonic "SIADH"):
- S — Surgery, Subarachnoid haemorrhage, CNS pathology (meningitis, stroke, trauma)
- I — Infections (pneumonia, especially Legionella; TB; lung abscess)
- A — Abscess / lung pathology (small cell lung carcinoma is the classic malignancy)
- D — Drugs (carbamazepine, SSRIs, cyclophosphamide, vincristine, NSAIDs, desmopressin, ecstasy/MDMA)
- H — Hormonal / others
Small cell lung cancer is the prototype ectopic-ADH tumour. Always rule out malignancy in unexplained SIADH.
Cerebral salt wasting (CSW) vs SIADH
A critical differential in neurosurgical/SAH patients — they look similar but management is opposite.
| Feature | SIADH | Cerebral salt wasting |
|---|---|---|
| Volume status | Euvolaemic | Hypovolaemic |
| Mechanism | Water retention | Renal sodium loss (natriuretic peptides) |
| Urine Na⁺ | High | Very high |
| Urine output | Normal/low | High (polyuria) |
| Treatment | Fluid restriction | Salt + volume replacement |
High-yield: Getting this wrong is dangerous — fluid-restricting a CSW patient worsens hypovolaemia and risks cerebral ischaemia. The discriminator is volume status.
Clinical features of hyponatraemia
Symptoms reflect cerebral oedema and correlate with rate of fall more than absolute level.
- Mild (130–135): often asymptomatic, subtle gait/attention deficits, falls in elderly.
- Moderate (125–129): nausea, headache, lethargy, confusion.
- Severe (< 120 or rapid): seizures, obtundation, coma, respiratory arrest, brainstem herniation.
Acute (< 48 h) hyponatraemia is far more dangerous than chronic because the brain has not had time to extrude osmolytes.
Management of hyponatraemia
Severe symptomatic (seizures, coma) — emergency
High-yield: Give 3% hypertonic saline — 100–150 mL bolus over 10–20 min, may repeat ×2 until symptoms improve, targeting a rise of 4–6 mmol/L acutely. Do NOT chase normal sodium.
Correction limits (memorise these numbers)
High-yield: Maximum correction = 8–10 mmol/L in the first 24 hours and 18 mmol/L over 48 hours. In high-risk patients (chronic, malnourished, alcoholic, hypokalaemic, liver disease) keep to ≤ 6–8 mmol/L/24h. Overcorrection → osmotic demyelination syndrome.
The classic Adrogué–Madias formula estimates the change in serum Na from 1 L of a chosen infusate:
Change in Na = (Infusate Na − Serum Na) ÷ (Total body water + 1)
(TBW = 0.6 × weight in men, 0.5 in women; 0.5 and 0.45 in elderly).
Cause-specific therapy
- Hypovolaemic: isotonic 0.9% saline restores volume → switches off ADH → water diuresis (watch for overcorrection here, an autocorrection trap).
- Euvolaemic / SIADH: first-line is fluid restriction (< 800 mL–1 L/day); add oral salt tablets / urea / loop diuretic; vaptans (tolvaptan) = selective V2-receptor antagonists for resistant SIADH or hypervolaemic states.
- Hypervolaemic (CCF, cirrhosis): fluid + sodium restriction, loop diuretics, treat underlying disease; tolvaptan can be used short-term.
High-yield: Tolvaptan must be started in hospital, is contraindicated in hypovolaemic hyponatraemia, and is limited to < 30 days with liver-function monitoring (hepatotoxicity). It causes free-water diuresis (aquaresis) without sodium loss.
Osmotic Demyelination Syndrome (ODS)
Previously "central pontine myelinolysis." Caused by too-rapid correction of chronic hyponatraemia — abrupt rise in tonicity shrinks brain cells that had adapted by losing osmolytes.
- Onset delayed by 2–6 days after correction (biphasic — patient improves then deteriorates).
- Features: spastic quadriparesis, pseudobulbar palsy, dysarthria, dysphagia, "locked-in" syndrome, behavioural change.
- MRI: symmetrical pontine "trident/bat-wing" hyperintensity; extrapontine sites (basal ganglia, thalamus) also affected.
- Risk factors: alcoholism, malnutrition, hypokalaemia, liver disease, Na < 105.
High-yield: If overcorrection occurs, re-lower the sodium using 5% dextrose ± desmopressin (DDAVP) to prevent ODS. Prevention beats cure — ODS is largely irreversible.
Key differentials checklist
- Translocational (hyperglycaemia, mannitol) — corrected Na is normal.
- Pseudohyponatraemia (lipids, paraproteins) — normal osmolality.
- Hypothyroidism and adrenal insufficiency mimic SIADH but are excluded by criteria 5.
- Primary polydipsia vs SIADH — urine osmolality is the splitter (< 100 vs > 100).
- CSW vs SIADH — volume status is the splitter.
Hypernatraemia (Na⁺ > 145 mmol/L)
Always a state of hypertonicity and almost always implies a water deficit relative to sodium. It signifies either impaired thirst, no access to water, or excessive water loss. Because thirst is such a powerful defence, sustained hypernatraemia occurs mainly in those who cannot drink: infants, the unconscious, the intubated, and the elderly/demented.
Etiology — classify by volume status
| Volume status | Mechanism | Causes |
|---|---|---|
| Hypovolaemic (Na & water lost, water > Na) | Hypotonic fluid loss | Renal (osmotic diuresis — hyperglycaemia, mannitol; loop diuretics), GI (diarrhoea — esp. osmotic in children), sweating, burns |
| Euvolaemic (pure water loss) | Free-water loss | Diabetes insipidus (central/nephrogenic), insensible/respiratory losses, fever |
| Hypervolaemic (Na gain) | Excess sodium | Hypertonic saline/NaHCO₃ infusion, salt poisoning, primary hyperaldosteronism, Cushing's |
High-yield: The single most useful test in hypernatraemia is urine osmolality. Low/inappropriately dilute urine (< 300, especially < 150) in a hypernatraemic patient = diabetes insipidus until proven otherwise. Concentrated urine (> 600–800) = appropriate renal water conservation → extrarenal water loss or salt gain.
Diabetes insipidus — central vs nephrogenic
| Feature | Central DI | Nephrogenic DI |
|---|---|---|
| Defect | ↓ ADH secretion | Renal resistance to ADH |
| Causes | Pituitary surgery, trauma, tumour, Sheehan's, idiopathic | Lithium, hypercalcaemia, hypokalaemia, genetic (V2/AQP2), demeclocycline |
| Water deprivation test | Urine stays dilute | Urine stays dilute |
| Response to desmopressin (DDAVP) | Urine osm rises > 50% | Little/no rise (< 10%) |
| Treatment | Desmopressin | Treat cause, thiazide + low salt, amiloride (lithium-induced), NSAIDs |
High-yield: The water-deprivation test followed by desmopressin is the classic discriminator. Copeptin assay is the modern alternative. Lithium is the commonest drug cause of nephrogenic DI; amiloride blocks lithium entry via ENaC.
Clinical features
Reflect cellular dehydration, again predominantly neurological: lethargy, irritability, weakness, hyperreflexia, twitching, seizures, coma. Rapid brain shrinkage can tear bridging veins → intracranial / subarachnoid haemorrhage, especially in infants. Intense thirst is the cardinal symptom if the mechanism is intact.
Management of hypernatraemia
Step 1 — Restore haemodynamics: if hypovolaemic/shocked, give isotonic 0.9% saline first to correct circulating volume.
Step 2 — Replace the free-water deficit:
Free-water deficit = TBW × ([Serum Na ÷ 140] − 1), where TBW = 0.6 × weight (men).
Replace with 5% dextrose or oral water; in milder hypovolaemia use 0.45% saline.
High-yield: Correct hypernatraemia slowly — maximum fall ≤ 10 mmol/L per 24 hours (≈ 0.5 mmol/L/hour). Rapid correction causes cerebral oedema, seizures and death (mirror image of ODS). For acute hypernatraemia (< 24 h, e.g. salt poisoning) faster correction up to 1 mmol/L/h is acceptable.
High-yield: Remember to account for ongoing losses in addition to the calculated deficit, and don't forget that the deficit calculation gives the volume of electrolyte-free water required.
Complications
- Hypernatraemia: cerebral haemorrhage (acute), and cerebral oedema from over-rapid correction (the dangerous iatrogenic complication).
- Untreated DI: severe dehydration, hypovolaemic shock.
Recently asked / exam angle
- Single-best-answer on urine osmolality: A euvolaemic patient with Na 122, low serum osm, urine osm 450, low uric acid → SIADH (and the malignancy to suspect is small cell lung cancer).
- Correction-rate vignettes: chronic alcoholic with Na 110 corrected to 130 in 24 h who then develops dysarthria and quadriparesis after 4 days → osmotic demyelination syndrome; MRI shows central pontine signal change. Management of overcorrection = re-lower Na with 5% dextrose + DDAVP.
- Drug associations: carbamazepine/SSRI → SIADH; lithium → nephrogenic DI; demeclocycline used to treat SIADH (induces nephrogenic DI).
- Formula questions: Adrogué–Madias (hyponatraemia) and free-water deficit (hypernatraemia) are directly testable.
- Neurosurgery patient with hyponatraemia + polyuria + hypovolaemia → cerebral salt wasting, treat with salt and volume (NOT fluid restriction).
- Hyperglycaemia correction factor (1.6 per 100 mg/dL) appears in DKA/HHS questions.
- Vaptan facts: tolvaptan = V2 antagonist, aquaresis, 30-day hepatotoxicity limit, contraindicated in hypovolaemia.
- Beer potomania / tea-and-toast with urine osm < 100 — a recurring "odd cause" stem.
Rapid revision
- Dysnatraemias are water problems; serum Na reflects water, not sodium content.
- Algorithm: serum osmolality → volume status → urine Na & urine osmolality.
- Hyperglycaemia = translocational (pseudo) hyponatraemia; add 1.6 mmol Na per 100 mg/dL glucose above 100.
- Urine osm < 100 in hyponatraemia → primary polydipsia / beer potomania; > 100 → ADH active (SIADH).
- SIADH = euvolaemia + low serum osm + concentrated urine + urine Na > 30–40 + low uric acid/urea; commonest tumour = small cell lung cancer.
- CSW vs SIADH: differ by volume status; CSW is hypovolaemic and needs salt + volume.
- Severe symptomatic hyponatraemia → 3% hypertonic saline 100–150 mL bolus, raise Na 4–6 mmol/L.
- Correction cap: ≤ 8–10 mmol/L/24 h (≤ 6–8 if high risk); overcorrection → osmotic demyelination syndrome (delayed 2–6 days, spastic quadriparesis, pontine MRI signal).
- Overcorrected? Re-lower with 5% dextrose + desmopressin.
- SIADH treatment: fluid restriction first; tolvaptan (V2 antagonist) for resistant cases — hospital start, < 30 days, hepatotoxic.
- Hypernatraemia = hypertonicity = water deficit; key test is urine osmolality; dilute urine → diabetes insipidus (lithium = commonest nephrogenic cause).
- Correct hypernatraemia ≤ 10 mmol/L/24 h with 5% dextrose/0.45% saline; too fast → cerebral oedema.