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GERICLINICS

GeriQBank · Paper II · Q4

Hyponatraemia

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Part II — Fluid, Electrolyte and Acid–Base Disorders
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Attempt it firstOutline your answer before revealing it — definition, causes, evaluation, management and the geriatric angle.Reveal answer

Hyponatraemia

7-Mark Note — 6 textbook points + 1 latest update = 7 points

Recurring question — asked ×3. Extra scaffolding provided below.

TEXTBOOK CORE — 6 POINTS

1.

Definition, severity and significance. Serum sodium <135 mEq/L; mild 130–134, moderate 125–129, severe or profound <125 mEq/L. It is the commonest electrolyte abnormality in hospitalised older adults and is described as "a serious and often overlooked problem of the older patient". Critically, elderly patients are more susceptible and may manifest cognitive impairment with even mild hyponatraemia.

2.

Why older people are predisposed. Impaired water excretion — minimum urine osmolality is only 92 mOsm/kg versus 52 in the young, and maximum free water clearance falls from 16.2 to 5.9 mL/min. In addition, infusion of hypertonic saline produces a greater rise in plasma vasopressin in older than in younger persons, and older adults are heavily exposed to the precipitating drugs.

3.

The three general causes. (a) Decreased renal blood flow with a decreased ability to excrete a water load; (b) diuretic administration leading to water intoxication — a condition rapidly corrected by discontinuing the diuretic; and (c) excess vasopressin secretion (SIADH), to which older adults are more prone. The drugs to interrogate: thiazides (the classic), SSRIs and other antidepressants (risk increases with age, female sex, low body weight and renal failure), carbamazepine, chlorpropamide and barbiturates (more frequent in older individuals), NSAIDs, PPIs, opioids and desmopressin.

4.

Step 1 of evaluation — is it true hypotonic hyponatraemia? Measure serum osmolality. Normal osmolality = pseudohyponatraemia (severe hyperlipidaemia, hyperproteinaemia, paraproteinaemia). High osmolality = translocational hyponatraemia (hyperglycaemia, mannitol infusion). Low osmolality (<275 mOsm/kg) = true hypotonic hyponatraemia — proceed.

5.

Step 2 — urine osmolality, then urine sodium, then volume status. Urine osmolality <100 mOsm/kg = appropriately dilute urine → primary polydipsia or low solute intake ("tea-and-toast" diet, beer potomania) — both common in the socially isolated older person. Urine osmolality >100 = impaired water excretion → check urine sodium: <20 mEq/L suggests hypovolaemia or an oedematous state (heart failure, cirrhosis, nephrotic syndrome); >30–40 mEq/L suggests SIADH, diuretic use, adrenal insufficiency or salt wasting. Always also check TSH and a 9 a.m. cortisol.

6.

Step 3 — treat by volume status, and correct slowly. Hypovolaemic → 0.9% saline and stop the diuretic. Euvolaemic (SIADH) → fluid restriction. Hypervolaemic → salt and fluid restriction with a loop diuretic; treat the heart or liver disease. Water restriction and hypertonic saline are indicated when the patient is symptomatic or the sodium level is below 120 mEq/L; in an emergency give 3% saline 100–150 mL over 10– 20 minutes, repeated up to three times until symptoms abate or sodium rises 4–6 mEq/L. This rapid correction should not exceed a 20 mEq/L rise during the first 48 hours (1 mEq/L/h), to avoid neurological damage and central pontine myelinolysis. Serum Na <135 mEq/L → measure serum osmolality ↓ Normal osm → pseudo High osm → translocational Low osm <275 → true (lipids, protein) (glucose, mannitol) ↓ continue ↓ Urine osmolality — <100 = polydipsia / low solute · >100 = impaired water excretion ↓ Urine sodium — <20 mEq/L = hypovolaemia or oedematous state · >30–40 mEq/L = SIADH, diuretic, adrenal, salt wasting ↓ Hypovolaemic Euvolaemic Hypervolaemic 0.9% saline, stop diuretic Fluid restriction ± second line Salt + fluid restriction, loop diuretic LATEST UPDATE (2023–PRESENT) — 1 POINT

7.

Correction limits have tightened, and deliberate re-lowering is now standard. Current practice caps correction at ≤8–10 mEq/L in the first 24 hours and ≤18 mEq/L over 48 hours, and at ≤6–8 mEq/L per 24 hours in patients at high risk of osmotic demyelination syndrome — malnutrition, alcohol use, hypokalaemia, liver disease, and initial sodium below 105 mEq/L, a risk profile that describes a large share of frail older inpatients. If the cap is breached, active re-lowering with 5% dextrose with or without desmopressin (the "DDAVP clamp") is recommended, and proactive desmopressin co-administration from the outset is increasingly used to make the rise predictable. Note also the danger of autocorrection: once a hypovolaemic stimulus or a thiazide is removed, vasopressin switches off and the sodium can rise dangerously fast on its own — so recheck sodium every 4–6 hours in the first day.

CURRENT PRACTICE UPDATE

Aspect Textbook Current recommendation

Maximum correction 20 mEq/L over 48 h (1 mEq/L/h) ≤8–10 mEq/L in 24 h; ≤6–8 in high-risk patients Overcorrection Avoid it Actively re-lower with 5% dextrose ± desmopressin Emergency therapy Hypertonic saline infusion 3% saline as 100–150 mL boluses, targeting a 4–6 mEq/L rise Exam approach: Write the textbook 20 mEq/48 h rule and the modern 8–10 mEq/24 h cap, and name osmotic demyelination syndrome (the current term for central pontine myelinolysis). Both together is the full-mark answer.

MEMORY ANCHORS & 15-SECOND SKELETON

Skeleton: Define and grade → why the old are vulnerable (diluting defect + vasopressin + drugs) → three general causes → serum osmolality → urine osmolality → urine sodium → volume status → treat by volume compartment → correction rate and osmotic demyelination.

Numbers: 135 / 130 / 125 / 120 · urine osm cut-off 100 · urine Na cut-offs 20 and 30–40 · serum osm 275 · 3% saline 100– 150 mL boluses · target rise 4–6 · cap 8–10 per 24 h · min urine osm 92 vs 52.

EXAMINER TRAPS

Diagnosing SIADH without excluding hypothyroidism, adrenal insufficiency and diuretic use — the commonest error in the whole topic.

Skipping serum osmolality and treating a pseudohyponatraemia.

Giving 0.9% saline to a patient with SIADH — the urine is more concentrated than the infusate, so free water is retained and the sodium falls further.

Forgetting the risk of autocorrection after the thiazide is stopped or volume is restored. Treating the number rather than asking "is this patient symptomatic, and is it acute or chronic?" — that question dictates everything.

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