Hyponatremia

Hyponatraemia is a serum sodium below 135 mEq/L and is the commonest electrolyte disorder in hospitalised patients, associated with increased morbidity, mortality, length of stay and cost.

Severity: mild 130–134 mEq/L, moderate 125–129 mEq/L, profound/severe below 125 mEq/L; by duration, acute (<48 hours) or chronic.

Older patients are more susceptible and may show cognitive impairment even with mild hyponatraemia — a fall in sodium, especially if rapid, can cause cerebral oedema, lethargy, seizures, coma and death.

Age-related tubular changes: reduced sodium reabsorption in the thick ascending limb producing “senile sodium leakage”, medullary hypotonicity, and inability to concentrate urine maximally.

Reduced plasma renin and aldosterone with blunted responses, plus elevated natriuretic peptides, enhance urinary sodium loss.

Exaggerated vasopressin response to a hyperosmolar stimulus with impaired baroreceptor-mediated suppression — older people over-secrete ADH.

Reduced renal blood flow and reduced ability to excrete a water load; salt-restricted diets and poor appetite compound the problem.

Drugs are the leading cause — thiazide diuretics (classic), SSRIs, SNRIs, tricyclics, carbamazepine and oxcarbazepine, antipsychotics, PPIs, NSAIDs, desmopressin, chlorpropamide, vincristine, ifosfamide, cyclophosphamide and opioids.

SIADH — from CNS disease (stroke, haemorrhage, infection, metastases), pulmonary disease (pneumonia, tuberculosis, tumour), and small-cell carcinoma of the lung as a paraneoplastic syndrome.

Hypovolaemic: vomiting, diarrhoea, diuretics, third-space losses, cerebral salt wasting, mineralocorticoid deficiency.

Hypervolaemic: heart failure, cirrhosis, nephrotic syndrome, advanced CKD.

Endocrine: hypothyroidism, glucocorticoid deficiency and abrupt withdrawal of glucocorticoid therapy.

Low solute intake: “tea-and-toast” diet and beer potomania — very relevant to socially isolated older Indians on rice-and-tea diets.

Pseudohyponatraemia (hyperlipidaemia, paraproteinaemia) and translocational hyponatraemia (hyperglycaemia, mannitol) must be excluded first.

Step 1: serum osmolality — exclude pseudo- and translocational hyponatraemia. Step 2: urine osmolality — <100 mOsm/kg suggests primary polydipsia or low solute intake. Step 3: urine sodium — <20 mEq/L suggests hypovolaemia or oedematous states; >30–40 mEq/L suggests SIADH, diuretics or adrenal insufficiency. Step 4: clinical volume status.

Diagnostic criteria for SIADH: sodium <135 mEq/L, plasma osmolality <280 mOsm/kg, urine osmolality inappropriately high (>500 mOsm/kg), urine sodium >20 mEq/L, clinical euvolaemia, and normal renal, adrenal and thyroid function.

Additional tests: thyroid function, 9 a.m. cortisol or short Synacthen test, blood urea and uric acid (low uric acid supports SIADH), chest imaging and CT head if a cause is not evident.

Severe symptoms (seizures, coma, respiratory arrest): 3% hypertonic saline 100–150 mL as an intravenous bolus, repeated up to three times as needed, aiming for a rapid initial rise of 4–6 mEq/L to relieve cerebral oedema.

Correction limits are critical: no more than 8–10 mEq/L in 24 hours and 18 mEq/L in 48 hours, and no more than 8 mEq/L/24 h in high-risk patients (alcoholism, malnutrition, hypokalaemia, liver disease, sodium <105 mEq/L) — to prevent osmotic demyelination syndrome.

Chronic asymptomatic hyponatraemia: treat the cause, stop the offending drug, and use fluid restriction (typically 500–1000 mL/day) with adequate salt and protein intake.

Second-line agents: oral urea 15–60 g/day (effective, safe, cheap), loop diuretic with oral salt, demeclocycline, and tolvaptan in euvolaemic or hypervolaemic SIADH with high ADH activity.

If over-correction occurs, re-lower the sodium with 5% dextrose with or without desmopressin; monitor sodium 2– 4 hourly during active correction.

Long-term consequences even of mild chronic hyponatraemia include gait instability, attention deficits, falls, osteoporosis and fractures — an important geriatric syndrome, not a laboratory curiosity.