Hyponatraemia

Hyponatraemia is defined as a serum sodium concentration <135 mmol/L. It is a disorder of water balance rather than just sodium balance. Severe hyponatraemia (<120 mmol/L) can cause cerebral oedema, seizures, and coma. The diagnostic approach focuses on assessing volume status. 1. Hypovolaemic (Low volume): Occurs with sodium loss (e.g., diuretics, diarrhoea, vomiting, Addison's disease). 2. Euvolaemic (Normal volume): Most commonly due to Syndrome of Inappropriate ADH (SIADH), hypothyroidism, or secondary adrenal insufficiency. 3. Hypervolaemic (High volume): Occurs in oedematous states where ECF is high but effective arterial blood volume is low (e.g., Heart Failure, Cirrhosis, Nephrotic Syndrome). SIADH criteria include low plasma osmolality, high urine osmolality (>100 mOsm/kg), and high urine sodium (>30 mmol/L). A critical management rule is that chronic hyponatraemia must be corrected at a rate no faster than 8-10 mmol/L per 24 hours to prevent Osmotic Demyelination Syndrome (ODS), a devastating neurological condition.

Sodium is the primary determinant of plasma osmolality. Hyponatraemia usually results from an excess of water relative to sodium. This is regulated by Antidiuretic Hormone (ADH), which is released from the posterior pituitary in response to high osmolality or low blood volume. ADH acts on V2 receptors in the collecting duct to insert aquaporins, increasing water reabsorption. In SIADH, ADH is released despite low plasma osmolality (caused by tumours like Small Cell Lung Cancer, CNS disorders, or drugs like SSRIs). In hypovolaemic states, the 'hypovolaemic stimulus' for ADH overrides the 'osmotic inhibition', causing water retention even as sodium is lost. When serum sodium falls, water moves into brain cells via osmosis, causing cerebral oedema. If sodium is replaced too rapidly, the sudden rise in extracellular tonicity pulls water out of brain cells too quickly, leading to the destruction of the myelin sheath (ODS), typically in the pons.

Mild hyponatraemia (130-134) is often asymptomatic. Moderate levels cause nausea, headache, and confusion. Severe hyponatraemia (<120) or a rapid drop leads to seizures, reduced level of consciousness (GCS), and respiratory arrest due to brainstem herniation. Clinical assessment of volume status is vital: Look for signs of dehydration (dry mucus membranes, low JVP, postural hypotension) suggesting hypovolaemia, or signs of overload (pitting oedema, raised JVP, crackles) suggesting hypervolaemia. In euvolaemic hyponatraemia, the patient looks 'wet neither in the tissues nor the pipes'. Potential underlying causes must be screened: Lung cancer (SIADH), heart failure, or medication use. ODS presents several days after correction with 'locked-in' syndrome, dysarthria, and dysphagia.

Bloods: U&Es (check Na+ and Creatinine), Serum Osmolality (confirms true hyponatraemia), Glucose (hyperglycaemia causes pseudohyponatraemia), Thyroid Function Tests (TFTs), 9am Cortisol (to exclude Addison's). Urine: Urine Osmolality and Urine Sodium (essential for differentiating SIADH from other causes). Imaging: Chest X-ray if SIADH suspected (look for malignancy).

General: Stop offending drugs (Thiazides, SSRIs). 1. Hypovolaemic: IV 0.9% Normal Saline; this restores volume and shuts off the ADH trigger. 2. Euvolaemic (SIADH): Fluid restriction (typically 500-1000ml/day); sometimes V2-receptor antagonists (Vaptans) or Demeclocycline. 3. Hypervolaemic: Fluid restriction and Loop diuretics. 4. Severe/Symptomatic: If seizures/coma, consider cautious Hypertonic (3%) Saline in a critical care setting to raise sodium by only 1-2 mmol/L/hr for a few hours. Monitoring: Re-check Na+ every 4-6 hours. If correction is too fast, consider giving IV Dextrose or Desmopressin to 're-lowering' the sodium.