Sodium is an extracellular cation. The renin angiotensin system is the major regulator of sodium concentration in the body. Decreased renal blood flow can lead to increased renin with consequent conversion of angiotensinogen to angiotensin І and then to angiotensin ІІ by angiotensin converting enzyme (ACE) in the lung. Angiotensin ІІ stimulates aldosterone production from the adrenal cortex leading to increased sodium reabsorption from the distal convoluted tubule. Water homeostasis through stimulation of thirst and antidiuretic hormone (ADH) also plays a crucial role in the determination of sodium concentration in the body.

Hyponatraemia is defined as the presence of serum sodium of < 136 mmol/L [1]. Hyponatraemia is the commonest electrolyte abnormality in in-patients [1] (prevalence ranging from 5 to 15 %) and is more prevalent in some groups of patients including the elderly and postoperative patients [2]. Hyponatraemia has been linked with prolonged in-patient stay [3] particularly in patients with metastatic malignancy and heart failure [4]. Hyponatraemia has been shown to be an independent variable of increased mortality [5, 6] and the increased mortality may be secondary to the acute electrolyte disturbance and its management or the underlying aetiology of hyponatraemia [7]. Acute hyponatraemia is defined as onset of hyponatraemia of < 48 hours duration and chronic as the presence of hyponatraemia > 48 hours duration [5]. Hyponatraemia is further classified as mild (130–135 mmol/L), moderate (125–129 mmol/L) and severe (< 125 mmol/L). Patients with hyponatraemia are usually symptomatic when serum Na < 120 mmol/L.

The diagnosis of hyponatraemia is under reported [8] as its signs and symptoms are non-specific and require a high index of clinical suspicion. The signs and symptoms of hyponatraemia depend on the duration of onset and the degree of severity [1]. The clinical spectrum of hyponatraemia may range from nausea, vomiting, weakness and lethargy to symptoms like falls and increased fracture risk, impaired memory and cerebral oedema [9]. Hyponatraemia may be more than just a biochemical entity and may be a marker of sinister underlying pathology [2] (e.g., presence of congestive cardiac failure, chronic liver disease and malignancy).

Hyponatraemia may be secondary to excess water (secondary to excess infusion of hypotonic fluids or isotonic fluids like dextrose that are metabolised to water), low solute (salt losing conditions), artefactual (analytical or contaminated sample with intravenous fluids), high concentration of osmotically active substances (e.g., glucose and mannitol) and SIADH (syndrome of inappropriate ADH secretion). The common causes of hyponatraemia are tabulated in Table 24.2. Institution of appropriate therapy depends on the underlying aetiology and can be dramatically different ranging from restricting fluid intake to administering fluids.

Plasma osmolality = 2× (serum sodium + serum potassium) + urea + plasma glucose mOsm/Kg. Plasma osmolality is predominantly determined by plasma cations- sodium and potassium. In hyponatraemia, the fall in extracellular tonicity leads to an osmotic pressure gradient with movement of water into the intracellular compartment and consequent cerebral oedema if hyponatraemia is acute in onset [2]. The cerebral adaptation to the development of hyponatraemia involves movement of sodium, potassium and organic osmolytes from the intracellular to extracellular compartment to reduce intracellular tonicity [2]. This adaptation may take upto 48 h and hence the need for more cautious correction of sodium in patients with chronic symptomatic hyponatraemia [2]. However, hyponatraemia is also seen in hyperosmolar states (i.e., hyperglycaemia) where there is movement of water from the intracellular to the extracellular compartment with dilution of serum sodium concentration.