Principles of management

Treat the underlying disorder: causes of hypernatraemia are given in Table 85.1, and management summarized in Figure 85.1.

Assess the volume status of the patient (Box 85.2) and review fluid balance charts. Is there polyuria (>3 L/day)? In diabetes insipidus, the serum osmolality is usually >300 mOsmol/kg in the presence of an inappropriately dilute urine, that is, urine osmolality is less than serum osmolality.

Check serum sodium, potassium, urea, creatinine, eGFR, calcium and plasma glucose, and serum and urine osmolality.

The choice of fluid and the route and rate of administration depend on the volume status of the patient and the chronicity of the hypernatraemia. Too rapid correction or overcorrection of hypernatraemia may result in brain damage. In mild to moderate hypernatraemia, treating the cause such as hyperglycaemia, or stopping diuretics may be sufficient to correct the derangement.

If the hypernatraemia is chronic (duration >24 h or unknown), aim for a rate of decrease of plasma sodium of no more than 0.5 mmol/L/h, and no more than 10 mmol/L/day, with a target plasma sodium of 145 mmol/L.

If the hypernatraemia has occurred rapidly over a few hours, then prompt correction decreases the risk of osmotic demyelination and improves prognosis without risk of cerebral oedema. Here it is usually appropriate to try to reduce the serum sodium concentration to about 145 mmol/L within 24 h.

Hypovolaemic hypernatraemia

If the patient has hypotension with signs of low cardiac output, give normal saline IV until systolic BP is >110 mmHg.

Then give half-normal (0.45%) saline or 5% glucose IV, or water PO, until the water deficit is corrected.

See Chapter 84 for management of hyperosmolar hyperglycaemic state.

Normovolaemic hypernatraemia

Correct the water deficit with 5% glucose IV or water PO. If the patient has central diabetes insipidus, give vasopressin; if nephrogenic diabetes insipidus, ask advice from a nephrologist.

Hypervolaemic hypernatraemia

This is rare. It may be seen when hypertonic sodium bicarbonate is given for the treatment of metabolic acidosis or hyperkalaemia, or following inappropriate administration of hypertonic saline, or the ingestion of salt. Hyperaldosteronism can cause mild hypervolaemic hypernatraemia.

If related to a hypertonic infusion, discontinue the infusion. Use a loop diuretic (or dialysis) to remove excess sodium.

Principles of management

Treat the underlying disorder: causes of hyponatraemia are given in Table 85.2, and management summarized in Figure 85.2.

Assess the volume status of the patient (Box 85.2) and review fluid balance charts. Check serum sodium, potassium, urea, creatinine, calcium and plasma glucose, with serum and urine osmolality and also check TSH and serum cortisol. Exclude pseudo-hyponatraemia, for example due to lipaemia or severe hyperproteinaemia. In normo-osmolar hyponatraemia consider also hyperglycaemia and sick cell syndrome.

In most cases, hyponatraemia is accompanied by low plasma osmolality (<280 mOsmol/kg) (hypo-osmolar hyponatraemia) and results from an excess of free water, almost always due to the activity of ADH at the renal collecting ducts. This is usually due to appropriate physiological stimuli of ADH secretion from the posterior pituitary, but occasionally to disordered regulation of ADH secretion, the syndrome of inappropriate antidiuretic hormone, SIADH (Table 85.3). SIADH is overdiagnosed. It is only SIADH if no appropriate stimulus for ADH exists. Hypothyroidism and adrenal insufficiency must be excluded before SIADH can be diagnosed. If SIADH is confirmed, arrange CT head/chest/abdomen and pelvis, to investigate for the cause.

Hypo-osmolar hyponatraemia can be categorized into three clinical groups: hypervolaemic, euvolaemic and hypovolaemic.

Rapid correction of hypo-osmolar hyponatraemia is only indicated if this is the cause of severe neurological abnormalities (reduced conscious level, coma, major seizures); it may result in osmotic demyelination of pontine neurons, especially if the brain has adapted to hyponatraemia. The risk of osmotic demyelination is increased in patients with liver failure, malnutrition and potassium depletion, and elderly women taking thiazide diuretics.

Accurate fluid balance assessment is difficult but critical to the correct management of hyponatraemia. Re-evaluate this if serum sodium is not correcting as expected.

Over-rapid correction of hyponatraemia can lead to catastrophic neurological consequences. Frequent evaluation of serum sodium concentration during treatment is essential to avoid doing harm.

Hyponatraemia with severe neurological abnormalities

Assess airway, breathing and circulation and take appropriate resuscitative action where necessary.

Check baseline investigations as above. Place a bladder catheter and send urine for sodium concentration and osmolality. Consider a central line for venous pressure monitoring.

Administer hypertonic saline. Infuse 150 mL 3% saline over 20 minutes. Recheck serum sodium after the infusion. Administer repeated 150 mL infusions of 3% saline. Aim to raise serum sodium by a maximum of 5 mmol/L in the first hour. Continue hypertonic saline infusions until either a) symptoms improve, or b) the serum sodium reaches 125 mmol/L. Aim to raise serum sodium by a maximum of 10 mmol/L in the first 24 hours and 8 mmol/L in subsequent 24 hour periods.

Use of selective vasopressin (V2) antagonists may be considered under expert guidance.

Hyponatraemia without severe neurological symptoms

If the patient has no symptoms attributable to hyponatraemia or is only mildly symptomatic (e.g. headache, nausea, lethargy), hypertonic saline should not be given.

Management depends principally on the patient's fluid status.

• Hypovolaemic hyponatraemia is managed with isotonic intravenous fluid, for example 0.9% saline, aiming for a correction rate of no greater than 12 mmol/L/day.
• Euvolaemic and hypervolaemic hyponatraemia are managed with fluid restriction. In euvolaemic hyponatraemia, oral sodium supplementation may be added if total body sodium is suspected to be deficient. This should be avoided in hypervolaemic hyponatraemia due to cardiac failure and cirrhosis. The selective vasopressin (V2) antagonists such as conivaptan and talvaptan may have a place here, but seek expert advice.

Hyponatraemia associated with glucocorticoid, mineralocorticoid or thyroid hormone deficiencies should correct on replacement.

Drugs associated with hyponatraemia should be stopped.

• Thiazide diuretics. Act via SIADH as well as via their effect on the Na⁺/Cl^- symporter of the distal convoluted tubule.
• Loop diuretics. Less able to cause hyponatraemia than thiazides since their action diminishes the medullary concentration gradient and limits the ability of the kidney to resorb free water as a result of ADH activity.
• Angiotensin-converting-enzyme inhibitors and angiotensin receptor blockers. They usually cause only mild hyponatraemia but limit the ability of the kidney to retain sodium to correct hyponatraemia.
• Antidepressants (tricyclic and SSRI), phenothiazine antipsychotics, quinolone antibiotics, non-steroidal anti-inflammatory drugs and protonpump inhibitors increase ADH secretion or potency.