Hyponatraemia: a complete guide to low sodium

Hyponatraemia is one of the most common reasons GPs refer patients to my clinic, and it is also one of the conditions where specialist input most directly changes outcomes. The mistake I see most often is treatment without first establishing the cause. This article walks through how I assess and treat low sodium in clinic.

Hyponatraemia, or low sodium, is the most common electrolyte disturbance in clinical practice. It affects up to 15 per cent of hospital inpatients and a meaningful proportion of older adults in the community. It is also one of the electrolyte disturbances where specialist input most directly improves outcomes. Mild hyponatraemia often produces no symptoms and resolves with simple measures. Severe or rapidly developing hyponatraemia can cause confusion, seizures, and coma. The wrong treatment, even for the right diagnosis, can be more harmful than the original problem.

This guide walks through what hyponatraemia is, what causes it, how it is investigated, and how it is treated safely. It also covers what patients can do to reduce their risk and what to watch for.

The normal range for serum sodium is around 135 to 145 millimoles per litre. Hyponatraemia is defined as a serum sodium below 135. It is usually classified by severity (mild, moderate, or severe) and by the speed of onset (acute or chronic). Mild hyponatraemia is generally a sodium of 130 to 134. Moderate is 125 to 129. Severe is below 125. The classification matters because the treatment approach depends on both how low the sodium is and how quickly it has fallen.

The symptoms of hyponatraemia depend on both severity and speed of onset. Chronic mild hyponatraemia often produces no symptoms at all and is picked up incidentally on routine blood tests. Slightly more advanced or more rapidly developing hyponatraemia can cause nausea, headache, lethargy, and unsteadiness. More severe forms cause confusion, drowsiness, falls, and ultimately seizures and coma. The brain is the organ most sensitive to changes in sodium because cells swell when the surrounding fluid becomes more dilute. The skull does not accommodate this swelling, and the resulting pressure produces the neurological symptoms.

The causes of hyponatraemia are many, and the right treatment depends entirely on identifying the cause. The standard approach to investigation classifies hyponatraemia by the patient’s fluid status: hypovolaemic (too little fluid), euvolaemic (normal fluid), or hypervolaemic (too much fluid). Each category points toward different causes.

Hypovolaemic hyponatraemia means low total body water along with proportionally lower sodium. Causes include diuretic use (particularly thiazide diuretics, one of the most common culprits in older adults), gastrointestinal losses such as vomiting or diarrhoea, third-spacing of fluid in conditions like pancreatitis, and rarely adrenal insufficiency. The treatment is generally to restore volume with appropriate intravenous fluids while addressing the underlying cause.

Euvolaemic hyponatraemia means total body water is roughly normal but sodium is relatively low. The classic example is the syndrome of inappropriate antidiuretic hormone secretion (SIADH), in which the body retains too much water relative to sodium. SIADH has many triggers including lung disease (pneumonia, lung cancer, chronic obstructive pulmonary disease), brain disease (stroke, trauma, infection, tumours), various medications (especially some antidepressants, antiepileptics, antipsychotics, and chemotherapy agents), and many acute illnesses. Other causes of euvolaemic hyponatraemia include hypothyroidism and the rare cerebral salt wasting syndrome. Treatment of SIADH typically begins with fluid restriction.

Hypervolaemic hyponatraemia means total body water is increased (with fluid overload) but the sodium remains relatively diluted. The main causes are heart failure, liver cirrhosis, advanced kidney disease, and nephrotic syndrome. These conditions all produce a state in which the body retains both water and sodium, but proportionally more water than sodium. Treatment focuses on the underlying condition along with appropriate fluid restriction and management of complications.

Medications deserve specific attention because medication-induced hyponatraemia is one of the most common forms. Thiazide diuretics (bendroflumethiazide, indapamide, hydrochlorothiazide) are perhaps the leading cause of community-acquired hyponatraemia, particularly in older women. SSRIs and other antidepressants are common triggers, especially in older adults. Antiepileptics including carbamazepine and oxcarbazepine can cause SIADH. Antipsychotics, opioids, NSAIDs, and certain chemotherapy agents are all on the list of culprits. Reviewing all medications is therefore a routine and essential part of investigating any case of hyponatraemia.

A particular form of hyponatraemia worth noting is exercise-associated hyponatraemia, sometimes seen in endurance athletes who consume large volumes of low-sodium fluids during prolonged exercise. This is a serious condition that can cause severe symptoms and even death. Prevention through appropriate fluid and electrolyte intake is the key.

Investigation of hyponatraemia begins with a careful history and examination, with particular attention to medications, recent illnesses, and fluid status. Laboratory tests typically include serum and urine osmolality, urine sodium, thyroid function, and adrenal function (a 9 AM cortisol or a synthetic ACTH test in selected cases). The combination of these results, along with the clinical assessment of fluid status, allows the cause to be identified in most cases.

Urine osmolality is particularly informative. A low urine osmolality (under 100 milliosmoles per kilogram) suggests the kidney is appropriately diluting urine, which points to either excessive water intake (primary polydipsia, exercise-associated hyponatraemia) or low solute intake. A high urine osmolality (above 100 milliosmoles per kilogram) indicates inappropriate water retention, suggesting either SIADH or a hypovolaemic state.

Urine sodium helps to distinguish causes further. A low urine sodium (under 30 millimoles per litre) suggests the kidney is appropriately conserving sodium, which fits with hypovolaemia, heart failure, or cirrhosis. A higher urine sodium suggests SIADH, salt wasting, or the effects of diuretics.

Treatment of hyponatraemia depends on the cause, the severity, and the speed of onset. The single most important principle is that sodium should not be corrected too quickly, particularly in chronic hyponatraemia. Rapid correction can cause a devastating brain injury called osmotic demyelination syndrome (also called central pontine myelinolysis). The safe rate of correction is well defined: no more than 8 to 10 millimoles per litre in any 24-hour period, and ideally less. Patients with severe chronic hyponatraemia who are corrected too rapidly can develop permanent neurological damage, even though their sodium is now normal.

For mild chronic hyponatraemia, treatment is generally conservative. The cause is addressed: medications are adjusted, fluid restriction is implemented if appropriate, and any underlying condition is treated. Severe hyponatraemia with significant symptoms (such as seizures or coma) may require controlled correction with hypertonic saline, but this is done in a specialist setting with very careful monitoring.

For SIADH, the treatment hierarchy starts with fluid restriction (typically to 800 to 1,000 ml per day). If this is insufficient, options include increased dietary salt and protein, urea supplementation, demeclocycline (an older option, less used now), and vasopressin receptor antagonists such as tolvaptan. The choice depends on the underlying cause, the severity, and the patient’s overall situation.

For patients on diuretics, the offending diuretic may need to be stopped or changed. For patients on antidepressants causing SIADH, the medication can sometimes be continued at a different dose, or a different antidepressant can be substituted. The decision involves balancing the benefit of the medication for the underlying condition against the risk of recurrent hyponatraemia.

For patients with chronic recurrent hyponatraemia, long-term management often involves stable fluid restriction, regular monitoring of sodium, and adjustment of any contributing medications. Specialist input adds particular value for cases that are unexplained, recurrent, or treatment-resistant.

For patients with hyponatraemia, the practical messages are clear. If your sodium is low, work with your doctor to identify the cause. Review your medications carefully and bring an up-to-date list to all appointments. Follow fluid restriction advice if it is given. Be alert to new symptoms such as confusion, headache, or unsteadiness, particularly during illness or after starting new medications.

I see private patients at Blackrock Clinic, The Beacon Hospital, Bon Secours Dublin, the Hermitage Medical Centre, and St Vincent’s Private Hospital. If you would like a consultation about your kidney health, you or your GP can contact my secretary through drrorymcquillan.ie. Most patients are seen within two to three weeks of referral.