Hyponatraemia (serum sodium <135 mmol/L) is common. Presentation can cover a broad spectrum of symptoms and signs. Severe hyponatraemia can be life threatening requiring emergency assessment and treatment. This guidance covers emergency management of severe symptomatic hyponatraemia.
Recognition of the patient presenting with severe and moderately severe, symptomatic hyponatraemia
The degree of biochemical hyponatraemia is classified in three groups:
Mild: 130–135 mmol/L
Moderate: 125–129 mmol/L
Profound: <125 mmol/L
Severity of clinical presentation may not match the degree of hyponatraemia: profound hyponatraemia may be symptom-free, while some patients with moderate biochemistry may have significant neurological symptoms and signs. For the purposes of this guidance, symptoms have been classified as follows:
Severe symptoms: vomiting, cardiorespiratory arrest; seizures; reduced consciousness/ coma (Glasgow Coma Scale ≤8)
Moderately severe symptoms: nausea without vomiting; confusion; headache
Mild or absent symptoms
The clinical status of the patient reflects the balance of a number of factors:
Biochemical degree of hyponatraemia
Rate of development of hyponatraemia
The intrinsic ability of the central nervous system to adapt to changing osmolar stress
The range and degree of co-morbidities
Severe symptoms are unlikely with serum sodium >130 mmol/L and alternative causes of neurological dysfunction should be considered in this context.
Treatment of the patient presenting with severe or moderately severe symptomatic hyponatraemia
See Fig. 1 for the recommended approach. Patients with severe symptoms require immediate treatment with hypertonic saline, irrespective of the cause of the hyponatraemia.
The decision to treat with hypertonic fluid and the supervision of treatment with hypertonic fluid should the responsibility of a senior clinician with appropriate training and experience. The aim is to achieve a 5 mmol/L rise in serum Na+ within the first hour, reducing immediate danger from cerebral oedema while minimising the risk of over-rapid correction and osmotic demyelination.
If the clinical status of the patient does not improve after a 5 mmol/L rise in serum Na+ in the first hour, we recommend taking additional steps as outlined in Fig. 2.
Managing over-correction of serum Na+
Over-correction of serum Na+ risks precipitating osmotic demyelination. The condition underlying the patient’s presentation with hyponatraemia may well change during the first 24 h with cause-specific intervention; the situation is dynamic. If the limit of 10 mmol/L in the first 24 h or 18 mmol/L in the first 48 h of treatment is exceeded, hypertonic fluid should be stopped. We recommend consulting a clinician with experience in managing over-correction who may wish to consider introducing hypotonic fluid, with or without concurrent anti-diuresis (3).
Differential diagnosis of hyponatraemia following emergency treatment
Measurement of urine osmolality and urine Na+ concentration are central to defining the aetiology of hyponatraemia. An algorithmic approach to establishing the cause of hyponatraemia, in-line with other recent guidance, is outlined in Fig. 3 (1, 4).
The document should be considered as a guideline only; it is not intended to determine an absolute standard of medical care. The doctors concerned must make the management plan for an individual patient.