Introduction
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
Biochemical assessment
The degree of biochemical hyponatraemia is classified in three groups:
Clinical assessment
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:
The clinical status of the patient reflects the balance of a number of factors:
Severe symptoms are unlikely with serum sodium >130 mmol/L and alternative causes of neurological dysfunction should be considered in this context.
Management decisions should be made on the basis of presenting clinical symptoms and signs rather than the degree of hyponatraemia (1, 2).
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).
Disclaimer
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.
References
- 1↑
Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier RW, Sterns RH & Thompson CJ. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. American Journal of Medicine 2013 126 S1–S42. (doi:10.1016/ j.amjmed.2013.07.006)
- 2↑
Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, Decaux G, Fenske W, Hoorn E & Ichai C et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. European Journal of Endocrinology 2014 170 G1–G47. (doi:10.1530/EJE-13-1020)
- 3↑
Mohmand HK, Issa D, Ahmad Z, Capuccio JD, Kouides RW & Sterns RH. Hypertonic saline for hyponatraemia: risk of inadvertent overcorrection. Clinical Journal American Society of Nephrology 2007 2 1110–1117. (doi:10.2215/cjn.00910207)
- 4↑
Grant P, Ayuk J, Bouloux P-M, Cohen M, Cranston I, Murray RD, Rees A, Thatcher N & Grossman A. The diagnosis and management of inpatient hyponatraemia and SIADH. European Journal of Clinical Investigation 2015 45 888–894. (doi:10.1111/eci.12465)