+1 Recommend
1 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      SOCIETY FOR ENDOCRINOLOGY ENDOCRINE EMERGENCY GUIDANCE: Emergency management of severe symptomatic hyponatraemia in adult patients

      1 , , 2 , 3 , the Society for Endocrinology Clinical Committee 4
      Endocrine Connections
      Bioscientifica Ltd

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          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: Mild: 130–135 mmol/L Moderate: 125–129 mmol/L Profound: <125 mmol/L 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: 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. 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. Figure 1 Patients with hyponatraemia presenting with severe symptoms. Recommended approach to the use of hypertonic sodium chloride. 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. Figure 2 Patients with hyponatraemia treated with hypertonic saline. Recommended approach if no improvement following 5 mmol/L rise in Na+ in the first hour. 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). Figure 3 Diagnostic algorithm for patients presenting with hyponatraemia. For use following emergency treatment.

          Related collections

          Most cited references2

          • Record: found
          • Abstract: found
          • Article: not found

          Hypertonic saline for hyponatremia: risk of inadvertent overcorrection.

          Data regarding dosage-response relationships for using hypertonic saline in treatment of hyponatremia are extremely limited. Objectives of this study were to assess adherence to previously published guidelines (limiting correction to 12 mEq/L per 24 h and in 9.7% was >18 mEq/L per 48 h. No patient's rate was corrected by >25 mEq/L per 48 h. Among patients with serum sodium <120 mEq/L, the observed increase in sodium exceeded the rise predicted by the Adrogué-Madias formula in 74.2%; the average correction in overcorrectors was 2.4 times the predicted. Inadvertent overcorrection was due to documented water diuresis in 40% of cases. The Adrogué-Madias formula underestimates increase in sodium concentration after hypertonic saline therapy. Unrecognized hypovolemia and other reversible causes of water retention pose a risk for inadvertent overcorrection. Hypertonic saline should be infused at rates lower than those predicted by formulas with close monitoring of serum sodium and urine output.
            • Record: found
            • Abstract: not found
            • Article: not found

            Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations


              Author and article information

              Endocr Connect
              Endocr Connect
              Endocrine Connections
              Bioscientifica Ltd (Bristol )
              September 2016
              5 October 2016
              : 5
              : 5
              : G4-G6
              [1 ]Department of Endocrinology Central Manchester University Hospitals Foundation Trust, Manchester Royal Infirmary, Manchester, UK
              [2 ]Leeds General Infirmary Leeds Teaching Hospitals NHS Trust, Blood Sciences, Leeds, UK
              [3 ]Department of Endocrinology University Hospitals of Leicester, Leicester Royal Infirmary, Leicester, UK
              [4 ]The Society for Endocrinology 22 Apex Court, Woodlands, Bradley Stoke, Bristol, UK
              Author notes
              Correspondence should be addressed to S Ball; Email: s.ball@ 123456manchester.ac.uk
              © 2016 The authors

              This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License .

              : 3 August 2016
              : 3 August 2016
              Emergency Guidance


              Comment on this article