Management of Severe Hyponatraemia in Children & Young People

Published by PIER Network Clinical Review Group • Ratified by Child Health Governance • Last updated: 08-2026

Introduction In children, a normal plasma sodium is 135-145mmol/L (though there may be regional variations in laboratory normal ranges of up to 2mmol/L). Hyp...

Introduction

In children, a normal plasma sodium is 135-145mmol/L (though there may be regional variations in laboratory normal ranges of up to 2mmol/L). Hyponatraemia is classified as acute (<48 hours) or chronic (>48 hours) (1).

The severity of hyponatraemia is defined as (1):

  • Mild hyponatraemia, 131-135mmol/L

  • Moderate hyponatraemia, 126-130mmol/L

  • Severe hyponatraemia, ≤125mmol/L

It is the most common electrolyte abnormality in children and associated with significant morbidity and mortality (2,3) but this can be reduced with prompt diagnosis and management (4).

The RCPCH published a hyponatraemia related deaths inquiry report in 2018 (2). This was carried out in response to five paediatric hyponatraemia related deaths between 1995 and 2001. Literature at the time cited more than 50 cases of serious injury or child death from this cause (5).

The speed of onset of hyponatraemia (rate of change of sodium) is a better predictor of risk of neurological compromise than the sodium level itself (6), due to rapid drops in sodium causing water to move from the extracellular compartment to the intracellular compartment to maintain osmotic balance, resulting in cerebral oedema. Children have a higher brain-to-skull size ratio with a smaller space in which the cerebral tissues can swell. This results in children being more prone to cerebral herniation than adults (7).

Current literature suggests that a 4-6mmol/L increase in plasma sodium is sufficient to reverse severe manifestations of acute hyponatraemia, however correction should not exceed 12mmol/L over the first 24 hours (4,7,8,9). Rapid sodium correction can result in osmotic demyelination syndrome (see later section). Correction should be more cautious in patients with chronic hyponatraemia, with a maximum correction of 4-8mmol/L over a 24-hour period (10,11).

Hyponatraemia is caused by water retention (e.g. excess water intake or impaired free water excretion), sodium loss or a combination of the two. It is more common for hyponatraemia to be due to retention of water diluting the plasma sodium than pure sodium loss. Therefore, hyponatraemia is commonly a disorder of water balance mediated by either appropriate or inappropriate arginine vasopressin (AVP) production.

  • For this guideline, we define severe hyponatraemia as a plasma Na ≤ 130mmol/L in a patient who is symptomatic. Symptoms include seizures, impaired consciousness, respiratory depression, hypertension, bradycardia, encephalopathy, headache, nausea and vomiting. Proceed immediately to <Figure 2> if this is the clinical situation.

  • The treatment for asymptomatic hyponatraemia can be found in <Figure 3>.

Purpose & Target Audience

To provide clinical guidance for all staff involved in the care and management of severe hyponatraemia in Children & Young people in the Wessex Region with the exception of Paediatric Oncology patients – for this patient group please use https://drive.google.com/file/d/1WdTyBNBxbR1myaCZG2jIkiunUpXokJDW/view

Assessment

Should be focused on:

  • Severity of symptoms. These primarily reflect the extent of neurological dysfunction (due to cerebral oedema) and can include nausea, vomiting, lethargy, confusion, agitation, headache, seizures and hyporeflexia. Coma and respiratory arrest can occur in severe cases.

  • Duration and onset of hyponatraemia: view previous results, thorough history of symptoms from family/carers, recent weights.

  • Additional important points to elicit in the history are water intake and presence of salt-craving

  • Ascertaining fluid status is essential: weight trend, physical examination, fluid balance and urine output.

Figure 1: Causes of Hyponatraemia by Fluid Status to Aid Diagnosis

Hypovolaemic

Euvolaemic

Hypervolaemic

  • Total body water decreased

  • Total body sodium decreased

  •  Urinary sodium > 20mmol/L suspect renal losses.

  •  Urinary sodium < 20mmol/L suspect extrarenal losses

  • Total body water increased

  • Total body sodium normal

  • Urinary sodium generally > 20mmol/L(12)

  • Total body water increased

  • Total body sodium increased

  • Urinary sodium > 20mmol/L consider AKI/CKD

  • Urinary sodium < 20mmol/L consider oedematous states

  • Gastrointestinal losses

  • Skin losses

  • Abdominal third spacing

  • Excessive enteral hypotonic fluid intake

  • Excessive intravenous fluid intake

  • Renal losses: tubulopathy, diuretics

  • Increased ADH secretion: pulmonary, trauma, endocrine (hypothyroid, low cortisol)

  • Oedematous states: nephrotic syndrome, heart failure, cirrhosis, hypoalbuminaemia

  • Hypoaldosteronism

  • Salt-wasting

  • SIAVP: inappropriately HIGH urinary osmolality (> 100 mOsm/kg) and low plasma osmolality (<275 mOsm/kg)

  • Acute kidney injury

  • Chronic kidney disease

  • Hyperglycaemia

  • Metabolic alkalosis

  • Medications: chemotherapy, antiepileptics, vasopressin, desmopressin

  • Obstructive uropathy

Investigations

As soon as possible:

  • Blood gas

  • Urea and electrolytes, bicarbonate, full blood count, serum albumin

  • Paired plasma and urine osmolality

  • Urinary sodium

  • Urinary creatinine

  • Blood glucose (if hyperglycaemia and hyponatraemia, consider DKA)

 

If new presentation and/or endocrine cause suspected, then also send:

  • Renin & aldosterone

  • Cortisol

  • ACTH, 17- ACTH, 17-OH-Progesterone and serum for storage.

 

Southampton Children’s Hospital:

  • There are 2 versions of a “hyponatraemia bundle” on CHARTS, pictured below. 

  • Again, if this is a new presentation, use the endocrine bundle which includes ACTH, 17-OH-Progesterone and serum for storage.

Rationale:

  • Paired urine and plasma osmolalities are required to diagnose syndrome of inappropriate antidiuresis (SIAD)

  • Urine osmolality may indicate whether water excretion is normal or impaired. Hyponatraemia is usually associated with plasma hypo-osmolality (osmolality <275 mOsm/kg). Suspect another osmotically active substance (such as mannitol or glycerol containing compounds) if plasma not hypo-osmolar.

  • If urine osmolality is <100mOsm/kg, hyponatraemia likely due to excessive free water

  • A low urinary sodium of <20mmol/L suggests body salt depletion and may be associated with intravascular volume depletion. Consider a non-renal cause of sodium loss.

  • Urinary sodium and fractional excretion of sodium (FENa - see below) may help to differentiate (but may not diagnose) the causes of hyponatraemia. However values in the 1st year of life can be misleading. 

  • Haematocrit and albumin can be useful indicators of volume status

Fractional excretion of sodium (FENa):

  • FENa = fraction of sodium filtered by the glomeruli that appears in the urine

    • FENa = (urine [Na+] mmol/L/ serum [Na+] mmol/L) x (serum [creatinine] µmol/L / urine [creatinine] µmol/L)

    • Used to help differentiate pre-renal disease (decreased renal perfusion) from intra-renal/post-renal causes

    • Limited in that it is only useful in acute kidney injury (not chronic kidney disease) and cannot be used in patients on diuretics

    • FENa <1% can be interpreted as normal, if >1% there may be excessive urinary sodium loss

    • Calculator:  https://www.mdcalc.com/calc/60/fractional-excretion-sodium-fena

Blood gas readings:

  • Sodium levels vary by measurement technique and whole blood sodium measurements obtained via point-of-care blood chemistry analysers (“blood gas machines”) on average  2-3mmol/L lower than central laboratory-based measurements (13,14). Clinicians should keep this variation in mind when managing patients with abnormal sodium values.

  • Hypercholesterolemia/hypertriglyceridemia can cause pseudohyponatremia on blood gas readings (15).

  • Always send formal urea and electrolytes (+ investigations mentioned above) when sampling from these patients. However, in the acute emergency situation, severe hyponatraemia on a blood gas reading should be acted on – do NOT wait for formal urea & electrolyte results. 

Management

The presence of clinical signs such as seizures, altered consciousness or respiratory depression is a medical emergency and should be treated using Figure 2.

All children should have a strict fluid balance including weight. Consider an in and out urinary catheter to collect samples or an indwelling catheter for accurate assessment of ongoing fluid status.

Hyponatraemic seizures may be refractory to anticonvulsant therapy. Treat seizures as per <APLS/PIER guideline> however do not delay sodium correction to facilitate this.

The SORT guideline for making up 3% hypertonic saline, when premade 2.7% hypertonic saline is not available, can be found at www.sort.nhs.uk.

Figure 2: Emergency Management of Severe Hyponatraemia

Algorithm: Management of Acute Severe Hyponatraemia. . Steps: Plasma sodium <130mmol/L and clinical signs: seizures, altered consciousness or respiratory depression: | call 2222: | 2ml/kg IV 2.7% sodium chloride (maximum 100ml) over 10-15 minutes. : If signs of impending brainstem herniation then administer over 2-3 minutes | Recheck plasma sodium on blood gas: send formal urea and electrolytes. Send repeat urine for osmolality, sodium and creatinine | Plasma sodium >125mmol/L or increased by 5mmol/L AND seizures terminated/improvement in clinical signs: | Re-assess volume status: Send repeat urine for osmolality, sodium and creatinine. Ongoing support in HDU/PICU setting: • Commence Plasmalyte (or 0.9% sodium chloride if not available). • A 4-6mmol/L increase in plasma sodium is sufficient to reserve severe manifestations of hyponatraemia. • Ensure that the rate of increase in plasma sodium does not exceed 12mmol?L in a 24 hour period. • Measure formal urea and electrolytes 4 hourly until plasma sodium > 135mmol/L | Whilst hypertonic salien is prepared, the follow should be done:: • Vascualar access: blood gas and glucose, urea and electrolytes, bicarbonate, FBC, LFT, plasma osmolality, renin and aldosterone. • SCH: use <hyponatraemia (bundle)> order set on CHARTS • Catheter: urine for osmolality, sodium and creatinine.

Figure 3: Management of Asymptomatic Hyponatraemia

Algorithm: Management of Asymptomatic Hyponatraemia. . Steps: At Any Point: : Plasma sodium <130mmol/L and clinical signs: - Seizures - Altered Consciousness - Respiratory depression | : Assess fluid status (as per Figure 1) | Medical Emergency 2222 and follow Figure 2: | HYPOVOLAEMIC: | EUVOLAEMIC: | HYPERVOLAEMIC: | Treat underlying cause: | : Administer intravenous fluid with Plasmalyte (or 0.9% sodium chloride if not available) at maintenance volume + replacement based on % dehydration | : Fluid restrict to 2/3 maintenance volume with enteral fluid where possible Consider oral sodium supplementation | : Ongoing monitoring of plasma sodium required in context of fluid status: - Sodium correction should be gradual and no more than 4-8mmol/24 hours - Check plasma sodium and fluid balance (including weight) at least 12 hourly.

Osmotic Demyelination Syndrome (ODS)

ODS can occur because of rapid sodium correction through osmotic stress leading to cerebral apoptosis and loss of myelin. It encompasses central pontine myelinolysis (CPM) and extrapontine myelinosis (EPM).

Clinical presentation occurs several days after a rapid rise in plasma sodium (>12mmol/24 hours).

Signs include:

  • Confusion

  • Delirium

  • Hallucinations

  • Tremors

  • Balance issues

  • Cranial nerve palsies

  • Dysphagia

  • However asymptomatic cases have been identified through MRI scanning of patients thought to be at risk. 

ODS is rare in paediatric patients, with death as an outcome in 9% of reported cases. It is thought to be underestimated and under-reported (16).

References

  1. National Institute for Health and Care Excellence. Hyponatraemia. NICE Clinical Knowledge Summaries https://cks.nice.org.uk/topics/hyponatraemia/ 

  2. RCPCH Hyponatraemia Related Deaths Inquiry Report 2018

  3. Adrogué HJ. Consequences of inadequate management of hyponatremia. Am J Nephrol. 2005 May-Jun;25(3):240-9.

  4. Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier RW, Sterns RH, Thompson CJ. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013 Oct;126(10 Suppl 1):S1-42.

  5. Moritz ML, Ayus JC. Preventing neurological complications from dysnatremias in children. Pediatr Nephrol. 2005 Dec;20(12):1687-700.

  6. Nakamura A, Nakayama T, Azegami T, Komatsu M, Hayashi K. Risk factors for neurological symptoms in hyponatraemic patients: a retrospective cohort study. Clin Kidney J. 2025 Nov 19;18 (12).  

  7. Zieg J. Evaluation and management of hyponatraemia in children. Acta Paediatrica. 2014. 103, pp. 1027–1034.

  8. Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, Decaux G, Fenske W, Hoorn EJ, Ichai C, Joannidis M, Soupart A, Zietse R, Haller M, van der Veer S, Van Biesen W, Nagler E; Hyponatraemia Guideline Development Group. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014 Feb 25;170(3):G1-47.

  9. Sahay M, Sahay R. Hyponatremia: A practical approach. Indian J Endocrinol Metab. 2014 Nov;18(6):760-71.

  10. NICE guideline: Intravenous fluid therapy in children and young people in hospital. NG29. 2015, updated 2020.

  11. Sterns R, Nigweakr M, Hix J. The treatment of hyponatraemias. Seminars in Nephrology 2009. Volume 29, Issue 3. P282-299.

  12. UpToDate, LLC. Urine sodium. Medscape https://emedicine.medscape.com/article/2088449-overview?form=fpf

  13. Levene I. Towards evidence-based medicine for paediatricians. Question 1: Is measurement of sodium from capillary blood accurate enough for clinical decision making? Arch Dis Child. 2014 May;99(5):481-2.

  14. Morimatsu H, Rocktäschel J, Bellomo R, Uchino S, Goldsmith D, Gutteridge G. Comparison of point-of-care versus central laboratory measurement of electrolyte concentrations on calculations of the anion gap and the strong ion difference. Anesthesiology. 2003 May;98(5):1077-84.

  15. Lea El Hage, Edmunds Reineks, Christian Nasr. Pseudohyponatremia in the Setting of Hypercholesterolemia. AACE Clinical Case Reports. Volume 5, Issue 2. 2019. Pages 172-174.

  16. Lalit R. Bansal, Timothy Zinkus. Osmotic Demyelination Syndrome in Children, Pediatric Neurology, 2019. Volume 97. 12-17, ISSN 0887-8994.

This clinical guideline was ratified for regional paediatric care across Wessex and Thames Valley. Return to all clinical guidelines.