Sodium - Hyponatraemia

This the most common electrolyte disturbance in hospital patients and commonly seen in the ED setting. Patients are usually stable and need no emergency treatment but when severe and acute of onset may be symptomatic and lead to decreased level of consciousness, seizures and death.

The most useful piece in the diagnostic puzzle is the rate at which the deficit occurred and usually it is never known.

  • Serum Na+ normal: 135-145 mmols l-1

  • Mild: 130-135mmols l-1

  • Moderate: 120-130mmols l-1

  • Severe: -1

Causes of hyponatraemia

First assess by volume:

  • Hypovolaemic patient: are the Na losses renal, from drugs or Addison’s Disease or from extra renal such as diarrhoea, vomiting, burns, third spacing or other trauma.

  • Euvoleamic then Syndrome of Inappropriate Antidiuretic Hormone (SIADH).

  • Hyervoleamic or volume overloaded then heart, liver or renal failure may be the cause.

Polydipsia of water particularly in association with some recreational drugs can lead to fatal hyponatraemia.

Hyponatraemia associated with Ecstacy (MDMA):

A relatively common and occasional fatal presentation is hyponatraemia associated with Ecstacy use, particularly in women. Manage symptomatic hyponatraemia with 3mLs/kg of 3% hypertonic saline. For more information see Further References and Resources below.

Symptoms of hyponatraemia

What symptoms occur at what level of sodium are dependent on at what rate the deficit was acquired. For example a patient get to 115 very slowly over a period of months to years and be asymptomatic, whereas if this deficit was acquired over a few days then this may lead to seizures.

Mild to moderate 120-135mmols l-1

  • Fatigue, muscle cramps

  • Nausea, anorexia, vomiting

  • Confusion, headache.

Severe Na

  • Convulsions

  • Coma

  • Focal neurological deficits.


Urine osmolality helps to differentiate between conditions associated with impaired free water excretion and primary polydipsia, in which water excretion should be normal (provided intact kidney function). With primary polydipsia, as with malnutrition (severe decreased solids intake) and reset osmostat, the urine osmolality is maximally dilute, generally less than 100mOsm/kg. A urine osmolality greater than 100mOsm/kg indicates impaired ability of the kidneys to dilute the urine. This usually is secondary to elevated vasopressin (ADH) levels, appropriate or inappropriate.

Serum osmolality readily differentiates between true hyponatremia and pseudohyponatremia secondary to hyperlipidemia, hyperproteinemia, or hypertonic hyponatremia associated with elevated glucose, mannitol, glycine (posturologic or postgynecologic procedure), sucrose, or maltose (contained in IgG formulations).

Urinary sodium concentration helps to differentiate between hyponatremia secondary to hypovolemia and SIADH. With SIADH (and salt-wasting syndrome), the urine sodium is greater than 20-40mEq/L. With hypovolemia, the urine sodium typically measures less than 25mEq/L. However, if sodium intake in a patient with SIADH (or salt-wasting) happens to be low, then urine sodium may fall below 25mEq/L.

In addition: Thyroid-Stimulating Hormone (TSH) and Serum Cortisol Levels - if hypothyroidism or hypoadrenalism is suspected.

Serum albumin, triglycerides, and a serum protein electrophoresis - may also be indicated for particular patients.

Source: Simon, E. et al. (2014) 'Hyponatremia Workup' Medscape.


Severe and Na+
  • Seizures

  • Coma / altered mental status

  • Focal neurological deficit

Treat as per ACLS guidelines, manage seizures in the usual way and in addition give hypertonic saline (3%), 1.5mLs/kg (100mLs for 70kg) over 10mins. If symptoms persist and other causes excluded then can repeat a further 1.5mLs/kg (100mLs) of 3% saline. In 70kg patient 100mLs will give approximately 2mmol/L elevation of serum sodium. Thereafter serum Na should be elevated no greater than 10 mmols in the first 2 hours and 18 mmol in the first 48 hours day to avoid Central Pontine Demyelinolysis.

The risk of Central Pontine Demyelinolysis is greatest in chronic hyponatraemia. In this group aiming for an overall increase in sodium of 5 mmol/L/day should be considered in discussion with your admitting team and intensive care unit.

Mild to moderate = most other patients

Managed with:

  • IV N/Saline (0.9%) hypovolaemic

  • Salt rich diet (where salt lose is diagnosed)

  • Fluid restrict to slowly correct chronic hyponatremia (SIADH)

  • Find and treat the cause

Further References and Resources

  1. Campbell, G. and Rosner, M. (2008) The Agony of Ecstacy: MDMA (3,4-Methylenedioxymethamphetamine) and the KidneyClinical Journal of the American Society of Nephrology, vol. 3, pp. 1852-1860.

  2. Hall, A. and Henry, J. (2006) Acute toxic effects of 'Ecstasy' (MDMA) and related compounds: overview of pathophysiology and clinical managementBritish Journal of Anaesthesia, vol. 96, no. 6, pp. 678 - 685.

  3. NSW Health Guideline - Infants and Children: Management of Acute Gastroenteritis (4th Edition, December 2014)

  4. Simon, E. et al. (2014) Hyponatremia WorkupMedscape.

  5. van Dijken, D., Blom, R., Hene, R. and Boer, W (2013) High incidence of Mild Hyponatraemia in Females Using Ecstasy at a Rave Party, Nephrology Dialysis Transplant, vol. 28, no. 9, pp. 2277-2283

  6. Spasovski et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Nephrol Dial Transplant (2014) 0: 1–39.

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