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AKA: hyponatraemia

Evaluation and management of low blood sodium in pediatric patients


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Causes of hypotonic (hypoosmotic) hyponatremia

Hypovolemic hypotonic hyponatremia

  • Net loss of sodium in excess of net loss of free water

  • Usually due to the administration of hypotonic fluid in the setting of fluid losses

    • Distinguished from SIADH because while the retention of free water is driven by ADH, this is β€œappropriate” in the setting of hypovolemia
    • Conditions associated with increased fluid losses:
      • Polyuria
      • Gastroenteritis
        • Secretory or osmotic diarrhea
      • Nasogastric suction
        • Drains/fistulas/ostomies
      • Skin (burns)
      • Respiratory
  • Diuretics

    • More common with thiazide diuretics than loop diuretics, as loop diuretics impair the medullary concentrating ability
    • Thiazide diuretics enhance water reabsorption (independent of ADH) and can lead to the production of urine with sodium greater than that of plasma, thereby causing hyponatremia independent of water intake
  • Less commonly due to salt wasting, which is also associated with hypovolemia

    • Mineralocorticoid deficiency
      • 21-hydroxylase deficiency, hypoaldosteronism (Addison disease)
    • Cerebral salt wasting
      • Extremely rare
  • Non-kidney (extrarenal) losses

    • Diarrhea
      • Particularly secretory diarrhea
    • Vomiting
    • Skin (burns, sweating)
    • Third-spacing (e.g., ascites)
    • Hemorrhage
    • Intense exercise

Euvolemic (isovolemic) hypotonic hyponatremia

  • Increased ADH states)
    • Primary SIADH
      • Nephrogenic syndrome of inappropriate diuresis (rare)
    • Hospitalization
    • Respiratory illness
      • Pneumonia
      • Bronchiolitis
      • Mechanical ventilation
    • Recent surgery
    • Pain
    • CNS injury/infection
    • Medications
    • Hypothyroidism
    • Cortisol deficiency
  • Reset osmostat (rare)
  • Exercise-associated hyponatremia
  • Water intoxication
    • Primary polydipsia (psychogenic polydipsia)
    • Forced water drinking (e.g., hazing rituals)

Hypervolemic hypotonic hyponatremia

  • Decreased effective circulating volume
    • ↓ kidney perfusion β†’ ↑ water retention
    • Cirrhosis, heart failure, nephrotic syndrome
  • Kidney failure
    • ↓ GFR β†’ impaired free water excretion

Signs and symptoms

  • Muscle weakness, gait disturbance
  • Malaise, fatigue
  • Headache
  • Encephalopathy: lethargy, confusion, coma
  • Ataxia
  • Seizures


  • Serum osmolality to confirm β€œtrue” hypotonic hyponatremia
    • Low osmolality = true hypotonic hyponatremia

      noteIn patients with hyponatremia in the setting of kidney failure, the serum osmolality may be measured as normal or high due to elevated serum BUN. However, there is a difference between the measured osmolality and the effective osmolality (i.e., the tonicity). Urea moves freely in and out of cells, and thus does not obligate the movement of water (i.e., it is not an effective osmole). Therefore, patients with azotemia may have true hypotonic hyponatremia despite a normal serum osmolality measurement.

    • Normal osmolality = isotonic hyponatremia (pseudohyponatremia)
      • Lab artifact due to increased fraction of solids in the plasma compartment (e.g., hyperlipidemia, hyperproteinemia)
        • Affects indirect ion-selective electrodes (as is typically used in main laboratory analyzers)
    • High osmolality = hypertonic hyponatremia
      • Sodium is displaced out of the plasma by the presence of other effective osmoles
        • While the sodium is actually low (and not merely measured as low, as with pseudohyponatremia), it is not clinically significant as the negative clinical effects of hyponatremia are due to the associated decreased serum osmolality rather than the hyponatremia per se
      • Causes:
        • Hyperglycemia
          • Glucose is usually a minor serum osmole as it is rapidly transported into cells, but in circumstances (e.g., diabetes, insulin resistant states) it can have a more significant impact on serum osmolality
        • Mannitol
  • Assess volume status
    • Consider aldosterone, cortisol, ADH (copeptin proAVP), ACTH, free T4 and TSH


  • Depends upon the cause, chronicity, and clinical status of the patient
    • Rapid overcorrection, particularly in chronic (β‰₯48 hours) hyponatremia, can cause osmotic demyelination

Acute hyponatremia with severe symptoms

  • Severe symptoms include seizures, loss of consciousness, lethargy, coma
    • Assess for other possible causes of symptoms such as intoxication, drug ingestion, or trauma
      • Exercise caution if alternative explanations for symptoms may be present, as this will cloud the assessment of treatment response
  • Treat with 3% (hypertonic) saline until symptoms resolve or serum Na has increased by >5 mEq/L
    • Dose: 2-3 mL/kg over 20 minutes, x1-3 doses
  • Once severe symptoms have resolved, proceed with more gradual correction of hyponatremia

Restore intravascular volume if necessary

  • Hyponatremia in children is typically associated with hypovolemia, in which cause there is a need to restore both water and electrolyte status
    • If clinically significant hypovolemia present, fluid resuscitation is the next priority
      • Bolus with 20-60 mL/kg of 0.9% (normal) saline

Correcting hypovolemic hyponatremia

  • Sodium deficit (in mEq) = Current total body water (TBW, in L) x ([desired change in plasma Na)
    • See: TBW calculator
      • Alternatively, crude estimate of TBW = 600 mL/kg (0.6 L/kg)
    • Desired change in plasma Na = (desired Na) - (current Na)
  • Replace with IVF, target rate usually 8-10 mEq/L per 24 hours
    • Do not want to increase serum Na by more than 0.5 mEq/L/hour

Euvolemic hyponatremia (SIADH)

  • Fluid restriction
  • Increasing solute load may allow for more liberal fluid restriction
  • Furosemide (Lasix)
    • May be more effective when combined with sodium supplementation