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CDHB

Hypernatraemia

Hypernatraemia (serum sodium>145 mmol/L) is due to a deficiency of water relative to solute (sodium) in the extracellular fluid and always represents a hyperosmolar state. Thirst and release of antidiuretic hormone are important defence mechanisms preventing hyperosmolar states. Therefore hypernatraemia is rarely found in alert patients with normal thirst and access to water. At risk groups include infants, the elderly, intubated patients, and those with altered mental status.

Symptoms - depend on time course (acute vs chronic) and level of sodium:

• Lethargy, weakness, irritability.
• Confusion, seizures, coma.

Causes

• Pure water depletion:
  • No water!
  • Hypodipsia either 2^o e.g., severe illness, dementia, coma or rarely 1^o hypothalamic injury.
  • Diabetes insipidus; cranial or nephrogenic. Hypernatraemia is only sustained if there is impaired thirst or lack of access to water.
• Depletion of hypotonic fluid i.e. loss of relatively more water than Na.
  • Renal loss:
    • Loop diuretic, osmotic diuresis (glucose, urea, mannitol).
    • Post-obstructive diuresis, polyuric phase AKI (acute kidney injury).
    • Intrinsic renal disease.
  • GI tract loss:
    • Vomiting, NG drainage, diarrhoea, laxatives.
  • Skin loss:
    • Burns, excessive sweating.
• Solute excess (uncommon)
  • Sodium: ingestion of sodium chloride, sea water, sodium bicarbonate infusion
  • Hyperalimentation: IV or parenteral nutrition

Approach to Hypernatraemia

Evaluation includes history to determine likely cause, clinical assessment of volume status (usually depleted except in rare cases of sodium overload) and neurological function. Investigations should include:

• Plasma electrolytes, urea, creatinine.
• Calcium. Calculate osmolarity [(2 x Na) + urea + glucose] (all mmol/L).
• Urine osmolality, sodium and glucose.
• Urine osmolality >700-800 mOsm/kg confirms normal ADH secretion and action and suggests non-renal fluid losses and/or a blunted thirst response.
• Low urine osmolality (<700 mOsm/kg) indicates a urine concentrating defect. Causes include solute diuresis (e.g., glucose), diabetes insipidus either cranial or nephrogenic (lithium, hypercalcaemia, severe hypokalaemia, congenital).
• Formal evaluation for diabetes insipidus requires a water deprivation test which should only be performed after initial fluid resuscitation and with close supervision. Please consult Endocrinology.

Management of Hypernatraemia

Cerebral adaptation to hypernatraemia occurs within hours, involves accumulation of intracellular electrolytes and organic osmolytes, and minimizes the potential reduction in cerebral volume - therefore, as with hyponatraemia, acute hypernatraemia is more likely to be symptomatic and should be more aggressively managed than chronic hypernatraemia (>24hr). Treatment involves administering hypotonic fluid and addressing the cause. Principles include:

• In acutely hypernatraemic and symptomatic patients (e.g., accidental sodium loading) rapid correction is appropriate, reducing Na by 1 mmol/L/hr to approximately 145 mmol/L.
• In patients with hypernatraemia of longer or unknown duration, a maximal correction rate of 0.5 mmol/L/hr is appropriate - targeted fall 10 mmol/L/day.
• The preferred route of administering fluids is oral, nasogastric, or subcut.
• Generally use pure water (orally) or 5% glucose - the lower the osmolality of the fluid, the lower the volume required for correction.
• Avoid sodium chloride 0.9% unless frank circulatory collapse.
• Remember to allow for ongoing fluid losses both incidental and obligatory.
• Use the following approach to estimate the amount of excess water required to return the serum sodium to 140 mmol/L in 60 kg patient with serum sodium 168 mmol/L:
  • 3 mL of electrolyte-free fluid/kg of lean body weight will lower serum sodium by 1 mmol/L.
  • thus in a 60 kg patient 180 mL electrolyte free fluid (3 mL/kg x 60 kg) will lower serum sodium by 1 mmol/L.

  if initial serum sodium is 168 mmol/L and target sodium is 140 mmol/L the electrolyte free fluid requirement is therefore 5 L or [180 mL x (168-140)]

• As a guide to the rate of fluid infusion, use the following approach:
  • Assume serum sodium will decrease by 1 mmol/L if 3 mL/kg infused per hour.
  • If desired decrease in serum sodium is 10 mmol/24hr, then initial rate of free water administration should be approximately 75 mL/hr, derived as follows:

    (3 mL/kg/hr x 60 kg x 10 mmol/L/day/24h per day)

  • To account for 40 mL/hr of obligate water loss in sweat and stool and 50 mL/hr of ongoing urinary free water loss, the total water prescription is 165 mL/hr (75+40+50).
• These are guidelines and frequent clinical and biochemical reviews are essential in patients with severe and symptomatic hypernatraemia; repeat sodium after 4-6 hours initially.
• For acute cranial diabetes insipidus (CDI) desmopressin (synthetic AVP) should be given parenterally in a dose of 1-4 microgram IM or IV with repeat doses as clinically required based on urine output and osmolality, usually 12-18 hourly. Consult Endocrinologists.
• Established CDI requires the use of desmopressin in a dose adjusted according to clinical need, usually 10-20 microgram daily by intranasal spray.

Topic Code: 3695