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Home | Articles | Electrolyte Disturbances | Hypernatraemia

Hypernatraemia

Last updated 26th April 2024

Mechanisms

  1. Hypernatraemia is a state of hyperosmolality. It primarily occurs as a result of water deficit or, more rarely, sodium gain.
  2. Hypernatremia is uncommon because the ensuing rise in plasma osmolality stimulates the release of both ADH and thirst, thereby minimizing further water loss and increasing water intake.
  3. In adults, it is most often due to water losses in older patients that are not replaced because of impaired mental status

Causes

  1. Reduced water intake:
    • Commonest cause is insufficient water intake in elderly with cognitive impairment
    • Hypothalamic lesions impairing thirst or osmoreceptor function
  2. Free water losses:
    • Central or nephrogenic diabetes insipidus (now called ADH deficiency or resistance)
    • Osmotic diuresis eg glucose in uncontrolled diabetes mellitus
    • Insensible & sweat losses e.g. in fever, exercise, severe burns
    • Gastrointestinal losses
  3. Excess sodium intake or administration of hypertonic sodium solutions

Clinical Features

  1. Symptoms occur because water moves out of the brain (mirror image of hyponatraemia)
  2. Symptoms are uncommon in chronic hypernatraemia (the common form of hypernatraemia) and only likely if hypernatraemia is acute
  3. Symptoms of hypernatraemic dehydration include lethargy, weakness and irritability. If severe, manifestations can include seizures, and coma.

Investigations

  1. Check the drug list to make sure desmopressin hasn’t be inadvertently stopped- Untreated ADH deficiency ( formerly known as Diabetes Insipidus) has resulted in preventable deaths
  2. Full electrolyte panel with glucose, calcium, urea and creatinine to assess for presence of uncontrolled diabetes mellitus, other electrolyte abnormalities, renal impairment.
  3. Measurement of serum and urine osmolality may give further clue to cause.
  4. If urine osm < plasma osm, consider diabetes insipidus (ADH deficiency/resistance)
  5. If urine osm > plasma osm, pure volume depletion not due to diabetes insipidus eg inadequate water intake, GI or insensible losses.


General Management

  1. Treatment should address the underlying cause (e.g. stop offending medication or fluids, treat fever) as well as replacing any free water deficit.
  2. Fluid replacement strategy is based on severity, volume status (hypo, hyper or euvolaemic), and duration of hypernatraemia (chronic if >48 hrs or unknown, acute if <48 hrs)
  3. Nearly all patients with hypernatremia will have chronic hypernatraemia, even those who present with acute changes in mentation who are discovered to have hypernatremia.
  4. Acute hypernatraemia is uncommon, occurring in patients with salt poisoning; in patients with ADH deficiency (diabetes insipidus) who acutely lose the ability to replace their water losses (eg, a patient with ADH deficiency (diabetes insipidus) who undergoes surgery and does not receive adequate intravenous water).
  5. The key is regular monitoring of serum sodium and adjusting the fluids accordingly.

Fluid Replacement

  1. Mild cases of hypernatraemia – replace missing body water with oral water (not electrolyte drinks) or glucose 5% IV.
  2. Severe cases of hypernatraemia eg Na >170mmol/L, give glucose 5% IV unless the patient is volume depleted and hypotensive, in which case give sodium chloride 0.9% IV before water replacement.
  3. It is important that the rate of reduction of serum Na does not occur more rapidly than about 10mmol/L per day.
  4. Reassess and record patient’s blood results and clinical conditions every 8 hours. Recheck serum Na after 2 L of fluid replacement, or after 8 hours at the latest.
  5. Patients should be handed over to the next shift to clarify monitoring and fluid requirements.
  6. If diabetes is simultaneously present, then BM monitoring is required and if the blood glucose is >30mmol/L then follow the Hyperglycaemic Hyperosmolar Guideline
  7. In complex cases, the free water deficit can be calculated and advice can be sought from Biochemistry to guide the rate of water replacement.

What Rate of Infusion?

  1. In acute (<48 hrs) – 3-6ml/kg/hour, aiming to correct sodium to near normal values within 24 hours. If severe symptoms – correct sodium by 2mmol/l/hour in first few hours followed by correction rate of 0.5mmol/l/hour
  2. In chronic (>48 hrs or unknown duration) – 1.35ml/kg/hour, aiming to correct sodium no faster than 0.5mmol/l/hour or 10-12 mmol/l/day

Hypernatremia Due to Correction of Severe Hyperglycaemia

  1. Serum sodium rises because of osmotic shift of water from extracellular fluid into cells and because of loss of electrolyte-free water in the urine as excess glucose is excreted.
  2. Because most of these patients are hypovolemic and hyperglycaemic, free water is usually administered as saline 0.45% at 6-12ml/kg/hr rather than dextrose 5%.

Content by Tina Grant. Updated by Chris Isles.