Hypernatremia resident survival guide

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Resident Survival Guide

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mounika Lakhmalla, MBBS[2]


Hypernatremia is an electrolyte disturbance consisting of an elevated sodium level in the blood. It is defined as a serum sodium concentration exceeding 145 mEq/L. This is a relatively common problem particularly among young children, older adults, and hospitalized/critically ill who depend upon others to control their water intake.


Life Threatening Causes

Conditions that may cause death or permanent disability within the next 24 hours

Common Causes

The most common cause of hypernatremia is not an excess of sodium, but a relative deficit of free water in the body. Hypernatremia can be caused by many disease processes and drugs.

  • Water loss into cells due to severe exercise or electroshock-induced seizures[3][4], an effect that is mediated by a transient increase in cell osmolality seizures.
  • Hypernatremia can also occur in cases of primary hypothalamic disease due to impaired thirst (hypodipsia) with or without concurrent diabetes insipidus.


Shown below is an algorithm summarizing the diagnosis of Hypernatremia:

Etiology of
Urine Osmolality <600
Urine Osmolality >600
If the criteria for renal loss & GI loss are not satisfied
Renal loss
Gastrointestinal loss
Insensible losses such as due to sweat, breathing, burn


Summary of Treatment for Hypernatremia based on Volume status

❑ Rapid correction ~ 2-3 mmol/L/hour
❑ Not exceeding 12 mmol/L/hour
❑ Slow correction ~ 0.5 mmol/L/hour
❑ Not exceeding 8-10 mmol/L/hour
Volume Status

❑ Fluid resuscitation with a balanced cryatalloid

❑ Then, 5% Dexterose/ Half saline

❑ 5% Dexterose

❑ No loop diuretic

❑ 5% Dexterose

❑ loop diuretic

  • It is important that we determine whether hypernatremia is due to
    • Gain of sodium or
    • Loss of free water or
    • Whether a combination of the 2 is present, which will be the case in most patients with ICU-acquired hypernatremia.
      • In any of these cases hypovolemia, volume resuscitation needs to be performed before efforts to correct hypernatremia take place (by the administration of isotonic solutions).
      • If a loss of free water alone is present, it should be treated by the administration of free water in the form of a 5% dextrose solution
      • 5% Dextrose is safe in terms of hemolysis.
      • Distilled water can be given via a central venous line, As an alternative to 5% dextrose.
  • If pure sodium gain is the case, natriuresis should be induced through the application of loop diuretics. At the same time, fluid loss during loop diuretic therapy must be restored with the administration of fluid that is hypotonic to the urine.
  • In critically ill patients who require renal replacement therapy, correction of hypernatremia can be performed by either intermittent or continuous renal replacement therapy.[5]
  • In case of serum glucose levels, which are hard to control, half isotonic saline can be used as an alternative to a 5% dextrose solution to avoid glucose lapses.
  • Addition of loop diuretics along with half isotonic saline to induce natriuresis is recommended.
  • Osmotic diuresis due to urea is often the cause of renal loss of free water and the consequent rise in serum sodium concentration in critically ill patients [6]. This phenomenon can be observed in patients who are tube-fed or in a catabolic state. High amounts of urea are generated and excreted in the urine. This process leads to the high renal output of osmoles and the consequent loss of water as in glucosuria.

Serum sodium > 145
Urine output
Low < 200
High urine osmolality
Urine osmolality
Hypotonic fluid loss
GI losses nausea, vomiting, renal losses, diuretics

Replace Both free water deficit as well as Current ongoing fluid losses.

Calculate the fluid deficit, or the water that the patient has already lost to get to their current sodium.
(% Body Water x Body Weight) x [(Current Na – Target Na)/Target Na]

Calculate the ongoing fluid losses which is how much free water the patient is losing daily as you replete.

Precision method is the electrolyte free water clearance:
Urine volume x (1- (Urine Na + Urine K) / serum Na)
Add ‘fluid deficit’ and ‘ongoing fluid losses’ to find the target water intake for the patient.
It is recommended that dividing by 24 hours and giving hourly as oral free water (preferred) or D5W if the patient is unable to drink or does not have an NG tube.
NOTE, large volumes of D5W may cause osmotic diuresis (through hyperglycemia) and worsen renal water losses.

Target rate for correction of hypernatremia: 10-12 mmol/day is commonly used[7].

A recent study showed no evidence that more rapid correction was associated with greater risk of mortality, cerebral edema, or adverse events[8]
Negative water
deprivation test
Osmotic diuresis
Collect urine for 24h and calculate a total daily solute excretion
(urine osmolality multiplied by total daily urine volume).

If the total daily solute excretion is >1000 mOsm/day,
then they have an osmotic diuresis (due to high protein feeding, glucosuria, or mannitol).
Glucose Diuresis: Urine Glucose > 250mmol/L or Urine dipstick positive for Glucose
Urea Diuresis: Urine Urea > 250mmol/L and Urine Glucose negative.

Osmotic diuresis can also be caused by Mannitol administration.
Diabetes insipidus
Increased urine osmolality
urine osmolality unchanged
Central Diabetes Insipidus
Nephrogenic diabetes Insipidus
Possible Etiologies include Traumatic brain injury, surgery, or Tumors.

Treatment Options include
Thiazide diuretics[16][17][18].
Indomethacin [20] .

Desmopressin is the preferred agent in almost all patients
and is required for symptom control.
Other drugs mentioned above are used in rare instances.

Low-solute diet with or without a thiazide diuretic
can be tried in cases of Partial DI and mild-moderate polyuria and nocturia.
Possible Etiology:Heriditary causes;Acquired causes like Drugs( lithium, foscarnet, amphotericin B, or ifosfamide);Infilterative disorders;Sickle Cell disease;Hypercalcemia, hypokalemia[23].

Thiazide diuretics in combination with a low salt diet have long been used to treat nephrogenic DI due to lithium.

More recent literature suggests that Acetazolamide may also be effective, and may be useful for patients whose nephrogenic DI is refractory to thiazides.[24].



  • Extreme care must be taken to avoid excessively rapid correction or over correction of hypernatremia, which might increase the risk of iatrogenic cerebral edema, with possibly catastrophic consequences.


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