Hypernatremia in Critical Care


by Patrick Neligan (c) 2002


What is it?

Extracellular fluid osmolality is determined by the sodium concentration. A serum sodium of >145mEq represents a hypertonic state. There is a net deficit of water in relation to sodium.

This may be caused by water loss or sodium gain.

1. Free water deficit (dehydration), caused, for example or diabetes insipidis.

2. Deficit of both sodium and water, with relatively higher water loss, caused, for example, by overaggressive diuresis. Potassium deficit may co-exist.

3. Sodium gain following administration of hypertonic fluids, such as sodium bicarbonate.

Why is it important in ICU?

Hypernatremia leads to profound thirst. Critically ill patients do not control over fluid intake and are not able to communicate their thirst to carers. Hypernatremia can be associated with significant neurologic sequelae: initially the brain shrinks due to volume depletion (this is, after all the mechanism by which we control intracranial pressure), which makes the blood vessels vulnerable to rupture. The brain adapts to dehydration by expressing more solute, which may lead to cerebral edema, neurological deficit or convulsions.

How do you manage it?

There are two steps: 1. Identify and control/reverse the source. 2. Correct the free water deficit / sodium excess

Step 1: identify the cause

Causes of hypernatremia in ICU:

Pure Water Loss

Large insensible losses: no humidifier on mechanical ventilator.

Diabetes insipidis – neurologic (associated with head injury, brain hemorrhage or meningitis) or nephrogenic (caused by lithium, demeclocyclin, amphoteracin B, heavy metal poisoning, hypokalemia and hypercalcemia).

Hypotonic Fluid Loss

Excessive diuresis with loop of osmotic diuretics.

Polyuric phase of acute renal failure



Nasogastric drainage.



Hypertonic sodium gain

Sodium bicarbonate infusion

Hypertonic saline administration.

Step 2: Correct the free water deficit / sodium excess

This can be achieved by either calculating the free water deficit and replacing water, or calculating the required rate of sodium reduction for the chosen infusate.

If your patient is becoming hypernatremic following therapeutic intervention (such as diuresis to correct fluid “overload”) this is a clear indication that the objectives have been achieved, even exceeded.  To correct hypernatremia, fluid and electrolyte losses must be restored. The rate of correction depend on the duration of hypernatremia: in general, for ICU patients, correction at a rate of 1 mmol Na/litre /hour is appropriate; if hypernatremia is prolonged, the 0.5 mmol Na/litre/hour is more advisable (to reduce the risk of rebound cerebral edema).

How do I calculate the free water deficit?

This is a useful equation for calculating how much free water the patient requires to return the serum sodium to normal:

0.6 x patient’s weight in kg x (patient’s sodium/140  - 1)

Where 0.6 x weight* = estimated body water, and 140 = desired sodium

So, for a 70 kg male with a serum sodium of 150 mEq/L = 3 litres (we will use this example in discussions below).

*This represents total body water (TBW) for young males; for females and elderly males multiply the weight in Kg by 0.5

My preference, where possible, is to replenish water losses enterally, and administration of an extra 100ml per hour of free water over two days, in this case, will certainly reduce the serum sodium towards the goal level. However, this is usually a luxury, and often the fluid and electrolyte deficit needs to be replenished by intravascular fluid administration. Any fluid can be used, either isotonic or hypotonic: however, the more hypotonic the fluid, the more rapidly the deficit will be replaced.

In the example above, we wish to reduce the patient’s serum sodium by 10 mEq/L – how much of what fluid do we use?

This depends on the amount of sodium in the chosen fluid, and then applying this figure to the formula below:

Change in serum Na per litre = Infusate Na – Serum Na / weight in Kg x 0.6 -1

Fluid (infusate)

Na Content

Change per liter in 70kg male with Na 150 mEq/L

Dextrose 5% in water


- 3.5 mEq Na / L

0.2% NaCl in D5%


- 2.7 mEq Na / L

0.45% NaCl


- 1.7 mEq Na / L

Lactated Ringers


- 0.5 mEq Na / L

We choose D5% (dextrose 5% in water). We wish to correct this patient’s sodium at a rate of 1mEq/L/hour: as each 1 liter will correct 3.5mEq, then the rate of fluid infusion is 1000ml/3.5 = 285ml/hour.

Clearly, for simple hypernatremia, the choice of fluid determines the volume required to correct the sodium abnormality (a much larger volume of LR is required compared with D5%).

What if the patient has been excessively diuresed, and now has hypokalemic metabolic alkalosis in addition to hypernatremia?

This type of patient has "contraction" alkalosis, caused by free water deficit. The patient is alkalotic due to an increase in the strong ion difference (SID between sodium + potassium versus chloride). Sodium must be retained to maintain ECF volume, so potassium is sacrificed in order to maintain electroneutrality. Frequently, however, contraction alkalosis features hyperkalemia, hyperuricemia and hyperchloremia. The treatment is free water replacement, with potassium repletion as necessary.
Hypochloremic metabolic alkalosis usually occurs in the face of a normal serum sodiums.

What is really important is that the cause of the problem is stopped: one cannot correct a fluid and electrolyte abnormality, while simultaneously administering diuretics.


   (1)    Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med 2000; 342(20):1493-1499.




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