Hypernatremia
Definitions & Key takeaways
Hypernatremia is a condition where the blood sodium levels are too high, specifically above 145 mEq/L. Having proper blood sodium levels is essential for the conduction of nerve impulses and the balance of water and minerals in the body. When the levels are too high, it can cause dehydration, seizures, coma, and even death.
The concentration of sodium depends on both sodium and water levels in the body. About 60% of our body weight comes from just water, and it basically sits in two places or fluid compartments—it either outside the cells in the extracellular fluid or inside the cells in the intracellular fluid.
The extracellular fluid includes the fluid in blood vessels, lymphatic vessels, and the interstitial space, which is the space between cells that is filled with proteins and carbohydrates.
One third of the water in the body is in the extracellular compartment, wheres two thirds of it is in the intracellular compartment.
Normally, the two compartments have the same osmolarity -- total solute concentration -- and that allows water to move freely between the two spaces.
But the exact composition of solutes differs quite a bit. The most common cation in the extracellular compartment is sodium, whereas in the intracellular compartment it’s potassium and magnesium.
The most common anion in the extracellular compartment is chloride, whereas in the intracellular compartment it’s phosphate and negatively charged proteins.
Of all of these, sodium is the ion the flits back and forth across cell membranes, and subtle changes in sodium concentration tilts the osmolarity balance in one direction or another and that moves water.
This is why we say “wherever salt goes, water flows”. So with hypernatremia, someone can have a high concentration of sodium in the extracellular fluid and therefore the blood, by either losing more water than sodium, or gaining more sodium than water.
Either way this increases the sodium concentration in the extracellular fluid, draws water out of the cells. When hypernatremia develops over a long period of time, the cells get time to adapt and they start generating osmotically active particle, which ends up preventing water from being lost via osmosis.
However, when hypernatremia develops acutely, the cells get no time to adapt, and the loss of water leaves them shriveled up and can cause them to die.
Now, there are several common causes of hypernatremia via water loss. All of us lose some free water everyday without even realizing it, for example through sweat as well as in the moisture breathed out during normal breathing.
Under normal conditions, this loss is replaced by the water we drink but this balance can be tipped when you have a high fever or exercise a lot on a hot summer day.
In those situations, you can have temporary hypernatremia which is easily fixed by drinking lots of water. Another way that the body can lose free water is through the kidneys.
When the nephrons filter blood and form urine, some of the water in the filtrate is reabsorbed in the distal convoluted tubule and the collecting duct.
When you’re dehydrated, the hypothalamus releases antidiuretic hormone also called ADH or vasopressin, which acts on receptors on the nephron to boost its ability to reabsorb water.
So if there’s brain damage affecting the part of the hypothalamus that controls the release of ADH, then ADH levels could fall and the nephron wouldn’t reabsorb as much water, meaning more fluid gets lost and the urine becomes more dilute, and the sodium concentration in the blood gets more concentrated.
This is called central diabetes insipidus because the fault lies centrally, in the hypothalamus. People with central diabetes insipidus make up for it by drinking more water, though those like infants who can’t drink water on their own can become severely hypernatremic.
Another possibility is that the hypothalamus makes ADH normally, but the receptors in the kidney stop responding to it. This time the fault is in the kidneys, so it’s known as nephrogenic diabetes insipidus.
Again the urine becomes dilute and the sodium concentration in the blood becomes concentrated, and just like central diabetes insipidus, people with this type also drink water to make up for the loss.
Alternatively, there might be brain damage that only affects the thirst center in the hypothalamus rather than the ADH secreting part of the hypothalamus.
Here, the kidneys aren’t losing water, but the person is drinks too little water while still losing some through sweat, urination, and breathing, again resulting in hypernatremia.
In rare cases, when there’s major damage to the hypothalamus, ADH may not get released and the thirst center may be destroyed, which means that the person will lose a lot of water in the urine and still won’t feel thirsty - a dangerous combination.
Instead of water loss, hypernatremia can also be caused by sodium gain. This happens most commonly when a patient in the hospital is being given sodium intravenously to help increase their sodium level, and too much is given too quickly.
Occasionally, this can also happen simply because somebody’s diet has too much salt. But in either situation, the kidneys usually do a good job of getting rid of too much sodium, so it only usually happens if there’s also some sort of kidney dysfunction alongside them.
Symptoms of hypernatremia are related to the underlying cause - for example, some patients may have signs of dehydration, whereas others may have signs of excess fluid in their tissues.
Long-standing hypernatremia typically causes fewer cause symptoms, because the cells have a chance to adjust, whereas acute hypernatremia can cause cell death, particularly in the central nervous system, resulting in serious problems like an altered mental status, seizures, or even a coma.
The first step in diagnosing hypernatremia is to figure out if a patient’s intravascular volume is low “hypovolemic” or normal “euvolemic”.
If a person is hypovolemic, they’re usually drinking too little water or sweating a lot, like on a hot day. In this situation, the kidneys are trying to hold on to water by peeing out thick, concentrated urine with osmolarity of over 600 mOsm/kg.
At the same time, the kidneys are also trying to preserve sodium so they have a urine sodium concentration less than 20 mEq/L.
If instead in a hypovolemic patient the kidneys aren’t functioning right and are losing sodium, then the urine sodium concentration will be higher than 20 mEq/L, and this could be because as a result of medications like osmotic and loop diuretics or even a kidney disease.
On the other hand, if a person is euvolemic, then it’s usually because their kidneys are dumping water, like in diabetes insipidus.
Their urine osmolality is usually below 300 mOsm/kg, and they have a urine sodium concentration less than 20 mEq/L. Treatment of hypernatremia depends on the underlying cause, but ultimately the goal is to reduce the sodium concentration.
Individuals with diabetes insipidus with a normal thirst mechanism can do this by drinking water. If intravenous fluids have to be given, it has to be done carefully to avoid complications like cerebral edema.
Alright, as a quick recap… hypernatremia is an electrolyte disorder that describes a high concentration of sodium in the blood, which can be caused either by losing too much water or gaining too much sodium.
Either way, hypernatremia can cause water to shift out of the cells, and in severe cases it can cause brain cells to shrink and die.
Diagnosing hypernatremia involves checking the volume status and measuring the urine osmolarity and urine sodium concentration.
Treatment generally involves slowly and carefully giving back free water to normalize the sodium concentration over time.
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