Approach to hypernatremia (pediatrics): Clinical sciences

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Introduction0:00–0:33

Hypernatremia is an electrolyte imbalance that occurs when the serum sodium concentration exceeds 145 milliequivalents per liter.
It typically results from increased water loss or decreased water intake, but in rare cases, it can be caused by an excess salt load.
Now, based on the volume status, hypernatremia can be classified as hypovolemic, euvolemic, and hypervolemic hypernatremia!
Okay, if a pediatric patient presents with chief concerns suggesting hypernatremia, you should first perform an ABCDE assessment to determine if they are unstable or stable.

Unstable patient0:33–1:49

If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and consider IV fluids. Next, put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry; and don’t forget to monitor your patient’s urine output!
Now, here’s a clinical pearl! Patients with an acute rise in serum sodium concentration can develop neurologic complications, such as seizures and coma.
Moreover, increased serum osmolality causes water to rapidly shift out of cells, causing the brain to shrink, subsequently stretching intracranial blood vessels.
In severe cases, blood vessels can rupture and result in intracranial hemorrhage. Also, be cautious when treating hypernatremia, since aggressive correction of serum sodium levels or giving aggressive fluid resuscitation can lead to rapid fluctuations in serum osmolality, resulting in cerebral edema.
Now, let’s go back to the ABCDE assessment and take a look at stable patients. In this case, obtain a focused history and physical examination and order a basic metabolic panel, or BMP.

Stable patient1:49–2:28

Your patient or their caregiver will typically report neurologic symptoms, like irritability, restlessness, and sleepiness.
Additionally, history often reveals a high-pitched cry in combination with increased thirst. Meanwhile, the physical exam may demonstrate increased muscle tone and brisk reflexes; while the BMP will reveal serum sodium levels greater than 145 milliequivalents per liter.
With these findings, you can diagnose hypernatremia, so your next step is to assess the patient’s volume status! First, let’s focus on hypovolemic patients!

Hypernatremia2:28–2:37

Hypovolemic Hypernatremia2:37–3:05

In this case, the physical exam will reveal signs of dehydration, like elevated heart rate and an orthostatic drop in blood pressure.
You may also notice sunken eyes, dry mucous membranes, decreased skin turgor, and a recent weight loss. These findings are highly suggestive of hypovolemic hypernatremia, so your next step is to assess the patient’s urine output and urine osmolality.If the urine output is reduced, meaning less than 1 milliliter per kilogram per hour, and urine osmolality is 750 milliosmoles per kilogram or greater, consider extrarenal fluid loss, such as insensible and gastrointestinal losses, or reduced fluid intake.

Extrarenal fluid loss/reduced fluid intake3:05–3:31

Keep in mind that these are the most common causes of hypernatremia in children.Now, first, let’s focus on hypernatremia due to insensible fluid losses!

Insensible losses3:31–3:59

These patients might have extensive burns, or they might be sweating excessively. Additionally, they could have a fever or require the use of a radiant warmer, phototherapy, or mechanical ventilation.
Any of these scenarios can be associated with insensible fluid losses, dehydration, and subsequent hypernatremia!Next up are gastrointestinal fluid losses.

GI losses3:59–4:44

These are usually associated with signs of gastrointestinal infections, like vomiting or diarrhea. Additionally, some patients might have an ongoing nasogastric suction, while others might be taking high doses of osmotic cathartics, such as lactulose.
No matter what the underlying cause is, your patient is losing excessive fluids over the gastrointestinal tract, which eventually results in dehydration, and again, hypernatremia!
Moreover, hypernatremia due to gastrointestinal loss represents the most common mechanism of hypernatremia in children and often occurs in combination with decreased free water replacement.Finally, let’s go over inadequate fluid intake!

Inadequate intake4:44–5:12

Some common examples include infants with poor intake due to difficulty breastfeeding, children with an impaired thirst mechanism from neurologic conditions, like holoprosencephaly, as well as infants who are unable to communicate thirst to their caregiver!
Any of these conditions can result in hypernatremia due to inadequate fluid intake.Now, let’s go back and take a look at patients who are presenting with elevated urine output, meaning more than 4 milliliters per kilogram per hour, and urine osmolality below 750 milliosmoles per kilogram.

Renal fluid losses5:12–6:39

In this case, consider renal fluid losses as a cause of hypernatremia. For instance, a child might take diuretics for conditions like hypertension, congestive heart failure, or bronchopulmonary dysplasia.
In these patients, hypernatremia is probably due to diuretic use! On the other hand, your patient might present with a history of uncontrolled diabetes mellitus with hyperglycemia, or a recent intravenous mannitol administration.
Glucose and mannitol are non-resorbable osmotic-active urinary solutes, and once filtered in the kidneys, they stimulate diuresis, eventually reducing the intravascular volume, which results in hypernatremia!However, if your patient recently had surgical correction of an obstructive uropathy, such as posterior urethral valves or PUV, there’s a high chance that hypernatremia occurred due to post-obstructive diuresis.Finally, if your patient has sickle cell disease, cystinosis, a recent acute kidney injury, or if they have acute tubular necrosis or ATN with polyuria, hypernatremia is probably caused by renal disease.Okay, moving on to euvolemic patients.
In this case, your patient or their caregiver may report polyuria, polydipsia, and secondary enuresis, which is loss of bladder control after a child has completed toilet training.

Euvolemic hypernatremia6:39–7:19

The physical exam typically reveals a normal heart rate without an orthostatic drop in blood pressure, as well as moist mucous membranes, normal skin turgor, and no weight loss.
This spectrum of findings suggests euvolemic hypernatremia, so your next step is to order a urine and serum osmolality, and measure the patient’s urine output.Let’s look at a urine osmolality of less than 300 milliosmoles per kilogram, with a serum osmolality greater than 300 milliosmoles per kilogram, and a urine output greater than 4 milliliters per kilogram per hour.

Diabetes insipidus7:19–8:46

This is highly suggestive of diabetes insipidus, which can be central or nephrogenic. In the central type, the pituitary gland is not producing enough vasopressin, which normally increases water reabsorption in the kidneys.
On the other hand, in the nephrogenic type, the pituitary gland produces vasopressin, but the kidneys are not responding.
In both scenarios, your patient is losing fluids from the kidneys, but they are also compensating for the fluid loss through increased fluid intake, therefore, there will be no dehydration!Here’s a clinical pearl!
If you suspect diabetes insipidus, but your patient’s urine and serum osmolality don’t meet diagnostic criteria, consider performing a water deprivation test.
After limiting your patient’s water intake, you can confirm the diagnosis if the urine remains excessively dilute despite no decrease in urine output, and if serum sodium increases.
Be careful not to perform this test if your patient’s serum sodium is already elevated, since water deprivation can quickly cause sodium levels to rise even more and exacerbate pre-existing hypernatremia!
Once you diagnose diabetes insipidus, the next step is to determine the type by performing a desmopressin challenge test.

Desmopressin challenge8:46–10:47

To perform this test, give your patient a synthetic vasopressin analogue called desmopressin and evaluate the urine osmolality after 1 hour.
If urine osmolality increases by more than 50 percent, that's a clear indication of vasopressin deficiency and that the kidneys respond normally to vasopressin, so diagnose central diabetes insipidus.
This form is caused by inadequate pituitary secretion of vasopressin, and usually occurs in the setting of head trauma, intracranial tumors like craniopharyngioma, anatomic pituitary or hypothalamus defects, or intracranial surgery.
However, if the urine osmolality increases by 50% or less, the kidneys are not responding to vasopressin, so you can diagnose nephrogenic diabetes insipidus.
This type can be caused by medications like lithium, or by renal tubular disease, such as in sickle cell disease. It can also co-occur with electrolyte disorders such as hypercalcemia or hypokalemia, and rarely, it can be inherited as an X-linked condition.Here’s another clinical pearl!
Normally, the posterior pituitary gland cleaves the pre-pro-vasopressin into vasopressin and copeptin, to release them into the circulation!
Now, you could try to measure the patient’s vasopressin blood levels to differentiate central from nephrogenic diabetes insipidus, but the thing is, vasopressin is quickly removed from the plasma and is really hard to measure!
For that reason, it’s better to measure copeptin since this peptide mirrors the concentration of vasopressin! During the copeptin test, low copeptin levels usually point towards central diabetes insipidus, whereas high copeptin levels indicate nephrogenic diabetes insipidus.Finally, let’s go over hypervolemic individuals.

Hypervolemic Hypernatremia10:47–11:13

These patients may report recent weight gain or shortness of breath, and their physical exam will typically reveal increased blood pressure, tachypnea, and peripheral edema.
These findings are suggestive of hypervolemic hypernatremia, so your next step is to obtain a urine sodium and creatinine level, and calculate the FENa.
If the FENa is 2% or greater, then consider the possibility of excessive salt ingestion or administration.For instance, the history may reveal that a caregiver mixed their infant’s formula improperly, or a child may have received an excess salt load from intravenous hypertonic saline or parenteral nutrition.

Excess salt load11:13–11:42

In this case, the cause of hypernatremia is an excessive salt load, which is a relatively rare cause of hypernatremia.On the other hand, the FENa values around 1%, decreased serum potassium, and elevated serum bicarbonate are highly suggestive of primary aldosteronism, also called primary hyperaldosteronism.Primary aldosteronism results from excess adrenal aldosterone production, which could be caused by a primary adrenal tumor, known as Conn syndrome, or from bilateral adrenal hyperplasia.

Primary aldosteronism11:42–12:24

Autonomous aldosterone production increases renal sodium and bicarbonate reabsorption and potassium excretion, which leads to hypernatremia, hypokalemia, and metabolic alkalosis.
These patients typically present with neuromuscular symptoms, such as fatigue, muscle weakness, muscle cramps, and paresthesias.
Alright, as a quick recap… Hypernatremia refers to a serum sodium concentration above 145 milliequivalents per liter. Based on volume status, hypernatremia can be categorized as hypovolemic, euvolemic, and hypervolemic.

Review12:24–13:23

For hypovolemic patients, assess the urine output and osmolality to determine if your patient has insensible or gastrointestinal fluid losses, or inadequate fluid intake; or if they have renal fluid losses.
For euvolemic patients, check the urine and serum osmolality to evaluate for DI, and once you confirm it, perform a desmopressin challenge to distinguish central from nephrogenic type.
Finally, for hypervolemic patients, calculate FENa to determine whether the cause of hypernatremia is excess salt ingestion or administration,