Approach to hypernatremia: Clinical sciences

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 patient presents with chief concerns suggesting hypernatremia, first, perform an ABCDE assessment to determine if they are unstable or stable.

If unstable, stabilize the airway, breathing, and circulation, obtain IV access, and consider giving your patient IV fluids. Next, put your patient on continuous vital sign monitoring, including blood pressure, heart rate, and pulse oximetry. Finally, be sure to monitor the patient’s urine output.

Now, here’s a clinical pearl to keep in mind! Acute hypernatremia develops in less than 48 hours, with symptoms ranging from mild, such as nausea, to severe neurologic impairment, such as seizures and coma.

On the other hand, chronic hypernatremia presents with no symptoms or only mild ones. This is because, in chronic hypernatremia, there's enough time for the body to adjust to electrolyte changes, which makes neurological symptoms less likely.

Finally, be cautious when treating hypernatremia since aggressive correction of serum sodium levels and aggressive fluid resuscitation can lead to rapid fluctuations in serum osmolality and subsequent cerebral edema.

Alright, now let’s go back to the ABCDE assessment and look at stable patients.

In this case, obtain a focused history and physical examination and order a basic metabolic panel. History might reveal symptoms like muscle weakness, increased thirst, polyuria, and polydipsia.

In extreme cases, the patient might even report a history of seizures.

Next, the physical exam might reveal blood pressure changes. Moreover, if the patient is hypervolemic, you might find elevated blood pressure, and if they are hypovolemic, you might notice orthostatic hypotension. Other important findings include brisk deep tendon reflexes, as well as sudden, brief muscle jerks called myoclonus.

Finally, if labs reveal a sodium level greater than 145 milliequivalents per liter, you can diagnose hypernatremia.

First, let’s focus on hypovolemic patients! Once you diagnose hypernatremia, assess the patient’s volume status! These patients will typically present with elevated heart rate, orthostatic drop in blood pressure, and signs of dehydration like 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 low and urine osmolality is greater than 600 milliosmoles per kilogram, you should assess the patient for adequate water intake!

If the water intake is normal, consider extrarenal losses. Patients with insensible fluid losses might have extensive burns, they might be sweating excessively, or they could have a fever. Any of these scenarios can also be associated with insensible fluid losses, dehydration, and subsequent hypernatremia.

On the flip side, in gastrointestinal losses, history will typically reveal signs of gastrointestinal infections, like vomiting or diarrhea. In some cases, 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 can experience GI losses, which eventually results in dehydration and hypernatremia.

Finally, let’s go over inadequate water intake. One example is low fluid intake, which can occur in individuals with severe dementia. However, some individuals could also present with impaired thirst mechanisms, which is especially common with hypothalamic lesions! These conditions are associated with inadequate fluid intake, subsequent dehydration, and hypernatremia!

Now, let’s go back and take a look at individuals presenting with elevated urine output and urine osmolality of 600 milliosmoles per kilogram or less.

In this case, consider renal fluid losses as a cause of hypernatremia!

For example, if history reveals the use of diuretics for the management of chronic cardiovascular conditions, such as hypertension and congestive heart failure, hypernatremia is probably due to diuretic use!

On the other hand, if history reveals diabetes mellitus; your patient reports polyuria, polyphagia, and polydipsia; and the labs show high glucose levels, think of uncontrolled diabetes mellitus.

Glucose is a non-resorbable osmotic-active urinary solute, and once filtered in the kidneys, it stimulates diuresis, eventually reducing the intravascular volume, which results in hypernatremia!

Now, here’s a clinical pearl to keep in mind! In hyperglycemia, there is an osmotic water shift from the intracellular to the extracellular space, which dilutes the serum and potentially creates a falsely low laboratory serum sodium value. However, over time, the kidneys remove all that excess water in the extracellular space, leading to dehydration and eventually hypernatremia.

In this case, you need to calculate the corrected sodium, which is equal to the measured serum sodium, plus 1.6 times the glucose concentration minus 100, divided by 100.

Similarly, the administration of mannitol, which is also a non-resorbable osmotic-active urinary solute that stimulates diuresis, can result in dehydration and mannitol-induced hypernatremia!