Approach to hypernatremia: Clinical sciences

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Introduction 0:00–0:35

Hypernatremia is an electrolyte imbalance that occurs when the serum sodium concentration exceeds 100 and 45 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.
Ok. If a patient presents with chief concerns, suggesting hypernatremia first perform an ABCD E assessment to determine if they are unstable or stable.

Unstable Patient 0:35–2:03

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 heart rate, BP 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.
All right. Now, let's go back to the ABCDE assessment and look at stable patients.

Stable Patient 2:03–3:04

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 BP changes.
Moreover, if the patient is hypervolemic, you might find elevated BP. 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.

Hypovolemic Hypernatremia 3:04–3:52

These patients will typically present with elevated heart rate, orthostatic drop in BP 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 mill osmoles per kilogram. You should assess the patient for adequate water intake.
If the water intake is normal. Consider extra renal losses.

Insensible fluid losses 3:52–4:16

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.

GI losses 4:16–4:47

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 causes.
Your patient can experience gi losses which eventually results in dehydration and hypernatremia. Finally let's go over inadequate water intake.

Inadequate water intake 4:47–5:15

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 mill osmoles per kilogram or less.

Renal fluid losses 5:15–7:58

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 nonresorbable osmotic active urinary solute that stimulates diuresis can result in dehydration and Mannitol induced hypernatremia.
Next, if your patient recently had surgical correction of an obstructive uropathy, there's a high chance that hypernatremia occurred as a result of post obstructive diuresis.
This type of hypernatremia typically occurs due to acute decompression of an obstructed ureter or bladder. Finally, if your patient has sickle cell disease, cystinosis or a recent acute kidney injury, the likely cause is renal disease.
Now, moving on to euvolemic patients. In this case, your patient will report polyuria and polydipsia while their physical exam will reveal a normal heart rate without an orthostatic drop in BP.

Euvolemic hypernatremia 7:58–12:05

Also, there will be no signs of dehydration, meaning they will have moist mucous membranes, normal skin turgor and no weight loss.
This spectrum of findings suggests euvolemic hypernatremia. So your next step is to order urine and plasma osmolality and measure the patient's urine output urine osmolality of fewer than 800 mill osmoles per kilogram, but usually less than 300 plasma osmolality of 300 mill osmoles per kilogram or greater and urine output above 50 mL per kilogram per 24 hours are suggestive of diabetes, insipidus, diabetes, insipidus can be central or nephrogenic.
In the central type, the pituitary gland does not produce 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, but they're also compensating for the fluid loss through increased fluid intake. Now, here's a clinical pearl to keep in mind 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 serum sodium increases but the urine remains excessively diluted.
Despite no decrease in urine output. 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 preexisting hypernatremia. Now, once you diagnose diabetes insipidus, the next step is to determine the type by performing a desmopressin challenge test to perform this test.
Give your patient the synthetic vasopressin analog desmopressin and evaluate the urine osmolality. After one hour.
If urine osmolality increases by more than 50% the kidneys are responding to vasopressin normally, which suggests vasopressin deficiency.
In this case, diagnosed central diabetes, insipidus, which usually occurs in the setting of head trauma. A cranial tumor or infiltrative conditions like sarcoidosis.
However, if the urine osmolality increases by 50% or less, the kidneys are not responding to vasopressin. So, diagnosed nephrogenic diabetes, insipidus.
This type can be caused by medications like lithium. It can also cour with electrolyte disorders such as hypercalcemia or hypokalemia.
Now, here's another clinical pearl. Normally the posterior pituitary gland cleaves the preprovasopressin 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 hard to measure for that reason, it's better to measure copeptin.
Since this peptide mirrors the concentration of vasopressin, low copeptin levels usually point towards central diabetes insipidus while high copeptin levels indicate nephrogenic diabetes, insipidus.
Finally, let's go over hypervolemic individuals. These patients often report recent weight gain and shortness of breath while their physical exam usually reveals elevated BP, tachypnea and peripheral edema.

Hypervolemic Hypernatremia 12:05–12:56

These findings are suggestive of hypervolemic hypernatremia. So your next step is to obtain urine sodium and creatinine levels and calculate the phena.
To calculate phena, you need to divide the product of the urinary sodium and serum creatinine by the product of the urinary creatinine and the serum sodium then multiply the dividend by 100.
Knowing the FNA helps to understand the handling of sodium at the level of the kidneys. If the FNA is 2% or greater, consider the possibility of excessive salt administration.

Excess salt load 12:56–13:29

For example, intravenous administration of hypertonic saline and parenteral nutrition can result in excess salt load and subsequent hypervolemic hypernatremia.
On the other hand, if your patient presents with phena values around 1% decreased serum potassium and elevated serum bicarbonate.
Think of primary aldosteronism. Primary aldosteronism results from excess adrenal aldosterone production, which could be caused by a primary adrenal tumor known as K syndrome or from bilateral adrenal hyperplasia.

Primary aldosteronism 13:29–14:07

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.
All right. As a quick recap hypernatremia refers to a serum sodium concentration above 145 milli equivalents per liter.

Review 14:07–14:53

Based on the volume status. Hypernatremia can be categorized as hypovolemic, euvolemic and hypervolemic hypovolemic hypernatremia can be caused by insensible or gastrointestinal fluid losses, inadequate fluid intake or renal conditions.
On the other hand, euvolemic hypernatremia is typically seen in diabetes, insipidus. While hypervolemic hypernatremia could be associated with excess salt administration or primary aldosteronism.
Approach to hypernatremia: Video, Steps, and Uses | Osmosis