Guest post: Understanding pseudohyponatremia

by Howard Rodenberg, MD, MPH, CCDS

A few years ago, there was a change of attitude within seizure medicine that manifested itself as new terminology. The older term “pseudoseizure” was replaced by the phrase “psychogenic non-epileptogenic seizure.” The theory behind the change is that the term pseudoseizure implies that the patient is consciously faking the seizure, while the latter suggests that maybe the person can’t help it, that their non-seizure seizure is a result of unconscious forces beyond their control.

I was initially taken aback at this, especially as pseudoseizures make for some of the most entertaining moments in the ED. Every ED doc has his or her own favorite pseudoseizure stories. Mine is the person who, while I was doing a sternal rub to assess her level of consciousness, interrupted her writhing long enough to open her eyes and shout, “Stop doing that! Can’t you see I’m unresponsive?” I got so good with psuedoseizures that there was one parent who would specifically ask for me, because I was the only one who could treat her daughter’s pseudoseizures. The magic words? “I know you’re not having a seizure. It’s okay to stop.”

When the new terminology came out, I thought that perhaps my view was overly negative, and that I might do well to adopt a new, more forgiving paradigm. So, I talked to a neurosurgeon I trusted and asked him about the psychogenic non-epileptogenic seizures. After a careful discussion chock-full of compassion and discernment, he proclaimed, “Sounds like a (expletive deleted, rhymes with ducking) pseudoseizure to me.”

Pseudohyponatremia, however, is something real, and something I’m seeing more often in my denials work. What usually happens is that a diabetic patient with profound hyperglycemia is also diagnosed with hyponatremia by the clinician, and the latter claim is rejected by the payer. As often as I think denials are justified with bogus reasons, this one I actually understand.

Hyponatremia—a decreased level of serum sodium—comes in several flavors. The most common is what we might call hypotonic hyponatremia. (The term “hypotonic” here refers to a true decrease in the tonicity of the serum, or the concentration of solutes—ions and molecules—within that fluid space. Sodium and sodium salts are the principal solutes within extracellular fluid.) This form of hyponatremia usually results from volume loss, such as with dehydration, vomiting or diarrhea; medical conditions such as heart failure and cirrhosis; and use of diuretic agents that inhibit the reabsorption of sodium within the kidney. Less common causes include the Syndrome of Inappropriate Anti-Diuretic Hormone Secretion (SIADH), advanced renal disease, and psychotic polydipsia with water intoxication,

To understand pseudohyponatremia, you need to go all the way back to high school biology and the processes of diffusion and osmosis. As you may recall, solutions on either side of a membrane want to be in balance with each other. So if you have a tank with two compartments, and you put some table salt in one side, over time it will dissolve and be distributed equally throughout the tank as long as the salt can penetrate the divider between both sections. The reverse of diffusion is osmosis, where a higher concentration of solute on one side of a divider pulls in water to achieve dilution and equilibrate the concentration of the solute on either side.

The same is true in the body. If the fluids within one body compartment contain a high concentration of any particular ion or molecule, and the surrounding fluids have a lower concentration of the same substance, they both want to be in balance with each other. Depending on the ability of the molecule to pass between the two spaces, either diffusion or osmosis occurs with the goal of equalizing concentrations within both spaces unless there are physical or physiologic barriers preventing it. Examples of these latter situations include a molecule that’s simply too big to get through a capillary wall, differences in the permeability of cell membranes such as the “blood-brain barrier,” and the active sodium-potassium pump that regulates neuronal cell activation and discharge.

Let’s see how this works when the patient has hyperglycemia. In this scenario, you have a large concentration of glucose within the intravascular space and a lower concentration in the surrounding interstitial tissues. The physics of osmosis will pull water into the serum to dilute the glucose in an attempt to equate the concentrations between the two fluid compartments. As it does, the incoming water also dilutes the sodium concentration within the plasma, resulting in a relative, “false” hyponatremia. This mechanism is why pseudohyponatremia might be better termed a “dilutional hyponatremia.”

(Why osmosis, where water is pulled in, and not diffusion where the glucose simply moves out? Recall that glucose can’t get out of the vasculature and into cells without the help of insulin. In diabetic hyperglycemic states, either there is lack of insulin or high levels of insulin resistance preventing the normal take-up of glucose.)

The exact relationship between serum glucose and serum sodium levels varies slightly within the literature. The traditional rule of thumb has been that for every 100 mg/dl that serum glucose rises over baseline, the serum sodium drops 1.6 meQ/l. Newer literature suggest the actual number may be higher, up to 2.4 mEq/L. If we split the difference at 2.0 mEq/L, a serum glucose of 600 mg/dl (5x a normal baseline of roughly 100 gm/dl) might drop the serum sodium by ten (from 135 to 125 mEq/L).

There are other solutes that can cause a similar dilutional hyponatremia. These include relatively large molecules that are unable to escape from the vasculature into the interstitial space. “Pseudohyponatremia” can also be seen with hypercholesterolemia, hypertriglyceridemia, and abnormalities in plasma proteins as found in multiple myeloma.

It’s important to keep pseudohyponatremia in your CDI toolkit when you run across hyponatremia in the patient with significant hyperglycemia, whether noted in the lab results or physician documentation. You can do the math by hand, but the easiest way to check is by using a free medical calculator app of your choice (I happen to be a big fan of MDCalc.) If the corrected figure is within your institution’s range of acceptable values, then you’re likely seeing pseudohyponatremia.

What do you do when there’s evidence for pseudohyponatremia but the clinician wrote a nonspecific “hyponatremia?” The best way to address this would be through a clinical validation query, and it might be useful to put the selected terms in some kind of frame of reference. One might list choices such as “pseudohyponatremia (often associated with hyperglycemia)” or “hypotonic hyponatremia (related to dehydration, diuretic use, or GU fluid loss)” in an effort to provide a clinical context for the atypical terms.

What do you do with a confirmed diagnosis of pseudohyponatremia? The answer is…nothing. Hot off the press, Coding Clinic, first quarter 2020, describes pseudohyponatremia as an abnormal lab finding inherent to another underlying condition. As such, pseudohyponatremia cannot be coded, and coding efforts should focus on identifying the inciting cause.

 Editor’s note: Rodenberg is the adult physician advisor for CDI at Baptist Health in Jacksonville, Florida. Contact him at howard.rodenberg@bmcjax.com or follow his personal blog at writingwithscissors.blogspot.com. Advice given is general. Readers should consult professional counsel for specific legal, ethical, clinical, or coding questions. Opinions expressed are that of the author and do not represent HCPro or ACDIS.