Na=Sodium (Normal range 134-145 meq/L)Hyponatremia, or low sodium, is quite common affecting estimates of 1.7-2.1% of the US population1. There are many causes of Hyponatremia (low serum sodium). For completeness, there are less common causes of Hyponatremia, such as the type associated with hyperglycemia (very high blood sugar) or seen with extremely high lipids or protein levels termed ‘’pseudohyponatremia’. These types are looked at and treated differently then the more common hypotonic Hyponatremia that most patients have.
It’s very important that we recognize something first, nearly all Hyponatremia is caused by the dilution effect of excess water in the blood. This excess water dilutes the sodium level to below 135 meq/L. It’s in this context that we discuss the major causes of Hyponatremia.
Lets start with medications. There are many medications that lead to Hyponatremia, thiazides diuretics being the most common culprits.
Other drugs commonly implicated are antidepressants and anticonvulsants. Street drugs such as ecstasy, bath salts, and amphetamines are also possible causes.
One question that is often brought up is, ‘doctor can I drink too much water?’
Answer, a resounding yes with some caveats.
Its relative to the solute or food you consume. Your kidney can usually do a great job of ridding your body of excess water. Even the great kidneys, however, have their limits. The lowest dilution the kidneys can ever get down to is 50. 50 what you ask? 50 milliosmoles/Liter (mOsm/L). This implies that your kidney needs at least 50 mOsm/L of ‘stuff’ to get rid of that Liter of water you drank. The ‘stuff’ is food like protein (Urea), salt and potassium. The average person eats about 900 mOsm per day. So consider that scenario of 50 osm/L. The implication here is 900 mOsm/50 mOsm/L is 18 liters a day of water one could excrete. That’s over 4 gallons! So if your eating normally you’d have to drink an awful lot to dilute your sodium. This is actually termed psychogenic polydypsia when it happens. On the other hand, if your not eating all that well, say only 250 mOsm/day, then it’s 250/50= 5 liters. Often however, as we age the kidney may only get down to 100 osm dilution. Now 250/100 is only 2.5 liters of water before you start diluting. This type of Hyponatremia is called ‘’tea and toast’ or ‘beer potomania’ (when it’s beer as the main liquid). So yes you can drink too much water even if your kidney is doing it’s very best. Now what if your kidney is getting the wrong signal?
Syndrome of inappropriate ADH secretion or SIADH is just that, inappropriate signal. ADH is anti-diuretic hormone, meaning when it’s around you anti diurese (make less urine). When ADH is on board the kidney holds water very tight and your urine turns darker and more concentrated. Over several days of drinking water and other liquids, your serum sodium will become diluted.
So what causes the ADH to be excreted?
Common triggers for ADH are nausea and pain; that’s why we often see SIADH after surgeries. Other triggers are Lung disease including cancer (especially small cell) and brain diseases such as stroke, bleed, or infection. These SIADH scenarios respond best to UreaAide™ because the Urea induces a nice osmotic diuresis. The osmotic diuresis will counteract the dilution effect and raise the serum sodium level.
Another cause of low sodium levels are true volume depletion from vomiting and diarrhea. Here your body will also excrete ADH but this time the signal is appropriate. This is termed effective arterial volume depletion. This type of hypovolemic Hyponatremia usually corrects with iv fluids.
Other reasons your sodium could be low include: heart failure, cirrhosis of the liver, hypothyroidism, and adrenal Insufficiency. These tend to be obvious in terms of heart or liver disease, however thyroid or adrenal must be considered and tested for.
As you see their are a lot of scenarios in which the sodium may drop and your doctor will work with you to figure out why. The key is making the correct diagnosis and then recommending the best treatment.
1. Am J Med. 2013 Dec; 126(12): 1127–37.e1.
doi: 10.1016/j.amjmed.2013.07.021
PMID:24262726