Nephrologists are often consulted for evaluation of hyponatremia. While there can be a lot of causes, the basic approach to diagnosis is simple. First, look at serum osmolality. Serum sodium concentration is considered a surrogate for tonicity of the extracellular fluid. As such, if the serum sodium is low, osmolality is expected to be low. But if it is not, think of other osmotically active substances as glucose (hyperglycemia) or exogenous effective osmoles such as mannitol or pseudohyponatremia (as in too much triglyceride or protein level [rare with the use of ion-specific electrodes by labs these days]).

Next look at urine osmolality. If it is high (arbitrary cut off >100 mOsm/kg), there is ADH (anti-diuretic hormone) activity going on in the kidney. Remember, hyponatremia is almost always due to water excess (thereby diluting sodium level) and not sodium deficit. If urine osmolality is low (<100), kidney is excreting maximally dilute urine but still not able to correct low serum sodium concentration – typically happens when the patient is taking too much water coupled with low solute.

Urine osmolality gives an idea about ADH activity. Beyond this, it is of not much help to distinguish between various causes. This is where physical examination (= POCUS) helps to objectively evaluate fluid status and narrows the differential.

Then look at urine sodium. It will be low (arbitrary cut off 20 or 30) if the kidney perceives the need to conserve sodium (as in true hypovolemia or hypervolemia with sluggish circulation/decreased effective circulating volume). Sometimes the kidney wants to conserve sodium but cannot (as in diuretic use, adrenal insufficiency) in which case, urine sodium will be high despite the patient being hypovolemic. On the other hand, urine sodium will be high if there is no need to conserve sodium (in euvolemia, kidney excretes whatever sodium the person takes in). Urine sodium is also influenced by the fluids patient may have received prior to consultation. Below is the simplified hyponatremia algorithm.

Basically, the most important thing that guides management is fluid status. The accuracy of conventional parameters such as weight, BNP, auscultation, checking for pedal edema, doctors’ feelings (“I feel the patient is dry!”) is limited. As POCUS is the new physical examination, let’s see how we can use it to discern fluid status.

Isolated lung and/or inferior vena cava (IVC) POCUS is popular among novice users, but they are only one piece of the puzzle. VExUS is a great addition but still does not complete the hemodynamic puzzle.

It is a common misconception that a small collapsing IVC is equal to hypovolemia. No, it is NOT.

So, how can we measure stroke volume at the bedside and incorporate it into clinical decision making? Here are pertinent infographics. Note that POCUS by definition involves interpretation of sonographic findings in the appropriate clinical context. Therefore, it yields best results when interpreted in conjunction with rest of the clinical and laboratory data.

Is there any evidence supporting POCUS use in hyponatremia? Yes, below is a table summarizing pertinent case reports published till date (May 2022). Click on the first author for the link. Is there any evidence, especially a randomized controlled trial demonstrating mortality benefit of using POCUS to evaluate hyponatremia? No, POCUS is only a diagnostic tool. Putting the probe on the body does not improve mortality, neither do auscultation nor touching the patient.

A recent prospective study evaluated the role of IVC in classification of hyponatremia. However, isolated IVC is subject to pitfalls as mentioned. Here is my letter explaining why.